Animal Medical Center of Southern California

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2340 S. Sepulveda Blvd., Los Angeles, California

Animal Medical Center

Cranial cruciate ligament (CrCL) injury is the most common cause of stifle lameness in the dog.

The diaphragm is the muscular separation between the chest and abdominal cavities that functions as a barrier and aids in respiration.

Pyometra is an infection of the uterus in dogs and cats.

A syndrome of exercise intolerance and collapse (EIC) is being observed with increasing frequency in young adult Labrador Retrievers

Male cats, especially those that have been neutered, can easily develop obstruction of the urethra because the urethral diameter is so small.

First, I may be a bit particular about terminology as there are many misperceptions and misrepresentations.

The spleen is a relatively large organ with wide-ranging and various functions

Today there are many options for consumers to purchase veterinary medications.

Acute gastric dilatation with or without volvulus is a life-threatening condition that is classically described in large or giant breed dogs with deep chests and appears to occur more frequently in older animals

Cranial cruciate ligament (CCL) injuries are among the most common reasons for pain, discomfort, and lameness of the stifle joint of the dog.

Medical lasers have become an integral part of medical practice because of their wide range of therapeutic applications including but not limited to relief of acute and chronic pain, the promotion of tissue repair and wound healing, and the reduction of inflammation.

Pathophysiology, Diagnosis and Treatment

Fractures of the tibia are relatively common in the dog and cat, with tibial diaphyseal fractures the most commonly encountered injury of this bone.

Anal glands are pouches or sacs, which are located near the anus. Every dog and cat has a pair of anal glands, one gland located on each side of the anal region.

Fractures involving the distal femoral physis are relatively common in immature dogs and cats with the greatest incidence occurring between the ages of 5 and 8 months.

Primary pulmonary neoplasia was diagnosed in 14 dogs presented to the California Animal Hospital for medical and surgical management of respiratory tract disease.

The most frequent reason for performing a total hip replacement (THR) is relief of pain and disability caused by severe degenerative joint disease secondary to hip dysplasia.

Surgical Treatment for the Immature Patient

Thoracolumbar intervertebral disc disease is a well-recognized entity in veterinary medicine.

The shoulder joint is the most mobile of all of the main limb joints.

Fractures of the humerus are relatively common in the dog and cat with approximately half of all humeral fractures occurring in the distal portion of the bone.

Considerable attention has been given to the topic of coxofermoral luxation in the dog primarily because hip luxation is a relatively common traumatic injury encountered in small animal practice.

The ductus arteriosis is a normal structure that is present in the canine fetal heart.

Pathophysiology and Diagnosis

Surgical Treatment for the Mature Patient

Medial patella luxation (MPL) is one of the most common stifle problems encountered in veterinary medicine.

Osteochondrosis (OC) is a pathologic process in growing cartilage.

Although medical therapy is often effective in treating otitis externa, chronic otitis externa may progress to end stage otitis necessitating surgical intervention.

Mast cell tumors (MCT) in dogs are very common, accounting for approximately 20% of all skin tumors in dogs.

Multiple myeloma or plasma cell myeloma, is a neoplasm of well-differentiated B cell lymphocytes typically originating from the bone marrow.

Injury to the sacroiliac joint in the dog and cat commonly occurs in association with fractures of the pelvis and pelvic limb.

Portosystemic shunting is a macroscopic diversion of portal blood from the liver into the systemic circulation, which most commonly occurs because of a congenital malformation of the portal circulation.

One of the most common medical complaints that we see in our office is dogs with skin infections, “hot spots”, or allergic dermatitis, also known as atopic (atopy) dermatitis.

Cushing’s disease describes a syndrome resulting from the overproduction of cortisol, a normal naturally occurring hormone in cats and dogs.

Diabetes mellitus (DM) is a disease process involving either an absolute or relative insulin deficiency resulting in hyperglycemia.

Tracheal collapse is a progressive, degenerative disease of the cartilaginous rings of predominantly older small and toy-breed dogs.

Laryngeal paralysis (LP) is a common disease process, which results in acute and/or chronic progressive respiratory distress.

Acupuncture has been practiced on animals almost as long as it has been practiced on people, with first reports of its utilization for the treatment of certain conditions in animals dating to as early as 3000 years ago in China.

Thymoma is an uncommon canine and feline neoplasm of thymic epithelial cells.

A tendon is a dense band of fibrous connective tissue which acts as an intermediary component in the attachment of muscle to bone.

Numerous methods of fracture fixation are available to the veterinary surgeon.

Total derangement or dislocation of the stifle joint is a serious injury usually caused by severe direct or indirect trauma to the knee.

While at first it might seem odd that pets are the recipients of cosmetic surgical procedures, upon further consideration it makes perfect sense.

Animals and people have similar neural pathways for the development, conduction, and modulation of pain.

The usual protocol for the initial treatment of muscle and tendon injuries includes rest, ice, compression, and elevation of the injured area.

It’s never an easy decision to make, but perhaps the kindest thing you can do for a pet that is extremely ill or so severely injured that it will never be able to resume a life of good quality is to have your veterinarian induce its death quietly and humanely through euthanasia.

Canine heartworm infection is widely distributed throughout the United States. Heartworm infection has been found in dogs native to all 50 states. All dogs, regardless of their age, sex, or habitat, are susceptible to heartworm infection. Although there are differences in frequency of infection for various groups of dogs, all dogs in all regions should be considered at risk, placed on prevention programs and frequently examined by a veterinarian.

This condition is commonly called tendon contracture even though the tendons don't actually contract. Rather, it is generally a soft tissue problem that involves the flexure tendons, the muscles, ligaments and joint capsules of the distal extremities.

Toxoplasmosis is an infection caused by the protozoan parasite Toxoplasma gondii that can threaten the health of an unborn child if a woman becomes infected with Toxoplasma for the first time while she is pregnant.

Snake bites are life threatening, extremely painful, expensive to treat, and can cause permanent damage even when the dogs survive. Dogs can encounter a rattlesnake anytime they are in rattlesnake habitat. You and your dog may live in rattlesnake habitat, or perhaps you travel through or frequently visit places where rattlesnakes are found.

Anyone who has ever battled fleas knows how difficult they are to eradicate.

As a veterinary specialist practicing in Los Angeles for the last twenty-five years, I have had a tremendous opportunity to work with the overwhelming majority of rescue groups here in the Los Angeles area.

Your puppy may start off playful and easygoing, but as she matures she may become more difficult to control.

As pets get older, they may develop new, undesirable behaviors.

Growing up with a dog can add a special dimension to your child’s life. You can help build the best possible relationship by taking some simple steps.

Puppy training should begin from the moment you bring your new pet home—it will go much faster and smoother when your pet is young.

Play helps prepare kittens to become great hunters and develops their social skills with other cats.

Most dogs cope well when left alone, but some show distress, anxiety, or panic when separated from the family.

While most cats are very clean and dependable in using a litter box, they may eliminate in undesirable locations for a number of different reasons.

Most puppies have a strong natural desire to investigate and chew.

Most cats, especially young kittens, have a strong natural desire to play and explore.

Most dogs get noisy when exposed to anything new or unusual.

It’s normal for a puppy to use her mouth during play and social interaction, but it’s certainly no fun having those sharp teeth embedded in your ankle or arm.

Puppies don’t come into our world with ready knowledge about humans or the world in which we live.

Your home has just been blessed with a new puppy who arrived cuddly, warm, and ready to be loved. Unfortunately, she did not arrive housetrained.

While most cats can be trained to use a litter box, it’s important that you help your kitten get off to a good start.

Dogs can become fearful of people because of inadequate handling and socialization during the first few months of life, previous unpleasant experiences with people, medical problems, or genetics.

Cats and kittens may exhibit fearful behavior for a number of reasons.

The Pathophysiology and Medical and Surgical Treatment of Cruciate Ligament Disease.

Cranial cruciate ligament (CrCL) injury is the most common cause of stifle lameness in the dog. CrCL deficiency results in both translational and rotational instability of the stifle joint that leads to the development of degenerative joint disease. The joint pathology, including the complex of biologic and biochemical events that lead to ligament degeneration and the concurrent development of osteoarthritis (OA), has been coined cruciate disease. CrCL deficiency in dogs is a multifactorial disease involving genetics, conformation factors, and an inflammatory component that together create an imbalance between the biomechanical forces placed on the ligament and its ability to sustain these loads, eventually leading to rupture and joint instability. Biology and biomechanics are inextricably linked in health and disease of the CrCL, and it is vital to consider both aspects concurrently to develop a comprehensive understanding as well as medical and surgical therapeutic approaches to successfully manage this common cause of lameness in the dog. Simply put, this means that all of the tissues comprising the joint must function together, biologically and biomechanically, in order to maintain joint health and to allow full, pain-free function and range of motion. The CrCL cannot be isolated from the synovium, caudal cruciate ligament, articular cartilage, menisci, or subchondral bone, and all of these components must be considered critical interrelated elements, which are essential for long term stifle function.

A definitive cause for CRCL disease remains unknown, but many presumed factors result in a final common pathway of abnormal biomechanics and abnormal biology causing OA and the clinical signs of lameness, pain, and limb dysfunction. The biologic components include inflammation, degradation and degeneration, impaired synthesis, and turnover of extracellular matrix and necrosis. The biomechanical components include instability of various types and degrees, muscle weakness and dysfunction, misalignment, conformational changes, altered kinematics, and distorted joint contact areas and pressures. While many of these components have been incriminated as causes of cruciate ligament disease, evidence is lacking with regard to any one factor being a sole causal agent. For this reason, all of these factors should be considered as potential components of a multifactorial disease process. The precise role each plays in the process and the nature and timing of each event is critical to improve our understanding of cruciate disease so that we can improve preventative, diagnostic, and therapeutic strategies, and treatment options for dogs afflicted with cruciate ligament injuries.

An excellent question with regard to the cause of CrCl injury is does cruciate disease result from abnormal biomechanics on a normal ligament, normal biomechanics on an abnormal ligament, or a combination of both? Currently, there is no definitive answer to this question. While acute, traumatic CrCl rupture occurs and is characterized by the absence of pre-existing degenerative signs (osteophytes, synovial hypertrophy, cartilage degeneration), other joint tissues are concomitantly affected (meniscal tears, multiple ligament injuries, bone bruising) such that the total clinical outcome is one of whole joint injury and damage. This type of injury is not representative of the majority of CrCl injuries in the dog. More commonly, cruciate injury includes a degenerative component (osteophytes, synovial hypertrophy, cartilage degeneration, periarticular fibrosis, subchondral bone sclerosis). This more common scenario implicates abnormal ligament biology as a driving force behind the eventual development of ligament failure; it does not exclude abnormal biomechanics as a primary force behind this abnormal biology. It is certainly possible that abnormal biomechanics initiates and perpetuates abnormal ligament biology sustaining a vicious cycle of stifle joint failure that is recognized as cruciate ligament disease.

Current thinking has focused on conformation of the proximal aspect of the tibia as the major contributor to abnormal stifle biomechanics leading to CrCL failure. While one study has reported a significant difference in tibial plateau angle (TPA) between dogs with and without CrCL disease, data from multiple studies contradict this, and there is no definitive evidence that either TPA or patellar tendon-tibial plateau angle is a significant risk factor for cruciate disease in dogs. When either of these angles is considered high based on reference intervals in dogs, theoretical considerations suggest there are increased CrCL strain and an increased shear component of total joint force. Thus, these components may contribute to the process of organ failure, but do not appear to be primary causal factors based on current best evidence.  Inherent instability is another potential abnormality that could be involved in the development of cruciate disease. Instability can be the result of dysfunction of passive stabilizers, dynamic stabilizers, or both. In the canine stifle, passive stabilizers include the cruciate ligaments, menisci, collateral ligaments, joint capsule, and articular contours. The dynamic stabilizers are primarily the quadriceps-patellar mechanism components and hamstring muscles, but also include other associated muscles and tendons. Collectively, all of the stabilizers work to help maintain stifle joint kinematics. It is naive to view and treat CrCL disease as a singular issue of cranial caudal instability. Whereas failure of any of the stabilizers can lead to loss of normal kinematics and stifle joint organ failure, compensation for failure of 1 stabilizer by others can occur so that functional kinematics can be maintained. Instability from various causes as well as anatomic abnormalities of all types, joint incongruity, neuromuscular problems, tissue composition abnormalities, and changes to articular contact areas and pressures all alter stifle joint kinematics and are responsible for cruciate disease. These may occur because of genetics, nutrition, single or repetitive traumatic events, activities and training, infectious or metabolic disorders, and/or various surgical manipulations of the limb. It is therefore imperative that these considerations are included in investigations to determine etiopathogenesis, diagnostic approaches, breeding plans, and treatments for canine patients. The nature and complexity of this multifactorial disease process invokes comparisons with canine hip dysplasia and elbow dysplasia.  This combination of anatomic, biomechanical, genetic, cellular, and biochemical factors involved in CrCL disease in dogs could appropriately be considered as components of a stifle dysplasia complex.

Developmental, infectious, immune-mediated, genetic, metabolic, hormonal, and primary cell and/or matrix disorders have been suggested as causal or associated factors in canine CrCL disease. Genetic components appear to be involved in certain dogs and may contribute to conformational changes associated with biomechanical causes of disease. Hormonal- and metabolic-related changes have recently been implicated in CrCL disease. Effects of early spay or neuter on growth plate function could contribute to conformational changes associated with cruciate disease. Cell and matrix disorders can involve a myriad of different tissues, processes, and mechanisms. The current major areas of focus are on the CrCL and its synovial sheath. A critical component to these disease mechanisms is that the CrCL is intra-articular but extra-synovial. This means that, in health, the CrCL is protected from the intra-synovial environment, and the intra-synovial environment is protected from the CrCL. Intra-synovial structures such as the articular cartilage, synovium, and menisci constantly communicate with the CrCL, but this communication is filtered by the synovial sheath. When this protective filter is lost, as it is in cruciate disease, the CrCL is exposed to the intra-synovial environment and tissues, and vice versa. Whether this exposure is of biological or biomechanical cause or both is not known, but it is clear that this does occur in the disease process and that it can have severe consequences for both ligament and joint health, including upregulation and release of inflammatory mediators and degradative enzymes, proliferation of cells, recruitment of inflammatory and immune system cells, and production of anti-collagen antibodies in many cases.

Abnormal biology and biomechanics definitely potentiate and exacerbate one another. Instability, anatomic abnormalities, muscle weakness, and altered contact areas and pressures can directly lead to inflammation, necrosis, and tissue degeneration. Tissue composition changes, cellular responses, and degradative enzyme production and release can directly result in altered kinematics, neuromuscular dysfunction, and malarticulation. Some of these competing forces result in positive responses that help to ameliorate or retard the detrimental effects of the other abnormal processes. Osteophytosis, muscle hypertrophy, and periarticular fibrosis are biologic responses that help counteract abnormal biomechanics because of dysfunction of passive stabilizers, tissue loss, and anatomic abnormalities. Articular and meniscal cartilage as well as subchondral bone can remodel to help compensate for changes in tissue structure and architecture from abnormal matrix turnover. Unfortunately, these adaptations do not appear to be sufficient to allow for healing or even functional compensation for the associated abnormal biology and biomechanics of the CrCL.

Cruciate disease in dogs involves a spectrum of potential causal factors, patient types, clinical presentations, risk factors, disease mechanisms, and rates of progression. Treatment strategies should address abnormal biology and biomechanics with the overall goals of decreasing pain, improving function, and retarding disease progression. Although there is not a currently available methodology for restoring joint kinematics to normal in dogs with cruciate disease, it is clear that addressing craniocaudal instability alone will never be sufficient for full return to long-term function.

The strategies that have supporting evidence as potential aids in augmenting the productive responses outlined above include joint lavage, complete assessment of joint pathology with comprehensive and accurate debridement, pharmaceutical and nutraceutical interventions, and physical rehabilitation modalities. Whereas none have sufficient evidence in support of blanket statements regarding their use, joint lavage, or washout, has been reported to provide benefits in terms of dilution of nociceptive, inflammatory, and degradative mediators. The utilization of platelet-rich plasma (PRP) is a new technology, which focuses on enhancing the healing response after injury of different tissue types. In recent years, several studies have described a complex regulation of growth factors for normal tissue structure and reaction to tissue damage and have demonstrated an important role for growth factor application in the healing of damaged tissue. PRP is a natural concentrate of autologous growth factors (platelet derived growth factor, transforming growth factor, platelet derived epidermal growth factor, vascular endothelial growth factor, insulin like growth factor, fibroblastic growth factor, epidermal growth factor) and cytokines, which aids in the regeneration of tissues with low healing potential. Platelets have a major role in the initiation of wound healing. They adhere, aggregate and release numerous growth factors, adhesive molecules and lipids that regulate the migration, proliferation, and function of fibroblasts and endothelial cells. PRP has been shown to accelerate tissue repair in soft tissues via mechanisms involving the further synthesis of signaling proteins that participate in cell mitosis and angiogenesis. Another important consideration is that in addition to stimulating the growth of new tissue, PRP application has been shown to decrease pain and inflammation in the degenerate area in which it is applied. The utilization of PRP has the capacity to optimize the healing environment. Because of its autogenous origin, easy preparation and excellent safety profile, PRP has tremendous potential to speed recovery in cases of tendon, ligament, muscle, and cartilage disorders. As all of these tissues are compromised to varying degrees in cases of cruciate ligament disease, the administration of PRP has the ability to improve stifle stability, diminish pain, and accelerate physiologic healing and reparative tissue processes involving the patellar tendon, cruciate ligament, and meniscus. The incorporation of PRP into the medical protocol for management of cruciate ligament pathology may affect the current debate regarding the debridement and removal of partially injured cruciate ligaments and menisci given its ability to stimulate healing in these notoriously refractory tissues.

Full exploration and assessment of the joint increases the likelihood of accurate and complete diagnosis of degree of synovitis, articular cartilage damage, meniscal pathology, and cruciate ligament pathology. Debridement of damaged and pathologic meniscal tissue can improve joint biomechanics, ameliorate pain, help to minimize further articular cartilage loss, remove a potential source of inflammatory and degradative mediators, and help prevent subsequent meniscal pathology. Therefore, complete debridement of diseased cruciate ligament may act to remove a nidus of inflammation and degradation, remove a potential source of pain, and improve observation and access to the menisci. Medications can have beneficial effects on inflammation, degradation, nociception, and synovial fluid rheologic and biologic properties. Physical rehabilitation can improve range of motion, muscle mass, and weight-bearing function in dogs with CrCL disease. These factors used in conjunction can augment the positive adaptational responses noted in canine CrCL disease, and some anecdotal evidence suggests that they may obviate the need for stabilization procedures for certain cohorts in the CrCL disease spectrum of patients. Certainly, these components should be considered for inclusion as part of a comprehensive management plan for all patients and clients. In conclusion, canine CrCL deficiency is a whole-joint disease, which should be considered organ failure in most affected dogs. Patients with CrCL disease are fighting biological and biomechanical factors that induce and perpetuate osteoarthritis and the clinical signs of pain, lameness, and limb dysfunction.

An unstable joint is thought to initiate cartilage damage and the subsequent degradation and inflammation disease mechanisms characteristic of secondary OA. Whereas biomechanics may be involved, the biology of intra-articular structures, including the metabolism of synovium, adipose tissue, tendon, and ligament, may also contribute to the initiation and progression of OA. Diseased CrCL is one possible contributing factor that is easily removed at the time of surgery. The normal CrCL is intra-articular but extra-synovial so that direct exposure and communication to synovial fluid and other joint tissues does not occur in health. Current evidence suggests that pathology of the synovial lining of the CrCL and exposure of ligament to the joint environment could be early events in canine cruciate disease. This evidence lends further support to the theory that the CrCL may be one of the primary initiators and perpetuators of OA and for this reason CrCL debridement deserves careful consideration as a component of comprehensive treatment. With the introduction of proximal tibial osteotomies (TPLO, TTA) for the treatment of cruciate disease, recommendations have been made to perform small arthrotomies for meniscal release alone, perform arthrotomy or arthroscopy with or without debridement of the CrCL or meniscal release, and avoiding exploration of the joint altogether. Some of these approaches leave the CrCL in the diseased joint and exposed to the intra-articular environment. Whether to provide complete debridement of the CrCL at the time of surgery or to leave the ligament in situ is debated among surgeons because the current best evidence in the literature neither clearly supports nor unequivocally dismisses the need for ligament debridement. Ligament pathogenesis is the complex series of events that change a normal, healthy ligament into a diseased, nonfunctional, and potentially torn ligament. Resulting changes have been evaluated in both the ligament cells as well as extracellular matrix and characterized on molecular, biochemical, histological, and gross levels. Many of the degradative molecules thought to be responsible for ligament pathogenesis are the same molecules that are known to be involved in the initiation and progression of OA. These molecules may have the potential to diffuse from the ligament and synovium into the synovial fluid in sufficient concentrations to contribute substantially to the overall disease process. The amount of matrix metalloproteinases (MMP) released and the time frame of exposure needed to produce disease in the ligament and other joint tissues is not completely understood, but both ligament and synovium appear to be contributors to synovial fluid MMP concentrations. It is very possible that MMP from CrCL could be involved in the initiation of OA in cruciate disease in dogs. There are numerous studies that implicate MMPs in ligament pathogenesis. Collagenases have been identified in CrCL at both the gene and the protein level. Gelatinases have also been characterized in a similar manner as have cathepsins and other related degradative enzymes. If these degradative enzymes can be released when ligament tissue is exposed to the joint environment, then they could play important roles in osteoarthritic processes in addition to enhancing further ligament degeneration. Also, if these molecules contribute to OA, then removal of ligament remnants may ameliorate disease progression. Some studies support the theory that intact and partially torn ligaments left within the stifle joint and exposed to the intrasynovial environment may serve as a nidus of degradation. While it cannot be definitively concluded that ligament is the major intra-articular structure contributing to the release of these enzymes, diseased ligament is, however, one potential contributing factor that can be easily removed through debridement at the time of surgery. This provides some initial evidence supporting complete debridement of the CrCL as a component of comprehensive treatment of cruciate disease in dogs. The variables in favor of debridement include removal of the inflammatory and/or degradative nidus and elimination of ligament nociceptors. Additionally, removal of the ligament improves examination, probing, and access to menisci. The variables against debridement include preservation of ligament mechanoreceptors and proprioceptors, avoidance of morbidity to other joint structures during debridement, and potential maintenance of some CrCL function. The difference observed between normal and intact ligaments suggests that large amounts of MMPs may be produced during the process in which normal ligaments become diseased. CrCL remnants exposed to the intra-articular environment have the potential to release degradative enzymes known to be involved in the initiation and progression of OA and debridement of these remnants as a component of treatment for cruciate disease in dogs deserves consideration. None the less, a separate study evaluating the subjective arthroscopic appearance of CrCL that were left partially intact at the time of surgery in a numerous canine patients treated by tibial plateau leveling osteotomy suggested that CrCL tissue remained visibly intact over a range of postoperative evaluation time points. Additionally, there was a decreased incidence of meniscal injury and articular cartilage damage associated with leaving the ligament intact.  Unfortunately, no data regarding the functional capabilities of these CrCL or the status of their cell and matrix composition or activities was provided and all peer-reviewed studies, which have examined these factors, have reported that functional healing does not occur, degradation and degeneration inevitably progress, and that subjective appearance of the CrCL is a poor indicator of disease status. It is obvious, however, from these two studies that additional research needs to be performed before firm recommendations regarding the removal of CrCL remnants can be made. What is known, however, is that CrCL remnants exposed to the intra-articular environment have the potential to release degradative enzymes known to be involved in the initiation and progression of OA and debridement of these remnants as a component of treatment for cruciate disease deserves consideration.

The presence of different tissue types and their superimposition limit successful diagnostic imaging of the stifle joint with a single modality. Radiographic signs of cruciate ligament disease include intraarticular swelling, cranial displacement of the tibia in the mediolateral view with tarsal flexion applied, and in chronic cases, OA changes. The tibial compression stress radiograph has been reported to be useful in the diagnosis of partial CrCL rupture. This radiographic projection requires the stifle to be in 90 degrees of flexion with manual flexional forces applied to the tarsus. Flexion of the hock joint allows the tibia to move cranially, so it can be evaluated with during this stress view.

Ultrasonography is useful for assessing cartilage abnormalities, meniscal tears as well as muscle, tendon, and ligament abnormalities. Diagnosis of CrCL rupture can be made by demonstration of the fluttering edges of the ruptured ligament. If the infrapatellar fat pad obscures observation of the ruptured CrCL, saline solution can be injected into the joint to create an anechoic window. OA changes appear as hyperreflective regions with irregular borders on the bone surface. The entire meniscus, however, is difficult to observe. Normally, the meniscus is inhomogeneous and congruent with the margins of the femoral and tibial condyles. Meniscal injury results in hyperreflective with hyporeflective areas that are irregular in shape and displaced. There are substantial limitations to the routine use of ultrasound in evaluating the stifle joint. Ultrasound images generally have low resolution and soft tissue contrast, which may make other imaging modalities such as MRI more useful.

The major advantages of MRI are its excellent image resolution, superior soft tissue contrast, acquisition of images in any plane, and use of a magnetic field rather than ionizing radiation. MRI evaluation of the internal architecture of the stifle joint affords many advantages over arthroscopy or arthrotomy and is the primary imaging modality when assessing for cruciate, meniscal, and articular pathology in people.  Because the stifle is a complex joint with various tissue types, differing image planes and sequences are typically used for complete evaluation. As mentioned previously, CrCL rupture is the most common cause of stifle OA in dogs and is frequently associated with damage to the medial meniscus. Complete evaluation of the menisci is impossible even with arthrotomy or arthroscopy because of anatomic constraints. Using either technique, the tibial surface of the menisci remains hidden from view, as does the integrity of internal meniscal structure. Additional meniscal surgery after surgical stabilization for CrCL deficient stifle joints may be needed because of undiagnosed meniscal pathology at the time of the initial surgery. Therefore, avoiding invasive inspection and handling of unaffected menisci at time of CrCL stabilization probably results in decreased postoperative morbidity, reduced incidence of surgically related complications, and less progression of osteoarthritis. However, missing a meniscal tear has been reported to result in persistent or recurrent lameness after CrCL stabilization, highlighting the need for accurate diagnosis of meniscal integrity at surgery. Because most meniscal tears are treated surgically, any positive MRI finding would result in an invasive intraarticular procedure to confirm the tentative diagnosis and to perform subtotal meniscectomy. Therefore any diagnostic test that replaces invasive inspection of the menisci has to be highly sensitive to reduce the incidence of late meniscal tears, and at the same time it must be of reasonably high specificity, because any false-positively scored meniscus will be inspected surgically, undoing the potential benefit of noninvasive preoperative diagnostics. In a recent study, low field MRI did not reach anticipated diagnostic accuracy for meniscal tears. The primary interest of this study was in evaluating low field MRI as a preoperative, noninvasive screening tool for triage of stifles as affected by meniscal tears requiring further invasive meniscal inspection and probably meniscal surgery and those where meniscal pathology could be excluded, preventing unnecessary invasive procedures. Currently, we cannot recommend low field MRI as a highly sensitive screening tool for meniscal tears in the context of CrCL surgery. Although less expensive and potentially more cost effective, low-field-strength MRI systems suffer from several technical limitations, including long acquisition times, poor signal-to-noise ratio, inability to obtain thin slices, and poor spatial resolution. The trend toward increased magnet strength (at least 3.0 T) to improve signal to noise ratio has continued in veterinary medicine despite increased purchase as well as cryogen and maintenance costs, because of the superior resolution and shorter scan times in an attempt to overcome this diagnostic dilemma.
As mentioned previously, progressive degenerative joint disease may contribute to ligamentous deterioration and precede actual ligament rupture in clinical cases of CrCL rupture in dogs. In both clinical cases and in experimental models of CrCL rupture in dogs, the location of the MRI lesions is typically the intercondylar fossa of the femur and in the intercondylar eminence of the tibia. This is thought to be in part related to abnormal stresses born by the remaining caudal cruciate ligament and subsequent sequellae in the cancellous bone subchondral region associated with its origin and insertion. Early detection of theoretical pre-CrCL rupture lesions by stifle MRI evaluation may therefore afford surgeons an early opportunity to intervene medically before subsequent anticipated CrCL rupture.

With CT technology, images can be manipulated, with a computerized process known as windowing, to reveal various structures based on tissue characteristics. Clinical advantages of using multidetector helical CT scanners include improved patient safety, enhanced accuracy and most strikingly, the ability to perform 3D image reconstructions with the option of creating surgical models to plan surgery for complex cases. In a recent report of CT Arthrography to assess intraarticular structures in dogs with naturally occurring stifle CrCL dysfunction, sensitivities and specificities were 96–100% and 75–100% respectively for the identification of CrCL rupture. In the same report, however, reviewers were less adept at discriminating torn meniscal fibrocartilage, with sensitivities of 13.3–73.3% and specificities of 57.1–100%.

The key to successful management of the diagnostic options available is to have a thorough understanding of the anatomy and tissue properties of region being imaged and to recognize the strengths and weaknesses of the modality being selected. Ultimately, a multimodality approach will likely provide a complete assessment of complex structures using the strengths of each modality to exploit the tissue characteristics of the structure being imaged.

Dogs with CrCL insufficiency frequently sustain damage to the caudal pole of the medial meniscus. Arthroscopy can be considered a highly accurate diagnostic tool, although meniscal tears might be overlooked, especially those that do not reach the surface and those on the tibial side of the menisci. This highlights the importance of thoroughly probing both sides of the menisci when performing arthroscopy. Using a stifle distractor to improve observation and probing of the medial meniscus is believed to further increase diagnostic accuracy.

Historically, total, partial, or segmental meniscectomy has been recommended as treatment for these meniscal tears. Persistent or recurrent lameness after CrCL stabilization has been attributed to meniscal tears missed on direct inspection either using arthrotomy or arthroscopy during joint stabilization and reportedly occurs in 6.3–17.4% of operated stifles. Such tears are referred as latent meniscal tears in contrast to postliminary meniscal tears which are thought to develop despite surgical stabilization of the CrCL deficient stifle. Treatment is directed at removing the torn parts of the meniscus and has an overall good prognosis. However, the additional surgery necessary to perform meniscectomy increases the risk for surgical complications, results in additional owner cost, and delayed treatment of the meniscal tear may lower the overall functional outcome after CrCL stabilization.

Resection of the torn meniscus ameliorates pain and improves short term function; however, meniscectomy accelerates progression of degenerative joint disease in the CrCL deficient stifle.  Although total meniscectomy and segmental meniscectomy result in supraphysiologic intra-articular contact pressures and articular cartilage damage, meniscectomies are still commonly performed in dogs. Conservative excision of damaged meniscal tissue by partial meniscectomy when appropriate has been recommended. To preserve meniscal function and mitigate progression of DJD, meniscal tears are often repaired in people. Meniscal repair has been described in dogs but is infrequently performed. Evaluating the ability of meniscal repair to restore meniscal function compared with partial meniscectomy would be important to help determine whether or not meniscal repair should be considered in dogs. Meniscal repair is unlikely to be beneficial if the repaired meniscal parenchyma is degenerate and has lost its internal architecture. Torn meniscal tissue that has lost its normal structure and mechanical function is unlikely to regain normal function. A recent study evaluated the mechanical behavior of meniscal tears in dogs and found that non-reducible bucket handle, flap, and degenerative tears each caused a 45% increase in peak contact pressure (PCP). Although the meniscal parenchyma of degenerative tears and flap tears is macerated, necessitating resection of the damaged tissue, vertical longitudinal tears and bucket handle tears with healthy meniscal tissue may be amenable to repair. Repair of suitable meniscal lesions in people improves joint contact mechanics. It is anticipated that repair of reducible bucket handle tears of the medial meniscus in dogs could restore the biomechanical function of the meniscus. Conserving meniscal tissue would be advantageous because degeneration of femoral and tibial articular cartilage is proportional to the amount of meniscal parenchyma excised.

Unfortunately, the meniscal parenchyma of the axial portion of bucket handle tears in dogs with CrCL insufficiency often has disruption of normal structure and material properties because the meniscus has been damaged from chronic impingement between the femoral and tibial condyles. Crushing of the meniscal parenchyma of bucket handle tears has been shown to result in an increase in PCP. Repair of chronic tears cannot be recommended because the material properties and geometry of the meniscus would be expected to be disrupted in chronic tears. Results from a recent study suggest that meniscal repair be considered for acute meniscal tears. Suture repair in dogs in this study reestablished normal PCP whereas partial meniscectomy caused a 55% increase in PCP. The repair techniques evaluated restored normal contact mechanics to the medial compartment of a stifle with a medial meniscal tear whereas partial meniscectomy caused a 35% decrease in contact area (CA), a 57% increase in mean contact pressure (MCP) and a 55% increase in PCP. Until further mechanical studies are performed on meniscal suture techniques in dog menisci, this particular study recommends a vertical or cruciate suture repair in order to prevent subsequent articular cartilage damage. Additional studies to assess the efficacy of meniscal repairs to alleviate pain and to potentiate successful healing need to be performed. Based on current results, consideration should be given to repairing peripheral tears involving the vascular zone of the meniscus if the parenchyma of the axial portion of the meniscus is normal. Partial meniscectomy should be considered for axially located tears and degenerative tears. Further work is needed to determine the optimal repair technique that should be used clinically in dogs based on fixation strength and ease of application.

Cranial cruciate ligament deficiency in dogs is a common and costly problem for which there are multiple treatment modalities. Whereas numerous techniques have been investigated, none have proven optimal in terms of technical ease, associated costs, prevention of secondary pathology, complication rate, complication types, or mid to long-term outcomes. No one technique for treatment of CrCL deficiency has been shown superior to others in terms of functional outcome. Surgical techniques for correction have focused on intraarticular repair, extraarticular stabilization, or osteotomy of the proximal tibia. In spite of the innumerable studies performed comparing the techniques currently available, none of the techniques have consistently exhibited superiority for clinical efficacy making technique selection the surgeon’s preference.
Technical modifications of the classic lateral suture stabilization (LSS) technique reflect changes in suture material, knotting, and attachment sites. Placing the suture caudal to the lateral fabella and curving distally to a drill hole in the proximal tibial crest has been the established technique but recently, attachment points craniodistal to the fabella and caudoproximal to the tibial tuberosity at the proximal aspect of the tibial plateau have been reported. These modifications are thought to improve suture isometry and thus overall impact on functional outcome after LSS. In addition, when assuming some degree of anisometry regardless of the exact type of LSS performed, loop tension pattern during range of motion might be related to the angle of stifle flexion at the time the suture is tied. In a recent study of LSS attachment sites, results indicated that irrespective of the precise point of lateral suture attachment, substantial changes in suture tension occur during a full range of stifle motion. This change in tension increases significantly with joint flexion. The study also found that tightening the suture with the stifle in 70 degrees of flexion results in the most even tension pattern within the lateral suture loop, but stabilizing the stifle using LSS at a flexed angle would probably allow persistent joint instability, as the suture loop tends to loosen at joint angles between 70 degrees and 160 degrees.

When interpreting tension within a lateral suture used to stabilize the CrCL deficient stifle, two aspects should be considered. First, any disproportionate increase in suture tension would increase the risk of premature suture failure, or if the suture does not fail, stretching of the suture loop might occur. Secondly, very high tension within the suture will probably over-constrain the joint, whereas a substantial loss of tension within the suture will certainly result in some degree of joint instability. For optimal tibial fixation, some studies suggest attaching the suture at a point just caudal or cranial to the digital extensor groove, at the most proximal aspect of the tibial plateau. However, using a bone anchor on the lateral condyle and a divergent drill tunnel just cranial to the digital extensor groove (LSS4) resulted in the highest peak to peak load (PPL) and maximal peak load (MPL) among four techniques recently investigated. Passing the suture around the lateral fabella instead of using a bone anchor at the lateral femoral condyle might allow for some soft tissue movement, potentially reducing high strains within the suture, but relaxation of the fabellofemoral ligament might occur in the long term, resulting in loosening of the LSS and recurrent joint instability. Based on data from this recent study, LSS2 might be the preferred method when attempting to stabilize the stifle with a lateral suture, as this method consistently resulted in the least change in suture tension. Even though LSS2 is only a slight modification of the traditional technique popularized by Flo, omitting the lateral branch of the suture loop may improve isometry. None of the 4 methods studied reached isometry in terms of maintaining a constant tension throughout passive stifle motion, potentially resulting in loss of suture tension at some joint angles with consequent joint instability. There is little information about the precise joint angle at which the suture should be tightened. For any suture fixation that is not isometric, securing the loop at a joint angle when the lateral suture loop is longest will result in the least increase in suture load during range of motion, but may allow some joint laxity during range of motion of the stifle. If the suture is tied at a joint angle when the loop is shortest, tightening will occur during range of motion potentially over-constraining the stifle and promoting early suture break down. Surgical texts mostly recommend tightening the suture at slight flexion of the joint or at a normal standing angle. A survey of veterinary surgeons revealed that 67% positioned the stifle at 140 degrees when the suture was tied, full joint extension was preferred by 19%, and only 5% had the stifle at 90 degrees of flexion, confirming the divergent opinions with regard to which angle might result in the best balance between MPL and maximal negative load (MNL). Clinically, tightening the suture at an angle between 100 and 135 degrees may reduce MPL on joint flexion, potentially limiting stretch of the suture-knot construct and therefore early destabilization of the joint. At the same time, this angle would preserve most of the tension within the suture when extending the joint. In summary, both the angle of flexion chosen while tightening the suture as well as the suture attachment sites when performing LSS changes the pattern of tension within the suture throughout a full range of stifle motion. However, regardless of LSS technique, a significant increase in suture tension occurs on flexion of the joint increasing the risk of suture breakage and irreversible stretch. This unwanted peak in tension on flexion of the joint might be reduced when tightening the lateral suture in a greater degree of extension.

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Lateral suture stabilization (LSS) techniques performed in stifles using an 80 lb nylon leader line and a custom made crimp. (A) Traditional technique according to Flo (LSS1); (B) modification of LSS1 with 2 parallel drill holes at the tibial crest (LSS2); (C) distal attachment of the suture through 2 divergent drill tunnels at the Gerdy’s tubercle (LSS3); and (D) distal attachment at the Gerdy’s tubercle. Proximal attachment with a bone anchor placed into the caudolateral cortex of the lateral femoral condyle, at the level of the distal pole of the lateral fabella (LSS4).

In an attempt to further refine LSS techniques, an extracapsular suture stabilization technique called the TightRope CrCL technique (TR), was developed in an attempt to address perceived shortcomings of the current techniques, and to specifically incur minimal morbidity, address all aspects of CrCL deficiency, allow for repeatable placement in the most isometric position possible, and consistently result in successful functional outcomes with low overall and major complication rates in a cost effective manner. The TR CrCL extra-articular stabilization technique was developed to provide bone-to-bone fixation of the prostheses using a stiff prosthetic material. Femoral and tibial bone tunnels are used to place a fiber tape prosthesis across the lateral aspect of the stifle. The suture is anchored to the femur and tibia using toggle buttons placed at the medial orifices of the bone tunnels.

The primary stimulus for development of the TR technique was patient safety, specifically low morbidity as well as rate and severity of complications. Some studies have indicated that tibial osteotomy procedures (TPLO, TTA) are associated with higher and more severe complications in dogs undergoing surgery for CrCL deficiency when compared to other techniques. In a recent study comparing TPLO to TR, TPLO was associated with numerically higher major and total complication rates compared with TR, but these differences were not statistically significant. However, surgery and anesthesia times were significantly shorter for TR compared with TPLO, which is consistently associated with lower morbidity.  The other preclinical aspect of the development of the TR technique was comparative mechanical testing. In this study, the TR device proved superior for all variables examined. The biomaterial used for the TR procedure is a Kevlar-like material which is currently used extensively in the human field for many orthopedic applications. This material has properties that make it stronger and less prone to failure than any other suture materials currently being used in LSS CrCl reconstructions. These superior mechanical properties combined with the theoretical advantages of bone tunnel fixation in both femur and tibia suggest that the TR technique may have potential advantages with respect to stifle stability and joint kinematics during formation of periarticular fibrosis compared with LSS techniques which rely on soft tissue fixation or point-fixation. However, clinical comparisons among LSS extracapsular techniques or in vivo assessment of joint kinematics after any of the surgical techniques used to address CrCL deficiency has yet to be performed. These data from this study suggest that the TR CrCL technique can be successfully performed in medium, large, and giant breed dogs with CrCL deficiency and result in 6-month outcomes which are not different than TPLO in terms of degree and level of pain and function, as well as subjective assessment of radiographic progression of OA. Duration of anesthesia and surgery was less for TR than TPLO and major and overall complication rates were lower for TR compared with TPLO. The TR technique is safe and effective and can be considered as a viable choice as part of the overall treatment plan for CrCL deficiency in dogs. The technical aspects of TR were a major consideration for clinical application from its inception. The toggle fixation mechanism and the use of guide wires placed using consistent anatomic landmarks followed by cannulated drilling allow the TR device to be safely placed such that the functional fixation points are in locations similar to those determined most isometric for the lateral aspect of the canine stifle based on radiographic assessment.

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Figure 1 Illustrations of a canine stifle with the TightRope CCL implant positioned and viewed from the cranial (A) and lateral (B) aspects. T, tubercle of insertion of the biceps tendon/iliotibial band (tubercle of Gerdy); L, tendon of origin of the long digital extensor muscle.

Despite widespread use of LSS stabilization in dogs, only a few studies have evaluated the biomechanical effects of this procedure. It would be important to define contact mechanics in stifle joints after LSS stabilization to understand and refine surgical treatment of CrCL insufficiency in dogs. Tension placed on anterior cruciate ligament grafts in people is widely accepted to be an important biomechanical factor influencing procedure success. Excessive tension can cause premature failure of the prosthesis, whereas insufficient tension may not provide adequate joint stability. Appropriate suture tension should neutralize cranial tibial thrust while allowing a normal range of motion, and restore normal kinematics and contact mechanics to the CrCL-deficient stifle. Results of a recent study confirmed that over tightening an extra-articular prosthesis when performing either TR or LSS stabilization technique increased lateral compartment pressures in the stifle joint, but lateral compartment pressure normalized when an axial load was applied to the joint. Nevertheless, the significant increase in contact pressure at higher suture tensions tested in the unloaded stifles would suggest excessive tightening of an extra-capsular prosthesis might result in elevated contact pressures during the early convalescent period after surgery, when dogs typically place limited weight on the affected hind limb. Early weight bearing after extra-articular stabilization of the CrCL deficient stifle may be important to resolve abnormalities in contact mechanics and kinematics, which were evident in this study. That study also established that extra-articular stabilization induced significant excessive external rotation of the tibia. It is likely that any extra-articular reconstruction technique causes malalignment of the femorotibial joint which may be mitigated during loading the stifle; however, an in vivo kinematic analysis would be needed to confirm that stifle alignment would return to normal with weight bearing. Ideally a prosthesis mimicking the CrCL should be secured at isometric locations, so that the distance between points of attachment remains constant as the stifle moves through a range of motion. Isometry of suture placement would prevent laxity or over constraint of the joint at different flexion angles. However, an extra-capsular prosthesis can never be truly isometric because the stifle does not function as a pure hinge joint. Tightening an extra-articular prosthesis in an effort to stabilize the joint eliminates the normal motion of the femur and tibia. In addition, alterations in the instant center of rotation may change the direction of surface velocity, causing compression of the joint surfaces at their point of contact. Results of this study substantiate that excessive tensioning of the extra-articular prosthesis is detrimental to lateral compartment contact pressures. The non-isometric placement of prostheses, such as in the LSS or TR techniques, could result in excessive or ineffective prosthesis tension at different joint angles. Ligament prostheses are high load-bearing structures that are subjected to impact loading. High loads caused by excessive postoperative activity, or severe joint instability may predispose to early elongation of the prosthesis. An over-tightened prosthesis cyclically loaded outside the range of its tolerance may loosen with weight bearing and have no impact on lateral contact pressures. Many variables such as variations in weight bearing, degree of periarticular fibrosis, stifle conformation, presence of meniscal pathology and meniscal treatment, body weight, and activity level would influence the cycling of an extra-articular prosthesis. In summary, over tightening of an extra-articular prosthesis, regardless of technique, can increase lateral compartment contact pressures when the stifle is unloaded. The optimal tension for TR and LSS is difficult if not impossible to define because of the many mechanical and biologic factors that may influence the effects and properties of the tensioned suture. None the less, tensioning an extra-articular prosthesis should be done cautiously. This finding is supported by a previous study that found that dogs that had satisfactory limb function after LSS had more cranial drawer motion and a greater range of motion than dogs that did poorly. In this study, the effect of tension was eliminated by axial load, suggesting that early weight bearing may mitigate abnormalities in contact pressures caused by excessive tension of an extraarticular prosthesis.
Increasing interest has emerged in use of tibial osteotomies for treatment of cranial cruciate ligament insufficiency in dogs. Rupture of the CrCL causes stifle instability, which predisposes the meniscus to injury and the stifle to degenerative joint disease. Loss of integrity of the CrCL results in an unrestricted cranial femorotibial shear force causing tibial subluxation during weight bearing.  Tibial osteotomies impart dynamic stability by altering the geometry of the stifle and thereby neutralizing the cranial femorotibial shear force. Dynamic stability can be achieved by decreasing the slope of the tibial plateau or by advancing the tibial tuberosity. Tibial plateau leveling osteotomy (TPLO) imparts craniocaudal stability by reducing the tibial plateau angle (TPA), whereas tibial tuberosity advancement (TTA) eliminates cranial tibial thrust by advancing the insertion of the patellar tendon and modifying the angle between the medial tibial plateau and the patellar tendon, which defines the patellar tendon angle (PTA). Despite widespread use of these osteotomy techniques, a perspective of how they affect both TPA and PTA has not been established. In 1983, Slocum described the internally generated femorotibial shear force that causes cranial tibial translation as cranial tibial thrust. Slocum’s theory suggests that the magnitude of cranial tibial thrust is dependent upon the angle between the tibial plateau and the joint compressive force, which was purportedly directed parallel to the tibial axis. Slocum proposed that the tibiofemoral shear force or CrTT was an internally generated force that caused the tibia to translate cranially (and is opposed by the CrCL). Slocum proposed that the CrTT in the normal stifle joint was primarily controlled by the caudally directed forces of the hamstring muscles. In this theory, the compressive forces across stifle joint were proposed to be parallel to the tibial axis, but because of the caudally directed TPS, compression between the joint surfaces resulted in cranial tibial translation. This theory was developed as the active model of the stifle; CrTT is created by compression between the femur and tibia, which acts through the functional axis of the tibia, and is dependent upon the amount of compression and the TPS. Axial compression of the limb is thought to generate a compressive force across the joint, and this resultant force can be reduced to 2 orthogonal components, one perpendicular and one parallel to the tibial plateau, the latter representing the CrTT . The CrTT is a result of the tibial plateau oriented at an angle to the axial compressive force. If the angle of the tibial plateau is reduced to zero, the joint compressive force and resultant force become the same, as the CrTT becomes zero, as this force vector is eliminated. Clinically, however, the plateau is not returned to 0 degrees, but has approximately 5 degrees of remaining slope. This concept relies on the hamstring muscles, which contribute to neutralizing this small remaining force. More recently, some researchers have suggested that the sum of the forces acting around a weightbearing stifle is directed parallel to the patellar tendon. Cranial tibial thrust, according to this model, is thus dependent on PTA. This model demonstrated that the tibiofemoral compressive force was approximately of the same magnitude, and oriented in the same direction, as the patellar tendon force, which resulted in a variable tibiofemoral shear force. This force was either anteriorly or posteriorly directed dependent upon the angle of knee joint extension or flexion, respectively. The point of neutral tibiofemoral shear force was termed the crossover point in this model, which occurred at a patellar tendon angle (angle between the tibial plateau and the patellar tendon; PTA) of 90 degrees.  Therefore, it was proposed that the direction and magnitude of the tibiofemoral shear force was determined by the PTA. Methods for measuring PTA have been reported using anatomic landmarks of the plateau segment (PTATP) or by estimating a tangent to the femoral and tibial condyles at their point of contact (PTACT). The method using the common tangent is stated to be more accurate because it estimates the inclination of the tibial plateau at the contact point between the femoral and tibial condyles. The common tangent is an estimation of the inclination of the plateau at the point of articulation between femur and tibia. Factors that may influence PTACT include the point of contact of the femoral condyle relative to the tibial plateau as well as the surface geometry of the plateau, which are ignored when making TPA measurements. Previous theoretical analysis demonstrated the importance of the radius of curvature of the tibial plateau in predicting forces along the cruciate ligaments. As previously suggested, PTACT may be a better measure for pre-operative planning of tibial osteotomies. Further clinical studies are needed, however, to evaluate the applicability and repeatability of using the PTACT to determine plateau rotation during TPLO, and to determine if TPLO rotation based solely on the PTACT will yield functional stability.

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Schematic representation of the tibiofemoral forces in the stifle joint, according to Slocum, before (A) and after (B)
tibial plateau leveling osteotomy (TPLO). The resultant compressive force (large white arrow) across stifle joint is parallel to the tibial axis. Using the tibial plateau slope (TPS) as the baseline, whereby the femur can move along this surface if the cranial cruciate ligament (CrCL) is deficient, the resultant force can be broken down into its 2 orthogonal components (small shaded arrows), one perpendicular and one parallel to the tibial plateau. The latter represents the tibiofemoral shear force (resulting in cranial tibial thrust [CrTT]). If the angle of the tibial plateau is reduced to zero, the tibiofemoral shear force vector becomes zero, and the joint compressive force and resultant force become one and the same.

The CrCL-deficient stifle is stabilized at a PTA of 90 degrees achieved with TTA when the stifle is positioned at a standing flexion angle of 135 degrees. This model takes into consideration both extensor mechanism anatomy and the geometry of the articulating surfaces of the stifle and therefore differs from Slocum’s theory in that the direction of the joint reaction force is dependent on the inclination of the patellar tendon. The primary difference between the 2 proposed mechanisms is the direction of the tibiofemoral compressive force. With TPLO, the force is proposed to be parallel with the tibial long axis, whereas with TTA it is proposed to be parallel to the patellar tendon. Variations in morphology of the proximal aspect of the tibia, and specifically patellar tendon insertion angle, may be relevant for preoperative planning of tibial osteotomies. Recently, it has been suggested that the proposed theoretical mechanism of action of the TTA can also be used to explain the mechanism of action for TPLO. Understanding how TPLO affects both TPA and PTA may provide insight about the mechanism of action of TPLO. In a recent study, the planning of TPLO rotation using the preoperative TPA or PTATP would have resulted in similar magnitude of plateau rotation. Variations in tibial tuberosity morphology in certain breeds, such as chondrodystrophic dogs, however, could influence the surgical planning of plateau rotation based on PTA. In addition, this study indicated that a PTACT of 90 degrees is achieved at a TPA of 12 degrees with the stifle in 135 degrees of flexion. This finding may help to explain the observation that dogs with TPA less than or equal to 14 degrees after TPLO had clinically acceptable results. Based on the calculation of PTACT, the point where the femorotibial shear force is neutralized corresponds to a plateau rotation lower than previously recommended. This result would support the speculation that TPLO to a TPA of 6 degrees overcorrects the cranial tibial thrust because of excessive rotation. The excessive rotation may explain the abnormal femorotibial contact mechanics that results after TPLO which may predispose to osteoarthritis. Performing TPLO rotations based on calculations using PTACT might result in less plateau rotation and mitigate the adverse alterations in femorotibial contact pressures previously reported.

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Schematic representation in the stifle joint of the tibiofemoral forces before (A) and after (B) tibial tuberosity advancement (TTA). The resultant compressive force (large white arrow) across stifle joint is parallel to the patellar tendon. Using the tibial plateau slope (TPS) as the baseline, whereby the femur can move along this surface if the cranial cruciate ligament (CrCL) is deficient, the resultant force can be broken down into its 2 orthogonal components (small shaded arrows), one perpendicular and one parallel to the tibial plateau. The latter represents the tibiofemoral shear force (resulting in cranial tibial thrust [CrTT]). If the angle of the tibial tuberosity is advanced cranially until the patellar tendon angle (PTA, angle between the tibial plateau and the patellar tendon) is reduced to 90 degrees, the tibiofemoral shear force vector becomes zero, and the joint compressive force and resultant force become one and the same.

Presence and progression of radiographic changes of OA in the stifle joint of the CrCL deficient dog has been reported after conservative treatment and after extracapsular or intracapsular substitution techniques, TPLO, and TTA. Radiographic soft tissue changes include joint effusion/capsular thickening, lateral and medial soft tissue thickening, intraarticular osseous fragments, and meniscal mineralization. Bony changes include osteophytosis and enthesiophytosis, subchondral sclerosis, subchondral cyst formation, and joint space narrowing, generally placing emphasis on presence and growth of marginal osteophytes. Patellar ligament thickening and patellar tendinosis have also been observed. Surgical techniques that change the geometry of the proximal aspect of the tibia, such as TPLO and TTA were specifically developed to restore functional stability of the stifle, prevent deterioration of the medial meniscus, and reduce the degree of secondary OA in the stifle joint with CrCL rupture. The initial hope that progression of OA could be minimized using these techniques has not been consistently realized. Whereas progression of OA is less in dogs after TPLO and TTA than after extracapsular stabilization, in general, progression of OA has been observed after both TPLO and TTA. Several studies have reported or suggested a lack of significant correlation between the radiographic appearance of OA and clinical evaluation of limb function. A recent study evaluating the presence of OA and limb function found that limb function, characterized by force plate analysis, improved markedly after TPLO and TTA in spite of the fact that OA characterized by bony changes progressed in approximately 55% of the treated stifles. The degree of radiographically visible OA and the progression of bone and soft tissues changes after TPLO or TTA did not correlate with functional outcome assessed by ground reaction forces. Therefore, radiographic scoring systems may not necessarily reflect the true severity of OA. Historically, much emphasis has been placed on the presence and degree of osteophytosis in evaluation of the clinical status of canine joints and the presence and progression of OA has been suggested as a true test of the value of the treatment of the injured CrCL. For this reason, control of OA has been listed as one of the primary surgical goals of repair of CrCL injury. However, achieving this goal remains elusive and this and many other reports note progression of OA after stabilization despite an acceptable clinical outcome.

Despite the differences in proposed mechanisms of action, clinical results appear comparable between TPLO and TTA. As previously mentioned, an argument could be made that the proposed mechanism of action for TTA can also explain the mechanism for TPLO. This can be observed after reduction of TPA via radial osteotomy and rotation of the proximal tibial fragment, as this also reorients the patellar tendon angle to less than or equal to 90 degrees. Obviously, different techniques are used to approach this mechanism from 2 different perspectives: (1) a radial cut of the proximal tibial plateau segment for TPLO, and (2) an osteotomy of the tibial crest performed in the frontal plane for TTA. For TPLO, the tibial plateau is moved to meet the force; alternatively, for TTA, the force is moved to meet the tibial plateau. In either case, it appears that the end result is the same: the tibial plateau and the patellar tendon become oriented at approximately 90 degrees to each other.

Success rates with CrCL repair are reported to be greater than 90% regardless of the surgical technique used. Historically, selection of a surgical technique has been based primarily on surgeon preference rather than definitive evidence that one technique might be better than another. Unfortunately, there is no study that demonstrates that TPLO is a better procedure than, for example, the extra-capsular stabilization; this despite much anecdotal opinion that the TPLO is a superior technique, especially for active, athletic dogs. Likewise, there are no data for functional evaluation of TTA other than similar anecdotal evidence that it is an effective technique in similar types of affected dogs. There are no peer-reviewed reports comparing the outcome of TPLO to TTA; however, anecdotal comments have been presented. The question that is raised is whether one or the other of these techniques (TPLO or TTA) might be a better choice for repair of the CrCL-deficient stifle joint, and if so, under what conditions would one choice perhaps be better than the other.

If it is accepted that tibiofemoral shear force is dependent upon the PTA (for either technique), then altering the direction of the patellar tendon force is the mechanism for obtaining dynamic joint stability. Based upon the proposed directions of the total joint force, either parallel to the patellar tendon (TTA) or to the functional axis of the tibia (TPLO), there may be a difference of as much as 10–15 degrees in endpoint after surgery. Based on this argument, it would appear that the TPLO overcorrects for the cross-over point compared with TTA. This proposed difference between the 2 techniques might be less than 10–15 degrees because of the craniocaudal translation of the femoral condyles and the contact point with the tibia during flexion/extension. During extension, the femorotibial contact point moves cranially; similarly, during flexion, it moves caudally. The effect of this varied positioning is yet to be evaluated, but a suggestion has been made that it should be considered when assessing the joint forces. These anatomic changes further minimize the difference between the calculated endpoints between the 2 techniques, perhaps only 5–10 degrees. The difference in endpoints after surgery raises the question as to whether it has any potential adverse effects. Because the primary stabilizer of the joint becomes the CaCL after either TPLO or TTA, could this theoretical difference put the CaCL at greater risk for subsequent injury with TPLO? It has been reported that the CaCL undergoes marked morphologic changes in CrCL-deficient joints, which may result in compromised material properties. Regardless, there is no clinical evidence that the CaCL is at risk for failure after either TPLO or TTA. There is only anecdotal information as to the risk to the CaCL with over-rotation of the tibial plateau with TPLO. From a theoretical standpoint, TTA would be correcting the tibiofemoral shear force closer to a neutral tibiofemoral shear force at full extension (approximately 135 degrees) during weight bearing, thus there may be less stress placed on the CaCL. It should be mentioned, however, that there is still no documentation as to the ideal point at which tibiofemoral shear is neutralized with either TPLO or TTA, and which of these techniques comes closer to this theoretical point. More information is needed about the possible risks to the CaCL over time, especially in its new role as the primary stabilizer to the joint.
Another point to consider is whether or not an anatomic alteration of the tibial plateau angle when performing a TPLO makes a functional difference with regards to altering the gait and/or placing additional stress upon the menisci because of this change in joint orientation. The tibial plateau remains unaltered with TTA, whereas with TPLO, the tibial plateau is effectively placing the joint in approximately 15–20 degrees of increased flexion. Based upon kinematic gait analysis, stifle and hock mechanics remain unaltered with TPLO during weight bearing; however, some changes can be seen in the swing phase of the gait. Therefore, gait seems to be unaltered with TPLO, assuming that the alterations observed in the swing phase have no functional or clinical ramifications. This assumption appears to be reasonable based upon the absence of weight bearing during this time frame. It has been theorized that because TTA does not alter the orientation of the articular surfaces, there would be no effect on gait; however, to date there has been no similar evaluation of gait with kinematics. Any alteration of the point of insertion of the patellar tendon into the tibia and any effect on gait mechanics remain to be investigated. After TPLO, the femoral and tibial articular surfaces are placed in a relatively increased flexed position. Altered flexion of these surfaces during weight bearing results in changes in the pressure distribution to the caudal compartments of the joint (medial greater than lateral), possibly affecting the menisci (especially the medial meniscus); this altered positioning may also reduce the space for the meniscus. Both factors may place the meniscus at a greater risk for injury. This was the rationale to perform a medial meniscal release when performing a TPLO.  More recently, however, it also has been shown that performing the meniscal release, or caudal pole hemimeniscectomy, in a CrCL-deficient stifle joint with a TPLO further changes and increases the pressure distribution in the medial compartment of the joint, an argument that would perhaps favor leaving the meniscus intact. Although there is no evidence that the increased stifle joint flexion predisposes the menisci to damage, it was proposed that TTA might provide less risk for such damage because of the unaltered joint position. This led to the original recommendation to leave the intact menisci in situ when performing TTA. To summarize, some studies seem to suggest that the caudal pole of the medial meniscus is at risk for trauma after TPLO, whereas not after TTA because the TTA does not change the geometry of the joint and the pressure distributions essentially remain unchanged. Debate remains as to whether or not to perform a medial meniscal release in both TPLO and TTA.

An important argument to preserve the menisci has to do with the important biomechanical functions of the meniscus and the role of this structure to stabilize the joint. The meniscus functions as a load-bearing structure to distribute the femoral condyle forces more uniformly over the tibial plateau. Meniscal release eliminates this function and results in increased areas of localized stress to the articular cartilage. As previously noted, there are studies that indicate that preserving the meniscus with either TPLO or TTA better preserves joint mechanics in the CrCL-deficient stifle joint and these studies suggest leaving the meniscus intact if it is uninjured. Alternatively, as the meniscus acts as a secondary joint stabilizer in the CrCL-deficient joint, with any persistent passive laxity the caudal pole of the meniscus may be more easily injured with a failure to fully neutralize the tibiofemoral shear forces. Sparing this structure from injury by performing a meniscal release has been suggested. However, it has also been noted that performing a meniscal release does not completely eliminate the possibility of subsequent meniscal tears. It has been reported that after TPLO with meniscal release, there is cartilage damage present on the tibial plateau and medial femoral condyle, confirming that subsequent articular cartilage damage does occur. These changes have been attributed to both iatrogenic surgical injury when performing the meniscal release as well as to loss of normal meniscal function. However, it has also been stated that there is little outward evidence of clinical dysfunction as a result of these changes, which is consistent with most clinical impressions. Despite the progressive effects of osteoarthritis in these dogs, clinical dysfunction is considered minor as opposed to that occurring with an injured meniscus; therefore, this argument supports the meniscal release in favor of possible future meniscal impingement. The question is the unknown frequency of meniscal injury at initial surgery, and the number of undetected tears at that time as opposed to tears occurring after surgery. These meniscal injuries have been defined as either latent (undetected) or postliminary (subsequent) tears. A recent study evaluating the rates of meniscal injuries in a consecutive series of 1000 dogs receiving TPLO surgeries indicated an incidence of primary meniscal injury (PMI) of 33.2%, and subsequent meniscal injury (SMI) of 2.8%. In this study, complete CrCL rupture was associated with higher incidence of PMI than partial CrCL rupture as previously reported. This supports a mechanically protective effect of the remaining portion of CrCL in partial tears. Meniscal release was not performed for menisci of normal appearance and texture in this case series because it was considered that the relative risk of SMI was more acceptable than potentially subjecting all dogs to more severe focal cartilage wear that might be anticipated after MMR or partial meniscal resection. Many recent studies have independently confirmed that medial meniscal release eliminates the function of a crucial articular structure and therefore is in contradiction with the principles of surgical stabilization of CrCL deficient stifles as it is likely that a combination of inflammatory and degradative mediators originating from the transected meniscus and biomechanical abnormalities from the surgically induced loss of meniscal function play a key role in the development of cartilage degeneration after MMR.

There is also the question as to whether the altered anatomy created by either of the procedures could result in other anatomic or functional changes within the joint. There have been a number of reports of patellar tendon thickening, or even patellar tendinitis after TPLO. It has been proposed that by rotating the tibial plateau, greater stress is placed on the patellar tendon compared with decreased stress to this structure after performing a TTA. The proposed increased stress (TPLO) versus decreased stress (TTA) on the patellar tendon can theoretically be explained by the change in lever-arm lengths to the patellar tendon after the osteotomies. If one considers that the CaCL becomes the primary stabilizer to the joint after either TPLO or TTA, the lever arm to the patellar tendon is the distance between the femorotibial contact point to the point of attachment of the patellar tendon to the tibial tuberosity. For TPLO, it is thought that this lever arm can shorten by as much as 10% compared with the intact joint, whereas, with TTA this lever arm can lengthen by as much as 10%. A shorter lever arm requires more force to move an object the same distance; conversely, a longer lever arm requires less force to similarly move an object. In this case, the object is the tibial tuberosity and the force is the quadriceps muscle pull on the patellar tendon. In other words, more force is required to extend the joint with a TPLO, and less force is required with a TTA. Regardless, there are no known clinical ramifications in dogs with mild to moderate patellar tendon thickening after TPLO, although a small percentage of dogs with severe patellar thickening have clinical signs consistent with patellar tendinitis. Regardless, there are no specific studies that have investigated this issue, clinically or experimentally, much less comparing the different techniques and their potential ramifications.

Both the TPLO and TTA are complex procedures, requiring appropriate preplanning and accurate execution of the details of the procedure. Preoperative planning for the TPLO must include a proper assessment of the angle of the TPS, such that precise surgical execution results in the desired postoperative TPA of 5-6.5 degrees. Preoperative planning for a TTA must include a proper assessment to ensure that advancement of the tibial tuberosity results in a PTA of 90 degrees. It is suggested that there is some variability in the postoperative outcomes with the TPLO and TTA despite an attempt to obtain precise preoperative measurements. With both TPLO and TTA, there probably is some amount of postoperative variability that will be tolerated, but the ideal clinical postoperative PTA or TPS is unknown.

As described, TPLO is a relatively invasive procedure where there is abundant circumferential dissection of the entire proximal aspect of the tibia, and a greater potential for injuring some vital structures around the joint. The substantial soft tissue dissection and limited coverage in the area of the proximal tibia may contribute to dead space and may predispose dogs to incisional complications. In addition, there are a number of surgical technical errors that can occur with TPLO. Placing the osteotomy too far cranial and/or distal will result in a higher than expected TPA postoperatively, and inadequate neutralization of the CrTT. Such malposition of the osteotomy also results in a small tibial tuberosity fragment, creating the possibility of a tibial tuberosity fracture. Placing the temporary holding pins (after initial rotation of the tibial plateau) too far distally into the tibial tuberosity may result in a stress-riser in this fragment, again predisposing this bone to fracture. Fibular fractures can result in excessive stresses placed on this structure during the rotation, or may occur as a result of stress-risers from drill holes into this structure.

The TTA is considered by many to be a simpler procedure than the TPLO. Similar comments regarding soft tissue dissection and limited coverage in the area of the proximal tibia may be made for TTA; however, the surgical dissection is confined to the cranial portion of the bone. There is much more limited possibility for iatrogenic surgical injury with TTA, but damage to the long digital extensor tendon is one potential consequence. There are a number of surgical technical errors that can occur with TTA. These issues include too small of an osteotomy fragment, shifting the patella distally, or predisposing to a patellar luxation with improper tibial tuberosity repositioning. A small osteotomy fragment does not allow adequate fork purchase as there is insufficient bone available. Another potential error is patellar malposition. Patellar luxation can result if attention is not paid to the plate contouring, ensuring that the tibial tuberosity is advanced cranially without changing the orientation within the sagittal plane. Any shift either medially or laterally could result in a malalignment of the quadriceps mechanism, and thus the resultant patellar luxation. Other issues may include poor plate position, either rostrally along the tibial crest or distally along the tibial diaphysis. When comparing TPLO to TTA, the difference in implants could be considered: commercially pure titanium is the norm with TTA versus stainless steel with TPLO. Pure titanium is touted as a more biocompatible implant with tissues as compared with stainless steel. Furthermore, the plate profile with TTA is very thin and provides less overall bulk in a position on the limb where soft tissue covering is limited to a thin muscle layer and skin. This may play a role in limiting soft tissue complications. The use of locking screw technology compared with conventional screw technology in TPLO has recently been investigated. A distinct advantage of locking screws is their ability to function as an internal fixator and maintain accurate osteotomy reduction without having a perfectly contoured plate. With conventional screws, if the plate is not accurately contoured at the time of screw placement, osteotomy reduction can be disrupted as the screws are tightened to achieve bone–plate friction. Less initial tibial plateau disruption has been reported with locking screws compared with conventional screws. Locking screws better maintain initial rotation of the tibial plateau segment if small gaps occurred between bone and plate. According to this study, locking screw technology resulted in improved   radiographic healing and TPA was better conserved when compared with similar fixation using conventional screw technology.

Some factors specific to the anatomic configuration of the limbs being operated need to be considered, from the standpoint of conformational issues that would make one procedure perhaps the better choice than the other. These include angular and torsional limb deformities, patellar luxation, and excessive TPS. Furthermore, the size of the dog may also play a factor. When performing a TPLO, rotation of the tibial plateau segment only to the level of the patellar tendon insertion on the tibial tuberosity has been suggested to ensure its role as a buttress support for the tibial tuberosity segment. Therefore, dogs with high patellar tendon insertion point would run the risk of the rotation of the tibial plateau segment to a point below the patellar tendon insertion, thus potentially leaving the tibial tuberosity more prone to fracture because of an absence of buttress support. Alternatively, in dogs with a low patellar tendon insertion point, much greater rotation could be obtained while continuing to preserve the caudal buttress behind the tibial tuberosity. In contrast, the tibial tuberosity may be at more risk for possible fracture with TTA in cases with a low patellar tendon insertion point, as a smaller plate is applied to the tibial crest and the usual position of the interspersed cage is above the most proximal position of the plate with little bone present for support. In dogs with a high insertion point, a larger TTA plate can be applied to the tibial crest, and the interspersed cage is placed within the gap, which remains buttressed with adequate bone and a larger plate that disperses all the forces to the tibial crest. It is suggested that cases with a high patellar tendon insertion point are more conducive to a TTA, whereas cases with a low patellar tendon insertion point are better suited for a TPLO. In any case, there are no experimental or clinical studies reported that support these assumptions.

Cases where there is excessive TPS are not conducive to TTA, because the procedure requires that the advancement produce a PTA of 90 degrees, which likely would result in a required amount of advancement beyond that obtained with the currently available implants. Additionally, there is a conformational deformity of the joint with excessive TPS that places it in a relative angle of hyperextension despite the limb itself not being in the extended position. TTA does not address this malformation, whereas the TPLO can correct it. The question remains, however, as to the maximal angle of the TPS that should be used as a guideline to consider whether to perform a TTA, although it has been proposed that angles greater than 27 degrees probably are not well suited for a TTA.

Angular and torsional limb deformities may be treated with either TPLO or TTA; however, TPLO may be better suited to make these corrections simultaneous with the rotational osteotomy. The concept of modification of tibial plateau leveling osteotomy as a widely recognized management modality for canine CrCL insufficiency to include simultaneous correction of frontal plane deformity and/or torsional deformity of the tibia has been previously introduced. Such modifications are routinely used in dogs with preoperative tibial deformity in order to prevent   subsequent development of postoperative gait abnormality or exacerbation of limb deformity during the TPLO procedure when the medial cortex of the calcaneus and the central patellar axis are not collinear in the sagittal plane. With minor angulation or rotation, these deformities can be addressed after rotation of the proximal tibial fragment, after it has been temporarily secured with a pin or K-wire, and before plate fixation. At this point in the procedure, an angular correction (stifle varus or valgus) can be performed by shifting the jig position along either the proximal or distal jig pin (a translation of the jig along the pin) so as to obtain limb realignment. Similarly, a rotational correction can be performed by bending one of the jig pins (usually the distal pin) while the jig is securely fixed to these pins. A recent study successfully utilized a TPLO with a medial opening crescentic osteotomy (TPLMOCO) in dogs with genu varum attributable to proximal tibia vara and/or tibial torsion. If a TTA was performed to correct the CrCL-deficient joint, a separate osteotomy would still be required. The disadvantage is that the medial side of the bone already has the plate positioned for TTA in the proximal one third of the medial tibial surface, which will interfere with subsequent additional medial plate fixation. Although a standard plate could be applied over the thin TTA plate, this is far from ideal and generally not recommended.

Patellar luxation requiring tibial tuberosity transposition, on the other hand, may be better suited for a TTA, as any desired transposition could be simultaneously performed with the advancement. In this case, the TTA plate is slightly over-bent to conform to the new laterally (or medially) transposed tibial crest. The limitation with the tibial tuberosity transposition and TTA, however, would be cases of patellar luxation that also had a significant angular/torsional deformity that also needed to be corrected at the same time. In the latter instance, TPLO would again be the better choice. In this instance, if there was a simultaneous rotational deformity this correction could result in appropriate alignment of the tibial tuberosity after the repositioning.

Both TPLO and TTA have been performed in dogs as small as 5 kg and as large as 92 kg. Size limitation for these techniques is dependent upon the availability of the appropriately sized implants. Both devices are produced in a variety of sizes such that they can accommodate almost any sized dog. One current limitation of the TTA may be the large distance of TTA that is required for some large breeds of dogs (not necessarily the heavier dogs, but rather the taller dogs, e.g., Great Danes). The widest cage currently available to support the osteotomy gap is 12mm. Whereas the cage can be moved further distally to increase the width of the gap, this must be done judiciously, as the tibial tuberosity above the cage may become prone to fracture because of a large stress-riser created above the cage.

Early diagnosis of a CrCL injury and treatment by either TPLO or TTA may be protective against further CrCL disruption lending stability to the joint and decreasing the incidence of meniscal injury and articular cartilage damage. One study has indicated that in joints where initially there was only partial CrCL tear with most of the CrCL appearing normal, that the CrCL remained intact after TPLO and the intraarticular structures appeared normal or near normal. By contrast, joints that initially had either complete disruption or a partial tear with the remaining CrCL judged incompetent developed a range of pathologic changes including mild fraying or complete rupture of the caudal cruciate ligament, postliminary bucket handle tears of the caudal horn of the medial meniscus and visible cartilage lesions. These findings suggest that TPLO has a protective effect on injured CrCL when there is some initial fiber disruption but most of the CrCL is intact and appears functional. The protective effect may result from decreased stress on the CrCL after rotation of the tibial plateau and subsequent transformation of cranial tibial thrust to a caudal tibial thrust. The elimination of cranial tibial thrust would likely lower strain within the CrCL reducing the possibility of further fiber tearing. As the remaining CrCL maintains the relationship of the femoral condyles relative to the tibial plateau, i.e., centers the femoral condyles within the confines of the menisci, the effect is a decreased incidence of meniscal injury and articular cartilage damage. These findings support the notion of early surgical intervention for cruciate ligament disease and against debridement of CrCL fibers in early injuries because of good functional outcome and the apparent protective effect of surgery on the remaining CrCL.

In conclusion, there are a number of apparent advantages/disadvantages in both TPLO and TTA procedures. TTA may correct the tibiofemoral shear force closer to the neutral point compared with TPLO, which might protect the CaCL from additional stress as the primary joint stabilizer. Another advantage of the TTA is the unchanged joint geometry and superior cartilage pressure distribution compared with TPLO. TTA may also be a less invasive, simpler surgical procedure with fewer potential technical issues with adverse effects. TTA may be more suitable in cases of patellar luxation. On the other hand, TPLO is a more versatile procedure than TTA in cases with excessive TPS, and in cases with a variety of angular and rotational limb deformities, including cases with concurrent patellar luxation. At this time, there are only a few studies that present reasonable scientific support for either procedure. A number of experimental and clinical studies are necessary to attempt to shed more light on these repair methods.

In summary, the stifle joint of dogs is an organ comprised of multiple tissue types that must work in concert to maintain joint health and function. Cruciate disease in dogs is caused by a spectrum of causal and risk factors that result in a final common pathway of abnormal biomechanics and abnormal biology causing osteoarthritis of the stifle and the clinical signs of lameness, pain, and limb dysfunction. It is vital to understand the components of the biologic and biomechanical pathologies to improve our understanding of cruciate disease in dogs so that we can improve preventative, diagnostic, and therapeutic strategies for our patients. As veterinary surgeons, it is important to consider and address as many aspects of the disease as possible and educate clients well with respect to the nature and progression of CrCL disease, preoperative, operative, and postoperative treatment components and options, and their roles in achieving a successful outcome for their dog. While surgical intervention is recommended in dogs afflicted by CrCL insufficiency, there is no evidence to support the notion that any one technique is clearly superior to the others at this point in time. Not only is it unclear as to which surgical technique is superior, it is also unclear as to whether or not the remnants of the diseased cruciate ligament should be debrided and removed from the intrasynovial environment. It is equally unclear as to whether or not aggressive manipulation, inspection and release or removal of meniscal tissue should be performed. When analyzed collectively, the innumerable studies presently available for review on cruciate ligament and meniscal disease fail to definitively prove which one surgical approach has the best short term and long term success rate with consistent return to full, pain free function.  As with many surgical procedures, it is at the discretion of the surgeon to select the technique that he believes is the most appropriate for the specific task at hand and their own experience/expertise.
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3 different views of Post Op TPLO


References
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Marino, DJ: Diagnostic Imaging of the Canine Stifle: A Review. Vet Surg 2010; 39:284-295

Bottcher P, Bruhschweinz A, Winkels P et al: Value of Low-Field Magnetic Resonance Imaging in Diagnosing Meniscal Tears in the Canine Stifle: A Prospective Study Evaluating Sensitivity and Specificity in Naturally Occurring Cranial Cruciate Ligament Deficiency with Arthroscopy as the Gold Standard. Vet Surg 2010; 39:296-305

Breshears LA, Cook JL: Detection and Evaluation of Matrix Metalloproteinases Involved in Cruciate Ligament Disease in Dogs Using Multiplex Bead Technology. Vet Surg 2010; 39:306-314

Cook JL, Luther JK, Beetem J et al: Clinical Comparison of a Novel Extracapsular Stabilization Procedure and Tibial Plateau Leveling Osteotomy for Treatment of Cranial Cruciate Ligament Deficiency in Dogs. Vet Surg 2010; 39:315-323

Fischer C, Cherres M, Grevel V et al: Effects of Attachment Sites and Joint Angle at the Time of Lateral Suture fixation on Tension in the Suture for Stabilization of the Cranial Cruciate Deficient stifle in Dogs. Vet surg 2010; 39:334-342

Tonks CA, Pozzi A, Ling HY et al: The Effects of Extra-Articular Suture tension on Contact Mechanics of the Lateral Compartment of Cadaveric Stifles Treated with the TightRope CCLs or Lateral Suture Technique. Vet Surg 2010; 39:343-349

Hulse D, Beale B, Kerwin S: Second Look Arthroscopic Findings after Tibial Pleateau Leveling Osteotomy. Vet Surg 2010; 39:350-354

Thieman KM, Pozzi A, Ling HY et al: Comparison of Contact Mechanics of Three Meniscal Reapir Techniques and Partial Meniscectomy in Cadaveric Dog Stifles. Vet Surg 2010; 39:355-362

Kim SE, Pozzi A, Banks SA et al: Effect of Cranial Cruciate Ligament Deficiency, Tibial Plateau Leveling Osteotomy, and Tibial Tuberosity Advancement on Contact Mechanics and Alignment of the stifle in Flexion. Vet Surg 2010; 39:363-370

Drygas KA, Pozzi A, Goring RL et al: Effect of Tibial Plateau leveling Osteotomy on Patellar Tendon Angle: A Radiographic Cadaveric Study. Vet Surg 2010; 39:418-424

Morgan JP, Voss K, Damur DM et al: Correlation of Radiographic Changes after tibial Tuberosity Advancement in Dogs with Cranial Cruciate-Deficient Stifles with Functional Outcome. Vet Surg 2010; 39:425-432  

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Fitzpatrick N, Solano MA: Predictive Variables for Complications after TPLO with Stifle Inspection by Arthrotomy in 1000 Consecutive Dogs. Vet Surg 2010; 39:460-474
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Medical and Surgical Treatment of Diaphragmatic Hernia in Dog and Cat.

The diaphragm is the muscular separation between the chest and abdominal cavities that functions as a barrier and aids in respiration.  Diaphragmatic hernia is a disruption of the diaphragm which allows abdominal organs to migrate into the chest cavity. Almost exclusively the result of blunt trauma to the abdomen, acquired or traumatic diaphragmatic hernia is a common injury in companion animals, with motor vehicle accidents being responsible for 85% of cases documented in one study. A rapid rise in intra-abdominal pressure following a forceful blow and failure of the epiglottis to remain closed, allowing the stabilizing effect of the air filled lungs to be lost acutely, is the classic explanation for diaphragmatic rupture. While diaphragmatic hernia can occur in any dog or cat, as most dogs and cats that suffer diaphragmatic hernias have been hit by a car or have experienced some other type of trauma, most dogs are young intact males, and most affected cats spend time outdoors. In most cases, acute diaphragmatic hernia results in significant respiratory difficulty.  The trauma which caused the hernia may also result in rib fractures, lung lacerations, and lung bruising.  These injuries may lead to pneumothorax, or hemothorax.  If abdominal contents have entered the chest cavity, this can further compromise the ability to expand the lungs.  If the initial insult is tolerated, a diaphragmatic hernia may be diagnosed later as an incidental finding in a relatively asymptomatic animal.  For these reasons, the clinical signs of diaphragmatic hernia vary from none to severe respiratory compromise and shock.  As mentioned previously, dyspnea is the most common clinical sign, and relates multifactorily to the presence of shock,  chest wall dysfunction,  the presence of air, fluid or viscera in the pleural space, decreased pulmonary compliance, edema, and cardiovascular dysfunction.  Cardiac arrhythmias are present in approximately 12% of small animals with diaphragmatic hernia.  Other common clinical signs include muffled heart and lung sounds, thoracic borborygmi, and evidence of trauma, such as abrasions. Chronically, abdominal organs, such as the liver or intestines can become adhered in the chest cavity and the animal may exhibit signs associated with liver or gastrointestinal disease such as vomiting or anorexia.

It is important to remember that loss of continuity of the diaphragm does not necessarily result in severe respiratory distress.  The cause of respiratory impairment associated with diaphragmatic hernia is multifactorial.  Hypovolemic shock, chest wall trauma, pleural fluid or air, pulmonary contusions, and cardiac dysfunction are factors that contribute to hypoventilation.  Other injuries such as rib fractures or flail chest may compound mechanical dysfunction.  Pulmonary compliance is decreased by pleural fluid, the presence of abdominal organs in the thorax, or pneumothorax.  Pulmonary hemorrhage, edema, and atelectasis reduce total lung capacity and functional residual capacity.  Myocardial contusion often accompanies other traumatic injuries and may decrease cardiac output.  When myocardial injury is concomitant with impaired ventilation tissue hypoxia can result.  Pain resulting from chest and abdominal contusion and accompanying injuries causes voluntary restriction of motion (thoracic excursion) and may therefore further compromise ventilatory capability. 

Chest radiographs must be taken to diagnose the disease, and to look for any other abnormalities.  In the normal animal, a diaphragmatic line, a cardiac silhouette, and air-filled lung fields are appreciated on chest radiographs.  In the case of diaphragmatic hernia, loss of the diaphragmatic line, loss of the cardiac silhouette, displacement of lung fields, and presence of abdominal contents within the chest cavity may be noted on chest radiographs. Most cases of diaphragmatic hernia can be diagnosed from radiographs.  However, fluid in the chest cavity can obscure the diaphragmatic line in the absence of a hernia.  Repeating chest radiographs after thoracocentesis is advisable but may not definitively show a diaphragmatic hernia. In this case, ultrasound may be helpful to differentiate abdominal organs from pleural fluid. Ultrasonographic evaluation is useful to identify abdominal viscera on the thoracic side of the diaphragm especially in the presence of pleural fluid because it enhances sonographic evaluation.  Ultrasound may identify abdominal organs, differentiate organs such as the spleen or liver from pleural fluid, and will sometimes identify the defect in the diaphragm.  Contrast radiography, performed by injecting contrast material into the abdominal cavity, and MRI or CT evaluation may also be helpful.

Initial stabilization of diaphragmatic hernia patients consists of medical therapy for shock and respiratory distress, possible antimicrobial utilization and close observation.  Adequate volume replacement is the best therapy for hypovolemic shock. However, volume overload can be as detrimental as hypovolemia, particularly in patients with traumatic diaphragmatic hernias because concurrent pathology such as atelectasis, pulmonary contusions, and physical compression of the lungs by fluid or organ entrapment predisposes patients to pulmonary edema. The resuscitation fluid of choice is the subject of much debate. Isotonic crystalloids have long been the mainstay of volume replacement in treating hypovolemic shock and probably remain the recommended fluid for initiating therapy; however, hypertonic saline, colloids, and combinations of these fluids offer many potential advantages in trauma patients, including effective low-volume resuscitation and less expansion of the interstitial space compared with traditional isotonic fluid therapy. Volume and speed of fluid replacement are dictated by cardiovascular parameters such as capillary refill time, pulse quality, mucous membrane color, and central venous pressure, as well as respiratory parameters such as ventilatory rate, auscultatory findings, and pulse oximetry. 

Signs such as dyspnea, cyanosis, tachypnea, tachycardia, reduced mentation, and postural changes such as an “oxygen hungry” stance (i.e., abducted elbows, extended head and neck, and open-mouthed breathing) are suggestive of hypoxia and should be treated quickly. Various modes of oxygen delivery are available . The actual method chosen depends on a number of factors, including patient size and temperament, available equipment and desired level of oxygen to be delivered. In patients with marked shunting, delivery of even 100% oxygen does little to correct arterial hypoxemia because shunted blood is never exposed to the higher alveolar oxygen tensions and therefore continues to depress PaO2 while the blood perfusing ventilated alveoli is already almost fully saturated and improves only minimally with exposure to 100% oxygen. However, some elevation of arterial oxygen content occurs (mainly in the form of increased dissolved oxygen), making oxygen therapy a useful aid in immediately treating dyspneic patients with traumatic diaphragmatic hernias.

Removal of pleural effusion may also improve ventilation in selected cases. Antimicrobials may be used during the preoperative period to prevent infection-related pulmonary problems.  Every patient with traumatic diaphragmatic hernia needs close observation, since rapid changes in ventilatory function may occur.  Patients failing to respond adequately to pre-surgical management or rapidly deteriorate despite appropriate management should be taken to surgery as soon as possible.

The timing of anesthesia and surgical correction of diaphragmatic injury may have an important effect on the outcome of treatment.  Approximately 15% of small animals with diaphragmatic hernia will die prior to surgery, and animals with diaphragmatic herniorrhaphy performed within the first 24 hours after injury have the highest mortality rate (33%).  The timing of surgical repair depends upon the extent of the initial cardiopulmonary dysfunction, the presence or absence of organ entrapment, the degree of compromised pulmonary function, and whether or not the animal’s condition is improving, stable, or deteriorating.  Diaphragmatic herniorrhaphy may require immediate surgery if aggressive supportive care cannot stabilize respiratory function.  Acute dilatation of a herniated stomach or strangulated bowel are examples of situations where emergency surgery may be indicated.  A herniated stomach can rapidly distend from aerophagia, decreasing pulmonary compliance and compress the caudal vena cava decreasing venous return resulting in a vicious cycle that can be rapidly fatal.  A herniated parenchymal organ such as the spleen may tear as it passes through the diaphragm causing acute hemothorax and a patient that may deteriorate rapidly after an initial response to shock therapy.  Most small animals with diaphragmatic hernia can be stabilized over 24 to 72 hours, therefore the presence of a diaphragmatic hernia, on its own, is not indication for emergency surgery.  Accompanying thoracic injuries such as pulmonary contusion will improve dramatically in 24 to 48 hours. The goal of initial management is to improve the cardiorespiratory status of the patient to improve their capability of tolerating the stress of anesthesia and surgery.

Induction of anesthesia in the diaphragmatic hernia patient is done with as little stress as possible and with the goal of quick control of ventilation.  Intravenous catheterization, appropriate intravenous fluid administration (crystalloid or colloid) and cardiorespiratory monitoring are important. Propofol is preferred because it allows rapid induction of anesthesia, quick intubation, and near immediate control of ventilation with assistance or by a mechanical ventilator.  Isoflurane is preferred for maintenance of anesthesia because a surgical plane of anesthesia is attained more quickly, it is associated with decreased recovery time, subjects the patient to less cardiac depression, and does not sensitize the myocardium to arrhythmias. Assisted ventilation is required soon after induction because the patient usually has decreased pulmonary compliance secondary to the presence of air, fluid, or abdominal viscera within the pleural space.  Inspiratory pressure should not exceed 20 cmH2O to limit potential barotrauma from pulmonary hyperinflation which may result in over-inflation of the lungs during surgery.  Rupture of pulmonary parenchyma, intrapulmonary hemorrhage, plumonary edema, and rarely pneumothorax may result.  Resolution of atelectic areas in chronically atelectic lungs during surgery may subject the lung to mechanical and reperfusion injury.  Damage from reperfusion in the collapsed vascular channels may disrupt capillary integrity causing fluid to leak into the interstitium resulting in reexpansion pulmonary edema within several hours after surgery.  Reexpansion of atelectic areas that will not inflate with 20 cm H2O will gradually re-expand over several hours with a continual negative pleural pressure of 10 cm H2O.

The preferred surgical approach is a ventral midline celiotomy, extending from the xiphoid process to a point caudal to the umbilicus. This exposure allows access to all regions of the diaphragm.  The incision should be large enough to allow exploration of the abdominal cavity because injury to other abdominal organs may be present and treatable concomitantly.  Most diaphragmatic tears are muscular and are located ventrally and may favor either the right or left side.  The liver, small intestine and pancreas are most commonly prolopsed into the thoracic cavity when the diaphragm defect is on the right side, whereas the stomach, spleen, and small intestine prolapse on the left side.  It is essential to examine the entire diaphragm because more than one tear may occur.  Should additional exposure be required to retrieve abdominal viscera adhered to structures within the thoracic cavity, surgical exposure can be improved by enlarging the rent in the diaphragm, paracostal extension of the celiotomy, and by caudal midline sternotomy.  Visibility of the diaphragmatic defect is enhanced by placing a pediatric Balfour retractor over the towel-protected abdominal incision.  Abdominal or pleural fluid is removed by suction.  The abdominal viscera are carefully retracted from the thorax using gentle traction.  Final, definitive positioning of the viscera is delayed until the diaphragmatic defect is closed.  Inspection of the lungs and pleural cavity is usually performed after the herniated contents have been retrieved from the pleural cavity.  Closure of the diaphragm is achieved with either absorbable or nonabsorbable suture material, in a simple-interrupted or simple-continuous pattern.  The least accessible part of the defect is closed first, taking care to avoid traumatizing the aorta, caudal vena cava, hepatic veins or esophagus.  On closure of the diaphragmatic defect, residual air is removed from the pleural cavity either by thoracentesis performed through the diaphragm using a 20 gauge catheter, three-way stop-cock, and 35 ml syringe or by placing a thoracostomy tube.  Exploration of the abdomen, with particular attention given to the previously displaced tissues, is performed.  Any lesions requiring attention are repaired.  Closure of the abdomen is achieved after definitive replacement of the abdominal viscera.

Postoperative considerations for the patient with a repaired diaphragmatic hernia include ventilatory support, analgesic administration, and close observation.  Ventilatory support is continued until the patient is adequately ventilating spontaneously.  Particular care is necessary when administering positive pressure ventilation during and after surgery, since trauma to the lungs from overzealous ventilation is a definite possibility.  Re-expansion pulmonary edema following re-oxygenation of chronically collapsed lungs is a major cause of perioperative death, particularly in animals with long-standing diaphragmatic hernias.  Reperfusion injury, with release of superoxide radicals which cannot be effectively scavenged, is thought to result in increased pulmonary capillary permeability and pulmonary edema.  Spontaneous ventilation in the postoperative patient is assisted by maintaining the patient in a forequarters-elevated position and the appropriate use of analgesics.  Analgesic administration is done to comfort the patient and to ease apprehension during recovery. 

The prognosis for animals presenting with a traumatic diaphragmatic hernia is variable depending on other injuries incurred.  Of the patients that survive to presentation, the timing of surgery will significantly affect prognosis.  Animals that have surgery greater than 24 hours after trauma have a lower mortality rate than those having surgery within the first 24 hours owing to resolution of shock after appropriate medical stabilization.  The proper utilization of medical stabilization followed by surgical intervention results in an overall success rate of over 90%. The most common complication following surgical intervention is the development or persistence of pneumothorax. While complications can occur in the immediate postoperative period, most are transient and self limiting and will resolve with conservative therapy.

 

Pyometra.

Pyometra is an infection of the uterus in dogs and cats. It is relatively common, affecting approximately 25% of unspayed female dogs and cats. It is a serious condition which results in a variety of clinical and pathological signs requiring emergency surgery to remove the infected uterus. While medical treatment is sometimes attempted for this condition, it is often ineffective, and can be dangerous. Although the disease has been recognized for decades, the true pathogenesis has still not been completely understood. It is generally recognized that progesterone and estrogen and their receptors have a role in the development of pyometra; however, the infection is triggered by bacterial involvement.  The cyclical hormonal influences of the female allow the uterus to go through changes that will be acceptable for fertilization of an embryo.  If bacteria are introduced into the uterus at a certain time during the cycle, hormonal regulation of the uterus allows the infection to start and become fulminate. If bacteria enter the uterus at the times when the protective physical barriers are breached, such as estrus, parturition, or immediately after parturition, the normal uterine defense mechanisms are likely to eliminate these bacteria.  However, the hormonal influences may not allow the body to clear the bacteria.  The bacteria typically cultured from the pyometra are bacteria that would be found in the areas of the intestines and vagina (E coli is the most common).  Therefore, many of the infections are considered either from an ascending infection from the vagina, a concurrent urinary tract infection or fecal contamination.  Certain bacteria are more virulent than others and therefore allow a bacterium that is normally found on the dog to develop into an infection. Pyometra is most commonly seen in intact dogs 4-8 weeks after estrus (mean time of 5.4 weeks); however, it can be seen 4 months post estrus as well.  Although seen less commonly, cats generally develop pyometra between 1-4 weeks after estrous. Pyometra generally occurs in older (7 to 8 years) intact bitches and queens; however, it may occur in younger animals that have been given estrogen (mis-mating shots) or progestins for estrus suppression.

If pyometra is allowed to continue untreated for a significant period of time, it can affect the entire body, leading to critical disease, shock and death. Because the infection can be so overwhelming, the reasons for presentation are not limited to the genital tract.  The animal can become so overwhelmed by the inflammation associated with the infection that the animal may die from its own uncontrolled inflammatory process. A dog with an open pyometra (the cervix is open) will often have vaginal discharge, which can look like blood, pus or mucus. Many dogs and cats will have a closed cervix and therefore the obvious sign of a bloody to mucopurulent, hemorrhagic vaginal discharge may not be present. Furthermore, many dogs will clean themselves, removing any trace of vaginal discharge before it is visible to an owner which makes detection more difficult. The most common clinical signs that are present in greater than 50% of cases include lethargy, depression, anorexia, fever, excessive water intake and excessive urination. Pale mucous membranes, vomiting, diarrhea, weight loss, abdominal distension, and inflamed eyes have been reported although much less frequently. Up to 16% of patients may have no clinical signs other than purulent vaginal discharge.  It is the bacterial infection of the uterus which causes increasing inflammation within the organ and leads to the systemic effects observed in the majority of patients. The severity of the resulting illness is greatly influenced by the degree of drainage from the uterus. If the cervix is closed, then fluids and toxins accumulate, with potential for toxic effects. Rupture or slow leakage from one of the uterine horns can release inflammatory products into the abdominal cavity, causing peritonitis. If the cervix is patent, or open, then drainage limits the accumulation of inflammatory products and bacterial toxins, and increases the likelihood of early recognition of the problem. The clinical signs of increased thirst and urination have been linked to the direct influence of bacterial toxins on the kidneys’ urine concentrating mechanisms. Bacterial infection and toxins may cause secondary damage to the liver as well. Endotoxic shock alters blood supply to all tissues and can disrupt normal blood clotting mechanisms. Microscopic blood clots or clumps of circulating bacteria can further impact upon the blood supply to vital organs such as the heart and brain, permitting seizures, cardiac rhythm disturbances and other grave consequences. The most life threatening complications associated with pyometra are sepsis and systemic inflammatory response syndrome (SIRS) /multiple organ dysfunction syndrome (MODS).  If an unspayed female dog or cat is exhibiting any of these symptoms, they should be evaluated immediately.

Diagnosis is based in part on the history, reproductive status, and clinical signs. Physical examination of the pyometra patient reveals abdominal distention, an enlarged, palpable uterus, vaginal discharge if the cervix is open, and lethargy. A closed-cervix pyometra more likely will result in the animal showing signs of septicemia, including shock, hypothermia, dehydration, vomiting, and collapse. Laboratory testing and imaging are frequently used to aid in the diagnosis. A complete general chemistry profile, complete blood count, urinalysis, abdominal radiographs, abdominal ultrasound and perhaps vaginal cytology analysis are performed in suspected pyometra cases. The dog’s complete blood count, or CBC, is influenced by the degree of drainage from the uterus. Patients with a closed cervix and limited uterine drainage are more likely to show significant elevations of or reductions in, the white blood cell count. The white blood cells are also more likely to appear immature or unhealthy in those patients. Red blood cell counts are often reduced; patients with chronic disease frequently have low-grade anemia. Dehydration can mask this feature by reducing the amount of water in the bloodstream; consequently, the red blood count appears higher than it really is. Blood urea nitrogen, or BUN, and creatinine reflect blood flow to the kidneys. The level of these nitrogenous waste products in the blood will frequently rise with dehydration and kidney dysfunction, which are common in patients with pyometra. Elevated blood protein levels and disturbed electrolytes will often reflect the state of dehydration. The urine may be very dilute, reflecting toxic influences on the kidneys, or well concentrated as an appropriate response to dehydration. The urine may contain bacteria or inflammatory cells, if collected after voiding, due to contamination by the vaginal discharge. If pyometra is suspected, urine samples are rarely collected directly from the urinary bladder, via needle aspiration, because of worries about perforation of the distended, fluid-filled uterus. Urinary protein levels may be elevated if the kidneys have been damaged by the presence of chronic infection The vaginal discharge can be examined microscopically for the presence of white blood cells and bacteria. Diagnostic x-rays of the abdominal cavity may demonstrate a fluid-dense tubular structure. A ground-glass appearance on the x-ray may suggest fluid accumulation around the diseased uterus if leakage has contributed to peritonitis. Ultrasound imaging will help to detect or verify the uterine enlargement and to define uterine size and wall thickness.

Pyometra necessitates immediate medical and surgical therapy. Those patients with a closed cervix may be more ill at the time of diagnosis. Intravenous fluids and antibiotics are routinely administered to patients that are severely ill, irrespective of the patency of the cervix. Potent antibiotics are given by injection, in combinations to target the most common bacterial pathogens. Supportive measures are customized for individual patient needs, according to the levels of shock, dehydration, electrolyte imbalance, organ dysfunction or cardiac arrhythmia. The patient is stabilized medically, if possible, to prepare for emergency ovariohysterectomy, or spay, to remove the infected uterus and the ovaries from the abdominal cavity. The prognosis with ovariohysterectomy can be as high as 90-100% if abdominal contamination is avoided during surgical intervention and shock/sepsis is managed appropriately perioperatively. It should be mentioned that a pyometra spay is considerably more challenging than a routine spay.  Special care has to be taken so that the infected, dilated, friable and easily breakable uterus does not rupture and spill its toxic contents into the sterile abdomen. If severe sepsis and organ failure develops, the prognosis can be grave.  Some patients may remain PU/PD (increased urination and water intake) and in a state of permanent kidney damage. Although surgery is considered the therapy of choice, very special case selection meeting certain criteria may allow valuable breeding bitches to be treated medically. Stable patients may be given prostaglandin f2-alpha by injection for several consecutive days to dilate the cervix, stimulate uterine contractions and to decrease the blood progesterone level. The dog must remain hospitalized for observation, monitoring for side effects of the prostaglandin or for worsening condition, and for continued antibiotic administration. Clinical improvement may be expected within the first 48-96 hours of medical treatment. Surgery should be considered for patients that deteriorate. If purulent vaginal discharge persists seven days after conclusion of treatment, or if other parameters indicate ongoing infection or uterine enlargement, then repeating the treatment may be advised, provided that the patient remains physiologically stable.  Dogs are susceptible to developing pyometra again after medical treatment; the recurrence rate is as high as 80%. In addition, the chance of successful subsequent breeding after medical management of pyometra is approximately 50:50. Because of the high rate of recurrence and diminished breeding capacity, even those dogs that have been successfully managed medically should receive an ovariohysterectomy when their breeding purposes are finished.

The majority of patients are released two to three days following an uncomplicated surgical procedure. Antibiotic therapy and pain management are continued for seven to 10 days after most procedures. It should be emphasized that pyometra is extremely easy to prevent.  An appropriately performed spay procedure between 6 months and one year of age will prevent the development of pyometra.  However, an inappropriately performed spay in which a portion of the ovarian tissue, uterine body or horn is not removed may result in what is called uterine stump pyometra. Ultrasound imaging is especially helpful in detecting stump pyometra. Surgical removal of the infected remnant is usually curative.  In conclusion, an elective spay procedure of the young dog or cat will virtually eliminate the possibility of pyometra from ever developing in the overwhelming majority of pets. Clearly, hormone administration for mismating events and estrus suppression should be avoided except for the absolute necessities, as avoidance of estrogen or progesterone administration will decrease the risk of pyometra in both young and mature pets. When pyometra does occur, the combination of aggressive and prompt medical and surgical intervention is successful in almost all cases.

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Exercise Induced Collapse Syndrome in Labrador Retreivers.

A syndrome of exercise intolerance and collapse (EIC) is being observed with increasing frequency in young adult Labrador Retrievers. It has also been observed in Chesapeake Bay retrievers and curly-coated retrievers. Affected dogs have been found in field-trial, hunt test, conformation, pet, and service lines.  Most affected dogs have been from field-trial breedings. Signs become apparent in young dogs as they enter heavy training, usually between 7 months and 2 years of age. Black, yellow and chocolate Labradors of either sex can be affected. Dogs with this condition are always normal at rest and are usually described as being extremely fit, prime athletic specimens of their breed with an excitable temperament and lots of drive. Affected dogs can tolerate mild to moderate exercise but 5 to 15 minutes of strenuous exercise induces weakness and then collapse. The first thing noted is usually a rocking or forced gait. The rear limbs then become weak and unable to support weight. Many affected dogs continue to run while dragging their back legs. Some of the dogs appear to be uncoordinated, especially in the rear limbs, with a wide-based, long, loose stride rather than the short, stiff strides typically associated with muscle weakness. In some dogs, the rear limb collapse progresses to forelimb weakness and occasionally to a total inability to move. Some dogs appear to have a loss of balance and may fall over, particularly as they recover from complete collapse. Most collapsed dogs are totally conscious and alert, still trying to run and retrieve, but affected dogs can appear stunned or disoriented during the episode. It is common for the signs to worsen for three to five minutes even after exercise has been terminated.  After 10 to 20 minutes of rest, however, they return to normal. A few affected dogs have died during exercise or while resting after an episode of exercise-induced collapse. Actual ambient temperature does not seem to be a critical factor contributing to collapse, but if the temperature is much warmer than what the dog is accustomed to, collapse may be more likely. Affected dogs are less likely to collapse while swimming than when being exercised on land. Body temperature is normal at rest in dogs with EIC but almost always dramatically increases at the time of collapse. Recently, however, a study showed that clinically normal Labrador Retrievers had similar dramatic elevations in body temperature after 10 minutes of strenuous retrieving exercise. Affected dogs may, however, take longer for their body temperature to return to normal after exercise. Affected dogs are not stiff, sore or painful during the collapse or after recovery. Massage of the muscles or palpation of the joints or spine is not uncomfortable. Nervous system, cardiovascular and musculoskeletal examinations are unremarkable as is routine blood analysis at rest and during an episode of collapse.

Symptomatic dogs are rarely able to continue training or competition. It seems that if affected dogs are removed from training and not exercised excessively the condition will not progress and they will be fine as pets. Littermates and other related dogs are often affected, but depending upon their temperament and lifestyle, they may or may not manifest clinical signs. Some affected dogs will never exhibit signs of EIC; this could be because they do not participate in high excitement strenuous activities or because they have a laid-back temperament. Severely affected dogs may collapse whenever they are exercised to this extent; other dogs only exhibit collapse sporadically and all of the factors important in inducing an episode have not yet been well established.  A few affected dogs have died during exercise or while resting immediately after a collapse of exercise-induced collapse so an affected dog’s exercise should ALWAYS be stopped at the first hint of an EIC attack.

        The genetics of the condition are only now becoming better established. Recent research has been conducted at the University of Minnesota analyzing DNA harvested from the blood of affected dogs and their relatives to perform a full genome scan in order to identify a genetic marker for EIC, and to find the genetic mutation causing EIC.  Because of their efforts, the chromosomal locus (site) of the mutation was found on chromosome 9, and the genetic mutation responsible for susceptibility to EIC was identified. This is a mutation in the gene for dynamin-1 (DNM1), a protein expressed only in the brain and spinal cord, where it plays a key role in forming synaptic vesicles containing neurotransmitters. DNM1 is not required during low-level neurological stimulation, but when a heightened stimulus creates a heavy load on release of CNS neurotransmitters (as with intense exercise, a high level of excitement and perhaps increased body temperature), DNM1 is essential for sustained synaptic transmission in the brain and the spinal cord.

EIC is an autosomal recessive syndrome. To be affected, a dog must have received the mutated version of the EIC gene from both parents . Thirty percent of all tested Labrador Retrievers carry the EIC gene. This is not a problem unless a breeder unknowingly breeds one carrier to another carrier and ends up with affected Labrador Retriever puppies. It can take up to 5 years for symptoms to appear, so it is important that breeders test for this gene. It is also important for buyers to educate themselves and learn about this debilitating problem. Ask your breeder if their dogs have been tested and find a breeder who has done so to prevent problems later on in your dog’s life. The most reliable way to be assured that you are buying an EIC Normal pup is to have the EIC test done on the pup, or to verify that the sire and dam have both been tested and are rated EIC NORMAL. Breeding dogs is a serious process. It affects the lives and well being of both the pups and the families that end up with them. Breeders have an inherent responsibility to protect the comfort and well-being of the dogs they produce. Responsible breeders are and have been responding to the challenge of improving the genetic health of our companions through the encouragement of better breeding practices and education of the public.

The best treatment in most dogs consists of avoiding known trigger activities and activities that involve intensive exercise in conjunction with extreme excitement especially in hot weather.  Most dogs that are retired from training/competition or trigger activities live the remainder of their life without any episodes of collapse.  Owners/trainers must always keep in mind the importance of ending exercise at the first sign of weakness/wobbliness if it does occur since these dogs are susceptible to collapse and death from EIC.

 

 

Urethral Obstruction and Perineal Urethrostomy in Cats.

Male cats, especially those that have been neutered, can easily develop obstruction of the urethra because the urethral diameter is so small.  The obstructions are often the result of mucous plugs of inflammatory material, or small crystals, calculi or “stones” that have passed down into the bladder and are now attempting to pass through the urethra.  The exact cause of the inflammatory materials and stone formation it not completely understood, though viral and/or bacterial infections and diet may play a role.

Most affected cats are within 1 to 10 years of age.  Initially cats may show signs of urinary tract inflammation, such as straining to urinate, frequent urination, blood in the urine, painful urination, or inappropriate urination (urinating somewhere other than the litter box).  These bouts usually resolve in 5-7 days but will recur in many cats within 6-12 months.  Once the cats become obstructed, they may attempt to urinate in the litter box or elsewhere but will produce no urine. Many owners may mistakenly believe that the cat is constipated. They may cry, move restlessly, or hide because of discomfort, and eventually will lose their appetites and become lethargic. Other signs of obstruction include depression, weakness, vomiting, and a lack of appetite, dehydration, and collapse. Complete obstruction can cause death of the cat in as little as a few days.  In addition to the above clinical symptoms, a cat with a urethral obstruction will have a large, painful bladder that is easily felt in the back half of the abdomen.

While the precise cause of the urethral obstruction may vary from cat to cat, the exact etiology has not been completely determined. Factors that may play a role in the development include viruses, bacterial infections, stress, strict confinement, genetics and diet. Cats that eat dry diets (and therefore get less water) or diets high in mineral content (magnesium, ammonium, phosphate, calcium), protein, or salt may be at an increased risk for developing urethral obstruction. Uroliths and urethral plugs are composed of variable quantities of matrix and a variety of minerals (including struvite, calcium oxalate, ammonium urate, calcium phosphate, and cystine). Knowledge of nutritional factors associated with the pathophysiology of uroliths and urethral plugs facilitates the modification of diets for the dissolution of several minerals contained within them.
In cats with signs of urinary tract inflammation and/or obstruction, complete blood work is performed to evaluate kidney function and to determine if there is any evidence of infection or other systemic illnesses.  A urinalysis is evaluated for crystal formation and the presence of infection and may be submitted for culture.  Radiography is performed to determine if calculi (stones) or other material are present in the kidneys or bladder. In some cases, contrast enhanced radiography and/or ultrasound evaluation may be indicated to determine if there are any anatomic causes for straining and bloody urination, such as cancer, a bladder wall defect or a stricture of the urethra.

Fortunately, most cats are successfully unblocked. Occasionally a cat is brought in soon after blocking and achieves an excellent urinary stream immediately after unblocking. These cats may be able to proceed without having to spend a few days in the hospital or without having to have the urinary catheter sewn into place. Most blocked cats do not fit into this category but is important to realize that some cats are able to avoid more aggressive treatment. In the majority of cases, after receiving an anesthetic, a urinary catheter is sewn in place and will stay in place for 2-3 days while the cat is hospitalized. Cats that are unable to urinate can have severe abnormalities in their kidney values and electrolyte levels. For these reasons, hospitalized patients receive intravenous fluid therapy to correct the acid-base, electrolyte, and renal abnormalities, as well as receiving pain management, antibiotic therapy and monitoring of the heart for abnormal rhythms. Unfortunately, some patients suffer irreversible kidney damage due to a prolonged obstruction. Often a urinary collection bag is attached to the catheter so that urine production can be measured. Sometimes, the bladder is filled with sterile fluid and flushed out to remove crystals, inflammatory debris, and blood.
If the cat is successfully unblocked, routine post obstructive management includes the administration of medications (antibiotics, pain management), dietary change, and consistent monitoring for signs of straining to urinate, bloody urination, and to be aware of the urine volume being produced and of bladder size, if possible. Because of the amount of stretching that can occur when an animal is completely obstructed, the bladder may be incapable of contracting for some time. Medications can be administered to help this condition once the risk of re-obstructing has decreased. Any loss of appetite or vomiting should be reported to the veterinarian at once. If there is any concern about re-blocking, the veterinarian can determine fairly easily if the cat has re-blocked. It is crucial to realize that the cat is at risk for re-blocking for at least a week or two from the time of discharge. This is because the irritation syndrome that led to blocking in the first place is still continuing and as long as the episode continues, blocking is a possibility.

Cats which have experienced multiple episodes of urethral obstruction requiring hospitalization and catheterization and in those cases where the obstruction cannot be relieved with the passage of a urethral catheter require a surgical procedure called a perineal urethostomy. In this surgery, the distal part of the penis is removed and the more expanded section of the urethra then is opened up and sutured to the surrounding skin to widen the urethral orifice.  A perineal urethrostomy will decrease the likelihood of future obstruction but will not prevent the symptoms of cystitis or lower urinary tract disease that already may be present. The potential complications of surgery include the development of bleeding or swelling at the surgery site (usually transient) and stricture (scarring and narrowing) of the urethrostomy site. This last complication may occur if the cat traumatizes the surgery site or if an incomplete dissection of the urethra to a point proximal enough to provide a wide stoma was not performed appropriately. In addition, urine leakage under the skin because of self induced trauma or an incomplete suture closure may result in bruising, infection, scar formation and stricture. To prevent self induced trauma, an Elizabethan collar is placed on the cat to prevent the cat from licking at the surgical site until the sutures are removed.  If the surgery is performed properly, it is unlikely that the cat will develop subsequent urinary obstructions. Though postoperative urethral strictures and secondary complications may be minimized by proficiency with an effective surgical technique, the removal of the distal urethra may result in recurrent bacterial urinary tract infections in some patients after surgery. Urinary tract infections caused by urease-producing microbes may induce struvite urolith formation. In other words, the surgery does not affect the formation of crystals (which result in the plug to begin with), but provides a wider passageway for their release outside the body. Thus, blockages should not recur, but bladder infections might. Thus, the prophylactic benefits of minimizing recurrent urethral obstruction by urethrostomy must be weighed against a long-term predisposition to recurrent bacterial urinary tract infection and urolith formation. For this reason, perineal urethrostomy should be limited to those patients with a history of multiple obstructive episodes and those in which successful relief of obstruction via passage of a urethral catheter is unsuccessful.

In summary, urethral obstruction is a medical and potential surgical emergency.  If the symptoms are noticed early and professional treatment is obtained immediately, a combination of medical and potential surgical intervention usually results in successful management of the condition and will prevent the subsequent development of life threatening symptoms.

 

Class IV Laser Therapy.

First, I may be a bit particular about terminology as there are many misperceptions and misrepresentations. Due to years of inferior products and exaggerated claims, we must be specific and accurate with our statements. So this is not a discussion of “Light” therapy. This is “Laser” therapy. More specifically, we are talking mainly about “high power Laser therapy”. Although “cold” lasers or “low level lasers” work on the same principles, they often do not have enough power to elicit a measurable or consistent clinical response in deep musculoskeletal conditions. Newer high-powered Class IV therapy lasers were just FDA cleared in the US in 2005. Their use has grown dramatically in the last two years.

The basics: The two key parameters that dictate the function or capability of any Laser are wavelength and power. Laser therapy works by a wavelength-specific form of photobiomodulation. Laser light in the red and near-infrared range is absorbed by specific chromophores in the body (cytochrome C oxidase/hemoglobin/water) and this has a positive effect on specific biological reactions. This photochemical reaction increases blood flow to tissue, stimulates the release of 02 from the hemoglobin delivered, and enhances the conversion of O2 to useful energy by cytochrome C oxidase in the production of ATP. This leads to improved cellular function and/or an increase in cell growth replication, repair, or production of beneficial biochemical compounds – enzymes, proteins, immunoglobulins, DNA/RNA. There are other physiologic responses to Laser light: A mild photothermal effect (with Class IV Lasers only!) helps with vasodilation, muscle relaxation, and nerve conduction. The photo-energetic effect can stimulate acupuncture points, and the photoelectrical effect can affect membrane-bound ion channels as well as induce changes in the intracellular and extracellular ion gradients. The clinical results of these cellular reactions are:

-Accelerated tissue repair and growth
-Faster wound healing
-Analgesia
-Decreased inflammation
-Angiogenesis
-Vasodilation
-Improved lympathic drainage
-Improved nerve function, axonal regeneration, neurologic repair
-Decreased fibrosis
-Immunoregulation/Immunomodulation
-Acupuncture stimulation
-Trigger Point modulation

Laser power is the rate at which the Laser energy is delivered. Although seemingly straightforward, the power question seems to raise the most discussion regarding appropriate parameters. The physics associated with laser penetration within non-pigmented tissue is well established and quantified by the rate of decay of an incident beam as it moves through tissue. It can be approximated by the “optical penetration” depth of a given wavelength – the distance into tissue to which photons of that wavelength will travel where the incident beam is decreased by 63%. The power argument is almost exclusively associated with therapeutic Lasers; all other types—surgical, aesthetic, dental, and industrial –follow the basic science and physics when determining proper power guidelines for use.

Classification of all Lasers is dictated by the FDA, based on the maximum power the Laser can deliver. It is used for guidance when discussing safety and the potential to cause harm/damage, especially to the eye. Most therapeutic lasers are class IIIa, IIIb, or IV. Class IIIb lasers produce

<500 mW of power ( ½ watt). Class IV Lasers are anything over 500mW of power. Class IV therapy Lasers are extremely safe. The main benefit of higher power is the ability to deliver enough photons at the surface (a larger total dose) to compensate for the power loss (decreased number of photons) reaching deeper tissues. This allows for a more direct photochemical response on these tissues. That is why there is a much more dramatic and consistent response to class IV Laser therapy vs. class III Lasers or LEDs (Light Emmitting Diodes). Lower dosages are used when treating superficial wounds/lesions and for acupuncture point or trigger point stimulation. Adjustable power output can make a Class IV Laser effective for superficial dermatologic lesions, deep musculoskeletal conditions…and anywhere in between!

Laser therapy has broad clinical applications for pain management, wound healing, reducing inflammation/swelling/edema, and rehab in both large and small animals. Measurable positive results can be seen consistently in the following conditions:

-Arthritis/DJD (Hip dysplasia)
-Muscle, ligament, and tendon injuries (Sprains, strains, and tears)
-Ulcerations and open wounds (Lick granulomas, Hot Spots, Abscesses)
-Acute and Chronic Ear Problems
-Post Surgical pain/healing/rehab
-Trauma/Fractures
-Neck and Back Pain (Acute and chronic)
-Neuromuscular disease/damage/degeneration
-Even some respirator, urinary, and GI conditions.

Notwithstanding years of research on the bio-stimulatory effects of Laser light, we are just starting to realize all the clinical applications. Exciting new possibilities include help with OCD (osteochondrosis desicans), chronic rhinitis/bronchitis, insect/snake bites, allergic reactions, chronic intestinal or urinary tract inflammation, bacterial/viral infections, and adjunct therapy to improve stem cell results and even potentially for the control/palliation of some tumors. There is optimism for neurologic trauma including concussions, brain ischemia and stroke, peripheral nerve damage, IVDD, and stenosis.

It’s worth emphasizing that Laser therapy does not just accelerate healing; it actually improves repair, regeneration and remodeling of tissue. Post-op complications are reduced. Muscle atrophy can be reversed. Type 1 collagen production yields better tendon and ligament strength and elasticity. There is a positive effect on neurologic function and axonal sprouting. The joint capsule, synovial lining/fluid, and cartilage all benefit. Therefore ROM, function, flexibility and mobility are all enhanced. The potential for re-injury is greatly reduced. Performance animals not only recover quicker but they can regain their competitive edge. Pets can get back to their daily routines and become an active member of the family again. These are exciting times. Like all technology, Lasers have become smaller, safer, more efficient and easier to use. Their broad range of applications makes them not just affordable but profitable –especially when treatments are delegated to the support staff. It’s no wonder that therapeutic Lasers are rapidly becoming an indispensable tool in our clinic.
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Before Laser Therapy
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One Week After Laser Therapy

The Indications for Medical and Surgical Management of Splenic Disease.

The spleen is a relatively large organ with wide-ranging and various functions.  In general, the spleen is tongue shaped, has a mottled reddish brown color and occupies the left cranial quadrant of the abdomen.  While the spleen is not essential for life, its contributions to maintaining bodily homeostasis are beginning to be better understood as research has begun to shed more light upon the pathophysiology of other disease processes which may affect splenic function.  The four basic tenets of splenic function include erythrocyte conditioning and maintenance, erythrocyte and platelet storage, extramedullary hematopoiesis, and plasma filtration for the presence of antigens.  Thus, removing the spleen should not be considered as a procedure without consequence. 

As an organ of erythrocyte maintenance, the spleen processes the final stages of erythrocyte maturation, detects and removes abnormal intracellular particulate matter during the process of pitting, and helps cull aged erythrocytes out of circulation.  Newly developed immature erythrocytes spend several days in the spleen where remaining intracellular material is removed, the cell membrane is reshaped into the typical disc, and the cell is reduced in size before joining the circulating blood pool.  During the process of pitting the macrophages detect and remove abnormal intracellular materials.  The pitted materials removed include but are not limited to intracellular parasites, remnants of nuclear material (Howell-Jolly bodies), denatured hemoglobin (Heintz bodies), and other types of intracellular debris.  The relatively large population of erythrocytes and leukocytes circulating within the spleen creates an anaerobic environment; this relatively anaerobic environment results in the cell membrane of damaged, abnormal and older erythrocytes to become less pliable.  These cells become too stiff and are therefore unable to undergo the deformation required to pass into the splenic sinuses.  Macrophages then cull these cells out of circulation to recycle the iron back to the bone marrow. 

While the reservoir capacity of the spleen for erythrocytes may vary from one species to the next, the canine and feline spleen have a large storage capacity estimated to fall between 10 to 20% of the circulating red blood cell mass.  In addition, the spleen can store up to 30% of the entire platelet mass.  Within the spleen there are three pools in which the red blood cells circulate.  The majority (~90%) of the circulating blood enters the rapid pool and traverses through the organ in about 30 seconds.  Approximately 9% of the red blood cells enters the intermediate pool and circulates through within eight minutes.  The remaining 1% traverses through the slow pool, which can take nearly an hour to complete its circulation through the spleen.  Under conditions of stress, hypoxemia, heavy exercise and excessive blood loss, up to 98% of the blood volume is shifted to the rapid pool through splenic contraction to significantly increase the blood volume.

During fetal development, the spleen functions as an organ of hematopoiesis.  Normally, these hematopoietic abilities cease at birth as the bone marrow assumes this role.  A limited capacity for hematopoiesis, however, is preserved in the adult animal.  While splenic extramedullary hematopoiesis is uncommon in the cat, in dogs splenic hematopoiesis can occur with any one of a number of disease processes in which the numbers of erythrocytes become compromised.  These processes include infiltrative myeloproliferative diseases, immune-mediated hemolysis, chronic inflammatory conditions, infectious diseases and malignant disease processes. 

As an organ of filtration the spleen is the single largest reticuloendothelial system in the body.  It plays a major role in filtering and clearing blood borne microorganisms as well as initiating an immunologic response to offensive circulating antigens.  In addition to phagocytosis and IgM production, other mediators of immunity are synthesized which enhance both neutrophilic phagocytosis and the activation of the complement pathway. While both the liver and spleen filter microorganisms, the splenic filtration is more effective in removing poorly opsonized bacteria. 

The processes that lead to splenic enlargement (splenomegaly) are varied. Splenic enlargement may be diffuse and generalized encompassing the whole spleen, or localized involving only portions of the spleen at one time.  It should be mentioned, however, that the mere presence of splenomegaly does not necessarily result from disease processes which require medical intervention.  Several different mechanisms which affect the splenic parenchyma may result in generalized splenomegaly.  These mechanisms include inflammation, cellular hyperplasia, congestive enlargement, or cellular infiltration.  The process which leads to inflammatory splenomegaly depends on the type of cells predominantly found in the enlarged spleen. Infectious splenitis is commonly associated with neutrophilia secondary to bacterial infections from various sources including but not limited to penetrating abdominal wounds, migrating foreign bodies, and by hematogenous means.  Protozoal, viral, and mycotic infectious organisms can also lead to infiltrations with various other inflammatory cells. As part of the reticuloendothelial system, the spleen may become hypertrophic and/or hyperplastic in response to blood-borne antigens, or through the destruction of erythrocytes.  This is the result of an increase in the lymphoreticular populations.  Common subacute and chronic disease processes which lead to hyperplastic splenomegaly include immune-mediated hemolytic anemia, immune-medicated thrombocytopenia, drug induced hemolytic anemia and hemobartonellosis.

Generalized splenomegaly can also be caused by various vascular changes which occur through both normal and abnormal physiological conditions.  Vascular distention secondary to smooth muscle cell relaxation in the splenic capsule is associated with certain sedatives and can lead to pooling of as much as 30% of the circulating blood volume. Congestion of the spleen is a common consequence of vascular outflow obstruction as seen in cases of torsion of the splenic vascular pedicle and in splenic and portal vein thrombosis.  Regardless, any pathologic process which lead to portal vein/caudal vena cava hypertension and any lesion which restricts venous blood flow away from the spleen will lead to generalized splenomegaly. 

Infiltration of the spleen by nonsplenic cells may also lead to generalized splenomegaly.  Extramedullary hematopoesis in the spleen commonly occurs when a pathologic process undermines the ability of the bone marrow to function normally or through any other various stimuli which requires the body to increase the red blood cell population.  Neoplastic cells of various lineages may infiltrate the spleen as either a primary tumor or as a metastatic disease.  Common neoplastic processes which typically produce generalized splenomegaly include myeloproliferative disease, lymphosarcoma, and mastocytosis.  In the cat, mastocytoma and lymphosarcoma are the most commonly observed neoplastic processes of the spleen. 

In contrast to generalized splenomegaly, localized splenic enlargement is a much more common occurrence in dogs than in cats.  In dogs, 51% of localized lesions are classified as non-neoplastic, whereas 48% are neoplastic.  While non-neoplastic masses are slightly more common than neoplastic masses, they are indistinguishable at the time of surgery.  As observed with any other neoplastic process, splenic neoplastic masses can be either benign or malignant and primary or metastatic.  The most commonly seen non-neoplastic splenic masses are hematomas and nodular hyperplasia.  Other causes of non-neoplastic causes of a splenic mass include abscesses, cysts and infarctions, but these lesions are very uncommon. 

Although splenic hematoma and nodular hyperplasia are categorized as separate entities, recent histopathologic evaluation of the two masses suggests that they are linked and represent a continuum.  A high percentage of non-neoplastic lesions contain elements compatible with both diagnoses.  Hyperplastic nodules in the spleen are composed of various cellular components including lymphoid, hematopoietic, and plasmacytic cell populations, whereas the splenic hematoma consists of hemorrhage, organizing fibrin, and degenerative erythrocytes.  The failure of marginal zone circulation secondary to nodular hyperplasia results in an accumulation of blood within the hyperplastic nodule, and may eventually lead to hematoma formation. 

The most commonly observed neoplastic lesion in the dog is hemangiosarcoma.  This malignant disease process carries a poor long term prognosis. Metastasis at the time of surgery is present in as many as 65% of the dogs.  Many other histologic types of cancer constitute the remaining canine splenic neoplasms, including leiomyosarcoma, undifferentiated sarcomas, fibrosarcoma, osteosarcoma, liposarcoma, myxosarcoma, chondrosarcoma, rhabdomyosarcoma, and malignant fibrous histiocytoma.  Cats develop different types of splenic tumors; lymphosarcoma, mast cell tumor, and myeloproliferative diseases accounted for 30% of neoplastic diagnoses, whereas hemangiosarcoma accounted for only 3%. 

The diagnostic evaluation of animals with suspected splenic disease begins with routine abdominal radiography.  The spleen is normally well visualized on plain abdominal radiographs, but there is a wide variation in its appearance.  On the ventrodorsal view the spleen is normally a triangular structure on the left side of the abdomen between the gastric fundus and the left kidney.  The size and location of the spleen are more variable on the lateral view; however, in general it has a triangular, oval, or rounded appearance and is caudal to the liver.  Radiographic splenomegaly can be secondary to generalized splenic enlargement or to a localized mass.  Splenic masses are the primary differential diagnosis for mid-abdominal masses in dogs and cats, however, other considerations are masses associated with the liver, intestinal tract, mesentery, adrenal glands, mesenteric lymph nodes, kidneys, or reproductive structures.  Ultrasonography constitutes the noninvasive procedure of choice to evaluate splenomegaly and to characterize the lesion and potential causes of splenic enlargement.  Abdominal ultrasonography can reveal diffuse splenomegaly, localized splenic masses, splenic congestion, and evaluate the abdomen for metastatic disease.  Color-flow Doppler ultrasound can detect vascular compromise with torsion of the splenic pedicle or portal vein congestion, as well as congestion secondary to cardiac or liver disease. Percutaneous sampling of the spleen is possible by fine needle aspiration with a low risk of significant complications.  Abdominal ultrasound can be used to guide the aspiration if the localized splenomegaly is not easily palpated.  Cytologic evaluation can be used to determine the need for surgery, further diagnostics, or therapy.  Although the ultrasound represents a major advance in evaluation of the spleen, it is not infallible. In some situations, the extent of the lesion or adhesions between the diseased spleen and adjacent organs can limit the diagnostic accuracy of ultrasonagraphy.  Both computed tomography and magnetic resonance imaging are useful for the evaluation of splenomegaly and concurrent underlying disease processes. Neither modality is commonly used in the diagnosis of splenic disorders because of the time and financial commitments involved in utilizing either one. 

The majority of the clinical signs of dogs and cats associated with disorders of the spleen are related to the underlying disease process.  These clinical signs may be vague and nonspecific and include anorexia, weight loss, abdominal discomfort and/or distention, vomiting, weakness/collapse and polyuria/polydipsia (PU/PD).  PU/PD is relatively common in dogs with marked splenomegaly, particularly in those with splenic torsions.  The mechanisms of PU/PD are not well understood, however, clinical signs usually resolve after splenectomy.

The most common splenic conditions which require surgical intervention include splenic laceration/trauma, torsion and the removal of splenic masses.  Splenic torsions occur most commonly in large/giant breed dogs with a deep chested confirmation.  The spleen rotates around its vascular pedicle and results in venous obstruction and eventually splenomegaly.  It is a condition commonly associated with gastric dilation-volvulus syndrome; however, it can occur as an isolated condition as well.  Splenic torsion can present either as an acute or a chronic condition.  Dogs experiencing the acute condition can exhibit significant abdominal pain and discomfort, excessive salivation and signs of cardiovascular failure which can lead to shock and collapse within several hours.  Patients experiencing the more chronic condition may present with non-specific signs of vomiting, anorexia, intermittent abdominal pain, abdominal distension, weight loss, and polyuria and polydipsia.  In general, laboratory findings usually do not contribute tremendously to the diagnosis. Packed cell volume may be in the low to normal range and concurrent thrombocytopenia may be present.  In addition, leukocytosis with neutrophilia may be present.  Anemia may be secondary to red blood cell destruction or splenic sequestration, whereas thrombocytopenia may be secondary to platelet sequestration or associated with the development of disseminated intravascular coagulopathy.  Hemoglobinuria is a common finding and pale mucous membranes are observed with both acute and chronic splenic torsions.  Regardless of the duration of the splenic torsion, surgical removal of the spleen is indicated. 

Substantial splenic trauma must be considered as a differential diagnosis for animals with hemoabdomen and a history of either blunt or penetrating abdominal injuries. While blunt abdominal trauma is thought to be the most common cause of splenic trauma, lacerations of the spleen can occur but with less frequency relative to blunt force. Whereas hemorrhage secondary to lacerations and blunt parenchymal lesions is not a major cause of morbidity in dogs and cats, trauma or lacerations involving the major splenic arteries and veins can be fatal, especially in the absence of medical support and surgical intervention.  The true impact of splenic hemorrhage secondary to laceration or blunt trauma remains to be seen and is underappreciated because a large portion of dogs and cats receiving fatal abdominal trauma may not present to a veterinary facility in a timely manner.  The presenting signs and laboratory and radiographic findings depend on the rate and amount of blood loss before presentation as well as the presence of concomitant injuries.  Supportive medical treatment including intravenous fluid administration, abdominal compression bandaging, and serial monitoring of the animal’s packed cell volume and circulatory status is the first line of stabilization.  Failing parameters are further treated by transfusion of appropriate blood products, and surgical intervention is considered when appropriate medical therapy fails to sustain stability of the patient.

The approach to treating splenic masses is based on clinical signs, the patient’s immediate medical condition, and the presence or absence of definable metastatic lesions on either thoracic and abdominal radiography and/or ultrasonagraphy. Echocardiography (ultrasound of the heart) is often recommended as up to 15% of dogs with malignant hemangiosarcoma may have tumor spread to the right atrium on initial presentation.  An ECG to look for arrhythmias may also be required especially after surgery.  Up to 24% of dogs with splenic hemangiosarcoma have arrhythmias and these may not be noted until after surgery.  While this may require treatment, most resolve within 24-48 hours. As mentioned previously, a dog with a splenic mass may display a variety of clinical symptoms which depends upon the underlying nature of the mass. Most dogs present initially with acute signs associated with tumor rupture and bleeding into the abdominal cavity.  If the mass is neoplastic, the patient can exhibit more systemic signs because of cachexic changes which can accompany malignancy. Regardless, if the mass is actively bleeding, the patient is considered an immediate surgical candidate as splenic removal is the only way to prevent continued intra-abdominal hemorrhage. Common clinical signs observed include decreased appetite or anorexia, weight loss, vomiting, abdominal distention with or without a fluid wave, abdominal discomfort, cardiac arrhythmias, pale mucous membranes, lethargy, and a palpable mass in 30-62 % of dogs. Whereas some factors, such as anorexia and hemoperitoneum are significantly more common in dogs with hemangiosarcoma, one third of all dogs with hemoabdomen have a benign hematoma; therefore, the presence of internal abdominal bleeding is not necessarily diagnostic of malignant cancer. Complete splenectomy is currently recommended for splenic masses.  A careful and complete abdominal exploratory is indicated to identify any possible metastatic lesions.  Metastasis of splenic tumors to the liver is common, and suspicious liver lesions should be sampled, and if possible, removed.  However, benign liver lesions such as extramedullary hematopoiesis and nodular hyperplasia are also common in dogs with splenic tumors and the surgeon must avoid the temptation to prematurely label a hepatic lesion as metastatic and therefore indicative of a malignant process. Basing immediate therapeutic actions on the presence of gross hepatic lesions can therefore result in an inappropriate diagnosis and prematurely lead to dogs being humanely euthanized when in fact they may have an excellent prognosis. Because more than 50% of splenic masses are benign, complete histopathologic evaluation and confirmation of a malignant process should precede a recommendation for euthanasia.  As the abdominal cavity is the main site of tumor recurrence, most dogs with malignant splenic cancer will die or be euthanized due to complications associated with progressive tumor growth within the abdominal cavity. Current standard treatment for dogs with hemangiosarcoma is surgery and systemic (intravenous) doxorubicin-based chemotherapy. Despite the most effective available treatments for this disease, most dogs will succumb to their tumor, and the average survival is approximately 6 months to one year. Other potential sites of metastasis can include the mesenteric, gastric, sternal and tracheobronchial lymph nodes as well as the prostate, diaphragm, lung, kidney, bladder, bone marrow, and intestines. 

In summary, while many general practitioners will visualize a mass effect involving the spleen and inform the client that their pet has a malignancy requiring euthanasia because of a poor prognosis, the truth is that this statement is accurate in only approximately 50% of the cases. As with any other organ the spleen is susceptible to the development of both benign and malignant disease processes. For this reason, many pets are inappropriately euthanized when in fact they may have a good to excellent prognosis with surgical removal of the affected spleen. As mentioned previously, regardless of histological origin both benign and malignant tumors can rupture without warning, and consequently lead to profuse blood loss, hypovolemia and eventual death. From a client’s perspective, one should understand that while the spleen functions to help maintain homeostasis of various bodily systems it is not necessary for survival. Depending on the stage of the pathologic state present, the splenic problem may or may not be life threatening without urgent care.  Appropriately staged diagnostic, medical and surgical intervention with or without adjunctive follow-up therapy may allow many pets the opportunity to achieve additional quality longevity free from pain or discomfort or to be completely cured.
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Intraoperative view of ruptured spleen

The Danger of Veterinary Internet Pharmacies.

Today there are many options for consumers to purchase veterinary medications. In the past, the veterinarian supplied prescriptive and non-prescriptive drugs and medications directly to the client. The rise of internet pharmacies has given the client the ability to buy medications indirectly through a third party. The advantage to the consumer has been better pricing and the convenience of home delivery, rather than having to visit their veterinarian’s office to fill or refill prescriptions. The disadvantages, mostly unknown to the consumer, includes but is not limited to a significant percentage of these online medications being counterfeit, near or exceeding their expiration dates, and they may very well not have been stored properly therefore significantly reducing their effectiveness, if not rendering them totally ineffective and/or endangering their pet. The reason for this is that the online pet pharmacies are not legally permitted to buy their supplies directly from veterinary pharmaceutical companies. They have to rely upon diverted merchandise from veterinary practitioners for the merchandise that they will then turn around and sell to pet owners. It is not illegal for veterinarians to sell their supplies to these companies, however, it is violating their contracts with the veterinary pharmaceutical companies to sell their drugs to these online pharmacies. The veterinary pharmacies do their best to police the situation, but it is obviously difficult to determine which veterinarians are violating their contracts by diverting drugs and supplies. When they succeed in determining when drugs are being diverted, that veterinary practice loses its ability to purchase products from that particular pharmaceutical company. Because these online pharmacies are dependent upon veterinarians diverting products, the quality and origin of these products has to be questioned.  If you are the type of veterinarian who needs to divert products in violation of your contract with the pharmaceutical companies in order to make a quick buck, then what type of reputable person are you? Would you try to make even more money by diverting poorly stored inventory? Would you knowingly divert counterfeit drugs? Is your ability to practice veterinary medicine that poor that you have to resort to being a middle-man to divert medications to generate a profit? Unfortunately, the answer to these questions is yes. At least twice monthly I receive offers from online veterinary pharmacies to start a new business relationship that they say is 100% legal and risk free. They tell me that this opportunity is a simple, no-risk profitable exercise. All I need to do is make one or two phone calls and they will take care of the rest. And it will be done totally confidentially. Really? This is the way legitimate companies operate? By the way, most of these companies are based in Florida; it’s not a coincidence. It’s a lot easier to distribute counterfeit medications arriving from the Caribbean when you’re that close to the source.

One of the main reasons why the veterinary pharmaceutical companies want their drugs distributed by a veterinarian and not a third party is to ensure that a proper veterinary-patient relationship is intact so that their products are not misused and/or prescribed inappropriately. In addition, quality control is maintained as the veterinarian is much more likely to store the medications properly and turn over their inventory on a regular basis to avoid buying in bulk and prescribing expired or soon to be expired medications. Maintaining distribution of an effective, quality product is not only important for your pet, it is important for the reputation of the company for its products to be seen as safe and effective when utilized in a proper manner. It is not about maintaining higher prices for their products. Most if not all veterinarians today will price match medications for their clients so that their clientele can purchase their pet’s medications at a more reasonable cost, all the while being assured that the drugs freshness or effectiveness has not been compromised and guaranteeing that the drug is not counterfeit. These are not trivial concerns. When it comes to purchasing veterinary drugs online, buyers should beware, says a top official from the Food and Drug Administration’s (FDA) Center for Veterinary Medicine. In fact, in a recently issued consumer alert, Dr. Martine Hartogensis, director of the FDA’s Office of Surveillance and Compliance, says that while some websites selling veterinary drugs represent legitimate businesses, others do not. In fact, FDA regulators have documented unscrupulous practices relating to the sale of unapproved and counterfeit pet drugs, dispensing of Rx drugs without a prescription and sale of expired drugs. Even the so-called legitimate businesses deal primarily in diverted products. And while the risk is present for consumers purchasing bogus, unapproved products through foreign and domestic pharmacies, “CVM is especially concerned that pet owners are going online to buy two types of commonly used prescription veterinary drugs—non-steroidal anti-inflammatory (NSAIDs) drugs and heartworm preventives.” Both drugs can be dangerous if given without involvement by veterinarians, Hartogensis reports.

If you’ve ever searched online for prescription pet medicines, you’ve no doubt seen eye-catching, attention-grabbing claims. They sound convincing in their promises of convenience and lower prices. But are these claims really true? Internet sites that sell pet drugs can be reputable pharmacies. However, others are fronts for businesses breaking Federal, State, and sometimes, International laws. Illegal online pharmacies may sell medicines that are counterfeit, outdated, mislabeled, incorrectly formulated, or improperly made or stored. These medicines may not contain the actual drug, or the correct amount of drug, may contain contaminants, may not work as well due to age or being stored in conditions that were too hot, cold, or humid, and may not have the proper directions for use. If you are unhappy with ordered products, in the end, you may find buying prescription pet medicines online more costly to your pet’s health and your wallet. If you find a cheaper medicine online, ask your veterinarian to consider matching the price. If the prices offered are dramatically different than the competition, the drug is most likely of dubious quality or origin. As mentioned previously, many veterinarians are willing to competitively charge based on the online price you’ve found (and can show proof of). You should also know that neither the drug maker nor your veterinarian will stand behind a product’s guarantee if you purchase the product online.

Counterfeit drugs are fake or copycat products that can be difficult to identify. The deliberate and fraudulent practice of counterfeiting can apply to both brand name and generic products, where the identity of the source is often mislabeled in a way that suggests it is the authentic approved product. Counterfeit drugs may be contaminated, not help the condition or disease the medicine is intended to treat, lead to dangerous side effects, contain the wrong active ingredient, be made with the wrong amounts of ingredients, contain no active ingredients at all or contain too much of an active ingredient, and/or be packaged in phony packaging that looks legitimate. Using medicine that contains an active ingredient that wasn’t prescribed may be harmful. The FDA continues to proactively protect consumers from counterfeit drugs. The agency is working with drug manufacturers, wholesalers, and retailers to identify and prevent counterfeit drugs. The FDA also is exploring the use of modern technologies and other measures that will make it more difficult for counterfeit drugs to get mixed up with, or deliberately substituted for, safe and effective medicines.

While online pharmacies can be an inexpensive and convenient alternative to purchasing these drugs through a veterinary office, pet pharmacies are not regulated the same way human pharmacies are. If the FDA and the DEA have trouble keeping human pharmacies on the level, what do you think the level of control aimed at online veterinary pharmacies is? These online outlets know that the legal ramifications of your pet’s drug reactions can’t touch companies of their size. As long as counterfeits and questionable expiration dates abound in the online pet drug marketplace, its buyer beware all the way.

Veterinarians and online pharmacies have had a rocky relationship from the start.
When online pharmacies first started selling medicines, many vets were worried that their already slim profit margins (even though vet care is expensive, most of what you pay your vet ends up going to his suppliers, his landlord, his employees, utility companies, the IRS, and regulatory agencies) would be reduced by the loss of income-generating drug sales. This concern has not panned out as expected. Well-managed veterinary hospitals do not derive much income from drug sales. In the hospitals where I have worked (and owned), medications were offered to clients more for their convenience than for our profit. And this makes sense. A veterinarian’s job is to manage the health of pets, not to sell drugs. So why is there a lingering animosity between vets and online pharmacies? Probably because some of my patients have received an expired or ineffective medicine from an online pharmacy, and I’m sure I’m not alone. My conversations with representatives from drug manufacturing companies assure me that this occurs on a relatively frequent basis. They also claim that some online pharmacies unwittingly distribute counterfeit medications that have no efficacy. In my opinion, if you order from a reputable online pharmacy the odds of receiving expired or counterfeit medicines are low, however, it does indeed occur on a regular basis.

In addition, working with online pharmacies can be very frustrating for a veterinarian. For instance, one internet pharmacy habitually refuses to write instructions on the drugs it dispenses. If a veterinarian sends a prescription to the pharmacy and indicates that the medicine should be taken twice daily, they will dispense the medicine with instructions to “take as instructed by veterinarian”. In the best case, this wastes the veterinarian’s time, as clients will call to ask how often the medicine should be given, when the information has already been provided to the pharmacy. In the worst case, it puts the patient at risk of being either over or under dosed. Another pharmacy routinely sends faxes to my office requesting authorization for prescriptions. I promptly fax back authorizations (after offering the client the opportunity to purchase the medication for the same price with the guarantee that it’s not counterfeit, diverted, etc). The next day, I often receive faxes from the pharmacy, written in a somewhat threatening tone, stating that they have not received my authorization. This confusion on the part of the pharmacy is very annoying, and it also causes me to lose confidence in their business in general. If they can’t manage their fax system, how can I expect them to dispense drugs accurately?

In summary, many pet owners are seeking lower prices for medications needed by their pets through the use of online pet pharmacies. The best way to assure yourself that the medication you purchase is safe, has been stored properly, is genuine and has not been diverted is to purchase the medication directly from your veterinarian. The products we sell on our veterinary website meet all of these criteria and are competitively priced for our clients, eliminating the need for them to search out and be scammed by the less than legitimate online pharmacies that are currently operating.

 

Gastric Dilation-Volvulus Syndrome.

Acute gastric dilatation with or without volvulus is a life-threatening condition that is classically described in large or giant breed dogs with deep chests and appears to occur more frequently in older animals. The highest incidence appears to occur in the Great Dane, Bloodhound, Irish Wolfhound, Akita, Standard Poodle, Weimaraner, Saint Bernard, Gordon Setter, and Irish Setter. Although there has been much debate whether dilatation or volvulus occurs first in the gastric dilatation volvulus (GDV) syndrome, it is plausible that either may occur primarily, as isolated cases of both conditions occur. Regardless of the sequence of events, once gastric distention and mal-positioning occurs, the compression of low-pressure (venous) intra-abdominal vasculature leads to cardiovascular, respiratory, and gastrointestinal compromise. Impaired perfusion causes secondary compromise of multiple organs. Elements of individual treatment regimes remain controversial, however, treatment strategies shown to yield the most successful outcomes combine aggressive emergency medical diagnostics and therapeutics with early surgical intervention and intensive postoperative critical care management.

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While rapid, significant gastric distention with gas and the ensuing cardio-respiratory dysfunction lead to the typical acute clinical picture, some dogs may have chronic, subtle gastrointestinal dysfunction. Multiple contributing factors have been identified and influence incidence within a genetically susceptible population. Although small dogs and cats can develop GDV, it is predominantly a syndrome of the large and giant breed dogs. Furthermore, having a first-degree relative with a history of GDV has been found to be a significant risk factor. It has been hypothesized that genetic predisposition to GDV may occur through inheritance of conformation, personality, or temperament that predisposes to the condition. An association between GDV and inflammatory bowel disease has been suggested, but the relationship is unclear. Anatomic studies have shown a correlation between increased thoracic depth-to-width ratio and incidence of GDV within certain breeds. It has been speculated that this conformation may inhibit eructation. Failure of normal eructation and pyloric outflow mechanisms may be a prerequisite for gastric dilatation. Stretching of gastric ligaments, as may occur with previous dilatation, the presence of an intra-abdominal mass or splenic torsion may facilitate development of the condition.

While still a matter of debate, dilatation likely precedes volvulus. Dilatation develops secondary to the accumulation of gas or fluid within the stomach, the outflow from which is obstructed. Obstruction may be caused by neoplasia, pyloric stenosis, the presence of a foreign body, or compression of the duodenum against the body wall by the rapidly expanding stomach. Prolonged gastric emptying, chronic dilatation secondary to pyloric dysfunction, and hypotonic gastric and pyloric musculature associated with the ingestion of large meals at protracted intervals have been incriminated in the pathogenesis of GDV, however, there is a lack of evidence for gastric emptying disorders in dogs that develop GDV. Overeating, postprandial exercise, and food type have all been incriminated as causes of GDV, but there remains a lack of evidence to support these assumptions. One study documented that an episode of stress occurred more frequently during the period immediately before development of a GDV than in a comparable disease-free population. The propensity to be influenced by a stressful event may be related to the personality of a given individual.

Distention of the stomach by gas may be associated with aerophagia, diffusion from the bloodstream, release of carbon dioxide after the reaction of hydrochloric acid and bicarbonate, or bacterial fermentation. Viewed from a caudal to cranial direction, the stomach rotates 90-360° in a clockwise fashion about the distal esophagus. The pylorus is displaced to the left of the midline, the duodenum becomes entrapped between the distal esophagus and the stomach, and the spleen may vary in position from left posterodorsal to right anterodorsal (depending on the extent of volvulus). If the volvulus is >180°, the distal esophagus becomes occluded. Gastric distention and displacement directly affect the cardiovascular, respiratory, and gastrointestinal systems. Secondary effects on these and other systems (i.e., metabolic, hemolymphatic, renal, and central nervous systems) ensue. Hypovolemic and endotoxic shock are the life threatening abnormalities in dogs with GDV, and an understanding of the cause of this state allows rational treatment. Severe gastric distention results in compression of the intraabdominal veins (caudal vena cava, portal vein, and splanchnic vasculature). This venous occlusion results in decreased venous return and increased venous pressure (splanchnic pooling and portal hypertension). The combination diminishes cardiac output and systemic blood pressure. The collateral circulation is unable to handle the venous return, leading to interstitial edema and loss of intravascular volume, which further contribute to poor perfusion of major organs. In addition, gastric distention prevents caudal displacement of the diaphragm and therefore impedes normal respiratory excursion. To compensate, respiratory rate and effort may increase. These efforts may become inadequate and eventually respiratory acidosis, due to impaired carbon dioxide clearance, might contribute further to the metabolic acidosis that exists secondary to poor tissue perfusion (lactic acidosis). Aspiration pneumonia may further exacerbate this respiratory compromise. The increased intraluminal gastric pressures impair flow through the gastric wall vasculature and this, combined with poor cardiac output, may lead to gastric necrosis. Avulsion, thrombosis, and stretching of the short gastric arteries are common and may further contribute to diminished perfusion of the stomach. Mucosal hemorrhage and necrosis are common. Susceptibility of the mucosa to damage by hypo-perfusion may be exacerbated by the acidic environment of the gastric lumen and high metabolic demands. Decreased gastric perfusion results in serosal hemorrhage and edema of the stomach wall, which begins in the fundus and spreads to the body of the stomach. Bacterial translocation from the stomach or other portions of the poorly perfused intestinal tract may lead to septicemia. Severe compromise to the gastric wall results in necrosis and perforation, with resultant peritonitis.

Cardiac arrhythmias, mainly ventricular in origin, occur in approximately 40-75% of patients with GDV. Several factors have been implicated in the cause of cardiac arrhythmias. Coronary blood flow in experimentally induced GDV is decreased by 50%. Histologic lesions compatible with myocardial ischemia are seen in both experimental and spontaneous GDV and may establish ectopic foci of electrical activity. Circulating cardiostimulatory substances such as epinephrine and cardioinhibitory substances such as myocardial depressant factor have also been implicated in the generation of arrhythmias. Acid-base and electrolyte imbalances are not seen consistently in dogs with GDV. Cellular hypoxia caused by systemic hypoperfusion may result in an increased production of lactic acid by anaerobic energy production, resulting in a metabolic acidosis. Blood pH may be normalized by a concurrent metabolic alkalosis caused by sequestration of hydrogen and chloride ions in the stomach lumen (causing a mixed acid-base disorder). Several pathophysiologic events may promote the development of hypokalemia, including the administration of a large volume of low-potassium fluids, sequestration of potassium within the stomach or loss through vomiting or lavage, hyperchloremic metabolic alkalosis with transcellular shifting, activation of renin-angiotensin-aldosterone system, and catecholamine-induced shifting of potassium into cells. Blood glucose levels may also fall in the later stages of shock as energy demands cannot be met by the inefficient production of adenosine tri-phosphate through anaerobic metabolism. Infarction of splenic arteries and thrombosis of splenic veins may occur, resulting in splenic necrosis. Disseminated intravascular coagulation (DIC) is seen frequently in dogs with GDV. Contributing factors include pooling of blood in the caudal vena cava, portal vein, or splanchnic circulation, tissue hypoxia, acidosis, endotoxemia, and sepsis.

Clinical signs may include an acute onset of restlessness, apparent discomfort, abdominal pain, repeated unproductive retching, excessive salivation, and abdominal distention. The abnormalities present on physical examination are manifestations of the circulatory and respiratory compromise that results from acute gastric distention and displacement. Dogs often present in cardiovascular and hypovolemic shock with depressed mentation, rapid and weak arterial pulses, cool extremities, pale mucous membranes, and prolonged capillary refill time. Tachypnea or dyspnea, or both, may reflect both discomfort and a reduction in tidal volume due to gastric distention. The abdomen can vary from unremarkable on palpation, to distended and firm, to tympanic. An irregular heart rate and associated pulse deficits may indicate the presence of cardiac arrhythmias. Decrease in venous return, cardiac output, and arterial blood pressure, as well as hypovolemic shock, are caused by compression of the caudal vena cava; sequestration of blood in dilated splanchnic, renal, and posterior muscular capillary beds; loss of fluid into the obstructed stomach; and a lack of water intake. Endotoxemia, hypoxemia, metabolic acidosis, and hypotension predispose to disseminated intravascular coagulation.

Diagnostic abdominal radiography is used to differentiate simple gastric dilatation from dilatation with volvulus and to rule out other medical conditions. The right lateral recumbent view is the view of choice. If possible, a dorsoventral view may also be taken to help delineate gastric position. Ventrodorsal positioning may lead to further cardiovascular compromise and may predispose to aspiration pneumonia should the patient regurgitate or vomit. The pylorus in a dog with GDV moves cranial to and is separated by soft-tissue opacity from the body of the stomach in the lateral projection and to the left of midline on the dorsoventral view. In comparison, the pylorus lies ventral to the fundus and to the right of midline in a dog without volvulus. Chest radiographs are also be indicated to rule out the presence of coexisting disease and/or aspiration.

The most important goal of treatment is the immediate correction of the circulatory, endotoxic and hypovolemic shock. Aggressive preoperative correction of cardiovascular collapse before surgery has dramatically improved patient survival to an overall rate of approximately 90%.  Fluid administration is initiated after placement of one or two large-bore (14 to 18 gauge) catheters in the cephalic or jugular veins. Complete hematologic and biochemical blood testing including a coagulation profile should be performed. Shock doses of crystalloid fluids (90 ml/kg) or a combination of isotonic crystalloids (20 to 40 ml/kg) and synthetic colloids (hydroxyethyl starch 10 to 20 ml/kg; or 7% hypertonic saline in 6% dextran-70 5 ml/kg IV over 5 to 15 minutes) should be administered to effect. After appropriate volume resuscitation, vasopressor therapy may be necessary to further alleviate hypotension. During the initial examination and initiation of fluid administration, supplemental oxygen should be administered, if possible, to optimize oxygen saturation of hemoglobin. Broad-spectrum antibiotic therapy should be utilized because affected animals are at high risk for bacterial translocation from the gastrointestinal tract to the bloodstream with resultant endotoxemia. Continuous electrocardiographic (ECG) monitoring should be performed and arrhythmias (typically ventricular) treated if they interfere with cardiac function and output; the arrhythmias that warrant medical therapy include but are not limited to multifocal premature ventricular contractions, a ventricular rate persistently >140 bpm, and the “R on T wave” pattern (a phenomenon that predisposes to ventricular fibrillation). If predisposing factors have been addressed and persistent ventricular arrhythmias warrant therapy, 2% lidocaine hydrochloride without epinephrine (1-8 mg/kg, slowly IV) is given and repeated if necessary. Continuous rate infusion (CRI) of lidocaine (30-80 µg/kg/min) may be indicated to control arrhythmias. Cardiac arrhythmias associated with GDV are often difficult to control. The lidocaine infusion was continued until arrhythmias improved, then it was slowly decreased over a 12-hour period by cutting the CRI in half every 6 hours. If the arrhythmia is poorly responsive to this therapy, procainamide (6-10 mg/kg, IV over 15 min) should be given.

Following initial stabilization, treatment goals include decompression of the stomach, repositioning and permanent gastropexy, and continued monitoring and treatment of medical complications.

Gastric decompression should be attempted simultaneously with or immediately after cardiovascular stabililization has commenced. Decompression will further improve cardiorespiratory function, however additional cardiovascular insult may occur because of the rapid release of endotoxins and ischemic by products into the circulation (reperfusion injury) as a side effect of appropriate and successful decompression. Gastric decompression usually can be accomplished with the passage of a well-lubricated orogastric (stomach) tube. The distance from the incisors to the xiphoid or costal arch should be measured and marked by a piece of tape on the stomach tube. This distance indicates the maximum length of tube that can be safely passed. Marking this length decreases the likelihood of passing the stomach tube through a devitalized stomach wall. The dog is positioned in sternal or lateral recumbency. A 2-in. roll of tape or an oral speculum is placed in the dog’s mouth, and the muzzle is closed around it. The tube can then be readily passed through the center of the roll of tape or the speculum. Some resistance is usually felt as the tube passes through the esophageal-gastric juncture. If resistance is met, the tube should be gently rotated while attempting to advance it. Undue force may tear the esophagus. Successful passage of a tube does not rule out concurrent gastric volvulus. Once the tube enters the stomach, gastric gas readily escapes. Excess fluid and ingesta are removed via gravity and suction. After the stomach has been decompressed, it should be lavaged with warm water or saline to remove any remaining debris.

In the event that the orogastric tube cannot be passed easily, many surgeons will recommend trocar insertion using a large-gauge, short needle or over-the-needle catheter in a region of the left cranial, dorsolateral abdomen. This should be performed in an area that exhibits the greatest tympany and that has been clipped and aseptically prepared. The main disadvantages associated with this procedure are increased surgical time and increased risk of abdominal contamination at the time of definitive surgical correction. My personal preference is to proceed to surgery immediately and to decompress the distended stomach after performing a ventral midline celiotomy using a blood collection set. In order to minimize the period of time between the initiation of anesthesia and surgical intervention, the patient is clipped and prepped prior to the administration of anesthesia while initial stabilization is being performed; a final sterile preparation is applied as the patient is transferred to the surgery room and as the surgeon is gowning. After utilization of the blood collection set to reduce the tympany present, the surgeon can more easily reposition the stomach into its normal anatomic position and help guide an orogastric tube into the stomach non-traumatically to completely decompress the stomach and remove any remaining fluid and/or ingesta.

While dogs with gastric dilatation in the absence of volvulus typically do not require immediate surgical intervention, gastropexy is recommended for these patients to help prevent the development of GDV in the future. Conservative treatment in these patients is tailored to the individual patient and should consist of the same aggressive medical stabilization upon initial presentation as described above and orogastric intubation as needed throughout the initial hospitalization. It is this surgeon’s opinion that upon stabilization a gastropexy procedure should be performed immediately in light of the extraordinary high recurrence rate and potential for the development of GDV and its more serious consequences. Continued periodic assessment of physical parameters (heart rate, EKG, peripheral pulse pressure and quality, mucous membrane color, capillary refill time, and gastric distention) as well as laboratory data (packed cell volume, total solids, acid-base status, and electrolyte values) should be performed to ensure treatment remains tailored to the individual patient’s response to therapy.

The goals of surgical management are to assess the integrity of the stomach and spleen, to reposition the stomach to its normal location, and to fix the stomach to the abdominal body wall in an attempt to decrease the likelihood of recurrence of volvulus. A midline celiotomy provides access to the stomach and visualization of the spleen and adjacent abdominal structures. Most often, the stomach and pylorus have shifted to the left (clockwise when viewed caudally to cranially), and the gastric fundus has shifted from its normal position in the left dorsal abdomen to the right ventral sector of the abdomen. With this type of rotation, the greater omentum is found draped over the cranial abdominal organs.

The stomach is decompressed by orogastric intubation (by the anesthetist with guidance by the surgeon) or via gastrocentesis as previously described and is rotated back into its normal position. The pylorus can be located by tracing the duodenum (identifiable by the attached pancreas) forward from the duodenocolic ligament. By gently bringing the pylorus back to the right of midline using one hand and using the other hand to push the body of the stomach dorsally, the stomach is derotated. The orogastric tube may then be used to completely decompress the stomach and empty ingesta.

Next, the stomach and the spleen should be assessed for viability and gastric resection or splenectomy performed as needed. Splenectomy is indicated only in those cases demonstrating vessel avulsion, thrombosis, infarction, or all three.  Although the spleen is generally involved in cases of GDV, its removal will not prevent recurrences. Partial gastrectomy is required when gastric necrosis has occurred, usually along the greater curvature. Gastric viability is assessed by examination of serosal color, palpation of gastric wall thickness, and preservation of arterial bleeding if incised. Gray or black coloration and palpable thinning of the stomach are signs of necrosis. Serosal discoloration within areas of viable tissue may improve dramatically within minutes of decompression and repositioning. Gastric resection may be accomplished by preplacing stay sutures to minimize or prevent additional abdominal contamination, followed by resection to bleeding tissue and closure. Whether hand-sewing or stapling (typically TA-90 or GIA-50) is used for closure, a second inverting suture line is recommended.  Invagination of necrotic tissue has also been used to treat gastric necrosis. Because this technique does not require opening of the gastric lumen, it is technically less demanding and is theoretically less likely to result in peritoneal contamination through gross spillage during partial gastrectomy or due to suture dehiscence; however, it should be noted that invaginated tissue may be prone to ulcer formation. Although there are risks associated with gastric resection and invagination, the devastating sequelae of perforation and peritonitis resulting from necrotic tissue that is not excised make it advisable to remove or invaginate any gastric tissue of questionable viability. Gastric necrosis has been associated with the development of several life-threatening complications including peritonitis, disseminated intravascular coagulation, sepsis, and arrhythmias.

Currently, the most widely used gastropexy techniques are incisional gastropexy (muscular flap), belt-loop gastropexy, circumcostal gastropexy and laparoscopically assisted gastropexy. The ideal gastropexy technique is simple to perform, permanently and predictably attaches the stomach to the abdominal wall in a correct anatomic position to prevent volvulus, does not interfere with gastric function, is associated with minimal intraoperative and postoperative complications, and requires minimal postoperative management of the treated dog. Each of the previously mentioned techniques has been assessed, and each has been found to be an acceptable method of performing a gastropexy. Tube gastrotomy, a once a popular technique, is associated with several problems.  In this procedure the gastric lumen is penetrated which can predispose the patient to a peritonitis postoperatively necessitating a second surgical procedure.  Refractory peritonitis is a complication which can lean to the demise of the patient.  The tube must remain in place for up to 10 days to allow time for formation of adhesions and thus, a potentially permanent attachment site. In addition, subcutaneous cellulitis and persistent stoma drainage are further supplementary complications. The aftercare requires additional hospitalization and adequate nursing care to prevent the tube from being removed prematurely either by the patient or subsequent to balloon rupture from contact with gastric juices. Finally, when compared with other techniques, tube gastropexy breaking strength is relatively low, and therefore recurrence of GDV is approximately 5 to 11% of dogs that undergo this type of surgery.

The circumcostal gastropexy has resolved most of the potential problems inherent with the tube gastropexy procedure. This technique provides a strong adhesion on the basis of findings in breaking-strength studies and results in a low GDV recurrence rate. The technique does not require penetration of the gastric lumen thus reducing the risk of iatrogenic peritonitis.  However, there is potential for pneumothorax secondary to penetration of the diaphragm or excess tension on the rib attachment causing the diaphragm to tear or for the rib to fracture.

Advantages of the incisional gastropexy techniques (muscular flap, belt-loop) are that the stomach lumen is not entered (reducing the risk of iatrogenic peritonitis), pneumothorax and/or rib fracture are no longer a concern and fibrous connective tissue cojoins the rectus abdominis muscle and stomach wall to form a strong, mature adhesion with extremely low recurrence rates for GDV.  The risks associated with the incisional gastropexy methods are more related to skill and technique; poor positioning or choice of attachment site can cause pyloric outflow obstruction or entrapment of adjacent abdominal viscera. My personal preference is to perform the muscular flap gastropexy as it is even less invasive than the belt-loop procedure as the seromuscular layer of a potentially devitalized stomach wall is not invaded to any extent. Having pioneered this gastropexy procedure over 20 years ago and having successfully employed it in hundreds of GDV cases with virtually no recurrence, I can personally attest to the outstanding success it has achieved in managing the GDV patient.

The goal in the immediate postoperative management period is to maintain tissue perfusion. Because of substantial fluid loss into the peritoneal cavity and GI tract, reasonably high fluid rates often are required for the first 48 to 72 hours. Mucous membrane color, capillary refill time, packed cell volume, total solid values, urine output, ECG, blood pressure, and acid-base balance should be monitored closely postoperatively. Dogs recovering well from surgery can be offered water first, and then a small amount of food if water is tolerated on the first or second day after surgery. These dogs can be weaned gradually off their intravenous fluids over 2 days. Because of the high incidence of gastric mucosal compromise, nonsteroidal antiinflammatory drugs are avoided, and histamine-2 receptor antagonists (ranitidine, cimetidine, famotidine) and coating agents (sucralfate) should be considered. All dogs should receive proper pain management consisting of but not limited to appropriate doses of hydromorphone, tramadol, fentanyl, and buprenorphine as necessary to alleviate pain.

In the past, mortality rates for dogs with GDV were approximately 50%. In a recent study, however, the overall mortality rate was 10%, and the postoperative mortality rate was 6.1%. The factor that was associated with a significant increase in overall mortality was the presence of preoperative cardiac arrhythmias. Additional factors that were associated with a significant increase in postoperative mortality were postoperative cardiac arrhythmias, splenectomy, or splenectomy with partial gastric resection. The factor that was most associated with a significant decrease in the overall mortality rate was time from presentation to surgery. Dogs that had gastropexy alone had a postoperative mortality rate of 3%. Dogs in which splenectomy was the only additional surgical procedure performed had a significantly higher postoperative mortality rate (15%) than dogs that did not require splenectomy. The postoperative mortality rate (9%) for dogs in which partial gastrectomy was the only additional surgical procedure performed was not significantly higher than the rate for dogs that did not have a partial gastrectomy. Dogs that had both splenectomy and partial gastrectomy had a significantly higher postoperative mortality rate of 20% compared to dogs that did not have both splenectomy and partial gastrectomy. This study documents that certain factors continue to affect the overall and postoperative mortality rates associated with GDV, but these mortality rates have decreased compared to previously reported rates. The fact that anesthesia and surgery time were less than half of those previously reported suggests that anesthesia and surgery times play a role in improved survival.

Many veterinarians have recently begun to advocate prophylactic gastropexy for higher- risk patients. Prophylactic gastropexy is performed to prevent the occurrence of GDV in predisposed dogs. The lifetime risk of certain dogs predisposed to develop GDV has been estimated to be between 4% and 37%. In contrast, the lifetime risk of development of GDV if a prophylactic gastropexy is performed in these dogs is 0.3%.  These dogs include, but are not limited to, large- to giant-breed dogs (especially Great Danes), dogs with a first-degree relative that has had GDV, excessively anxious dogs, and inappropriately rapid eaters. Other indications include a history of splenic volvulus and a chest shape that has a deep chest-to-width ratio Depending on the breed of dog, prophylactic gastropexy results in a 92% reduction in risk for development of GDV and a 2- to 30-fold reduction in lifetime mortality rates. On the basis of these findings, prophylactic gastropexy can be suggested for dogs of predisposed breeds because it decreases GDV-associated mortality rates.

Currently, prophylactic gastropexies can be performed via any of the previously described techniques (incisional or circumcostal). Each of these techniques requires a ventral midline incision and is considered an “open” major surgical procedure. Many owners and veterinarians consider such a procedure excessively invasive for a young healthy dog with an uncertain probability of developing GDV later in life. Issues associated with performing prophylactic gastropexy include invasiveness of the procedure, lifetime risk of an episode of GDV, and actual necessity of prophylactic surgery. More recently, minimally invasive alternatives have been described and are gaining interest among veterinary surgeons in an effort to decrease pain and potential morbidity associated with the more invasive open surgical approach. These include laparoscopic-assisted gastropexy, grid-approach gastropexy, and total laparoscopic gastropexy. The major drawback to these procedures is the need for expensive instruments for the laparoscopic technique, duration of the procedure, and possible increase in the risk of damaging other organs. Although potentially challenging, these procedures are advantageous in that they are associated with a decrease in incision size, decrease in the duration of hospitalization, decrease in morbidity, decrease in incisional complications, and improved cosmetic appearance, compared with results for conventional surgery.

In summary, while the gastric dilatation-volvulus disease complex is a true medical and surgical emergency, prompt and aggressive administration of appropriate medical and surgical intervention leads to successful case management the overwhelming majority of the time.

Dr’s Schulman interview with VPI Pet Insurance regarding GDV Syndrome

Cranial Cruciate Ligament Injury in the Dog.

Cranial cruciate ligament (CCL) injuries are among the most common reasons for pain, discomfort, and lameness of the stifle joint of the dog. While this may be true, the testament to our inability to decide on the most appropriate treatment regime is evidenced by the myriad number of techniques commended to repair a cruciate deficient stifle. The recognition and appropriate treatment of these lesions play an important role in the successful management of a small animal veterinary practice. It is the purpose of this as well as subsequent articles to address the causes, effects, and surgical options most suited to reconstruction of a clinically stable and fully functional stifle joint.

The CCL plays a vital role in the maintenance of stability of the stifle joint. It prevents cranial displacement of the tibia on the femur (which often leads to impingement of the caudal horn of the medial meniscus), prevents hyperextension of the stifle, and limits internal rotation of the tibia on the femur. These functions are directly related to the anatomic location and orientation of the CCL within the stifle joint and has lead to the belief that the technique for repairing the CCL should duplicate the ligament’s normal anatomy and function as well as maintain normal joint function.

The cruciate ligaments are dynamic structures and the mechanism of cruciate ligament injury is directly related to the function of the cruciate ligaments as constraints of joint motion. The most common mechanism of cruciate ligament rupture is excessive internal rotation of the tibia when the joint is partially flexed. In this position, the CCL is wound very tightly and is easily subject to trauma to the lateral side. In full extension, the CCL is quite tight, such that in hyperextension injuries, the CCL is the first structure subject to injury. Obviously, direct trauma can also induce CCL as well as other structural injury to the stifle joint. While excessive forces during the extremes of the aforementioned motions will result in acute CCL injury, chronic degenerative CCL lesions may also eventually result in rupture. Conformational deformities of the stifle (i.e. patella luxation) contribute to repeated excessive stress on the CCL, and in the obese animal, these stresses are increased. It has also been shown that ligament strength and stiffness decrease with age because of disuse, inactivity, and disease states. As the degeneration gradually progresses, the tensile strength of the CCL is reduced, making it even more susceptible to acute rupture. These changes are also associated with the normal aging process and may explain the increased incidence of ligament injury in dogs over 5 years of age. In addition, immune mediated processes may play a role in weakening and eventual failure of the CCL.

While acute complete rupture of the CCL is the more common scenario, partial CCL rupture is by no means uncommon. Because known trauma is lacking in the majority of dogs with a partial CCL tear, degenerative or immune mediated processes may be playing a more significant role in these cases. With complete ligament rupture, dogs typically develop a sudden severe lameness classically detected with cranial drawer sign or positive tibial compression test. With partial tears, mild to moderate lameness of acute onset is more likely, and a cranial drawer sign is elicited in only about 50% of the cases. The severity of the lameness will wax and wane over time and may respond to rest and analgesic therapy, but the condition gradually worsens over the course of several weeks to months. Accurate diagnosis of CCL injury is hampered by the fact that there is tremendous variability in eliciting cranial drawer motion, as it is based upon subjective evaluation and may vary from case to case depending on the type of lesion present and the length of time it has existed.

In dogs with acute complete rupture of the CCL, there is usually pain upon manipulation of the stifle, and a cranial drawer sign is elicited with the stifle flexed or extended. Excessive internal rotation of the tibia on the femur is detected and the stifle joint may be placed in a more full extension than is normally possible. Dogs that are apprehensive or tense may resist manipulation of the limb such that accurate evaluation of the amount of instability is impossible without resorting to sedation or anesthesia. In addition, over time, periarticular soft tissue fibroplasias may prevent manual detection of a cranial drawer sign, even under sedation. The radiographic presence of periarticular osteoarthritis at this stage, however, should support the diagnosis of a chronic CCL rupture. In dogs with partial CCL tears, the variability of the cranial drawer test results are due to the fact that the CCL is composed of a large caudolateral band and a smaller craniomedial band. The craniomedial band is taut throughout flexion and extension, while the caudolateral band is taut in extension only. Therefore, a solitary caudolateral band tear should not result in a cranial drawer sign at all, while a tear of the craniomedial band should result in a cranial drawer sign when the joint is in flexion only. In my experience, increased internal rotation is also evidenced with a craniomedial band tear as well. If rupture of the CCL is suspected and a positive cranial drawer sign cannot be elicited with the stifle in flexion or extension, or with the dog conscious or sedated, and the radiographs do not support a diagnosis, the next option includes and MRI, arthroscopy, or exploratory surgery.

It is an established fact that rupture of the cruciate ligament results in progressive degenerative changes within and around the joint and predisposes the contralateral joint to similar injury. It is for these reasons that the majority of veterinary surgeons agree that surgical correction of CCL rupture is preferable to conservative medical therapy and enforced rest alone. While some studies have indicated that dogs weighing less than 15kg can achieve at least good function without surgical intervention, these same studies conclude that if restoration of limb function and a normal activity level is desired, then surgical intervention is still warranted even in these smaller patients. With regard to partial rupture of the CCL, spontaneous healing of the torn fragment and/or restoration of full stability does not seem to occur, given the protracted clinical course seen in the majority of cases. If partial rupture is due to ongoing immune mediated mechanisms or other degenerative changes rather than trauma, it would seem reasonable to assume that the remaining intact portion is similarly affected and would eventually fail. In fact, most of the dogs suspected of having partial ligament tears initially eventually undergo surgical intervention within a few weeks or months when the ligament completely ruptures in spite of appropriate medical therapy and rest.

Surgical repair of the CCL has been and continues to be the topic of considerable interest, and the multitude of techniques and material used suggested for the surgical reconstruction can leave anyone confused. Basically, the procedures can be divided into the intraarticular versus extra-articular techniques and arthroscopy versus standard arthrotomy. These considerations will be discussed in the next article concerning surgical management of cruciate ligament injuries.

High Power Laser Therapy.

Medical lasers have become an integral part of medical practice because of their wide range of therapeutic applications including but not limited to relief of acute and chronic pain, the promotion of tissue repair and wound healing, and the reduction of inflammation.

Studies have shown that when photoreceptors at the molecular level are irradiated by lasers, the cells absorb energy from the laser light. Visible (red) light and Near Infrared (NIR) light are absorbed preferentially within the mitochondria and the cell membrane, activating a number of biological reactions such as DNA/RNA synthesis, increased cAMP levels, higher adenosine tri-phosphate (ATP) levels, increased protein and collagen synthesis, increased cell membrane permeability, blood and lymphatic vessel vasodilation, and cellular proliferation. The result is rapid regeneration, normalization, and healing of damaged cellular tissue. Thus, light is a trigger for the rearrangement of cellular metabolism.  As ATP is the “fuel” or energy source that all cells need to function and to stimulate self repair, these events then lead to a cascade of beneficial effects increasing cellular energy and health.

Despite more than 35 years of experience with therapeutic laser devices, some concerns remain as to the effectiveness of laser therapy as a treatment modality. Controlled clinical studies have demonstrated that while laser therapy is effective for many specific applications, the most common reason for poor clinical outcomes is related to low power or dosage. The previously available Class III Low Power Lasers simply did not generate the longer wavelengths of light or power output necessary to deeply penetrate tissue to be effective. The Class III or “low-level” lasers have a limited power output of up to 500 mW. The need for deeper penetration with less superficial absorption of laser energy coupled with the need for higher energy output levels has led to the development of Class IV, or “high-power” therapeutic lasers, which have been cleared for use by the FDA up to 7,500 mW.

Cells and tissues that are ischemic and poorly perfuse as a result of inflammation, edema, and acute or chronic injury have been shown to have a significantly higher response to laser therapy irradiation than normal healthy structures. The delivery of a high amount of laser energy and its ability to penetrate deep enough to stimulate these target tissues is the primary reason why Class IV laser therapy has been associated with much more positive therapeutic outcomes than the previously available Class III lasers. The deposition of a significant amount of energy into tissue and articular structures within a short period of time achieves optimal cellular stimulation to enhance wound healing and penetrate deep within the tissues to encourage healing within tendons, ligaments, muscles, nerves, dermal layers, joints, and even the periosteal layer of bone. This allows for a faster resolution to most orthopedic, soft tissue and dermatologic conditions.

During each treatment, laser energy increases circulation drawing water, oxygen, and nutrients to the damaged area.  This creates an optimal healing environment that reduces inflammation, muscle spasms, stiffness, and pain. As the injured area returns to normal, function is restored and pain is relieved. The biologic effects of Class IV laser therapy include:

  • Increased Circulation (angiogenesis): Photobiostimulation results in vasodilation and stimulates the formation of new capillaries within damaged tissues.
  • Immune Stimulation: Laser light stimulates the production of immunoglobulins and lymphocytes.
  • Reduction of inflammation
  • Pain relief: Lasers stimulate the production of endorphins, the body’s own natural morphine-like substance thereby increasing the threshold of pain perception.
  • Accelerated Cell Reproduction and Growth: This allows tendons, ligaments, bone and muscle to heal at an accelerated rate.
  • Stimulation of Nerve Regeneration
  • Increased Cellular Metabolic Activity
  • Reduced Fibrous Tissue Formation: Healing tissue fibers called collagen align themselves in a more linear, uniform, “normal” direction when exposed to laser light, reducing scarring and improving the tissue strength of newly healed wounds faster.
  • Accelerated Wound Healing: Photobiostimulation stimulates wound repair. Bacterial growth (and probably viral reproduction) are inhibited by exposure to laser light, making laser treatment helpful in treating non-healing wounds, contaminated wounds and burns.
  • Stimulation of Acupuncture Trigger Points

The goal of all laser therapy is to provide healing to the patient. In the case of an acute injury, aggressive therapy will result in the resolution of the condition in the least amount of time. If the condition is more chronic in nature, the laser therapy plan should be initially aggressive and then, a maintenance plan should be developed until the therapeutic goal is reached. Depending upon the condition being treated, laser therapy may be administered on a daily basis until the initial symptoms have diminished, at which point the therapy sessions can be reduced to twice a week, then at a weekly or biweekly interval as healing progresses. During the therapy session, the pet will become relaxed and may even appear to fall asleep. Because treatment is painless and quick, even the most nervous animal can be easily treated. The application of laser therapy is not just designed to manage pain, break the inflammatory cycle, and accelerate healing. It has the ability to alleviate the cause of the pain, inflammation, and pathologic change.

Currently, Class IV Laser Therapy is being utilized as a complementary and effective treatment solution for many patients’ needs.  Applications include but are not limited to wound care (surgical incisions, contaminated wounds and abrasions, burns, anal saculitis, perianal fistulas), dermatologic conditions (acral lick dermatitis, eosinophilic plaque, pyoderma, pododermatitis, acute and chronic otitis externa), musculoskeletal disorders (degenerative joint disease, intervertebral disc disease, hip and elbow dysplasia, tendon and ligament injuries, trauma, fractures, arthritis), neurologic disorders (peripheral nerve injuries, paralysis, degenerative myelopathy), gingivitis/stomatitis, and pain management. Class IV Laser Therapy can be easily integrated along with conventional veterinary care to provide the best possible care for a variety of conditions that previously appeared to be resistant to successful resolution.

 


\"s\"\Before Laser Therapy
\"s\"\One Week After Laser Therapy

 

Developmental Anomalies of the Canine Elbow Joint.

Pathophysiology, Diagnosis and Treatment

A high incidence of occurrence has been noted in the Bernese Mountain Dog, German Shepherd, Rottweiler, Golden Retriever, and Labrador Retriever. Other breeds affected are the Newfoundland, Saint Bernard, Mastiff, Springer Spaniel, Australian Shepherd, Chow Chow, Shar-Pei, Shetland Sheepdog, and some Terrier breeds. Typically, both elbows are affected. However, unilateral elbow dysplasia is also recognized.

Forelimb lameness is a relatively common presentation for the growing puppy with frequent presentation being the rule for some breeds. Although there are a number of developmental anomalies of the forelimb resulting in lameness, the focus of this presentation is restricted to those conditions most commonly referred to as elbow dysplasia.  The developmental growth of the canine forelimb coupled with the potential for trauma in the active playful puppy set the stage for the developmental anomalies that lead to elbow dysplasia. Since considerable joint degeneration can occur over minimal time, it is critical to be aware of the predispositions to and early symptoms of all forms of this disease. Ununited anconeal process, osteochondritis of the medial condyle of the humerus, and fragmented coronoid process are three conditions that may occur independently or concurrently in the same animal. The pathophysiology, diagnosis, and treatment of these three manifestations of elbow dysplasia are the subject of this report.

The canine elbow joint allows flexion and extension as well as a limited degree of supination and pronation. A common feature of UAP, OCD, and FCP is the presence of some level of elbow incongruity. Each of these conditions may then precipitate the secondary changes associated with degenerative joint disease. The time of occurrence of UAP, OCD, and FCP is usually between the ages of four and six months. At that time, the bones and joints are incompletely formed. In the elbow joint, an abnormally small curvature of the trochlear notch could result in a FCP through weight bearing forces transmitted via the humerus on an immature coronoid process lying above the level of the adjoining radius. For the same reason, the result could be an OCD lesion, caused by pressure exerted via the medial coronoid process on the opposite immature articular humeral cartilage, interfering with normal endochondral ossification. In dogs with a separate center of ossification of the anconeal process, stresses caused by the abnormally tight fit between the anconeal process and the opposite humerus, and present before union (ie-between the ages of 4-6 months), could cause microscopic movement at the level of the cartilage plate between the separate center of ossification and the ulna and result in a UAP. This developmental elbow incongruity is responsible for joint injury, which is manifested by continual cartilaginous breakdown and subsequent degenerative joint disease.

In FCP, the incongruous growth of the radius and ulna results in misalignment of the bones such that a tremendous amount of pressure is placed on the coronoid process, making it highly susceptible to the development of fractures or fissures. In addition, the location of the coronoid process at the medial extent of the articulation of the humerus, radius, and ulna make it prone to mechanical damage because of a shearing effect between the radial head and the coronoid during rotation of the forelimb, resulting in fragmentation of the coronoid process and potentially the development of a loose body. The cartilage damage induced by the erosion of the incongruent articular surfaces is usually manifested as an OCD lesion on the more medial articular surface of the humeral condyle.  As with FCP, UAP is a consequence of incongruent growth between the radius and ulna resulting in the anconeal process remaining ununited with the proximal ulna. Since the anconeal process can no longer provide support to the elbow joint because of its instability, articular instability and degenerative changes ensue.

The primary source of pain in elbow dysplasia is from the increased joint pressure, joint effusion, and loose cartilage fragments, which results from the destruction of the hyaline cartilage. These fragments induce synovitis, alterations in joint fluid consistency, and volume and joint instability, as the incongruent joint surfaces fail to properly bear weight. Characteristic of this degeneration is focal cartilage degeneration, proliferation of the synovial membrane, and formation of periarticular osteophytes. In advanced cases, erosion of the cartilage is so severe that subchondral bone becomes denuded and sclerotic. Chronicity causes capsular scarring and eventually a decreased range of motion in the joint with resultant gait changes.

The onset of gradual and variable clinical signs makes elbow dysplasia difficult to diagnose at an early stage in all cases. A combination of physical examination, gait analysis, palpation, radiography, nuclear scintigraphy (bone scans), or arthroscopy may be needed to adequately diagnose the syndrome. The most common symptoms associated with elbow dysplasia include limping or short striding steps in the forelimbs, difficulty lying down or rising, lying down with elbows abducted, warming out of lameness after minimal exercise, increased lameness after heavy exercise, and frequent shifting of weight with a noticeable head bob during ambulation.

Pain, crepitus, and swelling of the joint due to excess synovial fluid and capsule thickening may be elicited on palpation. A lateral deviation of the elbow when standing or walking may be observed, and the elbow usually exhibits a decreased range of articular motion. Although palpation and gait analysis are important means of detecting elbow dysplasia, any suspicion of joint disease should be confirmed by radiography. It is important to remember, however, that a decreased range of motion, lameness, and joint pain/effusion may be present before radiographic changes are evident.

Radiography of the affected joint should include standard anterior-posterior, medial to lateral, flexed lateral, and anterior-posterior medial to lateral oblique views to completely evaluate the joint. Initial osteophyte formation may be seen on the proximal anconeal process, medial epicondyle, medial humeral condyle, and medial aspect of the proximal ulna. High quality radiographs are essential for diagnosis, but it should be pointed out that even excellent radiographic technique might fail to adequately disclose signs of the disease being present. Mild cases are difficult to diagnose by radiography alone; lesions that do not appear through conventional radiography may be discerned through nuclear scintigraphy, MRI or CT scanning, arthroscopy, and/or standard arthrotomy.

Inadequate treatment of elbow dysplasia usually will lead to considerable degeneration of the elbow joint as well as the potential development of orthopedic problems in other joints due to resultant abnormal weight transfer during ambulation. Depending upon the degree and nature of the case and the physical expectations for the dog, elbow dysplasia may be treated with a multi-pronged approach including diet and exercise restriction, medical therapy and surgery via standard arthrotomy or arthroscopy.  Because it is inexpensive and non-invasive, medical therapy may be an effective method of treating minor elbow dysplasia cases, which exhibit mild or intermittent pain. Medical therapy is also indicated for those patients who, for any number or variety of reasons, may not be considered surgical candidates.  Medical therapy involves the administration of nutritional chondroprotectants (glucosamine, chondroitin, creatine, MSM), injectable chondroprotectants (Adequan), the utilization of steroidal and nonsteroidal anti-inflammatory drugs, pain management, acupuncture, physical therapy, platelet rich plasma injections, and Class IV laser therapy.  While medical therapy has limited applications by itself in those patients in obvious need of surgical intervention (since it does not eliminate either the original joint incongruity or the resulting histological trauma), medical therapy is a critical adjunct to arthrotomy and arthroscopy.

Several surgical approaches to the medial aspect of the elbow joint for the treatment of FCP and OCD have been described, requiring osteotomy, tenotomy, or transection of muscle. Although each technique provides good exposure of the medial coronoid process and medial humeral condyle, exposure is gained at the expense of additional surgical time and tissue manipulation. Longitudinal myotomy of the flexor carpi radialis provides rapid atraumatic access to the medial aspect of the elbow. The FCP is identified, dissected free, and removed. The medial humeral condyle is inspected for the presence of an OCD, and the lesion is curetted if present. In addition, gentle subchondral bone abrasion with microfracture of the involved surface may help liberate pluripotential stem cells, which serve to allow formation of an improved fibrocartilaginous weight bearing surface.  Treatment options for UAP include a lateral approach to the joint via a myotomy of the anconeal muscle and removal of the anconeus. There is evidence that proximal transverse osteotomy of the ulna may improve joint congruity and allow for the effective treatment of early UAP and FCP cases in young dogs. Ulnar osteotomy in young UAP cases may allow for the realignment of the ulna with the humeral condyle and the consequent reattachment of the anconeal process. Treatment of FCP by ulnar osteotomy must also involve the removal of the loose and degenerated bony fragments.

Increasingly, arthroscopic surgery is being utilized to treat elbow dysplasia. Loose coronoid fragments and OCD lesions may be effectively removed and curettaged less traumatically than standard arthrotomy. While the choice of surgical technique (arthroscopy or traditional surgery) may vary, the results are similar. Effective treatment of UAP, however, must still involve a standard arthrotomy.

While early surgical therapy is recommended, it should be mentioned that osteoarthritis may persist and progress despite appropriate surgical intervention and adjunctive medical therapy. The recent utilization of platelet rich plasma and Class IV laser therapy exhibit great promise in breaking this progressive cycle of degenerative joint disease. Because many of the degenerative changes that occur in elbow dysplasia are the result of joint incongruity, a few patients may progress to intractable disease, which may require the replacement or fusion of the joint. Total elbow replacement or arthrodesis of the elbow joint should be reserved for those cases that have progressed to massive cartilage damage and pain non-responsive to appropriate medical therapy. Most surgeons agree that the functional outcome after arthrodesis of the elbow is quite poor although pain in the joint was alleviated. A mechanical lameness results in almost all of these patients. In cases receiving total elbow replacement, each dog considered a surgical candidate had severe, daily lameness from chronic elbow osteoarthritis that was unresponsive to medical management. In many cases, surgery resulted in significantly improved limb function. The greatest disadvantage to elbow replacement, however, is that a serious complication can result in a second surgery that requires removal of the implant system. In the elbow, this leaves the surgeon with few options— generally arthrodesis, but amputation has also occurred following severe complications (neurogenic injury or untreatable infection). In lieu of amputation, some clients may elect for euthanasia because of the lack of medical or surgical therapy to return the pet to a comfortable, ambulatory gait.
 
Sliding Humeral Osteotomy (SHO) is a relatively new procedure that was developed specifically as a treatment for dogs with severe cases of elbow dysplasia with resultant medial compartment disease (severe cartilage loss in the medial aspect of the elbow joint). In many dogs with elbow dysplasia, the damage to the cartilage is confined to the medial (inside) half of the joint. The procedure begins by making a precise osteotomy through the humerus.  A specially engineered SHO plate is applied onto the upper section of the humerus.  As screws are applied to the plate and bone, the lower section of the humerus moves medially.  This slide shifts weight-bearing forces off the medial compartment and over to the healthy cartilage of the lateral compartment of the elbow joint, thus relieving the pain on the inside of the joint. This would give the damaged medial compartment an opportunity to heal with a layer of fibrocartilage. While stem cell therapy has been universally disappointing in stimulating this healing process, the utilization of Class IV laser therapy and platelet rich plasma may prove more rewarding. While numerous studies have confirmed that the SHO effectively shifts the weight bearing forces to the lateral compartment, the overall decrease in joint surface contact area suggests that these procedures may induce focal increases in pressure that may cause iatrogenic cartilage damage and continued lameness. Nonetheless, good to excellent results have been reported with this procedure, with the majority of dogs undergoing SHO having demonstrated a decrease in clinical lameness postoperatively while requiring less anti-inflammatory medication to remain comfortable. Considering the alternatives (total elbow replacement or fusion),  SHO may prove quite useful in helping to manage carefully selected patients with intractable pain and discomfort.

While the presence of multiple modalities of therapeutic options allow for a reasonable return to function, it is critical to determine the presence of elbow dysplasia before the joint deteriorates beyond repair in order to achieve the best possible prognosis. Ununited anconeal process, fragmented coronoid process, and osteochondritis all respond favorably if medical and surgical intervention is initiated early in the course of development and prior to severe degenerative changes.

Click here for a computed tomography report of elbow dysplasia
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Management of Tibial Shaft Fractures in Dogs and Cats.

Fractures of the tibia are relatively common in the dog and cat, with tibial diaphyseal fractures the most commonly encountered injury of this bone. Greater than 50% of the fractures occur in animals less than one year of age, reflecting an increased prevalence of traumatic incidents in younger animals. The various patterns of tribal diaphyseal fractures can in many instances be associated with the age of the animal involved. Non-comminuted and greenstick, or incomplete, fractures are more commonly seen in juveniles; while comminuted fractures are seen primarily in adults. The disparity in frequency of comminuted fractures in adults versus juveniles may relate to the increased brittleness of adult bone and the decrease in capacity of such bone to absorb the energy inflicted. Regardless of age, the most frequent fracture type is the spiral, oblique fracture.

Numerous methods of external and/or internal fixation have been advocated for the treatment of tibial diaphyseal fractures. The method of fixation ultimately employed is dependent upon the age of the animal and the severity of the fracture. Simple fractures may be effectively treated with closed reduction and external fixation, an intramedullary pin, a combination of cerclage and an intramedullary pin, bone plate, or Kirshner-Ehmer splints. Complex fractures are better treated with bone plates or Kirshner-Ehmer splints.

As previously mentioned, simple and/or non-displaced fractures may be successfully treated by closed reduction and coaptation, especially in immature animals. The main advantage is that blood supply to the fracture site is not disrupted by an open surgical procedure. In cases in which it is difficult to maintain a satisfactory reduction, placing through and through pins above and below the fracture site and then incorporating the pins in a cast is an especially useful technique which is simple to perform and has the additional advantages of preservation of soft tissues and blood supply to the fracture site. Complications associated with closed reduction and coaptation, including inadequate immobilization and/or incomplete reduction of fracture fragments, as well as muscle atrophy and prolonged joint immobilization have led to increased utilization of open reduction and internal fixation techniques for more complex tibial diaphyseal fractures.

Intramedullary pinning of tibial shaft fractures is a successful method of treating spiral and oblique fractures. Intramedullary pins provide excellent axial stability but minimal rotational stability, and when used alone to treat fractures, it should be applied to rotationally stable fractures only. An intramedullary pin in conjunctions with multiple full cerclage and/or hemicerclage wire may be used to provide additional rotational stability. A tibial intramedullary pin is best introduced just medial and caudal to the tibial tuberosity on the medial side of the patella ligament with the stifle flexed. While retrograde introduction of a pin from the fracture site into the proximal tibia can also be performed, if the pin is improperly placed, significant interference with stifle joint function can occur. Intramedullary pins should be removed as soon as the healing process is complete, and immature animals must be watched closely for the timing of pin removal.

External skeletal fixation devices may be applied to the tibia in a number of different configurations, depending upon the age and the size of the animal and type of fracture present. The techniques involved in the proper applications of external skeletal fixators will be the subject of a future journal article. The device may be used with intramedullary pins and interfragmentary screw fixation. External fixators are particularly useful in open fractures since the device affords rigid immobilization without invading the traumatized area. It also allows aggressive, frequent treatment of associated soft tissue wounds while maintaining rigid fracture fixation. Complications associated with external fixators include pin tract infections and pin loosening or breakage.

The repair of tibial diaphyseal fractures with bone plates is advantageous in a number of clinical situations. Plate fixation of tibial fractures is generally reserved for those fractures not associated with severely contaminated or infected soft tissue wounds. Bone plates may be placed as compression, neutralization or buttress plates, depending on the fracture configuration. In simple transverse or short oblique fractures, bone plates applied as compression plates establish early axial and rotational stability and encourage early return to activity. In spiral, oblique and severely comminuted fractures, interfragmentary compression is best achieved with individual lag screws through the plate. Following fracture reconstruction, the bone plate is applied as a neutralization plate to increase the stability of the fracture site. If complete fracture reconstruction is not attained, the fracture defects should be filled with an autogenous cancellous bone graft; and the bone plate is applied as a buttress plate. In multiple fracture patients, plate fixation of tibial shaft fractures is often more appropriate than other forms of internal fixation, as plates and screws afford the most rigid fracture stabilization and encourage early ambulation.

In summary, closed reduction and external fixation is used quite successfully on immature animals. Increased severity of fractures in immature animals leads to the use of intramedullary pins, wires, and external fixators. Bone plate application is used almost exclusively on fractures on adults. The frequent use of bone plates in the mature animal is related to the greater number of highly comminuted and severe fractures observed in the adult.

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Anal Gland Disease.

Anal glands are pouches or sacs, which are located near the anus. Every dog and cat has a pair of anal glands, one gland located on each side of the anal region. The openings to these glands are located just inside the anus very near the juncture between the anus and the skin at approximately 4 o’clock and 8 o’clock position. Anal glands in dogs and cats secrete a liquid substance, which is held inside of the sac until the animal defecates. In dogs and cats with normal anal glands, this liquid is normally expressed from the glands along with the bowel movement. Many animals will also express the contents of these glands when they become frightened, nervous, or excited. This expression will result in a foul smelling, dark colored liquid substance being seen near the rectum of the animal, under the tail, or on the floor or ground near the pet.

Dogs are more commonly affected with anal sac disease than cats, and small breed dogs are more commonly affected with anal sac impaction than large breed dogs. Older female dogs are more commonly affected with anal sac tumors. If the sacs do not empty normally, an impaction can occur. Symptoms of an impaction include “scooting” along the floor to attempt to empty the overfull sacs. This is more common in smaller breeds, but it can happen to any dog. Usually, it occurs because recurrent loose stools do not supply enough sphincter pressure to empty the sacs. It can also be caused by small anal sac openings or overactive glands. Other symptoms commonly noted are frequent licking of the anus or tail base, reluctance to sit, or sitting asymmetrically to avoid pressure on the painful anal sac, straining to defecate, difficulty defecating, production of ribbon-like stools, and painful swelling at the 4 o’clock or 8 o’clock locations around the anus.

When the anal glands become over-filled, it is possible to manually express them. External manual expression involves squeezing the area on either side of the anus to milk the fluid out of the glands. When expressed properly, the fluid from the glands will be visible exiting through the openings near the anus. Internal manual expression involves inserting a finger inside of the rectum of the dog and milking the fluid from the anal glands between two fingers, one inside the rectum and one outside. Similar to the external method, fluid will be visible exiting the anal gland openings when expression is accomplished successfully.

If intervention does not occur to empty the over-filled anal glands, eventually the fluid inside of the anal glands begins to change in consistency, becoming much thicker and more difficult to express. Left unexpressed, anal glands can eventually become infected and may even abscess and rupture, leaving an open, painful wound near the anus.

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Treatment for anal gland infections and/or abscesses may involve flushing the anal gland and treating with antibiotics, either systemically, topically, or both. Culture and sensitivity testing will determine the most appropriate antibiotic regime indicated to resolve the infection as expediently as possible.  Flushing the diseased anal gland may require sedation for the affected pet. In addition, pain medication may be necessary to relieve the discomfort for these dogs and cats. It is possible to surgically remove the anal glands from pets experiencing repeated anal gland issues. The staging of surgical removal is important as surgical removal in the presence of an acute rupture or infection increases the chances of complications, including but not limited to incomplete removal of anal gland tissue and spreading infection into previously unaffected tissue. Surgery is best performed after the infection is under control as visualization of the affected tissues is much more precise. Surgical removal of anal glands can lead to complications, which may include fecal incontinence if the nerves in the area of the anal glands are disrupted during the course of the surgery. This incontinence may be temporary or permanent. For this reason, an experienced surgeon is best equipped to perform the procedure in order to decrease the chance of postoperative complications.

Tumors of the anal sacs are uncommon in dogs, but can become serious problems because they can invade local tissues, such as the rectum, or metastasize to other organs, even when the primary tumor is still very small. Additionally, these tumors can cause increased blood calcium levels (hypercalcemia of malignancy) that can lead to kidney failure. Hypercalcemia of malignancy is detected in approximately 25% of dogs with anal sac carcinoma. Clinical signs may be associated with the primary tumor or with kidney disease resulting from hypercalcemia. Clinical signs associated with a primary tumor are similar to the signs observed for anal sac infections and include constipation, pain when defecating, straining to defecate, and bloody feces. Clinical signs associated with kidney failure from high blood calcium include lethargy, loss of appetite, vomiting, increased water intake, and increased urinations.

If a mass is felt in the area of the anal sac, it can be aspirated to determine if cancer cells are present. If anal sac carcinoma is confirmed, thoracic and abdominal radiographs and ultrasounds should be performed to search for evidence that the tumor has spread to the regional sublumbar lymph nodes or lungs. Blood chemistries and urine are tested to check for high calcium and any evidence of kidney damage since high blood calcium and subsequent kidney failure are associated with poor survival rates in animals with anal sac tumors.

Although a variety of treatment combinations have been reported, surgery is the only method that has been proven to influence survival of dogs with anal sac carcinomas. Surgical treatment includes removal of the primary tumor and, in some cases, also the sublumbar lymph nodes in the abdomen, which are affected by metastatic disease in half of dogs.  In addition to surgery, many oncologists recommend radiation and chemotherapy in an attempt to prolong survival of affected dogs. Due to the highly invasive nature of anal sac carcinomas and the possibility that aggressive surgical removal may lead to fecal incontinence, radiation is commonly used when complete (clean) surgical margins cannot be achieved.  Animals that present with hypercalcemia may need to be treated before surgery with intravenous fluid therapy, diuretics (to increase urine production), and corticosteroids or bisphosphonates to decrease blood calcium concentrations.

Prognosis and survival depend on factors such as the type of treatment, size of the mass, and presence of hypercalcemia and metastatic disease. In a recent study of dogs with anal sac adenocarcinoma, overall median survival was 584 days. Dogs not treated surgically had shorter survival times (median, 402 days).  Median survival is poorer in dogs with tumors larger than 4 inches (median survival, 292 days), hypercalcemia (median survival, 256 days), and spread to the lungs (median survival, 219 days).  Interestingly, metastasis to the abdominal lymph nodes was not found to affect survival.

In summary, because many of the clinical signs associated with anal gland infection can mimic those of an anal gland tumor or cancer, prompt and thorough evaluation of the rectal area is indicated whenever a pet is exhibiting signs of pain and discomfort in this region.

Surgical Repair of Distal Femoral Physeal Fractures in the Dog and Cat.

Fractures involving the distal femoral physis are relatively common in immature dogs and cats with the greatest incidence occurring between the ages of 5 and 8 months. Physel fractures have been classified by Salter and Harris into 5 categories: Type 1 traverse the physeal plate through the zone of hypertrophying cartilage; Type 2 involves the physis and continues through the mtaphysis; Type 3 involves the physis and continues through the epiphysis to involve the articular surface; Type 4 involves the articular surface, crosses the physis and continues into the metaphysis; and Type 5 a compression injury to the zone of resting cartilage of the physis.

Distal femoral physeal fractures are commonly Types 1 and 2; most physeal fractures in the dog are Type 2 while those in the cat are Type 1. This is due in part to the fact that the distal femoral metaphysis has four projections that correspond to four similar deep depressions in the epiphysis in the dog while in the cat, the projections are flatter and do not interdigitate as deeply with the corresponding epiphyseal depressions. Physeal fractures usually occur through the zone of hypertrophying cartilage, because this zone is characterized by large, vacuolated cells with minimal intercellular matrix.  Therefore, this zone is the weakest.

A variety of treatment methods have been described for repair of distal femoral physeal fractures including closed reduction and external fixation, normograde or retrograde placement of a single intramedullary pin with or without an anti-rotational Kirshner wire, multiple intramedullary pins, paired Rush pins, Steinman pins, or Kirshner wires employed in Rush pin technique, cross pins, bone plates, and lag screws. The ultimate goal of treatment should be accurate reduction and rigid stabilization of these fractures with as little iatrogenic damage to the germinal cells of the physis and their blood supply as possible.

While closed reduction and external fixation may be successful in selected cases, every attempt should be made to satisfactorily stabilize the fracture internally so that early return to function is achieved and restricted joint movement is avoided. When closed reduction and external fixation is used, a good result is the most that one can expect.

Surgical exposure for open reduction and internal fixation is achieved via a lateral parapatella approach with reflection of the patella medially. Interference with growth is a consideration in the selection of the method of repair; however, recent studies have suggested that premature closure of the physis occurs more commonly as a result of the initial trauma than the method of treatment employed. Distal femoral physeal closure normally occurs between six and eight months of age; as the majority of physeal fractures occur in dogs and cats greater than five months of age, over 90 percent of their skeletal growth has already been achieved by the time of injury. Therefore, in animals over five months of age, while some degree of femoral shortening may occur, the overwhelming majority of animals clinically accommodate shortening by a change in stifle or hock angulation. In dogs and cats under five months of age with substantial growth potential, the method of fixation chosen should provide adequate stabilization but should not mechanically bridge the physis. Early implant removal may minimize premature physeal closure. Any implant, which traverses the growth plate, will result in some degree of permanent damage to the growth plate. The least damage occurs when round, smooth, non-threaded implants are placed perpendicularly to the long axis of the growth plate.

Single intramedullary pin fixation, Rush pinning and modified Rush pin technique, and cross pinning are the most commonly employed techniques used to treat Salter Type 1 and 2 fractures. A single intramedullary pin should provide excellent alignment and stability if the opposing surfaces of the fracture interlock following anatomic reduction. However, in large dogs, single pin fixation may be inadequate to allow early use of the limb. In addition, femoral intramedullary pins existing the trochanteric fossa have been associated with sciatic nerve injury. Normograde pinning of distal femoral physeal fractures is less likely to induce sciatic nerve injury then retrograde pinning. Implant migration may also result in damage to the intra-articular surface of the stifle joint.

Although cross pin fixation works well, it is associated with more complications than other techniques including caudal malalignment and/or displacement of the distal fragment and quadriceps tie-down. In very immature animals, cross pin fixation may interfere with physeal growth because of the excessive pin angulation necessary for adequate stabilization.

Rush pins provide excellent fixation for distal femoral physeal fractures. Their disadvantage is the need for special instrumentation and the cost of the implants. Rush pins provide three point fixation, thereby increasing stabilization and making their application especially indicated in large dogs. If Rush pins are used in very immature animals, great care must be taken when driving the pins to prevent excessive compression of the germinal cell layer, which may result in growth arrest.

Steinman pins or Kirshner wires may be used in exactly the same way as Rush pins. Once the fracture is reduced, the pins are inserted laterally just cranial to the tendon of origin of the long digital extensor muscle, and medially on the distal medial bondyle symmetric to the later pin placement. The pins are alternately advanced in the medullary cavity. I prefer that the pins do not exit the trochanteric fossa so as to minimize the potential complication of sciatic nerve injury. Pre-bending the pins accentuates a three point fixation and results in rigid internal fixation and rotational stability. This technique can be used in very immature animals when fear of Rush pin compression of the germinal layer may be a factor. Such pins may be placed with relative minor trauma to the physis, and most animals continue to lengthen their femurs despite the pins through the growth plate. With proper alignment and internal fixation, an excellent result should be expected.

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Primary Pulmonary Neoplasia: The Results of Surgical Treatment in 14 Dogs.

Primary pulmonary neoplasia was diagnosed in 14 dogs presented to the California Animal Hospital for medical and surgical management of respiratory tract disease. Locations of the primary tumor were the right caudal (six), left caudal (five), right accessory (two), and right middle (one) lung lobes. Complete lobectomy of the affected lung lobe using a mechanical stapling device was performed in all cases. The tumor types observed were adenocarcinoma (six), bronchoalveolar carcinoma (six), anaplastic carcinoma (one), and epidermoid carcinoma (one). Of the 14 dogs undergoing exploratory thoracotomy, two died within a 72 hour postoperative time period. The remaining 12 dogs were monitored from two to 24 months (mean= 10 months) postoperatively to determine surgical complication and recurrence rates. No evidence of recurrence of pulmonary neoplasia has been observed in these dogs through the follow-up period.

Introduction:

Pulmonary neoplasms may be primary or secondary. Metastatic neoplasms of the lung are seen more commonly than primary tumors. The incidence rate of primary lung tumors has been estimated at 5.6 per 100,000 dogs. Although primary pulmonary neoplasia is relatively rare, as dogs continue to receive better medical attention enabling them to live longer, an increased incidence of these tumors may be observed.

The average age at the time of diagnosis is 10.5 years with the condition predominantly occurring in dogs seven years of age and older. breed or sex predisposition to primary lung tumors has not been identified. A higher incidence of primary tumors has been observed in the right lung lobes, with the right caudal lobe most frequently affected.

Any component tissue of the lung may be the site of origin of a neoplasm. The most commonly occurring primary lung tumors in the dog originate from the epithelium of the terminal bronchioli.

The majority of primary lung tumors are carinomatous. Based on histologic structure, most pathologists subdivide primary lung tumors into adenocarcinoma, bronchoalveolar carcinoma, anaplastic carcinoma, and carcinoid tumors. Other rare primary lung tumors include neoplasms arising from connective or lympathic tissue, and mesenchymal tumors.

The clinical signs associated with primary pulmonary neoplasia are usually vague and nonspecific. Symptoms observed may include loss of stamina, fatigue, anorexia and weight loss. Other clinical signs may include dyspnea, non-productive cough, hemoptysis, and lameness as a result of hypertrophic pulmonary osteoarthropathy. Occasionally, thoracic radiography reveals pulmonary lesions suggestive of neoplasia as incidental findings.

The prognosis associated with primary pulmonary neoplasia in the dog is dependent upon several factors, including (one) the severity of clinical signs, (two) the presence or absence of hilar lymphadenopathy, (three) the presence or absence of distant metastasis and (four) the tumor type.

The purpose of this paper is to describe the pathogenesis and clinical course of 14 dogs with primary pulmonary neoplasia and their responses to compete lobectomy.

Materials and Methods:

Exploratory thoracotomy was performed on 14 dogs with primary pulmonary neoplasia between January 1994 and December 1985. The dogs were elected for surgery based on the presence of a solitary mass involving a single lung lobe, with no evidence of distant metastasis or extrapleural involvement. A complete physical examination, as well as hematologic and biochemical blood analysis and urinalysis were performed in each case. Thoracic and abdominal radiographs were performed to eliminate the possibility of a primary neoplasm with pulmonary metastasis.

Complete lobectomy of the affected lung lobe using the TA 30 or TA 55 mechanical stapling deviceA was performed in each case. Examination for air leaks was made by flooding the cut surface with warm lactated Ringer’s solution. Leaks were managed with simple interrupted sutures using #2-0 polypropylene.

Following complete lobectomy, the thorax was lavaged, the remaining lung lobes were expanded to eliminate atelectasis, a chest tube was placed, and the thorax was closed. The chest was evacuated of all air and if there was no accumulation of air or fluid in the thorax over the next 24 hours, the chest tube was removed.

Representative sections of neoplastic tissue from each dog were submitted for histologic examination and classification based on the World Health Organization’s classification of pulmonary neoplasms in man.

Follow-up physical examination and suture removal were performed two weeks following surgery in all dogs. Follow-up thoracic radiography was performed at intervals of four to six months. All patients were followed from a minimum of two months to a maximum of 24 months.

Results:

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The results are given in Table 1. The average age of the dogs was 10.4 years (range = 3-14 years). There was no sex (seven male, seven female) or breed predilection. Clinical signs included coughing (five), dyspnea (three), and weight loss (two). There were no abnormal findings on physical examination in four dogs.

Of the 14 lung lobes removed, nine (64 percent) were on the right and five (36 percent) were on the left. Of those tumors affecting the right lung, six (67 percent) occurred in the caudal lobe, two (22 percent) occurred in the accessory lobe, and one (11 percent) occurred in the middle lobe. All five tumors affecting the left lung occurred in the caudal lobe.

Histologic examination revealed six adenocarcinomas (43 percent), six bronchoalveolar carcinomas (43 percent), and one epidermoid carcinoma (seven percent).

Two dogs died within a 72 hour postoperative time period because of cardiac arrhythmias non-responsive to anti-arrhythmic cardiac therapy.

Three dogs were euthanized because of unrelated causes (degenerative myelopthy – two, caudal cervical vertebral instability – one) and one dog died because of unrelated causes (renal failure). Survival time of these dogs ranged from four to 24 months (mean = 11.5 months). At the time of euthanasia or death, these dogs were asymptomatic from signs of recurrent respiratory tract disease.

Eight dogs are currently alive and free from signs of recurrent or progressive respiratory tract disease at two to 24 months (mean = 9.3 months) following surgery. Thoracic radiography performed every four to six months has revealed no evidence of recurrence.

Discussion:

Primary pulmonary neoplasms have been reported to occur predominantly in dogs over seven to eight years of age. The results of this study support this finding. No sex or breed predisposition to primary lung tumors have been identified. In this study, males and females were represented equally. Although no one breed was affected more frequently than others in this study, all of the dogs were medium to large size breeds with the exception of case #3. Further case studies were necessary to determine if this is either a significant trend or because of the predominance of medium to large breed dogs within our referral population.

Clinical signs associated with primary pulmonary neoplasia are often vague and nonspecific. It has been reported that as many as 33 percent of primary lung tumors are discovered during a physical or radiographic evaluation for another problem. There were no abnormal findings on physical examination in four of the 14 dogs (29 percent) in this study.

The most common clinical sign (five cases, 36 percent) was a non-productive cough. This is in agreement with the findings of previous investigators. Dyspnea (three cases, 21 percent) or weight loss (two cases, 14 percent) was the primary owner complaint in the remaining five cases.

It has been reported that the absence of clinical signs in man and dogs with primary pulmonary neoplasia is a favorable prognostic indicator. Because of the small sample size and length of the follow-up period a similar conclusion could not be drawn from the results of this study.

A number of investigators have reported a majority of primary pulmonary neoplasm affecting the right lung, with the right caudal lung lobe having the highest incidence of primary tumors. The results of this study are in agreement: 64 percent of the tumors were on the right side, with the right caudal lobe affected in 43 percent of the cases.

Histologic examination of primary lung tumors in dogs has indicated that nearly all lung tumors are malignant. Adenocarcinomas have been reported to be the most commonly occurring lung malignancy (75 to 83 percent). Epidermoid (squamous cell) carcinomas (six to 12 percent) are less common, as are anaplastic carcinomas (four to nine percent). This is in contrast to man, where squamous cell carcinoma (30 to 35 percent) is more common than adenocarcinoma (25 to 29 percent).

In this study, bronchoalveolar cell carcinomas (43 percent) occurred as frequently as adenocarcinomas (43 percent). Because of the small sample size, these results must be interpreted with caution. Anaplastic carcinoma (seven percent) and epidermoid carcinoma (seven percent) occurred less frequently.

In many dogs, the confirmation of primary lung tumor may be shortly followed by premature euthanasia. It is the authors’ opinion that surgery is often indicated in the treatment of primary pulmonary neoplasia. The results of this study demonstrate that surgical excision of the affected lung lobe can lead to prolongation of good quality life.

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Total Hip Replacement.

The most frequent reason for performing a total hip replacement (THR) is relief of pain and disability caused by severe degenerative joint disease secondary to hip dysplasia. Other reasons include hip fractures, chronic dislocation of the hip and acute dislocation of the hip that cannot be reduced because of hip dysplasia or soft tissue damage. The presence of any and all of the aforementioned conditions leads to hip joint laxity, subluxation (partial dislocation) and or luxation (complete dislocation) which ultimately leads to varying degress of degenerative arthritic change. Contrary to what one may think, many dogs with arthritic hip joints seem to function normally while others exhibit severe crippling disease. In addition, the severity of the clinical signs does not necessarily correlate with the degree of radiographic or pathologic changes seen. Breed and individual differences in temperament may also affect the amount of discomfort exhibited. Total hip replacement is now a well established procedure in veterinary orthopaedic surgery. Although there are some variations in technique and types of implant, most involve the replacement of the acetabulum with an ultra-high molecular weight polyethylene cup and the femoral head with a cobalt chrome ball and stem which are secured in position with acrylic (cemented) or porous coated implants resulting in normal or near normal function and activity.

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Clinical signs including lameness, reluctance to exercise and difficulty rising, using the stairs or jumping into and/or out of the car are often signs of hip related problems. Lameness of the hind limb varies from barely-detectable gait abnormalities to non-weight-bearing lameness. Lameness is usually especially evident after exercise periods. A “bunny-hopping” gait is often seen in affected young dogs and is characterized by simultaneous advancement of both hind limbs while running. Young dysplastic dogs often lay on their belly with limbs outstretched behind them. Pain is often elicited during full extension of the joint by a veterinarian. Hip dysplasia is not generally an acute lameness, but one of slow progression of lameness severity. It is not uncommon for dogs with hip osteoarthritis to have in addition, other orthopedic injuries. Many times it is these other problems that are the source of the lameness that prompted the visit to the veterinarian in the first place. The most common conditions which may mimic or be confused with clinically painful hips include cauda equine syndrome, cranial cruciate ligament tears, other rear limb arthritic conditions and neoplasia. Since dogs can have profound radiographic changes with arthritis and yet have few if any symptoms, any new lameness exhibited by such a dog, or sudden worsening of what had heretofore been a mild lameness, should prompt skepticism that it is due to the hips until proven to be so. Only when other causes have been excluded or treated should attention be focused on the hips and medical and surgical treatment such as THR be contemplated. 

Not all dogs with hip dysplasia or osteoarthritis require surgical treatment. The decision for performing a THR and the timing for joint replacement surgery depends on a number of factors, including the degree of clinical disability and discomfort, intended use of the dog, and the presence of other diseases or injuries. As mentioned previously the decision to perform THR is never based on radiographs alone, no matter how severe the changes appear. There can be a poor correlation between radiographic severity and clinical severity, and some dogs with terrible looking hips are yet functioning at a high athletic level with no apparent pain. So the decision to treat arthritic hips, with medicine or surgery, is always based on whatever clinical disability the patient is exhibiting.

Medical management to alleviate clinical symptoms is always attempted prior to surgical intervention as many dogs with degenerative arthritis can be kept comfortable and active with medical management. It is important to keep the patient at a normal body weight and to provide regular, controlled activity. Medical management includes the administration of steroidal or non-steroidal anti-inflammatories, muscle relaxants, poly-sulfated glycosaminoglycans (Adequan), hyaluronic acid (Legend), neutraceuticals (glucosamine, chondroitin, msm, creatine), omega 3 and 6 essential fatty acids, platelet rich plasma, Class IV laser therapy, acupuncture and physical therapy. If hip pain persists in spite of appropriate medical management, surgical therapy should be considered. The decision to intervene with surgery is based on the amount of pain, discomfort and lameness exhibited by the dog. Typically the patient has been refractory to medical therapy or has not returned to an acceptable level of performance. The decision to proceed with surgery should not wait until there is severe pain and/or loss of muscle mass as this may compromise the surgical result. Since total hip replacement results in near normal to normal function and activity, if medical treatment does not alleviate clinical symptoms, then surgical treatment is recommended. 

Surgical options include femoral head and neck ostectomy (FHO) with or without a biceps sling or total hip replacement. While the purpose of this article is THR, it is appropriate to diverge and mention the FHO procedure as this has been the contemporary surgical option to treat coxofemoral pathology in smaller dogs and cats. An FHO with a biceps sling removes the femoral head and interposes muscle between the acetabulum and femoral neck so that there is no longer bone rubbing on bone in the diseased joint. While this can relieve much of the pain, the loss of the normal ball-and-socket anatomic structure of the hip may result in a limb that will not function normal mechanically. Small, light-weight dogs and cats do better than large dogs with an FHO. The advantages of FHO include easier recovery, less risky complications, and less expense. If a femoral head and neck excision was performed previously, the results of total hip replacement are generally not as rewarding as cases receiving hip replacement initially.  An FHO can be converted into a total hip replacement, however, it is a technically demanding procedure with a higher complication rate than primary total hip replacement.  The longer the interval from the FHO to the total hip, the more difficult the total hip replacement becomes, with the best results occurring if the total hip replacement is performed early (4-6 weeks) after the FHO. Conversion of an FHO to a THR should not be recommended, as calcar support for the prosthesis is removed by the excision arthroplasty, there is a higher risk of infection and there may be inadequate muscular support for the prosthesis.

After FHO, especially in large dogs, the hindlimb is shortened to a variable degree, biomechanical function is altered, pain relief may be unpredictable, muscle atrophy with weakness is a common long-term finding and postoperative rehabilitation is prolonged. On the contrary, published reports of objective measures taken following THR in large dogs consistently document a return to normal function. The goal of THR is a pain-free joint that mimics normal biomechanics with excellent long-term function. THR is a common procedure used to treat degenerative arthritis and other hip arthropathies in large dogs, and it should be considered in smaller patients. Total hip replacement has historically been used in medium, large and giant breed dogs. There is now a much wider range of implant sizes, so it is available for small dogs as well. Truly, the only drawback to the utilization of THR in smaller patients is its expense and the fact that these smaller implants are usually cemented rather than porous-coated.

Total hip replacement techniques fall into two categories: Cemented and Cementless. Cemented THR provides fine short term, but less satisfactory long term outcomes. Cemented implants are held in place with an acrylic, but there may be break down of the interface between the cement and bone over time. For this reason, in the past, total hip replacement was only considered in older dogs. This was due to concerns with how long the cemented implants would remain stable. With the uncemented, porous-coated implants that we now use, break-down of the interface is unlikely and the high quality of the plastic of the cup will help it last for the life of the dog. Porous-coated implants become stable by in-growth of bone into their beaded surface in the first few weeks to months after implantation. Implants can be placed in young dogs with the expectation that they will provide a lifetime of pain-free function, and are preferentially indicated for hip replacement in young dogs.

In many dogs, both hips are arthritic. In most cases, the hip with the worse function is operated on first. This results in good to excellent function in about 75 percent of dogs. The other 25 percent remain somewhat lame on the opposite hip, and total hip replacement of the other side is considered in these cases.

Both hips are never operated upon at the same time because bilateral surgery increases discomfort and the risk of complications.  For this reason the two surgeries are separated by approximately 3-4 months in most cases. If function is good after the worse hip is replaced, the second hip may not need surgery and continued medical management may continue to alleviate clinical symptoms.

As there are risks inherent with any major surgical procedure, these risks should be thoroughly discussed with the client prior to surgical intervention. The current complication rate following total hip replacement is 2 to 5 percent. Complications are best treated when identified early. Significant complications include but are not limited to:

  • Dislocation of the prosthetic joint is rare, and is most likely to occur in the first 4 weeks after surgery. It may be corrected manually, but another surgery is often necessary.
  • Infection is a serious potential problem. If it occurs in the area of the wound, it is generally treated with antibiotics. If it occurs in the bone, removal of the prosthesis may be necessary.
  • Subsidence or sinking of the stem – a small amount of settling of the stem has no effect on function of the prosthetic joint. A large amount of subsidence or stem rotation may require surgical revision of the stem.
  • Fissure or Fracture of the femur – uncemented implants are hammered into place. Fissures can develop. If they are seen during surgery, wire is placed to prevent them from expanding. If they develop after surgery, they may lead to subsidence of the stem, or fracture of the bone. Another surgery would be required to manage this issue.
  • Loosening of the prosthesis is an uncommon problem with uncemented prostheses. If loosening is significant or progressive, the implant may need to be replaced or removed.

Most dogs are able to stand and walk on the new prosthesis within the first few days after surgery. While hospitalized, exercise is restricted to cage confinement with 10 to 15 minute walks under leash restraint twice daily. Most animals undergoing total hip replacement are hospitalized for a total of 3 to 4 days.

During the first month at home, the dog must have very limited activity. During this crucial period the joint capsule, muscles and tendons are healing, and helping to stabilize the hip. This means that dogs are allowed short walks only, and only on a leash. Otherwise the dog should be kept confined. Dogs should not run, play, jump, or climb flights of stairs. During this time, care should be taken to avoid activity on slippery surfaces, and stairs should be climbed only while the dog is under the direct control of the owner. Going up and down one or two steps to get outside is acceptable. Management at home will require strict supervision, and activity must be restricted in order to optimize surgical recovery. Adherence to postoperative restrictions can minimize potential complication. One month after surgery, supervised exercise can be gradually increased over the next 4 weeks. During this second month dogs are still limited in their activity, but can start increasing the length of their walks outside. At the end of 8 weeks, more normal activity is allowed. Between the second and third month activity is gradually increased so that by the end of the third month the dog is nearly back to normal function and activity. Vigorous, rough play or hard work is allowed after gaining strength and conditioning. Radiographic evaluation and orthopedic examination are necessary at 3 and 6 months after surgery, and every 2 years thereafter. This provides a history of the patient’s progress and may help to detect potential complications.

The majority of dogs are found to be more comfortable and have an improved quality of life following THR. Many owners report that their pet can do things they have not done since they were a puppy. Increase in muscle mass, improved hip motion, and increased activity levels are observed in most patients. Up to 95% of the dogs whose hips have been replaced return to normal or near normal ambulatory function. More than 95% of owners feel that their dog’s quality of life is significantly improved following THR. Although the state-of the-art equipment, implants, advanced technical expertise and training which go into the THR surgery are expensive, few other procedures are capable of so dramatically changing the quality of a pet’s life. It is for these reasons that THR is the surgical treatment of choice in both juvenile and adult dogs to obtain the best functional outcome when the pain and discomfort of degenerative arthritis is refractory to medical therapy.

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Canine Hip Dysplasia-Part 2.

Surgical Treatment for the Immature Patient

A number of different surgical techniques have been employed to treat canine hip dysplasia. The procedure, which is ultimately selected, should be based upon careful observation and evaluation of the individual patient. Criteria, which must be addressed, include: age of the patient; severity of subluxation (i.e., the angle of Wiberg); the angle of inclination and anteversion; the depth of the acetabulum; and the presence or absence of femoral head deformity and associated changes indicative of osteoarthritis.

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The surgical procedures most commonly recommended for treatment include: triple pelvic osteotomy; intertrochanteric de-rotational femoral osteotomy; excision arthroplasty with or without a bicep sling; and total hip replacement.

The advantages, as well as the indication for each of these procedures, will be discussed in this and in a future article.

The primary goal of surgical intervention for the treatment of canine hip dysplasia in the majority of immature patients is re-direction of the acetabulum. The restoration of hip stability promotes a more normal development of the hip and results in a decrease or halt of the osteoarthritic changes typically associated with degerenative joint disease.

Because the ultimate goal in a young dog is to help reshape the acetabulum so as to create more depth to accommodate the femoral head and save the hip joint, the technique of choice is the triple pelvic osteotomy (TPO). This procedure presupposes that the femoral component of the hip is normal. Triple pelvic osteotomy is not designed to correct the subluxation problems associated with coxa valga, i.e., increased angle of inclination or increased anteversion of the proximal femur. Such problems need to be addressed by performing a varus osteotomy and demonstrated, however, that if the acetabular component is repositioned such that normal congruency of the joint is maintained, the femoral changes will revert toward normal with time.

Fortunately, in my experience, femoral osteotomy is usually not necessary, although several studies have indicated that functional results tend to be less satisfactory in dogs having the largest angles of anteversion. Varus and/or intertrochanteric osteotomy is most appropriate in the young dog with subluxation and femoral dysplasia without acetabular dysplasia. As acetabular dysplasia is frequently present, these techniques are seldom employed as a sole means of surgical correction. As previously mentioned, the overwhelming majority of patients exhibit acetabular dysplasia, and the resulting new position obtained by a TPO produces adequate acetabular depth to provide hip stability. However, femoral osteotomy needs to be considered as an ancillary procedure in some cases.

The ideal candidates for a TPO are immature dogs with pain and/or lameness associated with hip subluxation. Since the purpose of the TPO is to prevent the development of degenerative joint disease, only those joints with minimal or no preexisting degenerative joint disease should be considered as candidates for the procedure. When radiographic changes of osteoarthritis are present, excision arthroplasty or total hip replacement may be indicated as the likelihood of success with a TPO is minimized.

The dog’s age is also an important consideration, as rapid breakdown of the dorsal acetabular rim occurs from 4 to 8 months of age in dysplastic puppies. For these reasons, the surgery should be performed prior to nine to ten months of age to achieve best results. However, if the other criteria mentioned previously have been met, good clinical results can still be achieved in older dogs.

Another prerequisite of surgery is the ability to reduce the hip while the patient is under general anesthesia. If the hip cannot be reduced and stabilized by the femoral abduction and internal rotation, there is a diminished chance of success that a TPO would produce good hip stability. Dogs with complete luxation of the hip (grade IV hip dysplasia) however, have been successfully treated with this procedure.

As with any other surgical procedure, numerous techniques and variations of TPO have been developed and used over the last several years to enhance success and minimize complications. The earlier techniques advocated a stair-step osteotomy of the ilium and internal stabilization consisting of screw and wire fixation with or without trochanteric osteotomy. More recently, techniques have employed straight osteotomy of the ilium and rigid internal fixation utilizing bone plates with or without ischial wiring. My own personal preference is to use an oscillating saw to perform the pubic, ischial, and ilial osteotomies through three separate skin incisions. The freely movable acetabular segment is then rotated and tilted into its new position, and rigid stability is achieved and maintained by application of a special pre-contoured bone plate.

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Routine post-operative care consists of confinement and restriction of exercise throughout the immediate post-operative period. Strict rest and confinement should eliminate the potential complication of loss of fixation. Other complications include constipation, urethral impingement, and sciatic nerve injury. Constipation is usually easily alleviated with administration of stool softener. Proper surgical technique should prevent complication related to urethral and/or sciatic injury. The overwhelming majority of animals will begin bearing weight on the operated limb within 24 to 48 hours, although significant additional time is required for complete healing.

All in all, triple pelvic osteotomy is an extremely successful treatment of choice for hip dysplasia in the immature dog. This high degree of success, however, depends upon the careful selection of surgical candidates and familiarity with the surgical techniques available.

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Intervertebral Disc Disease.

Thoracolumbar intervertebral disc disease is a well-recognized entity in veterinary medicine. The clinical incidence of intervertebral disc disease has been reported to be higher in the chondrodystrophoid breeds of dogs although disc degeneration occurs in all breeds. The pathophysiologic distinction between intervertebral disc disease in the chondrodystrophoid and nonchondrodystrophoid breeds has been reported in detail.

The severity of the spinal cord lesion resulting from intervertebral disk extrusion may be influenced by (1) the magnitude of the force of impact of the extruded disk material on the spinal cord; (2) the extent of the mechanical distortion of the spinal cord; (3) the chemical, neuronal, and vascular alterations within the spinal cord; (4) the rate of onset of spinal cord compression; and (5) the duration of attenuation.

Anatomy

The intervertebral disk is located between two adjacent vertebrae and acts as a “shock absorber” to handle forces along the spine. There are two parts of the disk which each work differently. The center portion, called the nucleus pulposus (NP), has a high water concentration and is positioned to help absorb the forces along the spinal column. The majority of the force of a compressive load is absorbed by the nucleus pulposus. The outer portion, the annulus fibrosis (AF), is more like a ligament. When forces impact the intervertebral disk, the nucleus pulposus spreads and transmits forces outwards to the annulus fibrosus, which also spreads. The annulus fibrosus, while flexible, is more rigid and maintains disk structure. When the forces along the intervertebral disk cease, the elasticity of the annulus fibrosus allows return to the normal shape of the disk. From the second to the tenth thoracic vertebra, the intercapital ligament between opposite rib heads lies ventral to the dorsal longitudinal ligament and dorsal to the disks. This thick ligament is thought to be the reason disk extrusion is uncommon in the cranial thoracic area. The paired vertebral sinuses lie in a ventrolateral position along the floor of the vertebral canal. Hemorrhage from the vertebral sinuses can accompany disk extrusion or can obstruct visualization during surgical decompression.

The intervertebral disk is found between all but the first two cervical (neck) vertebrae. Individually, an intervertebral disk is the largest organ in the body that does not get direct blood supply bringing nutrients and oxygen to and removing waste products from the cells of the disk. These functions are maintained mostly by diffusion from the end of the vertebral bones. This is a relatively inefficient process in relationship to the high metabolic activity of the cells that make up the intervertebral disk.

Disk degeneration is primarily a result of a breakdown in the process of diffusion leading to an environment in which the cells cannot maintain normal health and function. There is no clinical treatment that can prevent the degenerative changes, but daily controlled exercise can promote disk health by promoting diffusion in the spine.

Degeneration of the intervertebral disk leads to a change in function and chemical properties of the disk, which can result in progressive injury and failure (or rupture) of the disk. When the intervetebral disk fails, it usually does so in an upward direction into the spinal canal and this can lead to compression of the spinal cord.

Pathophysiology

Because most of the nervous system is inaccessible for direct examination, diagnosis of neurological problems depends on obtaining a good history, consideration of the species, breed, age, and gender of the patient, and conducting a thorough neurological examination in order to establish a neuroanatomic diagnosis.

There are two major types of disc disease in dogs. HansenType I disk degeneration is an early degeneration of the disk that is most commonly observed in chondrodystrophic breeds of dogs including the Dachshund, Shih Tzu, and Beagle. In this type of disk disease, as the disk ages, areas of the nucleus pulposus show signs of cellular necrosis, disintegration of the matrix, and calcification. The biochemical alterations associated with the degeneration of the nucleus pulposus are primarily a loss of water and proteoglycan molecules as well as an increase in collagen content. The poor biomechanical properties of the degenerating nucleus result in disruption of the lamellae of the annulus, which progresses until the calcified nuclear material erupts dorsally through the outer layers of the annulus and impacts on the spinal cord.  In this type of disk disease, it is not uncommon for the NP to extrude out of the center of the disk to result in rapid concussion as well as compression to the spinal cord. The age range of presentation is usually between two and twelve years of age, but peak incidence of dogs presenting with this type of disk disease is between 4-8 years of age, with an average age of 5.5 years of age.

Hansen Type II disk degeneration is associated with normal aging changes. This is most often seen in middle-aged to older large breed dogs including but not limited to the German Shephard.  The changes in Type II disk degeneration include alterations in the NP causing it to become similar in cellular properties and chemistry to that of the AF. In this type of disk disease, the primary physical change is tearing in the fibers of the AF and bulging or protrusion of the annulus fibrosus into the spinal canal. The degree of compression to the spinal cord can vary from minimally to severely compressed within the spinal canal. The onset usually involves more gradual progression of weakness, and often, the owner does not know exactly when it started. However, an acute and large disk extrusion is occasionally seen with this type of disk degeneration.

Whether the onset of disk extrusion is rapid or chronic, the compression to the spinal cord leads to neurological dysfunction. This can range from mild gait change and ataxia (incoordination of the limbs behind the spinal cord region affected) to weakness or even paralysis. It is not uncommon to see pain as the only presenting sign even when there is significant spinal cord compression. The extent of the clinical symptoms exhibited depends upon the length of time the disc has been herniated, the degree of compression of the spinal cord, the force of impact that the degenerated disc has on the spinal cord, and the rapidity of disc herniation and the resultant spinal shock and contusion to the spinal cord.

The most common sites for intervertebral disk extrusions in the dog occur between T11-12 and L2-3 (approximately 85% of all disc herniation), the cervical intervertebral disc C2-C3, and the L7-S1 intervertebral disc space in the lower back. Males are more commonly affected than females. Lumbosacral disc disease, a cauda equina disease at L7/S1, occurs most frequently in large breed dogs (e.g., Shepherd dogs) and is associated with Hansen type II disc disease, vertebral instability, and spinal stenosis, and the complex is called degenerative lumbosacral stenosis, a situation similar to sciatica in people.

Clinical Signs of Disc Disease

Clinical signs of intervertebral disc disease (IVDD) include spinal pain and varying degrees of neurologic deficits. Acute intervertebral disk extrusions are often characterized by the sudden onset of dysfunction of the spinal cord and pain. Chronic intervertebral disk extrusions are more common in large-breed dogs. With the latter form of disc compression, slow, progressive dysfunction without pain is common. The slow, progressive dysfunction associated with chronic intervertebral disk extrusions often times worsens in a rapid fashion as the compensatory limits of the spinal cord are exceeded. Spinal pain without paresis may cause the animal to be agitated, aggressive, or more vocal. Some animals will lie quietly refusing to walk whereas others will walk constantly or pace. Thoracolumbar IVDD may cause animals to walk with an arched back whereas dogs with cervical disk disease will be reluctant to elevate their heads or shake their ears. If there is compression on a nerve root, the animal may hold the affected limb up and have decreased weight bearing. Clinical signs of L7-S1 IVDD include pain upon rising, reluctance to jump up and down or negotiate the stairs, hesitancy to jump into or out of the car, and difficulty defecating. Some animals will have spinal pain as their only clinical sign. Clinical signs of spinal pain in our patient may improve, remain static, or progress depending on the disease progression. The clinical signs of spinal cord compression have been attributed to direct mechanical derangement of nerve tissue and hypoxic changes resulting from pressure on the vascular system in the spinal cord. Other causes for the neurologic signs include ischemia, edema, and reperfusion injury that may result in more severe spinal cord degeneration and hemorrhagic myelomalacia. Progression of neurologic clinical signs is correlated to increasing compression of the spinal cord. The larger, heavily myelinated fibers that mediate proprioception are affected first, followed (in descending order) by the intermediate sized fibers involved in voluntary motor function; the slightly smaller fibers that mediate superficial pain sensation; and, finally, the small unmyelinated fibers that mediate deep pain sensation. The spinal cord heals in the reverse direction with deep pain perception returning first, followed by superficial pain, voluntary motor control, and proprioception. Therefore, increasingly severe clinical signs occur in the following order: spinal pain, ataxia, paresis, paralysis, and loss of deep pain sensation. The ability to perceive superficial pain is typically lost at the same time that voluntary motor control is lost. Ataxia is the loss of coordination and is characterized by a broad-based stance and incoordination of the trunk or limbs in IVDD. Clinically, we may see crossing over of the limbs when walking or an over-reaching gait. Postural reactions may be diminished or absent with an ataxic animal. Paresis (weakness) and paralysis are measures of an animal’s voluntary motor ability. Gradation is arbitrary and may be characterized as mild, moderate, or severe. It is more helpful to describe if the animal can support weight or advance the limbs. The last modality lost is the perception of deep pain. An animal that has lost deep pain perception has a guarded prognosis and for the best possible outcome should be considered an emergency surgical candidate. Deep pain sensation is cerebral recognition of the painful stimuli and is different from the flexor reflex. An animal with no deep pain may retract their leg, but does not cry out, attempt to bite the examiner, or move away from the stimuli.

Diagnosis

Diagnosis of intervertebral disc disease is based upon the clinical presentation, history, and ultimately, the imaging findings. Survey radiography, myelography (contrast-assisted radiographs where a radiological contrast agent – dye – is injected into the spinal fluid to permit visualization of the otherwise radiographically invisible spinal cord on x-rays), contrast assisted computed axial tomography (CAT Scans), and magnetic resonance imaging (MRI) are utilized to diagnose intervertebral disk disease and accurately localize the compressive spinal cord lesion. Radiographic findings suggestive of IVDD include collapse or wedging of the intervertebral disk, deformities of the intervertebral foramina, and the presence of radiopaque material in or around the spinal canal.  While routine spinal radiographs may give us the suspicion of disk disease, the spinal cord and canal are not adequately visualized and significant spinal cord compression and injury are not identified in the majority of cases. The most accurate methods of diagnosis of spinal cord compression caused by IVDD require imaging of the spinal cord with myelography, computed tomography (CT), or magnetic resonance imaging (MRI). All of these methods require general anesthesia.

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MEDICAL AND SURGICAL TREATMENT

Neurological grading in canine IVDD is valuable to follow the progression of neurological deficits in time (improvement or worsening), to choose the mode of therapy, for prognosis, and for assessment of outcome after medical or surgical treatment.

NEUROLOGICAL GRADING IN CANINE INTERVERTEBRAL DISC DISEASE:

     
  • Grade 5: normal.
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  • Grade 4: cervical or thoracolumbar pain, hyperaesthesia.
  •  Grade 3: paresis (muscle weakness) with decreased proprioception, ambulatory (able to walk).
  •  Grade 2: severe paresis with absent proprioception, not ambulatory (not able to walk).
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  • Grade 1: paralysis (not able to stand or walk), decreased or no bladder control, conscious deep pain perception present.
  • Grade 0: paralysis, urinary and fecal incontinence, no deep conscious pain perception.

There is a diversity of opinion regarding treatment options for dogs with IVDD, but general guidelines can be used for selecting therapy. Decisions regarding when and if surgical versus medical treatment for spinal compressive disease is indicated depend primarily upon the severity of the neurological signs and the chronicity of the problem. In addition, treatment is modified in relation to the presumptive diagnosis, owner finances, and concomitant medical problems.

Patients with pain only (Grade 4) or pain with minimal neurologic deficits (Grade 3) can often be managed conservatively. It should be mentioned, however, that improper management of the dog with spinal pain with or without minimal neurologic deficits may result in the progression of clinical signs and a worse over-all prognosis.

Ideally, any significant spinal cord compression (Grade 2-0) should be relieved surgically. While medications and time may improve the animal’s comfort and neurological function, compression on the spinal cord of these magnitudes most likely will remain and result in continued spinal cord injury and prevent complete return to normal function.  Removal of the extruded nuclear material and hemorrhage crushing the spinal cord is necessary to allow for revascularization, removal of toxic by-products within the spinal cord, and resolution of swelling or edema. Decompression is based upon the location of the extruded nuclear material and hemorrhage based upon myelographic, CT, or MRI findings. For the majority of dogs, if done early, surgery will result in a good to excellent outcome. The outcome for decompression of spinal cords that have been compressed for months to years becomes more difficult to predict. Some factors that will affect the outcome are irreversible spinal cord injury (from acute concussion or chronic compression), the animal’s overall health, and whether there are multiple levels of disk extrusion with spinal cord compression.

Proper medical therapy for the IVDD patient includes cage rest, non steroidal anti-inflammatory therapy ( deramax, metacam, rimadyl), corticosteroid therapy (dexamethasone sodium phosphate, solu medrol, prednisolone), muscle relaxants (robaxin), pain management (fentanyl patches, oxymorphone, buprenex, gabapentin, tramadol), and gastrointestinal protectants (fametodine, zantac, pepcid, tagamet). Non-steroidal and steroidal anti-inflammatory therapy should not be combined in the same treatment plan because of the increased risk of gastrointestinal ulceration. While some may consider corticosteroid therapy controversial in treating intervertebral disk disease, my personal opinion, based on over 20 years of experience as a board certified surgeon, is to give steroids. Used intelligently and judiciously, my experience is that steroids have absolutely had a positive effect on a substantial number of our spinal patients.

While physical therapy and massage therapy probably will not prevent IVDD disease, they are very useful in helping patients recover from spinal cord injury. In fact, these methods may be as important as any other factor in ensuring maximal recovery. In cases where surgery is not performed, physical therapy and massage therapy must be limited to the least aggressive methods. Massage therapy improves muscle and joint flexibility, increases blood supply (improving nutrient delivery and waste removal), and help prevent or breakdown scar tissue formation. It also helps relax muscle spasms and aids in patient comfort levels. Massage therapy for animals should be performed by massage therapist trained in animal behavior and anatomy, under the supervision of your veterinarian. Many of the basic principles can be learned by the owner under proper instruction. While acupuncture cannot prevent IVDD disease and should be used with the same caution as relieving pain by conventional measures, acupuncture provides many beneficial effects in treating IVDD disease or following surgical correction during the healing process. Acupuncture is widely accepted as a method to provide analgesia without the side-effects of drugs. More recently, Class IV laser therapy may be employed in the multi-modal approach for those patients managed medically as well as surgically.

The medically managed patient must be observed frequently for deterioration of neurologic signs. Client education is an important component of the medical management regime. The client should be informed of the severity of the disease and of the fact that the signs may suddenly become progressively worse in which case surgical therapy is indicated. Recurrent episodes are frequent and are commonly more severe than the previous one. Recurrence of clinical signs after non-surgical treatment occurs in 40% of patients. Overall recovery in dogs with grade 3-4 deficits is 80% to 90%. Paraplegic dogs with grade 2-0 deficits non-surgical treatment is rarely the treatment of choice because of the low response rate, high rate of recurrence, neurological worsening during treatment, and development of complications. In dogs with grade 0 neurological deficits, the duration of absence of conscious deep pain sensation is an important prognostic parameter. Dogs with grade 0 neurological deficits should be regarded as emergencies and require surgery within 12-24 hours. When grade 0 neurological deficits persist beyond 24-48 hours the result of any treatment (surgical or nonsurgical) becomes minimal. Medical management has been shown to be as ineffective as surgical therapy in the majority of patients with sensorimotor paralysis for more than 24-48 hours. However, some clients do not consider euthanasia as an immediate alternative in these cases and may request some form of therapy.

The surgical approach taken to appropriately decompress the spinal cord is determined by the location of the herniated disc material within the spinal canal and the exact intervertebral disc space affected. In the cervical or neck region, a ventral or anterior approach is favored. The dorsal or posterior approach procedures are sometimes necessary; however, excessive muscle hemorrhage, increased surgery time, the difficulty of removing disk material from the ventral spinal canal, and prolonged postoperative care make this approach undesirable as a routine procedure. The ventral approach is less traumatic and requires less surgery time. The ventral-slot technique allows direct access to the extruded disk material and direct visualization of the affected spinal cord. The major disadvantage of the ventral-slot technique is the potential for hemorrhage associated with laceration of the venous sinuses.

Dorsolateral hemilaminectomy is the most common surgical treatment for thoracolumbar disc disease.

Hemilaminectomy best preserves the mechanical and structural integrity of the spine while allowing for excellent access and decompression. Dorsal laminectomy is not recommended in the thoracolumbar area because it causes considerable biomechanical instability and may lead to neurological worsening. In the lower lumbar area (L7-S1), however, dorsal decompressive laminectomy is the procedure of choice.

In addition to surgically decompressing the spinal cord to allow for spinal cord recovery, preventing further extrusions by the removal of the nucleus from the offending disk and other discs which can rupture is sometimes performed in breeds with a high incidence of repeat disc extrusions. This procedure is termed a fenestration. It is not a risk free procedure and in some cases can exacerbate the already existing clinical signs of spinal cord disease. It is also not a guarantee that the prophylactically fenestrated discs will not herniate at a later date as up to 20% of nucleus may be missed with this procedure. For these reasons, it is not commonly performed at our facility. Patients that are grades 2-0 are considered immediate surgical candidates. Grade 3-4 animals that have surgery performed within 48 hours have an excellent recovery rate to useful limb function (95%). Grade 0 animals (lose the perception of deep pain) that are operated on within 12-24 hours still have a fair to good prognosis for recovery (80-90%). If an animal has lost deep pain for more than 48 hours, a guarded prognosis should be given to the owner although one recent review indicated a 50% recovery rate.

The syndrome of myelomalacia is an important consideration in prognosticating the outcome of spinal trauma. Durotomy is performed when either an edematous spinal cord or discoloration suggestive of myelomalacia is present. Durotomy is ineffective as a method of treating compressive spinal cord trauma unless performed immediately (less than 2 hours) after the trauma has been suspected. Durotomy does, however, permit direct observation of the cord to see if myelomalacia is present. Myelomalacia occurs when severe, acute spinal cord trauma results in nearly complete destruction of nervous tissue. The cause and progression of myelomalacia is not completely understood, but the ischemia-reperfusion cascade results in lipid peroxidation and necrosis of myelin, and axons is suspected. Dogs with myelomalacia that have no deep pain perception and neurologic signs may progress cranial and caudal to the original injury. The typical clinical picture is an acute onset of paralysis with loss of deep pain followed by ascending and/or descending signs of neurologic dysfunction with ascending analgesia. Oftentimes, these patients are ill, febrile, and have extreme pain at the cranial edge of the lesion. Myelomalacia carries a hopeless prognosis.

Whether managed medically or surgically, paralyzed patients need to be maintained with excellent nursing care. Bladder management prevents urinary tract infections, overdistension, and urine scalding. The bladder needs to be expressed manually every 6-8 hours. If the bladder cannot be expressed, we recommend intermittent bladder catheterization using a sterile technique. Medication that assists with the ease of manual bladder expression include phenoxybenzamine and bethanacol,. These medications can be used together. Animals must also be maintained in a clean environment to prevent decubital ulceration (pressure sores). Frequent turning (every 4-6 hours) and proper bedding of sheepskin pads or foam “egg crate” bedding helps to lessen irritation. The skin needs to be closely monitored for the development of pressure sores as they are easier to prevent than reverse.

Postoperative recovery is often aided by the aforementioned medical therapy, controlled exercise and physiotherapy, acupuncture, and laser therapy afforded the medically managed patient. The best success rates combine medical therapy and surgical intervention. Functional improvement may be noted as early as 3-5 days following medical and surgical intervention. Continued gradual improvement over the following 4-6 weeks is expected. The prognosis for functional recovery is good for dogs with grade 2, 3, and 4 lesions irrespective of the treatment choice. Dogs with grade 1 lesions have better prognosis after surgical treatment than after nonsurgical treatment. In dogs with grade 0 lesions that are treated within 24-48 hours of onset, the animal has a chance of making a functional recovery.  Careful selection of surgical candidates should be based on the findings of a complete physical and neurologic examination, radiography, and specialized non-invasive diagnostic modalities (myelography, computed tomography, magnetic reasonance imaging). In conclusion, the combination of medical and surgical therapy yields an optimal recovery.
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Management of Shoulder Luxations in Toy and Small Breed Dogs.

The shoulder joint is the most mobile of all of the main limb joints. While its primary motion is in a sagittal plane, the shoulder has a significant amount of abduction and adduction, and internal and external rotation. Its stability is ensured by the joint capsule, the medial and lateral glenohumeral ligaments, and by large tendons located inside (tendon of origin of the biceps brachii muscle) or immediately outside the joint (supraspinatus, infraspinatus, teres minor, and subscapularis). The shoulder joint (or scapulohumeral joint) consists of a spherical humeral head articulating with a shallow glenoid fossa of the scapula. The stability of the shoulder joint is dependent on a complex interaction between active and passive mechanisms. The passive mechanisms (do not require energy expenditure by muscle) are the glenohumeral ligaments, the joint capsule, joint conformity, and the glenoid labrum. The active mechanisms (do require energy expenditure by muscle) are the muscles of the shoulder and the rotator cuff. The articular components of the shoulder are the glenoid cavity and the humeral head and they are connected by the joint capsule and the glenohumeral ligaments. It was previously believed that the rotator cuff muscles were responsible for maintaining joint stability; however, it is now established that the joint capsule and glenohumeral ligaments play a significant role in joint stability. The “cuff tendons” are four tendons that directly support the joint: the supraspinatus cranially, subscapularis medially, infraspinatus laterally, teres minor caudolaterally. The rotator cuff tendons act in concert with the joint capsule, glenohumeral ligaments and regional muscles to support the shoulder during movement. By contracting together, the cuff muscles press the humeral head into the glenoid fossa providing a secure scapulohumeral link. By contracting selectively, cuff muscles can resist displacing forces resulting from the contraction of the principal shoulder muscles.

Scapulohumeral luxation is an uncommon injury in dogs and rarely occurs in cats. The majority of luxations are medial or lateral, as cranial and caudal luxations are rarely observed. Trauma and congenital malformation are the most common causes of joint instability.  Medial luxation is the most frequently observed luxation.  Medial traumatic luxation may be seen in all type of dogs. It is associated with a rupture of the medial gleno-humeral capsule and ligaments and disruption of subscapularis muscle. In small breeds, medial luxation is often congenital and may be bilateral, with an important component being developmental laxity or insufficient development of the glenoid cavity, which prevents any successful reduction. Lateral luxation occurs most often in large size breeds after trauma. It is associated with a rupture of the medial gleno-humeral capsule and ligament and a rupture of the infraspinatus muscle tendon.

Affected animals may present with different degrees of lameness, which can range from mild intermittent to persistent unilateral forelimb lameness to complete non weight bearing lameness. After a traumatic luxation, the dog is usually non-weight bearing and holds the affected limb in flexion with external rotation of the foot. In contrast, dogs with a congenital luxation usually present as an intermittent to continuous lameness which is progressive in nature. Some dogs with congenital bilateral luxation however, show very little impairment in locomotion. On physical examination, the position of the greater tubercle and the acromial process are compared on both sides by bilateral palpation to reveal any sort of dissymmetry. The examination is performed with the dog in lateral recumbency and the affected shoulder uppermost. A cranial “drawer test” is performed to detect any possible cranio-caudal instability, in addition, the scapula can be immobilized with one had while the limb is abducted. Manipulation of the joint may or not be associated with crepitus, pain, muscle atrophy, possibility of reduction of the luxation, or some degree of ankylosis. The ability to abduct the limb away from the body for more than a 30 degrees angle is generally indicative of joint instability. In many cases, complete examination of the shoulder for signs of instability may need to be performed under anesthesia or heavy sedation. Flexion, extension, abduction, cranio-caudal translation, and rotational stability of the shoulder joint should be assessed. Normal range of flexion and extension are 40 degrees for flexion and 165 degrees for extension. Circumduction of the shoulder should not give rise to subluxation. Cranial and caudal translation should be similar in both shoulders. A normal abduction test is approximately 23 degrees; abnormal abduction is considered present when abduction exceeds this degree and there is a difference in abduction angle between the injured side and the normal side. When performing the abduction test, it is essential to maintain the limb in extension with the elbow in neutral position. If the elbow is externally rotated with the limb in extension, the shoulder joint will be internally rotated. The latter will give a false positive abduction test. To maintain the elbow in neutral position, the surgeon should place his thumb on the lateral surface of the olecranon caudal to the humeral epicondyle. Maintaining the thumb facing upward assures that the elbow remains in neutral position.

Radiographic examination is necessary to confirm the diagnosis. On the medio-lateral view, the displacement of the humeral head may not be easy to recognise unless it is a cranial or caudal luxation. Typically, on a medio-lateral view, the glenoid should overlap the humeral head with a medial luxation. Care should be taken to observe for possible fractures of the medial glenoid rim which would preclude conservative treatment via closed reduction. The cranio-caudal radiographic view is usually more diagnostic in cases of medial or lateral luxation. Care should be taken not to reduce the luxation by extending the limb cranially when positioning the dog for radiographic evaluation. Radiography also allows for the diagnosis of secondary degenerative joint disease lesions which have been reported to occur in 57% of all cases of shoulder instability. The existence of concurrent fracture may also be assessed. Mild cases of shoulder instability may exhibit few or no obvious evidence of radiographic change and may require bone scan, CT or MRI evaluation or arthroscopy for definitive diagnosis.

For an acute traumatic luxation, it is worthwhile to attempt closed reduction under general anesthesia. The surgeon extends the shoulder manually while lifting the humeral head into position with his free hand. If this is not accomplished easily, it may indicate a capsular flap that has fallen between the humeral head and glenoid thereby preventing reduction. In cases involving older luxations, an organized hematoma or fibrous mass may occupy the glenoid cavity preventing manual closed reduction. In either of the latter instances, open reduction will be necessary.  If the reduction is stable during gentle extension and flexion, the correct positioning of the limb is confirmed with radiography and the limb is bandaged. A Velpeau sling (flexed shoulder, humerus bandaged to the chest wall, then flexed elbow and antebrachium bandaged to the thorax) is used for medial luxation, while a non-weight bearing bandage in physiologic position is used for lateral luxation. Care must be taken that the sling holds the shoulder in a stable position. Too much internal rotation of the humeral head will cause redislocation. The most stable position is that of the forepaw rotated sufficiently to be near the opposite shoulder, thus promoting lateral positioning of the humeral head. Animals should remain immobilized in this fashion for 2 to 3 weeks. Results of nonsurgical treatment of scapulohumeral luxation depend on the magnitude of soft tissue injury, success of the splintage and compliance with activity restriction. If gentle manipulation after splintage and reduction results in reluxation of the joint, surgical stabilization is necessary.

Open reduction and surgical fixation has been used successfully extensively in cases of shoulder luxation that cannot be stabilized by closed reduction. Transposition of the biceps brachii tendon is the technique preferred for treatment of lateral, medial, and cranial shoulder luxation.

In cases of medial luxation, a caudo-medial transposition of the biceps tendon is performed. Surgically, a craniomedial parahumeral incision is made, beginning 4 cm dorsal to the shoulder joint and extending to a point midway down the humeral shaft. The skin and subcutaneous tissues are then reflected, and the medial border of the brachiocephalicus muscle is separated from the superficial pectoral muscle for the length of the incision and is retracted laterally. This exposes the superficial and deep pectoral muscles, the supraspinatus muscle, and the distal communicating branch of the cephalic vein. The insertion of the superficial pectoral muscle is transected down to the border of the distal communicating branch of the cephalic vein and is retracted medially to expose the deep pectoral muscle, which is incised in a similar manner along the length of its insertion on the humerus. This muscle is then retracted medially. The fascial attachment between the supraspinatus and deep pectoral muscles is also incised to allow full medial exposure of the shoulder joint At this point, the tendinous insertion of the subscapularis muscle, crossed by the tendon of the coracobrachialis muscle, is visible, as is the medial aspect of the joint capsule. The insertion of the subscapularis is elevated and detached from the lesser tubercle and is reflected medially. The tendon of the coracobrachialis muscle lays craniomedially and is retracted with the subscapularis. The tissues over the bicipital groove and the intertubercular ligament are transected, and the dorsal aspect of the joint capsule surrounding the bicipital tendon is incised to allow mobilization of the bicipital tendon from the intertubercular groove. At this point the joint may be inspected. The biceps tendon is held in its new position by a bone screw and a spiked washer or a U-shaped surgical staple which is implanted in such way so that the tendon is not compressed. The medial aspect of the joint capsule is reefed and closed routinely. The subscapularis muscle is tightened by advancing its free end anteriorly toward the crest of the greater tubercle of the humerus. It is sutured near the insertion of the deep pectoral muscle. The deep pectoral muscle is then closed over the greater tubercle to the fascia on the lateral surface of the crest and the deltoid insertion with interrupted sutures. The superficial pectoral muscle is closed over the deep pectoral muscle in a similar manner. The brachiocephalicus muscle is closed to the superficial pectoral muscle. The subcutaneous tissues and skin are closed routinely. The leg is placed in flexion in a modified Velpeau dressing for two weeks.

For cases involving lateral luxation, the technique of greater tubercle osteotomy and bicipital tendon transplantation mimics the method used for medial luxation; however, here the biceps tendon is repositioned on the lateral side of the shoulder joint to provide lateral “collateral” support. The skin incision and retraction of the superficial tissues are the same as for medial luxation. The brachiocephalicus muscle is retracted medially, exposing the cranial aspect of the proximal humerus and the insertions of the supraspinatus, deltoideus and superficial and deep pectoral muscles. The insertion of the superficial pectoral muscle is transected down to the border of the distal communicating branch of the cephalic vein, and the muscle is retracted medially, exposing the insertion of the deep pectoral muscle. The deltoideus muscle is transected in a similar manner. The exposed insertion of the deep pectoral muscle is elevated from the humerus and retracted medially, exposing the biceps brachii muscle and the tendon in the intertubercular groove. The intertubercular ligament is incised, and the biceps tendon is freed from the surrounding fascia and joint capsule. The greater tubercle is osteotomized so as to reflect dorsomedially the intact tendon of the supraspinatus muscle. The joint capsule is incised dorsally to free the full tendon of the biceps brachii to facilitate translocating it laterally on the opposite side of the osteotomized greater tubercle. The cut portion of the greater tubercle is replaced and fixed in position with two Kirschner wires. The dorsal joint capsule is closed and the capsular attachments near the intertubercular groove are sutured. Several sutures are placed through the bicipital tendon and the tendinous insertions of the supraspinatus, infraspinatus and teres minor muscles to immobilize the tendon. The muscles are reattached routinely as in the medial luxation. The limb is bandaged for 15 days with a nonweight bearing bandage. A velpeau sling promotes lateral translation of the humeral head so its use is avoided in patients with lateral luxation. 

In the case of a (much less common) cranial luxation, the biceps tendon is transposed cranially, into a groove created in the greater tubercular osteotomy site, then immobilized by returning the tubercle to its initial position and securing it with two Kirschner wires or pins. In cases of (even less common) caudal luxation, imbrication of the lateral and caudolateral joint capsule has resulted in good return to ambulatory function. In cases of recurrent surgical luxation, major degenerative joint disease, dysplasia of the glenoid cavity or extensive instability, excision arthroplasty or an arthrodesis may be required as salvage procedures required.

Open reduction and fixation using a biceps tendon transposition for medial and lateral shoulder luxations in the absence of concurrent fractures or significant joint abnormality has a good prognosis for success and return to normal to near normal function of the shoulder. Likewise successful closed reduction and fixation, when possible, has the same prognosis. Many studies report satisfactory results in greater than 90% of the cases managed with conservative medical and/or surgical intervention.

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Surgical Management of Lateral Humeral Condylar Fractures.

Fractures of the humerus are relatively common in the dog and cat with approximately half of all humeral fractures occurring in the distal portion of the bone. The overwhelming majority of distal humeral fractures involve the elbow joint and are classified according to their anatomic location. Lateral condylar fractures are common and may occur from either minor or severe trauma in dogs and cats of all ages. Because of the close proximity of the thoracic cavity, additional injuries such as pneumothorax, hemothorax, pulmonary contusion, traumatic myocarditis, diaphragmatic hernia, and thoracic wall trauma can occur concurrent with humeral fractures. These potential injuries should be identified and treated appropriately prior to repair of the humeral fracture.

The severity of the trauma sustained has been shown to influence the resulting fracture type. While severe trauma has been shown to result in simple lateral condylar fractures and the associated injuries previously mentioned, the majority of lateral condylar fractures result from minor trauma. The high incidence of condylar fractures resulting from minor trauma in immature animals may be explained by the relative weakness of the fusion zones of the principle centers of ossification of the developing distal humerus. A substantial number of condylar fractures, however, occur in adult animals. One study found an increased risk for male Cocker Spaniels over two years of age fracturing their humeral condyle with only minor loading forces. The findings of this study suggest that certain breeds of dogs may be predisposed to distal humeral condylar fractures after sustaining minor trauma equal to or only slightly greater than the loading forces generated by normal activity. Distal humeral condylar fractures are far more common in dogs than in cats. The rarity of condylar fractures in cats may be partially explained by their straighter condyles and relatively wider and thicker epicondylar crests.

Fractures of the lateral humeral condyle (capitulum) occur as abnormal compressive forces are directed upward through the radius. The condyle shears off the intercondylar area through the supratrochlear foramen and the lateral supracondylar ridge. Several factors are associated with the higher incidence of lateral versus medial condylar fractures. The capitulum is the major weight-bearing surface because of its articulation with the radial head. As forces are directed through the radius, they are transmitted directly to the capitulum. Fractures of the medial condyle (trochela) are less common because of its less frequent weight bearing position. In addition, the shape of the distal humerus is such that the capitulum sits off the midline of the central axis of the body, predisposing itself in injury. Finally, the lateral supracondylar ridge is smaller and biomechanically weaker than its medial counterpart.

Treatment of lateral condylar fractures should be directed at complete restoration of joint anatomy and function. Because these fractures are intraarticular, perfect reduction with interfragmentary compression is required for optimal postoperative function. Closed methods of reduction and external fixation cannot usually reduce the fracture fragments perfectly and prolonged immobilization of the joint, which is necessary for fracture healing may lead to joint stiffness. Closed reduction and stabilization using a condyle clamp to place a transcondylar screw through a stab incision is possible. The results obtained with this technique depend on the length of time since the injury occurred, the expertise and experience of the surgeon, the amount of swelling and edema present, and the amount of soft tissue interposed at the fracture site.

Open reduction and internal fixation are indicated for optimal alignment and stabilization of lateral condylar fractures and an early return to function. An early return to function will help alleviate elbow stiffness and degenerative joint disease. While several surgical approaches may be used to expose lateral condylar fractures, excellent exposure with minimal soft tissue dissection is achieved via a lateral or craniolateral approach to the elbow. The most common method employed for repair of lateral condylar fractures is a transcondylar lag screw with or without an additional crosspin for increased rotational stability.

Once the fracture site is adequately exposed, fibrin, clots, blood, and interposed soft tissue should be removed to allow perfect anatomic reduction of the articular surface. With the fracture reduced, a transcondylar hole is drilled beginning at a point juts cranial and ventral to the palpable lateral epicondylar crest. The drill hole is tapped, the later condylar fragment is over-drilled to create a gliding hole, and transcondylar lag screw is placed. In order to ensure central placement of the lag screw through the condyle, an alternate technique may be employed. The lateral condylar fragment is outwardly rotated and the gliding hole is drilled from the intercondylar fracture surface out through the lateral site of the condyle. The fracture is then reduced, the medial condyle is appropriately drilled, and tapped and a lag screw is placed. An anti-rotational Kirshner wire or Steinman pin is then driven from the lateral condyle and seated into the medial cortex of the distal humeral shaft. The elbow joint should be put through a full range of motion to assess stability and to check for crepitus.

I prefer to place the limb in a modified Bobby Jones dressing to help control swelling during the immediate post-operative healing period. The owners are advised to restrict the animal’s exercise for the first 6-8 weeks after surgery, while employing gentle, passive physiotherapy to help prevent elbow stiffness. When early surgical intervention, accurate anatomic reduction and rigid internal fixation are employed a good to excellent result should be expected.

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Surgical Management of Coxofermoral Luxations in the Dog.

Considerable attention has been given to the topic of coxofermoral luxation in the dog primarily because hip luxation is a relatively common traumatic injury encountered in small animal practice. Hip luxation is a relatively common traumatic injury encountered in small animal practice. Hip luxation is usually the result of blunt trauma with resultant disruption of the joint capsule and ligament of the head of the femur. The low incidence of hip luxation in dogs less than one year of age is due to the fact that the femoral capital epiphysis fuses to the femoral neck at about 11-12 months of age and that, prior to this time, trauma is more likely to cause a femoral epiphyseal separation. Numerous studies have indicated that a unilateral craniodorsal luxation is the most common injury seen.

The diagnosis of hip luxation is easily made upon physical examination and confirmed with survey radiography. While the affected limb may be held elevated, many patients will bear weight on the limb with the toes rotated laterally. Craniodorsal displacement of the greater trochante is evident as a noticeably increased distance between the trochanter and the tuber ishium, and a thumb held between these bony prominences will not be displaced laterally when the hip is rotated externally. Crepitus is usually detected upon palpation of the joint, and the affected limb will appear shorter than the contralateral limb when the dog is placed on its back and the limbs are extended caudally. Pelvic radiography will confirm diagnosis and demonstrate if there is the presence of pre-existing hip dysplasia or degenerative joint disease or concomitant injuries such as fractures of the femoral head and/or acetabular rim, all of which have a profound impact on the method of treatment selected and the ultimate prognosis.

Numerous techniques have been advocated for treatment of canine hip luxation. Closed reduction is the procedure of choice upon initial presentation of a patient with hip luxation if the luxation is not complicated by acetabular fracture, an avulsion fragment, or failed previous reduction. Closed reduction should be attempted as soon as possible after the injury, as there is a poorer prognosis for maintaining closed reduction if it is attempted more than 4-5 days post trauma. Maintenance of closed reduction may be achieved with application of a non-weight bearing Ehmer sling or insertion of a DeVita pin. Several studies have indicated a high failure rate associated with closed reduction and application of an Ehmer sling and so my personal preference is insertion of a DeVita pin. While sciatic nerve damage has been associated with this technique, in my experience, if the proper placement technique is utilized the danger of vital tissue injury is minimal. If stability is inadequate following closed reduction or if closed reduction can not be achieved, open reduction is indicated. The presence of osteochondral fragments, acetabular fractures, inversion of the joint capsule into the joint space, and the presence of debris (hemorrhage, fibrin, fibrous tissue) within the acetabulum, may preclude successful closed reduction. Another indication for open reduction is the presence of multiple orthopedic traumas where there is a need for immediate stable weight-bearing ability on the affected limb.

A number of surgical techniques have been described for management of hip luxation in the dog. These include replacement of the ligament of the head of the femur (transarticular pinning, toggle pin), extension of the acetabular rim with bone grafts or implants, reconstruction of or substitution for a damaged joint capsule (capsulorrhaphy, extracapsular suture stabilization), and the creation of extramuscular forces around the hip joint to maintain reduction (translocation of the greater trochanter). A combination of techniques may also be utilized in an effort to save the hip in difficult cases. In cases exhibiting an acetabular fracture, a significant avulsion fracture of the femoral head, pre-existing hip dysplasia, and/or the presence of degenerative joint disease, excision arthroplasty with a biceps sling or total hip replacement may be indicated. While all of these procedures have their inherent advantages and disadvantages, my procedure of choice for surgical treatment of canine hip luxation is capsulorrhaphy with trochanteric transposition. This technique is relatively simple to perform and avoids the potential complications of some of the other techniques including injury to vital structures, implant migration, pin breakage, foreign body reactions, and interference of implants with articular surfaces. Capsulorrhaphy with trochanteric transposition requires an adequate amount of intact joint capsule in which primary closure may be achieved and intact gluteal musculature to achieve internal rotation and abduction. Ideally, the joint capsule should be reconstructed and the greater trochanter advanced caudodistally to a decorticated bed while the hip is maintained in reduction, flexion, abduction, and internal rotation. In some hip luxations, the initial trauma may have resulted in extensive damage to the joint capsule and surrounding tissues such that a secure capsulorrhaphy cannot be performed. In these instances, extracapsular suture stabilization should be implemented to provide additional support during healing of the joint capsule. In most cases, a good prognosis is warranted for return of limb function when successful closed or open reductions are maintained post-operatively. Utilizing open reduction with capsulorrhaphy and trochanteric transposition as described above, early weight bearing ability is achieved and the technique offers an excellent chance of restoring a highly functional reduced hip joint without significant risk of complications or need for implant removal.

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Patent Ductus Arteriosis Surgery.

The ductus arteriosis is a normal structure that is present in the canine fetal heart.  Its purpose is to divert blood from the pulmonary artery (the vessel that brings blood from the heart to the lungs for oxygenation) directly to the aorta (the vessel that delivers blood from the heart to the rest of the body).  Therefore, the ductus arteriosis is present in the fetal heart to allow the majority of canine fetal blood to flow around rather than through the lungs.  This is necessary because the canine fetus lives in the fluid environment of the mother’s uterus, receiving oxygen from its mother’s bloodstream. The ductus arteriosus normally closes at the time of birth when the young animal begins to breathe, oxygen is obtained by the lungs and normal circulation is established. The problem occurs when the ductus arteriosus does not close.

With the condition patent ductus arteriosus (PDA), the ductus arteriosus does not close, causing abnormal blood flow through the heart and lungs. The result is a connecting vessel that allows blood to travel in a circular fashion from the left side of heart through the lungs and immediately back to the left side of the heart. The heart must work much harder to maintain a normal amount of blood flow to the rest of the body. This extra workload eventually causes the heart to fail.  The degree to which a patient is affected depends on the magnitude of the defect. This can range anywhere from a small blind pocket off the aorta which does not cause any problems, to varying degrees of abnormal blood flow through the ductus arteriosis between the aorta and the pulmonary artery.  Most commonly, there is a shunt from the left to the right side of the heart, with blood from the higher pressure aorta continuously shunted to the pulmonary artery. This means an increased volume of blood is sent to the lungs which results in fluid build-up (pulmonary edema) and volume overload of the left side of the heart. In some cases, however, the increased flow of blood into the lungs injures the pulmonary blood vessels. This can reverse the path of blood flow from right to left. In this case, un-oxygenated blood flows into the aorta. PDA is the second most commonly diagnosed congenital heart defect of dogs. It affects about 7 out of every 1000 puppies. The condition is usually inherited as a genetic trait. This condition most commonly affects the Miniature Poodle, Collie, Maltese, Shetland sheepdog, German Shepherd, Cocker Spaniel, Pomeranian, Yorkshire Terrier and Labrador Retriever. Female dogs are predisposed.

Clinical symptoms of the disease include: coughing, reduced tolerance of exercise, loss of weight, and eventually, congestive heart failure. Affected puppies initially appear normal, although they are usually smaller and play less vigorously than their littermates. Typically, there are no clinical signs until congestive heart failure develops. This leads to fluid accumulation in the lungs that causes the previously described clinical symptoms. In most cases, clinical signs develop within a year. About 60% of affected dogs will die without surgical treatment.

Patent ductus arteriosus is diagnosed by history, auscultation of a “machinary” heart murmur on physical examination, cardiac enlargement and pulmonary edema on chest x-ray, and visualization of the defect with cardiac ultrasound (echocardiagram). The majority of cases are first diagnosed upon the initial visit to a veterinarian when the characteristic heart murmur is detected on routine physical examination.

When caught early and following treatment with successful closure of the PDA, most dogs live a normal life. Unless there are complications from other heart defects or heart failure has already developed, there is rarely any future need for medication. While special circumstances can influence the prognosis, most cases are straightforward.

The conventional treatment is surgery, which should be performed shortly after the diagnosis is confirmed. Dogs as young as 8 weeks are considered surgical candidates, and it is recommended to carry out the procedure when the dog is between 8 and 16 weeks of age. There is no benefit to delaying surgery. In fact, the chances of a dog developing heart failure or suffering irreversible damage to the heart muscle only increase with time. Anesthetic and surgical risks become greater as the heart fails and the heart and lungs become irreversibly damaged. Medical therapy may be necessary prior to and immediately after surgery if significant clinical symptoms are present.  Dogs with a right to left shunting PDA are to be treated medically as surgery cannot be successfully performed in these pets. The polycythemia caused by right to left shunting is treated periodically by phlebotomy, which is removing blood to control the red blood count and viscosity of the blood. When surgery is not an option, and heart failure has occurred, drug therapy with furosemide, enalapril or benazepril, and digoxin is often prescribed. A salt-restricted diet is enforced. Aspirin, indomethacin, and other prostaglandin inhibitors sometimes used to close the PDA in premature human babies do not work in dogs and should not be given to close the ductus because the canine ductus lacks the smooth muscle capable of responding to these drug therapies.

Historically, surgical ligation has been the standard method of correction. Surgery consists of performing a thoracotomy on the left side of the chest through the third or fourth intercostal space to gain access to the surgical site. The standard technique has been to dissect immediately cranial and caudal to the ductus and then carefully create a passage on the medial aspect of the ductus by blind dissection with right-angle forceps and tying off the patent ductus. Operative success should be greater than 90 percent, even in the smallest dogs, and the prognosis is excellent for a normal life if surgery is completed early. Although highly successful, surgical ligation is associated with some operative morbidity and mortality.

The least invasive treatment available is to feed a coil via a catheterized large vessel into the patent ductus arteriosis to block the flow of blood through it.  However, depending on the size of the patient, anatomical and other factors, not every case is a candidate for this procedure.  In these cases, open heart surgery to ligate the patent ductus ateriosus closed is necessary.  If the patient is reasonably stable immediately prior to treatment, prognosis tends to be fair to good with treatment. 

While traditional surgery to close the PDA has a very high success rate, more recently, thorascopic PDA occlusion using Titanium ligating clips or a custom-designed thoracoscopy clip applicator has been described. Although technically demanding, minimally invasive PDA occlusion via thorascopy is a safe and reliable technique in dogs; however, preoperative measurement of the diameter of the PDA is crucial to determine if complete closure with metal clips can be achieved. Assuming the diameter of the PDA is amenable to clip ligation, minimally invasive thorascopic PDA occlusion can be considered as an alternative to occlusion via conventional thoracotomy.

More recently, minimally invasive transcatheter techniques have been employed for PDA occlusion. Transarterial PDA coil embolization is a safe, less invasive alternative for PDA occlusion. This procedure involves catheterization of the femoral artery under general anesthesia. An angiogram is then performed to delineate PDA morphology and facilitate coil selection. Coils are commercially available and composed of surgical stainless steel with prothrombotic poly-Dacron fibers. Coil occlusion has been widely accepted as a relatively safe and effective treatment for PDA in dogs, although careful patient selection is helpful in achieving a high success rate. Important patient factors that affect successful coil occlusion include the size and morphology of the ductus and the patient’s body weight. The standard arterial approach for PDA coil embolization requires placement of a 4-French sheath introducer into the femoral artery. The estimated minimal patient body weight needed to safely introduce this device is ∼2.5 kg, although there is variability associated with operator experience as well as the breed and age of the patient. Coils are advanced through a catheter into the PDA under fluoroscopic guidance until satisfactory angiographic occlusion is documented. Patients are then recovered and released the following day. This procedure requires substantial technical expertise and specialized equipment.

Many devices are available to close a PDA, and in each case, the device that is used is determined by the size of the PDA.  For narrow PDAs, a vascular coil, as described above, can be used to close the vessel.  Larger PDAs can be closed by canine ductal occluders (CDO) or vascular plugs.  To place any of these devices, a small incision is made allowing entry into the femoral artery and then the device is threaded through the artery to close the PDA. The Amplatz canine duct occluder (ACDO) is a nitinol mesh device with a short waist that separates a flat distal disc from a cupped proximal disc. The device is designed to conform to the morphology of the canine patent ductus arteriosus. PDA dimensions are determined by angiography, and a guiding catheter is advanced into the main pulmonary artery via the aorta and PDA. An ACDO with a waist diameter approximately twice the angiographic minimal ductal diameter (MDD) is advanced via the catheter using an attached delivery cable until the flat distal disc deploys within the main pulmonary artery. The partially deployed ACDO, guiding catheter, and delivery cable are retracted until the distal disc engages the pulmonic ostium of the PDA. With the delivery cable stabilized, the catheter is retracted to deploy the waist across the pulmonic ostium and cupped proximal disc within the ductal ampulla. Tension on the delivery cable is released, and correct ACDO positioning and stability are confirmed by observing that the device assumes its native shape, back-and-forth maneuvering of the delivery cable, and a small contrast injection made through the guiding catheter. The delivery cable is detached and removed with the guiding catheter. To assess for any residual ductal flow, an angiogram is performed at the conclusion of the procedure, followed by Doppler echocardiography. PDA occlusion in dogs with the ACDO is straightforward and extremely effective across a wide range of body weights, MDDs, and ductal morphologies.

In conclusion, prompt and appropriate diagnosis and treatment of this congenital, hereditary cardiac disorder is associated with an excellent long term prognosis. Both standard surgical and minimally invasive transcatheter techniques can be utilized at the surgeon’s discretion to achieve success.

Canine Hip Dysplasia-Part 1.

Pathophysiology and Diagnosis

Canine hip dysplasia (CHD) is an inherited developmental disorder of the coxofemoral joint commonly affecting many of the larger breeds of dogs. Patients with clinical signs referable to CHD are regularly presented for evaluation and treatment, and selection of the most appropriate medical or surgical therapy requires a comprehensive orthopedic evaluation of each individual. The purpose of this series of articles is to describe the pathophysiology of the disease and the techniques employed for its successful diagnosis as well as the indications for the multitude of surgical procedures utilized to treat the condition.

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The cause and pathogenesis of canine hip dysplasia are still poorly understood; however, numerous studies over the last 15 years have indicated that CHD is a developmental disorder and that multiple factors can influence or modify the expression of the disease. No specific genetic pattern of inheritance has been demonstrated; however, the pattern of inheritance is multi-factorial. The spread of hip dysplasia is centered around the genetic transmission and heritability of a particular body size, type, confirmation, and growth pattern. The occurrence of hip dysplasia has been reduced by breeding dogs that have radiographically disease-free joints and by selecting dogs for breeding based on family performance and progeny selection. Unfortunately, many factors affect the choice of dogs used in breeding programs and breeding dogs for desirable traits (i.e., large size, temperament) may result in the inadvertent selection of dogs predisposed to CHD. Therefore, while CHD is a heritable disease, controlled breeding programs have only reduced the prevalence of hip dysplasia, but the disease has not been eliminated.

Dogs with the highest incident of hip dysplasia are large, rapidly growing and maturing breeds with a heavy body confirmation. It has been speculated that slow growth and late maturation favors the completion of ossification and development of the joint before the hips are subjected to possible injury from excessive extrinsic forces, especially excessive body weight. Rapid growth and early weight gain may result in disparities of tissue development triggering a series of events leading to subluxation, hip dysplasia, and degenerative joint disease. While the role of nutrition has been thoroughly investigated, diet has not affected the occurrence or course of CHD other than the mechanical effect of increased or decreased weight upon the hip.

Several hormones have been implicated as playing a role in causing CHD, including estrogen and relaxin. Based on the results of several studies, there is no evidence that hormonal influence (within the biologic range) is associated with the development of spontaneously developing hip dysplasia in the dog.

A causal relationship between pelvic muscle mass and/or muscle myopathies and hip dysplasia has also been advanced. The disparity between primary muscle mass and/or failure of the muscles to develop and reach maturity at the same rate as the pelvis may lead to alterations in the function of pelvic muscles and the development of CHD. There are substantial evidence that the consequence of hip joint laxity. Joint laxity is thought to precede hip joint remodeling and degenerative joint disease. The possibility that joint laxity may be associated with or influenced by pelvic muscle mass and/or maturation as well as by the anatomic structures important in maintaining hip stability (i.e., ligament of the head of the femur, joint capsule, joint confirmation) has been extensively explored. The available evidence, however, does not single out any one factor or variable, which would lead to increased joint laxity. In conclusion, the confirmation and stability of the hip is governed by a number of factors which influence the congruency of the articular surfaces between the femoral head and acetabulum, the integrity of the joint capsule and ligamentum teres, combined with the overall mass and strength of the associated pelvic musculature. The failure of one or more of the orthopedic or soft tissue supporting structures leads to joint laxity with stretching and confirmational change of the aforementioned structures, progressive subluxation, hip dysplasia, and resultant degenerative joint disease.

The clinical signs of hip dysplasia are many and varied, ranging from minimal to pronounced pain, lameness, and disability. Symptoms may be seen as early as four weeks of age, but are generally not detected until 4-6 months of age. Physical examination must include gait analysis, palpation, and precise radiography of the hip.

Observation of the gait may disclose a weight bearing lameness, which is more severe after exercise, a stilted or swaying rear limb gait, an audible “click” when walking, or walking with an arched back. There may also be pain and/or crepitation present upon manipulation of the hip and evidence of poorly developed musculature of the hind quarters.

Palpation of the hip has been utilized to determine the presence or absence of joint laxity and early CHD, especially in immature dogs. The ability to accurately quantitate hip joint laxity should provide key diagnostic and prognostic information for affected dogs. There are, however, a number of concerns, which must be addressed relating to the accuracy of palpation as a method of diagnosis. Palpation is at best a subjective evaluation and is influenced by practitioner experience, positioning of the dogs, amount of forced applied, and whether or not the dog is anesthetized. As of yet, an objective method of determining the amount of joint laxity of subluxation in dogs manifesting symptoms of CHD prior to the development of detectable radiographic changes. The two most common procedures employed are the Bardens’ method and the test for the Ortolani sign, both of which are described extremely well in the article authored by Chalman and Butler. The Bardens’ test detects movement of the femoral head in and out of the acetabulum as the femur is lifted horizontally. Elicitation of an Ortolani sign may be performed with the patient in either dorsal or lateral recumbancy. During testing, the application of pressure along the femoral shaft will subluxate the femoral head dorsally. As the limb is abducted, the femoral head will reseat within the acetablulum. The resulting sound and vibrations or “clicks” produced by this reseating is a positive Ortolani sign. The degree of grading residence of “click” gives an appreciation of the severity of the existing pathology. Dogs with extensive pathology, however, may have a negative Ortolani sign because distortion of the acetabular rim combined with a thickened joint capsule and osteophyte production may lead to an extremely limited range of motion. In these cases, however, radiographic evidence of joint distortion exists and diagnosis should be straightforward.

Although observation of the gait and palpation of the hip can indicate the possibility of CHD, radiographic examination is used to establish the diagnosis in the majority of cases. Historically, radiographic evaluation consists of a symmetric ventrodorsal radiograph of the pelvis and femors with the hind limbs extended and parallel to each other. Lateral pelvic views contribute minimally in the assessment of possible CHD. A major deficiency in this standard radiographic view is the failure to adequately delineate the weight bearing portion of the acetabulum. In addition, this hip extended position may mask the true potential hip joint laxity because in this position, the joint capsule tightens and may act to drive the femoral head into the acetabulum. The dorsal acetabular rim radiographic view has been recommended to evaluate the dorsal rim of the acetabulum for damage and secondary changes to show acetabular filling and congruency of the hip and to correlate palpation of joint laxity and crepitation with radiographic appearance.

The primary radiographic signs of CHD are a shallow acetabulum and a small flattened femoral head. The dorsal acetabular rim recedes and becomes less concave, and increased joint space and subluxation or luxation of the femoral head is observed. As dysplasia progresses, joint instability, synovitis, and cartilage degeneration increase as evidenced by radiographic indication of osteoarthritic changes including femoral neck and acetabular osteophyte development, sclerosis of subchondral bone, subcondral cysts of the femoral head, and ossification of the joint capsule.

While one study reports excellent success in obtaining pelvic radiographs of dogs for hip dysplasia without sedation or anesthesia, chemical restraint is usually employed to achieve proper positioning. Once again, while anesthesia allows for proper positioning, the effects of anesthesia on the relaxation of tissues in the hip joint region and how this may affect radiographic diagnosis of CHD needs to be taken into consideration.

In conclusion, CHD is a developmental disorder, the expression of which is influenced by a multitude of factors. Gait analysis, palpation, and radiography are indicated to establish a correct diagnosis, but incipient disease may be difficult to identify because interpretation of the aforementioned diagnostic procedures can be subjective and requires a great deal of skill and expertise for accuracy.

In the next article, we will discuss the treatment of the young growing dog with hip dysplasia. The third article will address treatment of the mature dog with secondary osteoarthritic changes and degenerative joint disease.

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Canine Hip Dysplasia-Part 3.

Surgical Treatment for the Mature Patient

Although it is highly preferable to diagnose and treat canine hip dysplasia (CHD) in the immature patient, numerous dogs are presented with initial clinical signs of pain and lameness associated with hip subluxation once they have achieved maturity. While triple pelvic osteotomies are routinely performed on mature dogs with no or minimal pre-existing degenerative joint disease with a great degree of success, when moderate to severe radiographic changes of osteoarthritis are present, excision arthroplasty with or without a biceps sling or total hip replacement (THR) is indicated as the likelihood of success with a triple pelvic osteotomy is minimized. The purpose of this article is to discuss the advantages and disadvantages as well as the indication for each of these procedures.

Any discussion about the operative procedures utilized for degenerative disease of the canine coxofemoral joint must be preceded by mention of the fact that the procedure ultimately performed depends upon the surgeon’s experience and training. While this seems intuitively obvious, surgeons are extremely adamant in their views (also intuitively obvious) about which procedure is beset for management of degenerative hip dysplasia in the canine. While some surgeons consider a femoral head and neck excision, a salvage procedure one step short of an amputation, others feel that the inherent risks involved in a THR do not warrant its utilization as a form of treatment. In light of this fact, the discussion of the operative procedures available will proceed from the least aggressive to the most aggressive options rather than from worst to best or visa versa.

Femoral head and neck ostectomy (FHO) is a relatively simple procedure that has been used frequently to eliminate the pain experienced by dysplastic patients. Because the procedure does not reconstruct an intact coxofemoral joint, normal function of the joint is not restored. While the formation of a false joint often alleviates pain and produces increased weight bearing ability on the affected limb, post-operative sequellae including shortening of the affected limb, muscle atrophy, decreased range of motion of the pseudoarthrosis and continued pain, and/or lameness is not uncommon after simple excision of the femoral head and neck. Although these residual clinical signs may result from the biomechanical alterations associated with the formation of a false joint, they may also be attributable to persistent abnormal contact of the proximal femur with the pelvis. For these reasons, various modifications of the standard technique for excision arthroplasty have been developed to prevent bone on bone contact between the cut surface of the femoral neck and the acetabulum.

My own clinical observation has been that in dogs receiving excision, arthroplasty of the femoral head and neck alone increased morbidity, and generally overall, poorer results are achieved than if an ancillary, interpositional procedure is concurrently performed. It is therefore my own personal preference to discourage utilization of a simple FHO for treatment of degenerative joint disease of the canine hip and to rely instead on an ancillary interpositional procedure in combination with an FHO or total hip replacement. While a variety of tissues including the joint capsule and the deep gluteal and biceps femoris muscles have been mobilized to prevent bone on bone contact between the pelvis and the cut surface of the femoral neck, utilization of the biceps femoris allows for a wider and thicker flap of muscle to be mobilized easily for translocation.

The advantages and disadvantages of performance of a biceps sling compared to a simple FHO have been debated for a number of years. Surgeons that discourage its utilization argue that the increased operative time and potential morbidity (i.e., increased swelling or edema of the operated limb, wound infection, sciatic nerve entrapment), outweigh any potential benefits including excellent coverage of the ostectomy site, to decreased bone on bone contact, and the promotion of early post-surgical use of the limb.

Over the course of the last nine years, I have had considerable exposure to and experience with the biceps sling, and my clinical impression is that these patients, while perhaps not being restored to a totally normal state, fare far better than if a simple FHO had been performed. In fact, the overwhelming majority return to at least good, if not excellent, function over a relatively short period of time, free from pain, discomfort, and crepitation at the ostectomy site. Excision arthroplasty of the femoral head and neck utilizing a biceps femoris muscle sling is certainly an effective alternative to total hip replacement.

Total hip replacement is a rewarding method of treatment for canine hip dysplasia as the best approach to restoring normal hip function is to reestablish as closely as possible normal joint configuration. While standard operative procedures have been in use for more than 15 years, recent advances in surgical technique and modifications of the implants themselves have led to greater acceptance of the procedure as complication rates have decreased and long term success has been documented. The hesitancy to recommend THR as the primary means of treatment of canine hip dysplasia outside of limited availability and cost has been the potential for complications including prosthesis dislocation, deep infection, loosening of the implants, femoral fracture, and sciatic neuropraxia. Once again, by paying strict attention to detail, the potential for complications following THR is minimized and excellent long-term success rates can be achieved, clearly demonstrating the THR is an effective method of treating canine hip dysplasia.

In conclusion, it should be mentioned that patient selection for any of the aforementioned procedures is of the utmost importance. A dog that has hip dysplasia but has clinically sound ambulatory function is not a candidate for surgery. Many dogs function with minimal pain or impairment on medical management alone, despite tremendous bony changes. Others, with what appear to be minimal lesions, are severely hindered. It follows then that a reasonable effort at medical management must have been tried and failed. The point of medical failure must be clearly recognized, however, because continuing medical therapy after these treatments have become ineffective decreases the chances for surgical success. In addition, an accurate neurologic examination is mandatory, as many myelopathies co-exist in dysplastic dogs. If there is the presence of neurologic degeneration, the dog should not be considered a surgical candidate.

In response to the poor results consistently obtained with excision arthroplasty in large dogs, my recommendation is to avoid this procedure as a treatment for hip dysplasia and to rely instead on a biceps sling surgery or a total hip replacement. The determination of which of these two procedures to use depends upon the client’s expectations for return to function and the degree to which they are willing to accept the potential limitations and/or complications associated with each procedure.

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Management of Medial Patella Luxation in the Dog & Cat.

Medial patella luxation (MPL) is one of the most common stifle problems encountered in veterinary medicine. It is a more common orthopedic problem in the dog, but has been reported frequently in the cat.  MPL may be caused by trauma or congenital malformations (with the latter being far more common) or may occur secondary to fracture disease and/or surgical intervention. Congenital MPL is most commonly observed in the toy and miniature breeds of dogs and also in the Abyssinian and Burmese cats and causes minimal, if any, to severe gait abnormalities.  The degree of deformity and, therefore, subsequent dysfunction varies markedly within the affected population and within the approximately 50% of the patients with bilateral involvement. Many affected animals are presented at approximately six months of age with the owner describing a skipping or hopping type of gait or an animal that is intermittently non-weight bearing on one limb or the other. The problem is usually transient with the dog or the cat returning to apparently normal function within a short period of time. Although medial patella luxation may be present in cases with acute severe lameness, it is usually a chronic problem, and therefore, other causes of acute onset of stifle pain (i.e. cruciate ligament injury) should be carefully ruled out. Other animals are presented as adults with a history of acute onset of lameness with minimal trauma or with the frequently severe and complicated secondary stifle changes due to chronic abnormal stress.  There are also a certain portion of the affected population that present for routine physical examination with severe grades of MPL, to which the owner responds, “What do you mean he has bad knees, he’s never limped a day in his life.”

Various etiologies have been suggested for congenital medial patella luxation; however, it is generally agreed that MPL is a multi-factorial disorder of pelvic limb conformation.  Depending upon the severity of the individual case, various combinations and degrees of the following features may be observed: (1)intermittent or permanent medial patella luxation, (2)medial displacement of the quadricep’s group with or without muscular contraction, (3)limited extension of the hip and stifle, (4)decreased antiversion, (5)coxa vara, (6)external rotation and/or torsion of the distal femur, (7)internal rotational laxity of the tibia and/or medial torsion of proximal tibia and lateral torsion of the distal tibia, (8)medial displacement of the tibial tuberosity and crest, (9)real or artifactual lateral bowing of the distal femur with increased caudal and medial concavity, (10)lateral angulation or tilting of the femurotibial joint space, (11)shallow or absent trochlear groove, (12)femoral and tibial condylar asymmetry, (13)genu varum, (14)redundant or stretched lateral joint capsule, (15)contracted or inadequate medial joint capsule, (16)cartilage fibrillation or erosion on the articular surface of the patella, (17)erosion on the medial aspect of the dysplastic medial femoral condyle, (18)meniscal, cranial cruciate and lateral collateral ligament changes, and lastly, (19)degenerative joint disease.

While these derangements are common in cases of MPL in the dog, abnormal shape of the femur, tibia, or both has not been observed in cats with MPL.  Some cats, however, do exhibit shallow trochlear grooves and medial deviation of the tibial tubercle.  Because of the broad range of clinical lameness and degree of deformity present in this syndrome, no one surgical procedure is appropriate for all affected patients.  Numerous surgical procedures have been described for the repair of medial patella luxation, and determining the most effective combination of procedures to utilize is quite a challenge. The goal of surgery is to realign the quadricep’s extensor apparatus and to, therefore, stabilize the patella in the trochlear groove and return the animal to at least good, if not excellent function. A grading system, based on the severity and types of deformity present provides the basis for a rational surgical approach.  For each grade of malformation, the following discussion will present the surgical techniques and treatment rationale recommended for the treatment of MPL in the dog and cat at the current time.

Grade 1 MPL - The anatomy of the stifle joint is almost normal and the patella luxates only when the joint is extended and lateral digital pressure is applied; the patella reduces spontaneously.  Because these patients have a normal to near normal stifle joint, minimal if any clinical signs are observed when the animal is presented. It is difficult to recommend a surgical intervention on a clinically normal animal based on the assumption that these animals may be prone to future abnormalities and injuries, and it is my opinion that they are not operated unless they become clinically symptomatic.  In most, if not all, cases of Grade 1 medial patella luxation, all that is needed is the creation of a lateral restraint to prevent medial displacement of the patella.  This is accomplished by either lateral imbrication of the joint capsule or placement of an antirotational suture around the lateral fabelle and through a tunnel drilled in the tibial tuberosity.  In a small number of cases, a medial retinacular release may also be required.

Grade 2 MPL - The patella usually resides within the trochlear groove; however, it will luxate upon flexion of the joint (or digital pressure) and remains luxated until relocated by digital pressure or active flexion and extension of the joint. These animals usually present with some degree of gait abnormality because of the presence of some angular and torsional deformity, and degenerative changes are more likely to develop over time. In these cases, soft tissue procedures alone are usually not capable of restoration of function. A trochleoplasty, medial retinacular release, and lateral imbrication are usually sufficient to overcome the problem; however, if the tibial tuberosity is deviated medially, a tibial crest transplant is also indicated.

Grade 3 MPL - The patella is luxated most of the time, but may be reduced temporarily while the limb is extended.  The angular rotational and torsional deformities are more severe than in Grade 2 MPL, and a corresponding increase in clinical signs of lameness are observed.  All of the previously mentioned procedures will probably be necessary to correct Grade 3 MPL; however, the rotational instability of the tibia will still need to be addressed.  Placement of an antirotational suture around the lateral fabelle and through a tunnel drilled in the tibial tuberosity is usually indicated to help correct a Grade 3 MPL.

Grade 4 MPL - The patella is luxated period, and no amount of manual pressure of full limb extension will result in reduction.  Thankfully, this grade is the least commonly encountered, as the bony and soft tissue derangements are terribly severe and the previously mentioned techniques are inadequate to correct the problem. These cases usually require tibial and/or femoral corrective osteotomies to restore alignment of the stifle joint.  In the majority of cases, only a derotational proximal tibial osteotomy is required to correct the malalignment of the distal tibia and paw, which results from derotation of the proximal tibia by imbrication suture.  In some severe cases, however, a cuneiform osteotomy of the distal femur may be necessary to help further align the quadricep’s extensor apparatus.  As mentioned previously, as Grade 4 MPL is not encountered frequently; these corrective osteotomies are not usually necessary and should be used reluctantly, only in severe cases, and in my opinion, as a salvage procedure. These procedures should not be performed if there is the presence of permanent interarticular change (i.e. meniscal remodeling and/or cruciate or collateral ligament changes) as surgical intervention in an attempt to return the animal to more normal function may, in fact, make it worse, which brings us to another important point, namely, timing of the surgical procedure in order to achieve the best functional results.

Once clinical lameness has been recognized, surgical intervention is warranted. In cases where severe bone distortion is not a component of the problem, surgery should be performed early to prevent the continued degeneration of the joint, which normally occurs, and to prevent excessive strain and stresses from developing on the cranial and caudal cruciate ligaments, which will result in their further deterioration.  In those cases with evidence of bone distortion, early surgical intervention is a necessity, as the effects of continual growth distortion cannot be ignored.  In regard to specific surgical technique, the aforementioned procedures are relatively straightforward with the exception of the corrective osteotomies.  The only real choice to be made is how to perform the trochleoplasty.  The older, more standard procedure requires excision of trochlear cartilage and some subchondral bone to achieve proper trochlear depth and maintenance of patella alignment.  As hyaline cartilage does not regenerate, the exposed bone which results is fast covered by granulation tissue which undergoes metaplasia to fibrous tissue and finally fibrocartilage, which is frequently thin, incomplete and of variable quality. With the advent of the more advanced techniques currently available, this approach can no longer be recommended.

A second technique relies on elevation of the trochlear cartilage and removal of subchondral bone with subsequent replacement of the hyaline cartilage. This technique is applicable to dogs under 5 months of age, as cartilage elevation becomes more difficult as the animal ages, as the articular cartilage adheres more tightly to the underlying subchondral bone.  In the trochlear recession wedge technique, the femoral trochlea is depressed while maintaining the normal hyaline cartilage surface, and has provided excellent results in dogs of all ages.  An advantage of the recession wedge technique is that trochlear patella articular cartilage contact is maintained, accounting for a quicker return to full function of the limb.

Most recently, trochlear block recession (TBR) has been described in the veterinary literature as an alternative to trochlear wedge recession (TWR). In this technique, the surface of the recessed osteochondral block is rectangular, rather than a wedge which tapers to a point proximally and distally. The rectangular shape preserves a larger area of hyaline articular cartilage as well as a greater width to the trochlear recession proximally. Therefore, the value of this procedure is its ability to increase proximal pafuctellar depth, increase patellar articular contact with the recessed proximal trochlea, recess a larger percentage of the trochlear surface area, and to better resist patellar luxation in an extended position as compared with TWR.

The TBR was proposed as an alternative to the TWR as a method to increase recession of the proximal trochlea, which is important in the clinical treatment of patellar luxation. With the limb in a flexed position, there are no significant differences between TWR and TBR. As the patella most easily luxates when the stifle is extended and the patella is in a more proximal location within the trochea, performance of a TBR will increase proximal patellar depth and therefore increase patellar articular contact with the recessed proximal trochlea to better resist patellar luxation with the limb in an extended position as compared with TWR.

In conclusion, a variety of surgical techniques are available for correction of the various grades of medial patella luxation and a combination of procedures is usually necessary to optimize return to function.  Once clinical lameness is observed, rapid surgical intervention should be considered to help prevent the often-severe debilitating soft tissue and orthopedic changes, which result in premature development of degenerative joint disease.

The utilization of medical therapy in conjunction with surgical intervention affords the best clinical response. Medical therapy should include but not be limited to the administration of pain management medications (opiods and opiod transdermal patches, non-steroidal anti-inflammatories), neutraceutical supplements (glucosamine, chondroitin, msm, etc), polysulfated glycosaminoglycans (Adequan), acupuncture, physical therapy, Class IV laser therapy, and platelet rich plasma administration. With proper medical and surgical intervention, the majority of animals with patella luxation tendencies can be returned to at least good if not excellent, normal function.

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OCD of the Shoulder Joint: Pathogenesis and Surgical Treatment.

Osteochondrosis (OC) is a pathologic process in growing cartilage. Its main feature is a disturbance of endochondral ossification that leads to excessive retention of cartilage. The increase of epiphyseal volume, in growing animals, occurs through endochondral ossification within the epiphyseal cartilage. Multiplication of cartilage cells within a germinal layer leads to thickening of the growth cartilage towards the metaphysis. As the cartilage grows, the cells left in the newly formed matrix undergo a maturation, or degenerative process, while the ground substance becomes mineralised. Capillary buds then invade the mineralised cartilage from the metaphysis, following a front of chondroclasts that remove the cartilage. The latter is then replaced by bony tissue, synthetized by osteoblasts around the buds. Thus, normal growth of long bones results from a precise balance between cartilage growth and its gradual replacement by bone. Osteochondrosis can occur in any particular point within the cartilage and lead to a failure of the phenomena allowing capillary invasion and replacement of the cartilage by bone. Consequently, the cartilage tissue becomes abnormally thickened in that area. The process can be self-limiting. In this case, it remains clinically silent, although it may be detected as an incidental finding on survey radiographs. It may, on the other hand, evolve into a more significant lesion, associated with inflammation and clinical symptoms: this is referred to as “osteochondritis dissecans” (OCD). In shoulder OCD, the caudal aspect of the humeral head is usually affected. The epiphyseal cartilage is avascular, so that it only receives its nutrition via osmosis from the synovial fluid. In cases of OCD, the cartilage thickens markedly and the diffusion of nutrients into its deeper portion is poor, leading to degeneration and necrosis of the fragile cartilage cells. A fissure may develop at the necrotic site. Initially limited to the depth of the cartilage, it gradually extends towards the articular surface. This micro-fracture corresponds to the osteochondritis stage and is referred to as ‘dissecans’ (‘dissecting’) due to the formation of cartilage flaps separating from the subchondral bone. If a flap is completely detached, it may become free within the joint, forming one or more ‘joint mice,’ which may become localised in any joint recesses, though more particularly in the caudal recess or in the bicipital groove in the shoulder. A joint mouse can occasionally be gradually resorbed, or increase in size and become mineralised. Cartilage fissuring and the resulting cartilage breakdown products released into the synovial fluid contribute to inflammation and pain.  Invasion of the cracks by synovial fluid, thus coming into contact with subchondral bone also promotes inflammation. Clinical signs of lameness may occur at this point as lameness and pain become evident once synovial fluid establishes contact with subchondral bone. Osteochondrosis is a common and serious problem in many breeds of dogs. Large and giant breeds, especially Great Dane, Labrador Retriever, Golden Retriever, Newfoundland, Rottweiler, Bernese Mountain dog, English Setter, and Old English Sheepdog are most commonly affected. The age of onset of clinical signs is typically 4-8 months of age and bilateral shoulder involvement is seen in up to 67% of cases presented for evaluation. Males are more commonly affected than females.

The cause of OCD is considered to be multifactorial. Trauma, hereditary factors, rapid growth, nutritional factors and ischemia all seem to contribute to the pathogenesis of OCD. The initial clinical symptoms exhibited by dogs afflicted with OCD may be subtle and difficult to detect. Often times the dog may demonstrate nothing more than stiffness after rest which resolves relatively quickly, but typically the lameness worsens with exercise. The severity of clinical signs does not always correlate with the extent of the radiographic evidence of disease.

There may be episodes of spontaneous improvement for one or several weeks but the pain persists despite anti-inflammatory or analgesic therapy. Manipulation of the limb yields marked pain upon hyperextension of the scapulo-humeral joint and, to a lesser degree, upon forced flexion or deep palpation of the caudal joint recess. An accurate diagnosis is usually achieved with survey radiography, a mediolateral projection being most useful. The shoulder joint should be isolated as well as possible to improve visualization of the caudal aspect of the humeral head. The affected limb is radiographed with firm traction placed on it to pull the shoulder cranially and ventrally to avoid superimposition of the neck and thorax.  The opposite limb is pulled caudally to avoid any radiographic overlap while the affected thoracic limb is being evaluated. The typical radiographic appearance of OCD consists of an altered subchondral bone contour in the caudal aspect of the humeral head. It may be surrounded by a sclerotic bone area characterised by increased radiodensity and loss of trabecular pattern.

Conservative treatment (non surgical) is controversial for this condition. Regardless of the conservative approach used, a higher percentage of dogs go on to have permanent lameness and secondary joint changes associated with osteoarthritis when conservative treatment is used instead of a surgical approach. Conservative management of OCD usually consists of a combination of exercise restriction, body weight management, symptomatic pain management with analgesics and either steroidal or non-steroidal anti-inflammatory drugs, neutraceuticals and regimes of polysulfated glycosaminoglycans. The recent additions of Class IV laser therapy and platelet rich plasma administration to the conservative treatment regime show promise in alleviating the progressive arthritis usually observed with the conservative approach but definitive clinical studies have yet to be performed. None the less, the medical treatments described above are recommended in the post operative recovery period to enhance and optimize the outcome of surgery.

It is generally agreed that surgical intervention is the best treatment option in order to prevent continued degeneration of the joint. Given the course of the disease and the associated problems described earlier, it is probably not surprising that the treatment of choice for most cases of OCD is surgical removal of the cartilage flap as well over 90% of dogs diagnosed with OCD of the shoulder have a successful recovery with surgery.  The caudo-lateral approach between the acromial and the scapular part of the deltoid muscle, with cranial retraction of the teres minor and caudal retraction of the teres major is sufficient to provide adequate visualization of the lesion. This approach via a longitudinal myotomy of the acromial head of the deltoid was developed because of the minimal surgical trauma caused by this approach. Prior to its development, other more traumatic approaches (osteotomy of the acromial process, tenotomy of the infraspinatus and teres minor, etc), were being utilized but they were associated with a much higher post-operative morbidity. I’m proud to say that the technique was developed while I was a surgical resident and is still considered the least invasive approach to the shoulder joint for the treatment of OCD in use today (Schulman, A.J.; Lusk, R.; Ettinger, S.J.; Lippincott, C.L.:  Longitudinal Myotomy of the Acrimonial Head of the Deltoid:  A Modified Approach for the Treatment of Osteochondritis Dessicans in the Dog.  JAAHA 1986; 22: 475-479.). Once the affected area of the caudal humeral head is visualized, the cartilage flap is cut free and all the abnormal cartilage around the lesion is trimmed with a curette to create vertical walls. Aggressive curettage of the floor of the lesion is of questionable value. Multiple drill holes are created in the bed of the lesion (forage) with a 1-2mm drill or a small kirschner wire to allow bleeding to occur in the subchondral bone. This enhances the migration of pleuropotential stem cells into the damaged area to stimulate the formation of fibrocartilage in the articular surface defect. The joint is then lavaged to help flush out any remaining debris, including free fragments of cartilage which should always be looked for in the caudal cul-de-sac of the joint. The prognosis for shoulder OCD is usually excellent. Dogs with this disease often return to normal function after surgery, unless the lesion has been long-standing and significant degenerative arthritis has already set in.

Minimally invasive arthroscopic approaches are also successfully utilized to manage OCD lesions of the shoulder in addition to the standard arthrotomy approach described above. Surgical arthroscopy allows enhanced visualization of intra-articular structures and is also associated with limited postoperative morbidity.  Arthroscopy entails less disruption of the periarticular soft tissue and decreased soft tissue disruption leads to less postoperative pain.  This is especially true when multiple joints are involved and are operated arthroscopically under the same anesthetic procedure. Whether the standard arthrotomy or arthroscopic approach is utilized, the response of OCD to surgical intervention is rapid and rewarding. A good to excellent prognosis is warranted in the overwhelming majority of cases when combined with appropriate postoperative medical therapy.


Jean-Pierre Genevois: Shoulder Osteochondrosis-Shoulder Synovial Chondromatosis-Shoulder Dysplasia. Main Proceedings, 27 WSAVA Congress.

Schulman, A.J.; Lusk, R.; Ettinger, S.J.; Lippincott, C.L.:  Longitudinal Myotomy of the Acrimonial Head of the Deltoid:  A Modified Approach for the Treatment of Osteochondritis Dessicans in the Dog.  JAAHA 1986; 22: 475-479.

 

Total Ear Canal Ablation with Curettage of the Bulla for End State Otitis Externa.

Although medical therapy is often effective in treating otitis externa, chronic otitis externa may progress to end stage otitis necessitating surgical intervention. Unsuccessful medical therapy for otitis externa may be due to the presence of horizontal or vertical ear canal neoplasia or polyps, generalized dermatological disease, simultaneous otitis media, and/or interna or irreversible hyperplastic ear canal disease. Total ear canal ablation combining bulla osteotomy and curettage is the surgical technique of choice in patients that have chronic, non-responsive ear disease that is unsuitable for or non-responsive to lateral ear canal resection.

While total ear canal ablation with bulla osteotomy (“TECA/BO”) may be the technique of choice, it is also a technique that should not be taken lightly, as post-operative complications can and do indeed occur. These complications are attributable to the technical difficulty of the surgical procedure and the potential for post-operative infection because of bacterial contamination of the surgical site, the most common post-operative complications encountered include facial nerve paralysis, head tilt, nystagmus, ataxia, hearing loss, hypoglossal nerve dysfunction, Horner’s syndrome, cellulites, abcessation, fistulation and/or dehiscence, and/or recurrent infection. In the majority of cases, the manifestation of these complications is temporary, however, because of the potential for long-term disability, excellent client communication is essential prior to surgical intervention. In addition, in those cases exhibiting aural manifestations of generalized dermatological disease, the client should be informed that persistent topical and/or systemic therapy may be indicated to control head shaking, pruritus, and odor even after aggressive surgical intervention.

In light of the association of otitis media with chronic end stage otitis externa, bulla osteotomy and curettage is indicated in conjunction with TECA to provide drainage of the tympanic bulla and reduce the post-operative complication rates experienced when TECA is performed alone. The surgical procedures advocated to achieve tympanic drainage are either ventral or lateral bulla osteotomy with curettage. In my experience, lateral bulla osteotomy is preferable to ventral bulla osteotomy because the patient does not have to be re-positioned after the TECA procedure. In addition, less soft tissue dissection is required of both procedures are performed through a single incision. Although it is difficult to perform a valid comparison of the two techniques because of the variability of the clinical features present in each case, the overall rates of recurrence or persistence of drainage appear to be lower when the lateral approach is utilized.

As mentioned previously, a high rate of complications may be observed if excellent attention to detail is not achieved throughout the surgical procedure. Facial nerve dysfunction may result from stretching or transecting the nerve because of its close association with the horizontal ear canal as it exits the stylomastoid foramen. Meticulous dissection of tissues as close to the perichondrium as possible should be performed to help prevent iatrogenic trauma. This perichondrial dissection sounds easier than it is, because the distortion of normal ear anatomy caused by fibrosis, ossification, and perioral abcessation make dissection difficult and may prevent visualization of the nerve. Iatrogenic damage to the structures of the middle and inner ear can occur during bulla curettage resulting in Horner’s syndrome, nystagmus, head tilt, and/or ataxia post-operatively. While affected tissue must be removed to reduce the risk of continued infection, gentle curettage avoiding the dorsomedial compartment of the bulla may help reduce the incidence of neurologic complication.

In an effort to achieve complete yet gentle curettage, I use sterile cotton swabs instead of a curette to remove the inflammatory tissue and associated debris from the bulla. Complete removal of the offending tissue is easily accomplished using the gentle curettage because of the degree of inflammation and infection of the epithelium of the middle ear is such that the tissue usually strips away from the bulla cleanly. Gentle yet copious lavage will usually remove any tags of tissue missed initially. Bacterial contamination of the surgical site is a given and thorough debridement and lavage must be performed to decrease the risk of post-operative sequelae. Cellulitis, drainage, fistulation, and reinfection is usually due to incomplete removal of the infected tissue, inadequate drainage, or primary closure of the surgical site. In order to avoid these complications, I place a penrose drain within the bulla and allow it to exit the ventral aspect of the incision to achieve optimal ventral drainage In addition, the incisional edges of tissue are not primarily closed, but are incompletely opposed with loose tacking sutures to allow the defect to fill in with granulation tissue.

The head is then bandaged and rebandaged as necessary (usually every 2 to 3 days) to prevent the accumulation of blood, pus, or serum within the wound. Drainage is maintained until the drain is non-productive, which is usually by the seventh day post-operatively. At this stage bandages may be changed every 5-7 days until contraction and reepithelialization is complete, which usually takes an addition 7-14 days.

Utilization of complete curettage, thorough debridement, lavage, drainage, and delayed closure affords an excellent opportunity for successful management of chronic otitis externa with a single surgical intervention. If reinfection and fistulation eventually develop, surgical exploration for remnants of infected cartilage or epithelium is required, as antibiotic therapy alone is usually fruitless and only ends up delaying the inevitable. If exploration is performed, a ventral bulla osteotomy is strongly recommended as fibrosis and loss of normal tissue plains makes identification of the facial nerve even more difficult.

In conclusion, TECA/BO and curettage is an effective means of treating end stage otitis externa. Long-term results are usually good to excellent and adherence to the principles outlined above will help minimize the occurrence of the unfortunate complications that can accompany surgical management for this disease.

Canine Mast Cell Tumors.

Mast cell tumors (MCT) in dogs are very common, accounting for approximately 20% of all skin tumors in dogs. For most dogs, the underlying cause promoting the development of the tumor is not known. Mast cells are specialized cells derived from stem cells in the bone marrow and play an important role in helping an animal respond to inflammation and allergies. They are found distributed throughout the body, predominantly near blood vessels, nerves, and beneath the skin. Mast cells become activated when antigens bind to receptors on their surface, and subsequently release several biologically active chemicals stored in their granules when stimulated including histamine, heparin, seratonin, prostaglandins, proteolytic enzymes, and other pro-inflammatory molecules. Although these chemicals are vital to normal bodily function, they can be very damaging to the body when released in chronic excess. These chemicals can cause systemic problems that include gastric ulcers, internal bleeding, and a range of allergic manifestations.

Mast cell tumors can arise from any skin site on the body and can have a variety of appearances. MCT most commonly are seen as solitary lumps or masses in or underneath the skin; occasional dogs can have multiple masses. MCT can look like just about anything ranging from benign-appearing lumps, to more angry or ulcerated lumps, masses with a stalk, or focal thickenings in the skin. MCT may change quickly in size because of reactions around the mass and release of their vasoactive compounds. In most cases, evidence of a MCT is easily generated by examination of a fine-needle aspirate of the suspect mass, and aspiration is advised before removal of a mass to determine if it is a MCT, a finding that would demand a more aggressive surgical removal than for other more benign skin masses. Often, obtaining blood for a complete blood count and biochemical profile, buffy coat analysis, and a urinalysis will be advised as these can help assess overall health and provide information that potentially influences treatment recommendations. The CBC may reflect low or high white blood cell count, low platelet count, and/or elevated mast cell counts. The buffy coat is diagnostic (although subject to false-positives) and reflects mast cells circulating in the bloodstream where they are ordinarily not found in large numbers. A positive buffy coat suggests bone marrow involvement. Other tests may include lymph node aspirate, bone marrow aspirate, x-rays, and ultrasound evaluation.

As mentioned previously, canine mast cell tumors are among the most common skin tumors, which occur in dogs. Boxers, Rhodesian ridgebacks, Pugs, Boston terriers, Pit-bull terriers, and Weimaraners are at high risk (4 to 8 times more than the population) for developing MCT. Shar-Peis, particularly young dogs, are predisposed to developing MCT, and these tumors are often poorly differentiated and act more aggressively biologically than in other breeds.

One characteristic of mast cell tumors is the tendency for them to change in size, even on a daily basis. A tumor that gets bigger and smaller, seemingly on a whim, may be a MCT. Another idiosyncrasy is the potential of the tumor to produce “Dariers sign” if poked and prodded. Handling these tumors - even a routine veterinary palpation or needle aspirate - can cause a heavy release of histamine that results in swelling, redness, itchiness, and/or hives. Symptoms are variable, depending on the location of the tumor and the degree to which it has developed and/or spread. Signs of systemic involvement may include: loss of appetite, vomiting, bloody vomit, diarrhea, abdominal pain, dark or black feces, itchiness, lethargy, anorexia, irregular heart rhythm and blood pressure, coughing, labored breathing, various bleeding disorders, delayed wound healing, enlarged lymph nodes.

Most mast cell tumors are considered locally invasive and can be difficult to remove completely because of the extent of local spread. The behavior of mast cell tumors is a reflection of their grade. When evaluating the tissue sample obtained from surgical removal of the mast cell tumor, the diagnosis of mast cell tumor will be confirmed, the mast cell tumor will be staged, and the width of the tissue margins, which are free of tumor will be measured. Staging and the width of the tissue margins which are free of tumor cells together with the location of the mass, the health of the dog, and the grade of the mast cell tumor will determine whether further treatment with radiation therapy or chemotherapy will be recommended.

Mast cell tumors have 3 grades. Tumor grade is associated with the degree of differentiation of the mast cells. Grade I tumors are well differentiated and are the least aggressive and least likely to metastasize (spread to other organs). Complete surgical excision of Grade 1 MCT is usually curative. Grade 2 tumors are moderately differentiated and the prognosis and treatment options are perhaps the most complicated and difficult to predict. Grade 3 tumors are poorly differentiated, very aggressive with a high likelihood of metastasis. They carry the poorest prognosis but are fortunately the least common grade encountered. Mast cell tumors show a predilection to spread to regional lymph nodes, liver, spleen, and bone marrow.

Grading of mast cell tumors, however, is very subjective. In one study, mast cell tumors were graded by a group of pathologists, and frequently, there was disagreement regarding the grade even amongst board certified pathologists. In many cases, perhaps a better method of determining how malignant or benign a mast cell tumor will behave is to have a proliferative study performed. This includes PCNA (proliferating cell nuclear antigen), AgNOR (agyrophilc nuclear oganizing regions), and Ki67. Tyrosine kinase receptors (a receptor for mast cell growth factor) are also important and tests related to this include cKIT mutations and KIT staining patterns.

Because mast cell tumors prefer to metastasize the above mentioned sites, staging a dog with a mast cell tumor entails collecting cells from the regional lymph nodes for microscopic examination, imaging the thorax and abdomen (radiographs, abdominal ultrasound, ) for evidence of enlargement of the mesenteric lymph nodes, liver or spleen, and an assessment of potential bone marrow involvement, either via a bone marrow aspirate for microscopic examination, or examination of the white blood cells for circulating mast cells.

Surgical removal is the mainstay of treatment of canine mast cell tumors. Presurgical treatment with histamine blockers and/or steroids is recommended to prevent complications of mast cell degranulation during manipulation of the tumor mass for the duration of its removal. Because of their locally invasive behavior, wide margins of what appears to be normal tissue around the tumor needs to be removed to increase the likelihood that the tumor has been completely removed. Approximately 2-3 cm margins and one fascial plane of depth are attempted as surgical margins.  Recent research has shown that 1-2 cm clean margins of a grade 1 or 2 mast cell tumor can be curative.  For mast cell tumors that were not or because of location could not be completely removed with wide surgical margins, radiation therapy is often the best treatment for residual disease. Radiation therapy after surgical removal appears to be beneficial and may reduce the incidence of reoccurrence and increase survival rates. Radiation is most useful when the tumors have not spread to multiple areas of the body. Radiation therapy, however, is expensive and there may not be a facility able to offer this option within a convenient distance in many locations. Chemotherapy is sometimes used to treat mast cell tumors, but chemotherapy is usually reserved for dogs with grade 3 tumors. Mast cell tumors are notoriously unpredictable tumors with regards to response to chemotherapy, and chemotherapy for metastatic mast cell neoplasia does not offer consistent results. If the mast cell tumors have spread to multiple areas, combinations of anti-cancer drugs are commonly used along with surgery and radiation. These include vinblastine, lomustine, vincristine, doxorubicin, mitoxantrone, cyclophosphamide, and L-asparginase. These are all heavy-duty chemotherapy drugs with potential side-effects that include severe immunosuppression, vomiting, diarrhea, and/or liver damage. Palladia is a tyrosine kinase receptor blocker; the proliferative panel may be helpful to determine if the patient will respond to this type of medication. The tumor should be positive for cKIT mutations for this drug to be potentially effective. Unfortunately, mast cell tumors do not respond well to these drugs and several recent studies seem to demonstrate very limited efficacy in conjunction with surgery. It is important to remember that, while radiotherapy and chemotherapy are potentially useful adjuvant forms of therapy, aggressive surgery remains the mainstay of treatment for canine MCT and is sufficient to successfully treat the majority of MCT encountered in practice.

In addition to surgery, radiation therapy, and/or chemotherapy management of the tumors, many dogs will benefit from the administration of medications that tend to help fight the secondary local and systemic effects of the tumor. These usually include steroidal drugs like prednisone, and anti-histamines like Benadryl, Pepcid, or Zantac. These medications prevent the undue side-effects of histamine release commonly encountered in dogs with MCT.

Several prognostic factors (in addition to grade or stage) have been identified. Boxers have a higher percentage of low grade tumors compared to most other breeds (It is important to recognize, though, that a high grade mast cell tumor will behave just as aggressively in a boxer as in any other breed.) Smaller tumors and tumors that remain relatively static in size for prolonged periods (months or years) carry a better prognosis. Tumors that remain confined to the skin without metastasis to regional lymph nodes or distant sites carry a better prognosis. The presence of multiple cutaneous tumors does not affect long-term prognosis. Systemic illness (anorexia, vomiting, melena, gastrointestinal ulceration) is usually a reflection of a larger tumor burden and therefore carries a worse prognosis. Tumors located on the muzzle have a higher rate of spread to regional lymph nodes and therefore carry a more guarded prognosis. Historically, it has been suggested that tumors located in the inguinal area, perineum, and scrotum carry a more guarded prognosis, but this is based solely on anecdotal evidence, and two recent studies have refuted this claim.

The prognosis for completely removed grade I and grade II tumors is excellent. Even with complete surgical removal, however, because of the tendency of MCT to exhibit multicentric origination, new lesions may appear elsewhere, which are not the result of actual metastatic spread. For this reason, multiple surgeries over time may be necessary to control the disease process. The prognosis for incompletely removed grade I and II tumors treated with radiation therapy after surgery is also excellent with approximately 90-95% of dogs having no recurrence of tumor within 3 years of receiving radiation therapy. The prognosis for dogs with grade III tumors is considered guarded as local recurrence and/or spread is likely in most dogs. If your dog is diagnosed with a grade III MCT, most likely chemotherapy will be recommended as at least part of the protocol and a guarded prognosis is warranted.

Multiple Myeloma.

Multiple myeloma or plasma cell myeloma, is a neoplasm of well-differentiated B cell lymphocytes typically originating from the bone marrow. Neoplastic cells can metastasize widely, having a predilection for bone and resulting in osteolysis. The malignant transformation of a single B cell can secrete a homogenous immunoglobulin product known as paraprotein, which will mimic the structure of normal immunoglobulins. Overabundant production of paraprotein, consisting of any of the immunoglobulin classes, will appear as a sharp, well-defined peak or monoclonal gammopathy on serum electrophoresis.

The most frequently encountered multiple myelomas secrete IgG or IgA paraproteins; however IgM myelomas (macroglobulinemia) have also been diagnosed in companion animals. Light chain disease is caused by plasma cell overproduction of the light chain segment of the immunoglobulin complex, consisting of either the lambda or kappa light chain. These proteins are referred to as Bence-Jones proteins and are the most commonly observed immunoglobulin fragments in the monoclonal gammopathies. There are rare instances where a malignant plasma cell neoplasm will be nonsecretory. These tumors occur in approximately 1% of all cases of multiple myeloma and are referred to as nonsecretory multiple myeloma. In this type of neoplasm, malignant plasma cells produce either fragments or intact monoclonal immunoglobulins but do not secrete them from the cell. In rare cases of nonsecretory multiple myeloma, recognizable immunoglobulins are not produced.

Multiple myelomas have been described most commonly in dogs, humans, and cats. They account for

< 1% of all malignant canine tumors, ~ 8% of all malignant hematopoietic tumors in dogs, and 3.6% of all primary and secondary bone tumors diagnosed by biopsy. There is no current evidence suggesting any age, sex, or breed predilection; however, older dogs are most commonly affected with a mean age of 8 to 9 years. Multiple myeloma is even less common in cats with a median age of 12 to 14 years and possible male predisposition. The cause of multiple myeloma in companion animals is largely unknown although genetics, viral infections, chronic immune stimulation, and exposure to carcinogens have been identified as possible contributing factors.

The clinical manifestations of multiple myeloma are highly variable and may affect multiple organ systems. The pathologic conditions associated with multiple myeloma are related to the effects of the circulating paraprotein as well as organ or bone marrow dysfunction due to neoplastic infiltration. The presentation of a patient with multiple myeloma will depend on the type of neoplastic cell, type of immunoglobulin produced, location of the tumor, and severity of growth and infiltration. Affected dogs can exhibit signs of lethargy, weakness, lameness, bone pain, hemorrhage (e.g, petechiae on mucous membranes, gingival bleeding, and epistaxis), polyuria / polydypsia, and/or neurologic deficits. Other presenting signs of disease may include hypertension, ophthalmic abnormalities (e.g., venous dialation with sacculation, retinal hemorrhages, and retinal detachment), neurologic dysfunction (including seizures), organomegaly, and suggestion of multiple organ failure.

Hyperviscosity syndrome.
Hyperviscosity syndrome is an increase in the viscosity of the blood secondary to the high concentrations of circulating paraprotein, clinically manifesting in neurologic signs, retinopathy, and cardiomyopathy. IgA and IgM are most often associated with hyperviscosity syndrome because of their structure and size (IgA dimers and IgM pentamers). Cardiomegaly and cardiac disease may result secondary to increased cardiac workload and myocardial hypoxia caused by hyperviscosity. In a study of cats with multiple myeloma, two-thirds of the cats had cardiomegaly on thoracic radiographs and nearly half had a heart murmur.

Osteolysis.
Bone lesions associated with multiple myeloma include discrete radiolucent lytic areas (punched-out appearance) or diffuse osteopenia and commonly affect the axial skeleton and long bones. These lesions may be associated with severe bone pain, spinal cord compression, pathologic fracture, and hypercalcemia. However, only 50% of dogs have radiographic evidence of bone disease. And although cats are reported to have skeletal lesions (8% to 67%), the true incidence of lytic lesions in cats is unknown.

Bone lesion detection improves with focused imaging on specific regions or bones vs. routine survey abdominal and thoracic radiographs. In people, conventional radiography remains the gold standard imaging technique. Computed tomography and magnetic resonance imaging may also be useful; however, nuclear scintigraphy is generally not recommended since myeloma patients have inadequate skeletal uptake of technetium-99 secondary to osteoblast dysfunction.

Hemorrhagic diathesis.
Patients with multiple myeloma can manifest unique hemostatic disorders that predispose them to hemorrhage. Mechanisms include paraprotein-induced thrombocytopath, in which protein coating of platelets leads to platelet dysfunction and paraprotein interference with clotting factors. Other potential causes of bleeding include abnormalities in the formation and polymerization of fibrin, tissue fragility associated with amyloidosis, hypervolemia secondary to hyperviscosity syndrome, and thrombocytopenia. About one-third of dogs and cats with multiple myeloma have clinical signs of bleeding, most commonly epistaxis, intraocular hemorrhage, and gingival bleeding. These patients may have prolonged prothrombin and partial thromboplastin times and about 50% of cats and 30% of dogs are thrombocytopenic.

Cytopenias.
Patients with multiple myeloma can develop anemia from a variety of causes including chronic disease, hemorrhage due to coagulopathy, myelophthisis, and red blood cell destruction. Normocytic, normochromic, and nonregenerative anemia is one of the most common findings on a complete blood count (CBC); two-thirds of dogs and cats are affected. Pancytopenia may be seen in patients with marked bone marrow infiltration with neoplastic cells.

Hypercalcemia.
Hypercalcemia in cases of multiple myeloma can result from osteoclastic bone resorption, hypercalcemia of malignancy, or hyperglobulinemia. Bone stores of calcium can be released by osteoclasts secondary to cytokine secretion by myeloma cells (e.g. lymphotoxin, tumor necrosis factor alpha, interleukins 1, 3, and 6). Myeloma cells can also secrete parathyroid hormone-related peptide, resulting in paraneoplastic hypercalcemia of malignancy. Hyperglobulinemia results in calcium binding by the paraprotein increasing the total calcium concentration while the ionized calcium concentration remains normal. Ionized calcium measurement is, therefore, needed to confirm true hypercalcemia in patients with multiple myeloma.

Renal disease.
Renal disease occurs in about one-third of dogs and cats with multiple myeloma. Renal insufficiency is most commonly associated with excessive light chain production or hypercalcemia. First, excessive light chain production overwhelms the catabolic capacity of the renal tubular cells and the free light chains complex with proteins to form tubular casts leading to renal tubular obstruction. Endocytosis of light chains by tubular cells also induces cytokine release and inflammation resulting in further renal damage. Second, hypercalcemia can lead to prerenal azotemia secondary to antidiuretic hormone inhibition and eventual renal mineralization. Other potential causes of renal disease include amyloidosis, pyelonephritis, and decreased renal perfusion secondary to hyperviscosity syndrome.

Bacterial infection.
Increased susceptibility to bacterial infection is common in patients with multiple myeloma and infections can be life-threatening if not addressed. Immunodeficiency can be secondary to myelophthisis (which results in leukopenia), decreased production of functional immunoglobulin, and compromised B cell function.

Clinical signs and symptoms may be present for up to 1 year before a definitive diagnosis of multiple myeloma is made. Patients can also present with recurrent infections, non-regenerative anemia, pathologic bone fractures, and/or seizures. Complications secondary to multiple myeloma may include renal failure, infections secondary to immunosuppression, clotting disorders, chronic anemia, cardiac insufficiency, and neurologic dysfunctions such as senility.

A diagnosis of multiple myeloma may be made if there is radiographic evidence of osteolysis, there is a population of greater than 20% plasma cells in bone marrow aspirates or biopsies, a monoclonal gammopathy on serum electrophoresis exists, and/or Bence-Jones protinuria is present. Recent studies suggest that in cats’ visceral organ infiltration be included in the diagnostic criteria. Further studies suggest a primary extramedullary origin for neoplastic transformation in cats with multiple myeloma vs. primary intramedullary neoplastic transformation as accepted in the dog myeloma model.

Multifocal radiolucent lesions within the bone may be seen in ~ 40% of dogs suffering from multiple myeloma. In contrast, osteolytic lesions rarely are seen in cats. The bones most commonly involved in canine multiple myeloma include the spine, pelvis, ribs, skull, and proximal extremities. Malignant plasma cell tumors present in the bone marrow are often osteolytic. The presence of these tumors directly induces bone resorption by production of osteoclastic-activating factor from neoplastic cells. Osteolysis is also induced secondary to paraprotein binding of ionized calcium, which initiates secretion of parathormone (PTH) from the parathyroid gland. PTH acts directly on the bone to increase serum calcium concentration.

Survey radiographs may reveal focal, multifocal, or diffuse osteoporosis-type lesions approximately 3-4 weeks after bone changes have occurred. Clinically, the patient may present with pathologic fractures, rear limb lameness or paresis, or bone pain. Myelograms are an effective means of visualizing the changes to vertebral bodies, especially when the patient presents with rear limb lameness or paresis. Most commonly, the myelogram will show extradural compression of spinal cord in the area of the lesion. Plasma cell tumors producing IgM often infiltrate the spleen, liver, and lymph tissue rather than bone. Whole body survey radiographs may detect enlargement of these organs and tissues.

Dogs and cats with multiple myeloma may experience moderate to severe pain, and eliminating it should be a priority. Pain may be relieved by treating the underlying cancer and providing various analgesic therapies and supportive care. Antibiotic therapy may be needed to treat concurrent infections, such as urinary tract infection or bacterial pyoderma, as these can progress to life-threatening infections if left untreated. Intravenous fluid therapy is often needed initially to correct dehydration, improve cardiovascular status, and manage hypercalcemia and azotemia. Treatment with isotonic saline solution is preferred over other crystalloid replacement fluids in the initial management of hypercalcemic patients. Bisphosphonates, such as pamidronate, may be useful in managing hypercalcemia as well as reducing bone pain and decreasing osteoclastic bone resorption. Evaluation of blood urea nitrogen and creatinine concentrations in conjunction with urine specific gravity should be performed before using this medication since it is potentially nephrotoxic. The recommended dose of pamidronate is 1 to 2 mg/kg given intravenously in dogs and, anecdotally, 1 mg/kg given intravenously in cats every 21 to 28 days. This medication should be diluted in saline solution and administered as a slow infusion over two hours to minimize renal toxicosis. Bisphosphonates are an essential component of therapy for multiple myeloma in people, and their use is associated with significantly reduced skeletal-related events and improved survival times. Plasmapheresis is the best immediate treatment for hyperviscosity syndrome. Although rarely performed in veterinary medicine, this procedure involves withdrawing anticoagulated blood, separating blood components, removing the plasma, and reinfusing the remaining components with crystalloid fluids. Packed red blood cells or platelet-rich plasma transfusions may be required if marked hemorrhage or thrombocytopenia is present, respectively. Neoplastic plasma cells are sensitive to irradiation, and radiation therapy is a highly effective palliative treatment for multiple myeloma since it can relieve discomfort and decrease the size of the mass or tumor burden. Indications for radiation therapy include painful bone lesions, spinal cord compression, pathologic fracture (after fracture stabilization), or a large soft tissue mass.

Although a cure is unlikely, multiple myeloma can be a rewarding disease to treat since chemotherapy can greatly extend the quality and duration of life. The chemotherapy drugs most often used are alkylating agents, usually melphalan, combined with prednisone. However, eventual relapse during therapy is anticipated. In dogs, the recommended treatment protocol is melphalan administered orally once daily at a dose of 0.1 mg/kg for 10 days and then 0.05 mg/kg once daily until the disease relapses or myelosuppression occurs. Prednisone is given concurrently at a dose of 0.5 mg/kg given orally once daily for 10 days and then 0.5 mg/kg every other day for 30 to 60 days, at which time prednisone is discontinued. Pulse-dose therapy with melphalan has also been described, in which melphalan, at a dose of 7 mg/m2, is given orally once daily for five consecutive days every 21 days. The most common side effects associated with melphalan therapy are myelosuppression and delayed thrombocytopenia. A CBC should be performed every two weeks for the first two months of treatment and then monthly.

Combined melphalan and prednisone therapy can also be used in cats; however, cats appear to be much more susceptible to myelosuppression. The recommended treatment protocol is 0.1 mg/kg (or 0.5 mg total dose) melphalan given orally once daily for 10 to 14 days and then every other day until clinical improvement or leukopenia develops. A maintenance dose of 0.5 mg given every seven days is then recommended. Prednisone or prednisolone is given concurrently at a dose of 0.5 mg/kg orally once daily. If leukopenia develops, melphalan therapy should be discontinued until white blood cell counts return to normal; then, maintenance therapy may be attempted at the same or a lower dose.

Other chemotherapy agents used to treat multiple myeloma include chlorambucil and cyclophosphamide either alone or in combination with melphalan. In sick myeoma patients, in which a faster response to treatment is needed, cyclophosphamide may be administered intravenously at a dosage of 200 mg/m2 once at the time that oral melphalan therapy is initiated. Lomustine (CCNU) has also been used in combination with prednisone to treat multiple myeloma in cats.

In dogs with relapsing multiple myeloma or resistance to alkylating agents, single agent doxorubicin or the VAD (vincristine, Adriamycin [doxorubicin], and dexamethasone) protocol can be considered. This protocol combines vincristine (0.7 mg/m2 intravenously on days 8 and 15), doxorubicin (30 mg/m2 intravenously every 21 days), and dexamethasone sodium phosphate (1 mg/kg intravenously on days 1, 8, and 15); however, the reported duration of response to this protocol is only a few months.

The overall response rate for dogs treated with melphalan and prednisone chemotherapy is 92%, with 43.2% of dogs achieving a complete response and 48.6% achieving a partial response. The median survival time of dogs treated with this drug combination is 540 days, which is significantly longer than the survival time of 220 days in dogs treated with prednisone alone. Negative prognostic factors in dogs include hypercalcemia, light chain proteinuria, and extensive lytic bone lesions.

Response to therapy and duration of response appear to be more variable in cats. Factors associated with a more aggressive form of the disease and poor prognosis include bone lesions with pathologic fracture, anemia, light chain proteinuria, azotemia, and poor response to treatment. When treated with melphalan and prednisone chemotherapy, four cats classified as having aggressive disease had a median survival time of five days, whereas the median survival time of five cats with less aggressive disease was 387 days. Other studies have shown overall less promising results with a shorter duration of response to treatment and a survival time of six months or less in treated cats. In cats with multiple myeloma and other related disorders, the degree of plasma cell differentiation is significantly correlated with survival. Cats with well-differentiated tumors (< 15% plasmablasts) have a median survival of 254 days, whereas cats with poorly differentiated tumors (≥ 50% plasmablasts) have a median survival of 14 days.

In summary, multiple myeloma is a rare neoplasm in both cats and dogs. Conditions associated with multiple myeloma include hyperviscosity syndrome, bone lesions, hypercalcemia, renal disease, cytopenias, hemorrhagic diathesis, and increased susceptibility to bacterial infection. Multiple myeloma does not appear to have the same biologic behavior in dogs and cats and is best viewed as a heterogeneous disease with a different prognosis, clinical course, and response to therapy both within and between species. Although a good clinical response may be achieved with chemotherapy, eventual relapse of disease is to be expected.

Management of Sacroiliac Fracture/Luxation in the Dog and Cat.

Injury to the sacroiliac joint in the dog and cat commonly occurs in association with fractures of the pelvis and pelvic limb. Substantial soft tissue injury and neurologic dysfunction may also be present. A patient with a sacroiliac fracture/luxation has in all probability sustained a significant external blow to the pelvis, and because of the probability of multiple fractures and soft tissue injuries, a thorough physical and neurologic examination must be performed.

The sacroiliac joint is a combined synovial and cartilaginous joint which functions as a supportive bridge between the appendicular and axial skeletons. Because the pelvis and sacrum form a rigid rectangular or boxlike unit, unilateral displacement of the sacroiliac joint cannot occur without associated pelvic fractures or a pelvic symphyseal separation. Unilateral separation of the sacroiliac joint occurring in conjunction with other severe orthopedic injuries is much more common than bilateral sacroiliac joint injury. Few unilateral sacroiliac injuries are associated with ischial and/or pelvic fractures alone.

Clinical signs exhibited by the patient obviously depend on the severity of the trauma as well as the extent of the associated injuries. Caudal abdominal herniation, urethral laceration, intestinal perforation, urinary bladder rupture, diaphragmatic hernias, and pulmonary contusions have all been associated with fractures of the pelvis. It is imperative that associated soft tissue injuries be diagnosed, as they affect treatment and prognosis. The patient may be ambulatory or nonambulatory, depending on the nature of the associated orthopedic and/or neurologic injuries.

In fracture/luxation of the sacroiliac joint in dogs and cats, treatment is either conservative or surgical. Current recommendations indicate conservative treatment in subluxations or in complete luxations when the patient is ambulatory and exhibits minimal discomfort. Before a course on conservative therapy is chosen, a neurologic examination should indicate that there are no functional deficits of the lumbosacral trunk and/or sciatic nerve. Complications of conservative management include increased cranial or medial displacement of the hemipelvis and obstruction of the pelvic outlet. Conservative treatment may also prolong the period of instability and lameness and prolong the period of patient discomfort and client concern. In addition, if marked displacement is present, asymmetry of the acetabulae may result in an abnormal gait posttrauma.

Open reduction and internal fixation is indicated for fracture/luxations when one or more of the following clinical or radiographic signs are present: 1) marked instability and displacement of the hemipelvis, 2) neurologic deficits attributable to the luxation or 3) obstruction of the pelvic outlet is observed. Surgical intervention is of particular value when associated orthopedic injuries are present, as surgical stabilization allows the patient to become ambulatory earlier and provides a better prognosis for the return to a normal gait.

In light of the fact that the overwhelming majority of sacroiliac fracture/luxations are associated with additional orthopedic injuries, my personal preference is to opt for early surgical repair. Even in cases of unilateral fracture/luxations with minimal associated orthopedic injuries, in my experience surgical intervention returns these animals to a normal gait more quickly and with a shorter convalescent period than if conservative therapy was chosen.

Sacroiliac fracture/luxations may be surgically repaired by either a dorsolateral or ventrolateral approach. The approach chosen may be dictated by the presence of additional pelvic injuries requiring open reduction and interal fixation, or surgeon preference. Both approaches provide adequate exposure for visualization of the sacroiliac joint.

Stabilization of sacroiliac fracture/luxations is most commonly accomplished with lag screw fixation. The two most important variables in the technique of lag screw fixation affecting sacroiliac stability are screw location and depth of screw placement. Screws placed within the sacral body have the lowest rate of loosened fixation compared to other areas of the sacrum. Proper positioning within the sacral body is also essential to prevent injury to the nerve roots within the spinal canal, and the lumbosacral trunk or sciatic nerve ventral to the sacral body. With regard to depth of screw placement, a cumulative screw depth/sacral width of 60% or more significantly reduces the likelihood of loosening of the fixation. While some authors have suggested that 2 screws be used routinely for sacroiliac stabilization, in all feline and most canine sacrums there is room for only one properly placed screw within the sacral body. In the giant breeds of dogs, a second screw or an intramedullary pin may be placed, but the placement of this additional screw or pin within the sacral body is dependent upon the accuracy of placement of the first screw. In addition, a recent study did not demonstrate a difference in the number of loosened fixations when one or two screws were used.

When a sacroiliac fracture/luxation occurs, most if not all of the fibrocartilage remains attached to the lateral surface of the sacral wing. When placing lag screws for fixation, the location of the sacral body must be determined by palpation as well as by the anatomical landmarks of the sacral wing. Screw placement should always be just caudal to the sacral wing notch.

Postoperative care should include restriction of exercise for a period of 6-8 weeks. A mild laxative may be administered, if bowel movements appear to be painful during the immediate postoperative healing period. A significant number of sacroiliac fracture/luxations repaired with lag screw fixation may loosen and result in loss of reduction and sacroiliac instability. The guidelines for location of screw placement mentioned here should improve the results of fixation and allow for a better prognosis for return to a normal gait and conformation.

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Portosystemic Shunts.

Portosystemic shunting is a macroscopic diversion of portal blood from the liver into the systemic circulation, which most commonly occurs because of a congenital malformation of the portal circulation. Blood flow to the liver may be decreased by up to 95% of normal in shunt patients, resulting in a bypass of the body’s normal homeostatic liver detoxification mechanisms. Additionally, this lack of normal blood flow results in a deficiency of oxygenated blood, insulin, and growth factors that the liver requires for normal growth and function.  The anomalous connections may occur between the portal vein and the caudal vena cava, azygous vein, renal vein, phrenic vein, internal thoracic vein, and the umbilical vein remnant.  As mentioned previously, in most cases, the shunt is congenital in nature; however, there are cases of acquired shunting secondary to an increase in portal hypertension. 

The liver carries out a number of important functions, including but not limited to the synthesis of glucose, glycogen, cholesterol, lipoproteins, albumin, fibrinogen, bile acids, and detoxification of the blood to remove hazardous circulating chemicals, bacteria, and bilirubin. In addition, the liver functions as a reservoir to store important nutrients, minerals, vitamins, and hormones. All of these functions are significantly impaired in patients with portosystemic shunts. The degree of impairment is in direct correlation with the percentage of blood bypassing the liver.

Portosystemic shunts may be either intra or extra hepatic in nature. Congenital extrahepatic portosystemic shunts are most common, accounting for 61% to 94% of congenital shunts and are most prevalent in the smaller terrier breeds. They are frequently observed in the Maltese, Yorkshire Terrier, Shih Tzu, Dachshund, and Poodle. Congenital extrahepatic shunts are also frequently observed in cats. The Persian and Himalayan breeds are over represented; however, mixed breed cats may also be affected.  Acquired Intrahepatic shunts represent between 6% and 40% of congenital shunts and are more common in large and giant breeds of dogs such as Irish Wolfhounds and Golden Retrievers. Hepatic microvascular dysplasia is an unusual form of intrahepatic portosystemic shunting in which no gross vascular abnormality can be identified. This rare condition is associated with somewhat milder clinical signs and appears to be the consequence of a developmental abnormality; it has a higher prevalence in Cairn Terriers, suggesting a hereditary basis. Since that time, this anomaly has been seen in many other smaller dog breeds. Clinical signs and diagnostic evaluations are similar to those discussed below, but no surgically identifiable or radiographically identifiable shunt is seen. The shunting is at the level of the hepatic portal vein capillaries, and thus, not correctable surgically.

Portosystemic shunts are most commonly observed and diagnosed while the animal is young, often less than six months of age. The affected pets are smaller in stature, have poor quality hair coats, appear weak, and often exhibit neurologic abnormalities. Particularly bizarre behavioral signs or loss of intellectual function, unpredictable bouts of maniacal or aggressive behavior, staggering, pacing, circling, head pressing, blindness, deafness, tremors, seizures, and coma may be seen. Other signs include pica and polyphagia. In many cases, the clinical signs have an episodic nature; they are present for a few hours to a day or two and the animal returns to normal. The clinical signs are often meal related neuro-encephalopathic signs or somnolence, nausea or vomiting, diarrhea or constipation, polyuria and polydipsia, intermittent fever, ptyalism, and signs attributable to ammonium biurate urolithiasis (chronic urinary tract infections, prolonged or difficult urination). Any dogs or cats in which a uric acid calculus is identified should be evaluated as a possible PSS case (except for Dalmations and Bulldogs). Dogs with portosystemic shunts also have increased susceptibility to infections because of the decreased function of their hepatic mononuclear phagocytes which serve to clear toxic cells from the body. Minor bite wounds, tick bites, subcutaneous infections, lacerations, and even vaccinations may lead to illness requiring hospitalization. The severity of clinical signs in symptomatic patients is highly variable and is largely affected by the quality of food being consumed and the percentage of shunting present.

The diagnosis of PSS is often suspect on presentation of the afore mentioned clinical signs, history, and physical examination.  The diagnosis is confirmed by performing laboratory testing, which includes complete hematology, serum chemistry, urinanalysis, abdominal radiography, and pre and post prandial bile acid values. Hematologic evaluation may indicate microcytosis with or without a mild non regenerative anemia and a leukocytosis secondary to infection. Serum chemistry evaluation may indicate decreases in glucose, albumin, cholesterol, blood urea nitrogen, and total protein values because of decreased production and capacity for storage by the smaller than normal liver. An increase in certain liver enzyme values including the serum ALT, AST, and ALP, can be observed because of injury to the hepatic cells.  Increased serum bile acid concentrations taken either after an overnight fast or 2 hours after a meal are usually strongly suggestive of a shunt abnormality.

A definitive diagnosis of intrahepatic, extrahepatic, or microvascular PSS is made with varying combinations of contrast radiography, ultrasonography, scintigraphy, CT scan, or MRI angiography. This generally requires specialized imaging techniques, and it is appropriate that these pets be referred to appropriate specialists. Survey radiographs normally taken in general practice veterinary facilities is an important first step because it may indicate the presence of a small liver and urinary bladder stone formation consistent with a presumed shunt abnormality.

Contrast radiography is a procedure whereby a marker dye is injected into the jejunal vein or splenic parenchyma, which provides excellent imaging of portal blood flow.  The procedure requires general anesthesia and laparotomy to be performed and, as such, often performed in combination with surgical correction (so that the dog has to be anesthetized only once) and is often referred to as operative mesenteric portography. This procedure was the diagnostic technique of choice prior to the emergence of the non-invasive imaging techniques currently utilized in specialty practices such as the Animal Medical Center of Southern California.

Ultrasonography is a useful, noninvasive tool for acquiring information about the liver and circulatory system as well as the detection of portosystemic shunts. The exact location of intrahepatic shunts may be more amenable to diagnosis via ultrasound examination. Abnormalities observed upon ultrasound evaluation of pets with intrahepatic shunts include microhepatica, decreased numbers of hepatic and portal veins, detections of the anomalous vessel, and the presence of renal and bladder uroliths. Unfortunately, extraheptic shunts are more difficult to diagnose using ultrasound because of obscurity of the lesion from the surrounding visceral organs. 

Nuclear scintigraphy is an advanced non invasive technique which is currently the state of the art procedure used to evaluate portal venous shunting.  In this technique, after the animal receives a warm water enema, the colon is infused with technetium 99m pertechnetate.  The animal is scanned with a gamma camera and the images are registered.  In normal animals, the radiochemical is transported through the portal system to the liver.  In animals with PSS, a greater percentage of the radiochemical is carried to the heart.  The deviation in the time curve provides the diagnosis of the presence of a shunt; however, it does not definitively prove its anatomical location.  Normal dogs have a shunt fraction of less than or equal to 15 % whereas dogs with PSS have a shunt fraction of 60% or greater.  An inaccurately low result can be caused by poor absorption of the radiochemical by the colon, excessive fecal material in the colon, or poor administration technique.  A false positive result is occasionally observed with rectal administration of the radiochemical as uptake by the caudal rectal artery may be misinterpreted as an increased absorption indicative of an extrahepatic shunt.

MRI angiography and CT scan both provide excellent three dimensional images of the shunt.  Both modalities require a general anesthesia and can be cost prohibitive.  There are many other techniques available; transjugular retrograde portography, cranial mesenteric angiography, exploratory laparotomy, etc…The choice is often dependent on the patient’s stability, the urgency for surgical correction, availability, and physician preference.

Once a diagnosis is made, there are two standard management options: surgical ligation of the shunt and/or medical management of the effects of shunting. Surgery is the treatment of choice where feasible; however, the decision to pursue medical management should be made on a case-by-case basis depending on the type and location of the shunt, the age of the animal, and the severity of clinical signs. There may also be significant financial considerations on the part of the owner. Hepatic functional failure tends to progress in most animals that are diagnosed prior to one year of age. Even though medical therapy may keep them relatively asymptomatic, they eventually become refractory to medical management and succumb to their disease. Thus, surgical attenuation or ligation of the shunting vessel is the best therapeutic option in order to provide reversal of signs, and long duration quality survival. The objective of surgery is to redirect shunting blood back into the liver providing hepatic parenchyma with hepatotropic factors necessary for normal growth and metabolism.

Every patient diagnosed with a PSS should be appropriately medically managed prior to surgical intervention in order to provide more strength and stability to the patient in anticipation of undergoing an invasive surgical procedure.  Initially, the correction of fluid and electrolyte abnormalities, glucose imbalance, and hepatic encephalopathy are of utmost importance. Other pre-operative goals include minimizing lower urinary tract disease and reducing the metabolic load on the liver. The chief components of medical management strategies are dietary modifications and the administration of oral antibiotics. 

Dietary protein is restricted because it is a significant source of nitrogenous wastes and toxins that are in part responsible for symptoms of hepatic encephalopathy. Other additional toxins are derived from the bacterial flora found within the large intestine which is responsible for the production of ammonia and ammonia by products. The production of these toxins is reduced by limiting the total amount of protein ingested and ensuring that the dietary protein ingested is high quality and biologically available with little waste protein being generated during digestion. The utilization of these diets results in the reduction of the amount of waste protein that reaches the large intestine, thereby decreasing the substrate load the colonic bacteria have available to produce circulating toxins. Further reductions may be attained by feeding smaller meals more frequently to maximize the digestive capacity of the small intestine. These special high quality, lower total protein, high caloric diets are ideal because they provide a balanced protein-calorie intake, which is important for the control of hepatic encephalopathy. Including dietary fiber in the daily ration assists in acidifying the colonic environment and limiting toxin production and also acts as a mild laxative to increase the elimination of toxic factors in feces. Lactulose, a soluble fiber, is often prescribed as a supplement for this purpose. Antibiotics are used in most cases to reduce the bacterial population within the large intestine that are responsible for the production of circulating neurotoxins.

Surgical ligation of the shunt vessel is a sophisticated technique which requires an experienced surgeon and support staff in order to best ensure a successful surgical outcome. At the Animal Medical Center, our Board Certified Surgeon has successfully diagnosed and treated PSS patients for over 27 years. A thorough exploratory laparotomy is performed.  All the viscera in the abdomen are gently explored. The venous drainage system is explored and the shunt located.  Single extra hepatic shunts are usually identified as tortuous, abnormal vessels. The most common locations for an extrahepatic shunt include an abnormal vessel visualized rostral to the renal veins at the level of the caudal vena cava, along the greater or lesser curvature of the stomach, along the venous drainage of the spleen, and an abnormal vessel coursing dorsally to the azygous vein and disappearing beneath the diaphragm.  The shunt is ligated as close to it’s insertion site as possible so that the blood flow from potential tributaries of the shunt is redirected.  More specifically, portacaval shunts are occluded at their termination at the caudal vena cava and portoazygous shunts can be occluded at the abdominal side of the diaphragm. 

A potentially fatal complication from shunt ablation is portal hypertension, which occurs when intrahepatic vessels are unable to cope with the additional volume of blood that is diverted to the liver after closure of the shunt vessel. Failure to recognize and alleviate hypertension and resulting pain can lead to the development of bloody diarrhea and endotoxic shock leading to death in 2 to 24 hours after surgery. Approximately 40-68% of dogs and cats that undergo shunt attenuation can only tolerate partial ligation. Before permanent ligation, the shunt is temporarily occluded using gentle digital pressure for 3-5 minutes and the portal and systemic blood pressures are carefully monitored for hypertension and the intestines and pancreas are inspected for signs of cyanosis indicative of the inability of the body to cope with the redistribution of blood flow through the liver. These complications were much more prevalent when shunt attenuation was accomplished by ligature placement around the shunting vessel. In order to decrease the incidence of complications observed with the older technique of immediate, complete occlusion of the shunting vessel by ligature placement, an ameroid ring constrictor was developed.  An ameroid ring is made of casein on its inner side and stainless steel on the outside.  The casein interior is composed of a hygroscopic substance that slowly swells as it slowly absorbs fluid from the abdominal cavity.  The ameroid ring is placed around the shunt vessel and locked in a closed position. The resultant inward swelling causes the vessel to gradually occlude over a 4-5 week period.

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Dogs generally have dramatic clinical and biochemical improvement following shunt correction. They are usually clinically improved within 24 to 48 hours. Follow-up function studies significantly improve, but rarely return to normal post-operatively. Occasional animals will have persistently abnormal, but improved, ammonia tolerance tests or slightly elevated bile acid values but remain clinically asymptomatic and require no special therapy. A number of post-operative portal angiograms have been reported and all show improved portal circulation of the liver, but the perfusion pattern is aberrant. The overall prognosis for dogs with single extrahepatic shunts appears to be excellent if they survive the surgery and immediate post-operative period. For intrahepatic shunts, the outlook is more guarded, but numerous successful surgeries have been performed by surgeons knowledgeable in the intricacies of this procedure. If urinary calculi cannot be removed during the surgery to correct the shunt, they may be either removed at a later date or managed medically. Spontaneous dissolution of renal calculi (presumed to be ammonium urate) following shunt correction alone may be observed. Calculi present in the bladder may also be successfully dissolved using a combination of a reduced purine diet (Prescription diet-u/d) combined with allopurinol, 10 mg/kg every 8 hours, and sufficient sodium bicarbonate to alkalinize the urine. Calculi may disappear in 4 to 12 weeks on this therapy. Recurrences of calculi should not be a problem once the shunt is corrected, as metabolic abnormalities causing increased urinary ammonia and uric acid excretion should cease.

Immediate postoperative therapy should include fluid therapy, temperature and blood pressure monitoring, packed cell volume, total protein and glucose testing. All dogs undergoing surgical ligation should continue to receive medical therapy as discussed above for 2 to 4 weeks post- operatively.  Liver regeneration occurs rapidly and return to normal to near normal hepatic function can be observed by 8 weeks post-operatively.

In conclusion, the portosystemic shunt is a common disease process encountered in dogs and cats. While the origin of the disease is obscure the disease is considered to be congenital; however, breed predisposition does exist, indicating a hereditary origin. Symptoms vary but all result in central nervous system disorders called hepatic encephalopathy. Puppies and kittens that fail to maintain the same growth rate as their siblings are suspect. Specific urinary crystals develop due to increased concentrations of ammonium. The degree or percentage of vessel shunting may explain why some animals are without symptoms until later in life. Small liver size coupled with bizarre neurological signs in young dogs and cats is highly suggestive of the disease. Medical or surgical treatment is available; however, without corrective surgery an animal will eventually succumb to the progressive disease process. Prompt and effective surgical intervention utilizing an ameroid constricter and medical management results in effective and long lasting alleviation of the clinical signs induced by this congenital anomaly.

Canine Allergic Dermatitis: Causes and Treatment Options.

One of the most common medical complaints that we see in our office is dogs with skin infections, “hot spots”, or allergic dermatitis, also known as atopic (atopy) dermatitis. Unlike people who react to allergens most commonly with nasal symptoms and/or hives, dogs react with skin and/or gastrointestinal problems. This is because there are a higher proportion of mast cells, which release histamines and other vasoactive substances in the face of an allergic challenge, in the skin of dogs. These problems may range from poor coat texture or hair length, to itching and chewing, to hot spots and self-mutilation, gastrointestinal pain and discomfort, diarrhea, and flatulence. Allergies may also play a part in chronic ear infections. The most common causes of canine allergic dermatitis are flea allergy, food allergy, inhalant or contact allergy, and allergy to the normal bacterial flora and yeast organisms of the skin. To make matters more difficult to diagnose and treat, thyroid disease may add to the problem as well.

Canine atopic dermatitis (allergic dermatitis, canine atopy) is an inherited predisposition to develop allergic symptoms following repeated exposure to some otherwise harmless substance, an “allergen”. Most dogs begin to show their allergic signs between 1 and 3 years of age. Due to the hereditary nature of the disease, several breeds, including Golden Retrievers, most terriers, Irish Setters, Lhasa Apsos, Dalmatians, Bulldogs, and Old English Sheep dogs are more commonly atopic, but many dogs, including mixed breed dogs can have atopic dermatitis. Atopic animals will usually rub, lick, chew, bite, or scratch at their feet, flanks, ears, armpits, or groin, causing patchy or inconsistent hair loss and reddening and thickening of the skin. The skin itself may be dry and crusty or oily depending upon the dog.  Dogs may also rub their face on the carpet; ear flaps may become red and hot. Because the wax-producing glands of the ear overproduce as a response to the allergy, they get bacterial and yeast (Malassezia ) infections of the ear.

In order to overcome these frustrating symptoms, your veterinarian’s approach needs to be thorough and systematic. Shortcuts usually will not produce results and only add to owner frustration and canine discomfort.

Inhalant and Contact Allergies
Substances that can cause an allergic reaction in dogs are much the same as those that cause reactions in people including the pollens of grasses, trees and weeds, dust mites, and molds. A clue to diagnosing these allergies is to look at the timing of the reaction. Does it happen year round? This may be mold or dust. If the reaction is seasonal, pollens may be the culprit.

Food Allergies
Many people don’t suspect food allergies as the cause of their dog’s itching because their pet has been fed the same food all its life and has just recently started having symptoms. However, animals can develop allergies to a substance over time, so this fact does not rule out food allergies. Another common misconception is that dogs are only sensitive to poor quality food. If the dog is allergic to an ingredient, it doesn’t matter whether it is in premium food or the most inexpensive brand on the market. One advantage to premium foods is that some avoid common fillers that are often implicated in allergic reactions.

Flea Allergies
This type of reaction usually is not to the flea itself, but rather to proteins in its saliva. Interestingly enough, the dogs most prone to this problem are not dogs who are constantly flea ridden, but those who are exposed only occasionally! A single bite can cause a reaction for five to seven days, so you don’t need a lot of fleas to have a miserable dog.

Staphylococcus Hypersensitivity
Bacterial hypersensitivity occurs when a dog’s immune system overreacts to the normal Staphylococcus (Staph) bacteria on its skin. It appears that bacterial hypersensitivity in the dog is more likely to occur if other conditions such as hypothyroidism, inhalant allergy, and/or flea allergy are concurrently present. Bacterial hypersensitivity is diagnosed through bacterial culture and examination of a biopsy sample. Microscopically, there are certain unique changes in the blood vessels of the skin in bacterial hypersensitivity.

Diagnosis

Allergy testing is the best diagnostic tool and the best road to treatment for dogs that are suffering from moderate and severe allergies. There are several different testing methods available. The most common is a blood test that checks for antigen induced antibodies in the dog’s blood. Intradermal skin testing may also be performed.  In this method of testing, a small amount of antigen is injected into a shaved portion of the dog’s skin. This is done in a specific pattern and order so that if the dog shows a small raised reaction, the offending antigen can be identified.  After a period of time (hours), the shaved area is examined to detect which antigens, if any, created a reaction.  Allergy testing is performed to develop a specific therapy for the allergic animal.

Treatment

Medicated Baths
Many medicated shampoos have compounds in them that are aimed at soothing injured skin and calming inflammation. In addition, frequent bathing (weekly to every other week) of the dog can remove allergens from the hair coat, which may contribute to skin allergy flare-ups. The medicated baths we recommend are those that actually contain antimicrobial and antifungal agents as well as ingredients that allow the skin to be bathed on a more frequent basis without drying it out. Application of a rinse afterwards also helps to prevent drying out of the skin and hair coat.

Antihistamines
Antihistamines can be used with good safety in dogs. About one third of owners report success with antihistamines.  These medications tend to have a variable effect between dogs. For some allergic dogs, antihistamines work very well in controlling symptoms of allergic skin disease. For other dogs, very little effect is seen. Therefore, a minimum of three different types of antihistamines should be tried before owners give up on this therapy. Examples of antihistamines commonly used for dogs include Benadryl, Chlortrimeton, Atarax, Claritin, Zyrtec, and Clemastine.  However, antihistamines are considered to be worth trying in most cases since the side effects associated with antihistamines is low, and they are typically inexpensive medications.

Antibiotics and Antifungal Medications
Antibiotics are frequently needed to treat secondary skin infections. Anti-fungal medications are frequently needed to treat secondary yeast infections.

Flea Control
For dogs with this problem, a strict flea control regime must be maintained. The best flea control options include the use of products such as Advantage, Revolution, Frontline, Comfortis, and Sentinel.

Supplements
The Omega-3 and Omega-6 essential fatty acid supplements work by improving the overall health of the skin. These fatty acids are natural anti-inflammatory and anti-oxidative agents. They reportedly are helpful in 20% of allergic dogs. My own experience puts this figure a little higher. They are certainly worth a try because they are not harmful and have virtually no side effects. Omega-3 fatty acids are found in fish oils and omega-6 fatty acids are derived from plants containing gamma-linolenic acid (GLA). These supplements are different from those sold to produce a glossy coat. Products that contain both omega-3 and omega-6 fatty acids include Allergen Caps and Halo.

Hypoallergenic Diets
Allergies develop through exposure, so most hypoallergenic diets incorporate proteins and carbohydrates that your dog has never had before. As mentioned previously, the quickest and best way to determine which foods your dog may or may not be allergic to is through diagnostic allergy testing. As dairy, beef, and wheat are responsible for 80% of food allergies in dogs, these items should be avoided. Novel protein sources used in hypoallergenic diets include venison, egg, duck, kangaroo, and types of fish not usually found in pet food. Carbohydrate sources include potatoes, peas, yams, sweet potatoes, and canned pumpkin.

Hydrolyzed protein diets are diets in which the protein source has been synthetically reduced to small fragments. The theory behind feeding a hydrolyzed protein source is that the proteins in the food should be small enough that the allergic dog’s immune system will not recognize the protein fragments and will not mount an immune response resulting in an allergy.

Most pets with food allergies respond well when switched to a store-bought hypoallergenic diet, but occasionally an animal suffers from such extreme allergies that a homemade diet is the only option. In this case, the diet should be customized with the aid of a veterinarian.

Corticosteroids and Immunosuppressive Agents
Cortisone products such as prednisone, prednisolone, and dexamethasone reduce itching by reducing inflammation. These medications are not without side effects, so they need to be used judiciously in treating skin allergies. Steroids should be considered only when the allergy season is short, the amount of drug required is small, or to relieve a dog in extreme discomfort. Side effects can include increased thirst and appetite, increased need to urinate, and behavioral changes. Long-term use can result in diabetes and decreased resistance to infection. In some dogs, long term, low-dose alternate day therapy is the only management protocol that successfully controls the atopic pet. This protocol should be used only as a last resort after all other methods have been exhausted to avoid the potential long-term complications of the medication.

Cyclosporine (Atopica) is a medication, which seems to be fairly effective at reducing the inflammation associated with skin allergies and calming the immune system of the affected dog. However, the pricing of cyclosporine may be prohibitive for larger breed dogs.

Immunotherapy (Hypo-sensitization)
Allergy shots are very safe, and many people have great success with them; however, they are very slow to work. It may be six to twelve months before improvement is seen. Once the allergens for the dog are identified, an appropriate immunotherapy is manufactured for that specific dog, and treatment can begin. After the offending antigens are identified, then a mixture of these antigens can be formulated into a hyposensitizing injection. Depending on the type of agents used, these injections will be given over a period of weeks to months until the dog or cat develops immunity to the agents. After initial protection, an occasional booster may have to be given.

Environmental Control
If you know which substances your dog is allergic to, avoidance is the best method of control. Even if you are desensitizing the dog with allergy shots, it is best to avoid the allergen altogether. Molds can be reduced by using a dehumidifier or placing activated charcoal on top of the exposed dirt in your house plants. Dusts and pollens are best controlled by using an air cleaner with a HEPA filter. Air conditioning can also reduce circulating amounts of airborne allergens because windows are then kept closed.

Thyroid Medication
Healthy skin and a normal hair coat are the result of many factors, both external and internal. There are several glands in the body responsible for the production of hormones that are vital for the regulation of other body functions as well as a normal skin surface and hair coat. Hypothyroidism may result in poor skin and hair coat, including hair loss or abnormal hair turnover, dull or brittle hair, altered pigmentation, and oily or dry skin. A blood test is the simplest and most direct way to tell if your dog is hypothyroid. Thyroid testing may include all or part of the following:

Baseline T4 Test or Total T4 (TT4): This is the most common test. Dogs with a failure of the thyroid gland will have a lowered level of the T4 hormone. However, there are other conditions that can cause the T4 to decrease, so if this test comes back positive for hypothyroidism your vet should recommend an additional blood test, either the T3 Test or the Baseline TSH test.

Baseline TSH Test: Measures the level of Thyroid Stimulating Hormone. In combination with the T4 or T3 test, it provides a more complete picture of the hormonal activity of your dog’s thyroid gland.

Free T4 by RIA (radio immunoassay): The Free T4 test using RIA techniques does not appear to be more or less accurate than the above TT4 test.

Free T4 by ED (equilibrium dialysis): This test may provide more accurate data on the level of T4 hormone in your dog’s bloodstream.

Baseline T3 Test: In combination with the T4 or TSH test, these two blood tests can give a clearer picture of the hormone levels found in the bloodstream. This test is not reliable when used alone. The T3 Test should always be given in combination with one of the other blood tests.

TSH Response Test: In this test, the veterinarian takes an initial measurement of the thyroid hormones in your dog’s bloodstream and then injects Thyroid Stimulating Hormone (TSH) into the vein. After 6 hours, a blood sample is drawn and the level of T4 is checked. If your dog has hypothyroidism, the level of T4 will not increase even after the TSH is injected. This is an expensive test and is being used less often due to decreased production by the manufacturers.

Hypothyroidism is treated with a daily dose of synthetic thyroid hormone called thyroxine (levothyroxine). Blood samples will need to be drawn periodically to assess the effectiveness of the dosage and make any adjustments necessary.

Successful management of the atopic, allergic dog is sometimes complicated and frustrating because multi-modal management is necessary in the majority of cases to control the allergic flare-ups.  Proper diagnosis by a veterinarian and owner compliance and follow up care is essential to maximize the chances of curing or at least controlling the severely affected allergy patient.

Cushing’s Disease.

Cushing’s disease describes a syndrome resulting from the overproduction of cortisol, a normal naturally occurring hormone in cats and dogs. This overproduction results in a constellation of clinical signs and is also known as hyperadrenocorticism. It is seen mostly in dogs; cats are rarely affected. Middle-aged and older dogs are most commonly diagnosed, and the disease is slightly skewed toward females.

Overproduction of cortisol can result from either excess activity of the adrenal glands themselves or from excess stimulation of the adrenal glands to make cortisol caused by the release of the hormone ACTH by the pituitary gland in the brain. The most common form of Cushing’s disease is caused by the over production of ACTH by a pituitary gland tumor in the brain that in turn controls the volume of cortisol produced by the adrenal glands. This is called pituitary-dependent Cushing’s disease and is responsible for approximately 85% of the cases observed. A smaller percentage of dogs (15%) with Cushing’s disease have a tumor of one of the adrenal glands, which is responsible for the over production of endogenous cortisol. This disease state is known as adrenal-dependent Cushing’s. A small percentage of cases are caused by the over administration of glucocorticoids (iatrogenic Cushing disease) also known as steroids, while the pet is being treated for a steroid responsive disease process.

Cortisol affects the function of many organs in the body, so the signs of Cushing’s disease may be varied. The most common symptoms by far are excess hunger, excess urination, and excess thirst. Less common symptoms include an increase in panting, a pendulous abdomen (“sway belly”), exercise intolerance, weight gain, physical changes to the sexual organs, and symmetrical hair loss. Hair loss caused by Cushing’s disease occurs primarily on the body, sparing the head and legs. The skin is not usually itchy as it is with other skin diseases. If you pick up a fold of skin on a dog with Cushing’s disease, you may notice that the skin is thinner than normal. The pet may have fragile blood vessels and may bruise easily. A veterinarian may also note skin masses called comedones, an enlarged liver, an oily coat, and muscle wasting.

As previously mentioned, approximately 85% of Cushingoid dogs exhibit pituitary dependent Cushing’s syndrome. Most cases are caused by a benign tumor of the pituitary gland. The excessive ACTH produced by the pituitary gland tumor stimulates the adrenal glands to produce disproportionately high amounts of cortisol. Cushing’s syndrome results when the pituitary gland is unable to slow down its stimulatory messages when enough cortisol is present because of the presence of this particular type of brain tumor. As a result, the pituitary gland keeps encouraging the adrenal glands to make cortisol, a vicious cycle ensues, and Cushingoid symptoms result. The normal part of the pituitary gland shuts down, and the abnormal cells now function autonomously. In cases of adrenal dependent Cushing’s disease (15%), an adrenal tumor is responsible for the excess production of cortisol. In these cases, the normal pituitary gland senses the excessive production of cortisol and decreases its production of ACTH in an attempt to limit the amount of cortisol produced. Unfortunately, these adrenal tumors function independently of the levels of ACTH produced by the pituitary gland. While the causative mechanism is different, the result is the same, the over production of circulating cortisol.

Excess cortisol causes a host of problems. It acts on water balance, causing excess thirst and urination. It causes protein breakdown, so patients become weak and lack muscle mass while feeling very hungry. Normal skin function is disturbed and thinning, fragility, and changes to the skin and coat ensue. These patients are more susceptible to skin infections, hypertension, and the formation of blood clots.

Cushing’s disease is successfully diagnosed through a number of well-choreographed diagnostic tests. A normal blood panel and urinalysis often yields the first clues by reflecting changes in certain liver values as well as the presence of dilute urine. Radiographs may indicate an enlarged liver, thinning bones, and/or changes to lung tissue. Many of these animals will have high blood pressure. If the disease is suspected, one of two paths can be pursued. Most commonly, veterinarians will begin with what is known as an ACTH stimulation test. In this test, an analog of the pituitary hormone (cosyntropin) is given intravenously to stimulate cortisol release into the bloodstream from the adrenal glands. Cortisol levels are measured immediately before and 1 hour after administration of the cosyntropin. A normal animal will have low levels of cortisol before the cosyntropin is administered and moderately higher levels afterwards. Animals with Cushing’s disease will have higher levels before administration and very high levels afterward. This test is approximately 85% effective at identifying the disease, but less effective at identifying pituitary dependent versus adrenal gland dependent disease. The ACTH stimulation test is the gold standard of tests for the diagnosis of iatrogenic Cushing’s disease. For this reason, a dexamethasone suppression test is often performed after Cushing’s syndrome has been diagnosed by the pre and post ACTH stimulation test. The low dose dexamethasone suppression test is considered an excellent test with an estimated 90-95% ability to diagnose Cushing’s disease. A fasted dog has a blood sample taken as a baseline in the morning. A small amount of dexamethasone, a synthetic glucocorticoid, is injected, and follow-up blood samples are taken 4 hours and 8 hours later. In a normal patient, this steroid injection will signal the pituitary gland to decrease its production of ACTH and the adrenal glands will cease their production of cortisol. It essentially tells the brain and the adrenal glands that enough steroids are present in the body, so there is no need to be active at that time. Cushingoid dogs will not suppress blood cortisol in response to the dexamethasone injection because their feedback mechanisms are not working properly as explained above. This test does not differentiate between forms of Cushing’s disease (adrenal vs. pituitary), although it may be suggestive. Dogs that suppress at 4 hours and rebound at 8 hours usually have pituitary tumors. Once a dog has been diagnosed as Cushingoid, the high dose dexamethasone suppression test can be used to differentiate between forms of Cushing’s. Similar to the low dose dexamethasone test, a fasted dog has a baseline blood sample taken in the morning. The dog is then given a larger dose of dexamethasone. Blood samples are taken 4 hours and 8 hours later. A dog with an adrenal tumor will not suppress at all. The adrenal tumor simply doesn’t “care” about the level of blood cortisol; it keeps manufacturing cortisol. A dog with a pituitary tumor still has some limited ability to respond to feedback and thus should respond to a high dose of dexamethasone with a suppressed cortisol level. Approximately 15%-20% of dogs with pituitary tumors will not suppress on a high dose dexamethasone test; these dogs generally have large pituitary macroadenomas.

In this way, a dexamethasone suppression test is best for differentiating between pituitary-dependent and adrenal-dependent hyperadrenocorticism. Additional testing may be necessary to distinguish the cause of excessive cortisol production and include but are not limited to tests measuring baseline cortisol values, urinary cortisol:creatinine ratios, abdominal ultrasound to examine the adrenal glands, and computed tomography (CT) or MRI evaluation to examine the pituitary gland and/or adrenal glands.  Because no one individual test yields all the necessary information about a patient with Cushing’s disease, most doctors will perform more than one test to accurately diagnose a case of pituitary dependent versus adrenal dependent Cushing’s disease.

As previously mentioned, there is no one single test to diagnose Cushing’s disease. The history, physical exam, and results of initial blood and urine tests often provide a strong suspicion for the presence of Cushing’s disease. Laboratory tests that are most commonly altered by Cushing’s disease are an increase in white blood cell count, increase in the liver enzyme ALP (also called SAP or serum alkaline phosphatase), increased blood sugar (although not as high as the blood sugar levels of diabetic patients), increased cholesterol, and dilute urine. 

Radiographs of the abdomen often indicate a larger than normal liver. Occasionally, the x-ray will indicate dystrophic calcification in the area of one of the adrenal glands that is suggestive of an adrenal tumor. Ultrasound of the abdomen may reveal enlargement of both adrenal glands in pets with pituitary-dependent Cushing’s or enlargement of just one of the adrenal glands in pets with an adrenal tumor. The adrenal glands are NOT always seen during an ultrasound exam in pets with Cushing’s. In some pets with an adrenal tumor, the ultrasound or CT/MRI evaluation may indicate the tumor infiltrating into large blood vessels close to the affected adrenal gland or metastatic spread of the tumor into the liver.

Once a diagnosis has been made, there are several treatment options. Treatment depends on the type of Cushing’s disease, as well as on the overall health of the canine patient. As many dogs with Cushing’s are elderly and may have concurrent health problems, treatment can be complicated.  In some cases, the owner may elect to wait to treat until symptoms are severe enough that they interfere with a patient’s quality of life. For example, a dog with hair loss and no other symptoms may not be candidate for aggressive treatment, but will be if he develops additional clinical signs. Thus, a decision to treat Cushing’s disease is made with the owner and the veterinarian and takes substantial labwork as well as the patients’ current status and quality of life into consideration. Many veterinary internal medical specialists believe that no dog should be treated unless it has obvious and worrisome clinical signs.

 If Cushing’s disease is caused by an adrenal tumor, the logical approach is to surgically remove the tumor and the affected adrenal gland. These tumors tend not to recur on the remaining adrenal gland. In theory, this can cure adrenal-based Cushing’s disease, and the prognosis is very good for dogs with benign adrenal tumors. Dogs may be treated with ketoconazole or trilostane for 8-16 weeks prior to surgery to try to minimize the symptoms of Cushing’s disease, as one significant symptom of Cushing’s is delayed wound healing. There are high risks associated with adrenalectomies, and given that patients are often elderly dogs, this may deter an owner from pursuing this treatment route. Unfortunately, approximately 50% of adrenal tumors are malignant and may have already metastasized to the liver or lungs or invaded the major arteries and veins in the immediate region by the time they are discovered.

Pituitary tumors are not removed surgically in veterinary medicine. These tumors tend to be very small and slow-growing and cause little or no damage on their own, aside from overstimulating the adrenal glands. With these canine patients, the symptoms themselves are treated and not the root cause. Pituitary macroadenomas may be treated with radiation in an attempt to shrink them and thus relieve the neurological symptoms caused by their presence and the pressure they place on brain tissue.

The current treatment of choice in most cases is administration of a drug called trilostane (brand name Vetoryl). Trilostane acts by inhibiting cortisol production, so that levels in the blood are lower. Trilostane is generally given at a tapering dose as the patients’ symptoms subside. Vomiting and diarrhea are the most common side effects, but are seen far less frequently than with other drugs used in this disease. Trilostane, however, is the only drug associated with necrosis, adrenal rupture, acute bleeding, related illness, and/or death.

Lysodren (Mitotane, o.p’DDD) was, until the advent of trilostane, the most commonly used drug for pituitary-dependent hyperadrenocorticism. It is also used, albeit with less effectiveness, in treating adrenal-based Cushing’s. Lysodren selectively destroys adrenal cortex tissue, the cells that produce glucocorticoid hormones. An initial week or so of daily lysodren (a loading or induction phase) damages the adrenals enough to bring cortisol blood levels within normal ranges and make Cushingoid symptoms begin to abate. Thus, even though the pituitary gland may be secreting surplus ACTH and excessively stimulating the adrenals to release more cortisol, the adrenal glands simply cannot respond. Dogs are then be maintained on once or twice a week lysodren dosages for the remainder of their life. Half of dogs will relapse and need another round of daily lysodren. Sometimes dogs fail to respond to lysodren either from the start or after having been on it for some time. Lysodren is effective, yet it carries a great potential for serious side effects. If too much adrenal tissue is destroyed, a dog can be given permanent Addison’s disease, hypoadrenocorticism (the opposite of Cushing’s). This occurs inadvertently in approximately 5% of dogs given lysodren. More typically, a dog will experience a lysodren reaction in which cortisol levels are acutely too low. This occurs in approximately one third of canine patients and can be reflected in inappetence, vomiting, diarrhea, muscle weakness, wobbliness, lethargy, or even collapse and death. As with trilostane, mitotane has been associated with adrenal necrosis but has not been linked to adrenal rupture. Less than 1% of dogs experience fatal complications. Owners must carefully monitor dogs taking lysodren and respond to such adverse reactions by stopping the lysodren and administering prednisone. Also, dogs on lysodren must receive periodic ACTH stimulation tests to monitor their blood cortisol levels. Thus, treating with lysodren requires a greater than average owner commitment to monitoring their dog.

Ketoconazole is an antifungal drug, which is less commonly used than either trilostane or mitotane. While it controls the disease by inhibiting the synthesis of cortisol, it is only effective in approximately 50-75% of cases. It also commonly causes nausea, lethargy, and diarrhea. This is considered in the treatment of dogs with either pituitary-dependent or adrenal-based hyperadrenocorticism who cannot tolerate trilostene or lysodren or who do not respond to either of these two drugs. Ketaconazole is an oral anti-fungal medication with the unusual side-effect of suppressing hormone production. That side-effect is sought-after when using Ketaconazole for treating Cushing’s disease. This drug is given daily, and it can be prohibitively expensive to use. It has the advantage of being safer than lysodren, as it does not cause permanent adrenal tissue damage. Any effects it has on hormone production are fully reversible.

L- Deprenyl (Anipryl, selegiline) acts via a different pathway, known as the hypothalamic-pituitary axis, but its’ efficacy has been questioned. This is the most controversial of the drugs to treat Cushing’s disease. Anipryl does not affect the adrenal glands directly. First marketed for dogs as a psychotropic medication to help senile dogs think more clearly (canine Alzheimer’s), Anipryl allegedly stabilizes the balance of brain chemicals. It reduces ACTH production by functionally increasing dopamine levels. Approximately 70-80% of Cushingoid dogs responded favorably to the drug in clinical trials, yet actual practicing veterinarians are skeptical of its effectiveness. One endocrinologist claimed that it is very effective for only about 15% of dogs with pituitary-dependent Cushing’s. Others report a response rate closer to 40%. The effectiveness seems to be related to the specific location of the pituitary tumor itself. Anipryl is expensive and takes 1-3 months to evidence effects. Nonetheless, Anipryl is extremely safe and cannot cause Addison’s disease. Anipryl has no effectiveness at all in treating adrenal-based tumors.

All treatment options require a strong relationship and excellent communication between the owner and the veterinarian. For most treatment choices, potential side effects can be monitored at home, but patients must come in to the clinical setting for periodic ACTH stimulation tests to monitor their response much more accurately. Clients should be educated so that they are able to recognize if a patients’ dosage is too high or too low. It is important to note that dogs and cats rarely die of Cushing’s disease. Rather, the disease is treated because its manifestations can severely affect a patients’ quality of life. The goal in treating the disease is not cure, but rather control of symptoms. Patients with Cushing’s disease can lead long happy lives with prompt detection, proper care and appropriate monitoring. The goal of treatment, therefore, is to improve quality of life and perhaps lengthen life, except in situations where an adrenal tumor can be completely removed or where a dog can be weaned off external sources of cortisone. Again, as many Cushing’s patients are elderly and have concurrent health issues, hyperadrenocorticism is a serious condition, and maintaining a dog with Cushing’s disease requires vigilance and commitment on the part of the owner. In summary, Cushing’s disease is a common condition in older dogs and is often mistaken for signs of normal aging. Although most dogs with Cushing’s disease cannot be cured, their quality of life (as well as the owner’s quality of life) can be improved, and their lives may be extended with early intervention. It is often possible to successfully manage this disease for years. It thus behooves the pet owner to become familiar with the typical signs of Cushing’s and the treatments available.

Diabetes Mellitus.

  • Type I DM is comparable to insulin dependent diabetes mellitus (IDDM) in humans. It is characterized by beta cell destruction (in the pancreas) leading to absolute insulin deficiency. This usually occurs via cell-mediated autoimmune processes and is associated with multiple genetic predispositions and poorly defined environmental factors. It results in low insulin concentrations with impaired insulin secretion following a glucose load. Treatment requires insulin injections. Type I DM is the most common form of DM in dogs.
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  • Type II DM is similar to non-insulin dependent diabetes (NIDDM) in humans and is characterized by an impaired ability to secrete insulin as well as insulin resistance. Triggering causes include obesity, genetics, and insular amyloid deposition. Some cases can be managed with dietary therapy and oral hypoglycemics while others require insulin. Type II DM currently is thought to account for the majority of cases of feline DM.
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  • Type III DM is a condition whereby medications or concurrent insulin antagonistic diseases (hyperadenocorticim/Cushing’s disease, acromegaly, diestrus) interfere with insulin action and cause glucose intolerance, which can lead to DM. It is similar to impaired glucose tolerance in humans and is initially characterized by hyperinsulinemia. This type of DM may resolve or become overt depending on the situation.
  • The peak incidence of DM in dogs occurs at 6 - 9 years of age. Genetic predisposition has been noted in some breeds. The most common breeds are German Shepherds, Schnauzers, Beagles, and Poodles. Golden Retrievers and Keeshonds are more prone to juvenile DM. Gender is a factor in dogs with females being 3 times more likely to develop DM than males.  Most cats are over 8 years of age when diagnosed. Genetics may play a role in some breeds. Neutered males are affected most frequently in addition to obesity being a risk factor.

    Clinical Signs:

    The onset of diabetes is usually very gradual and easily missed by the owner until it is quite advanced. Common clinical signs of DM include an increase in water intake (polydypsia), an increase in urination (polyuria), an increase in food intake (polyphagia), and weight loss although some animals will still be obese upon presentation. Cataract formation is common in dogs with DM, but rare in cats. Cats may have icterus (jaundice) due to concurrent hepatic lipidosis and/or pancreatitis, but icterus is not common in dogs unless they have pancreatitis. Cats may also develop a peripheral neuropathy characterized by plantigrade stance to the pelvic limbs; such neuropathies are rare in dogs. Diabetes mellitus has been associated with immune suppression, retinopathy, hypertension, hypotension, and proteinuria. 

    Diagnosis

    Normal blood glucose (BG) is 80 - 120 mg/dl. The diagnosis of DM is based on persistent fasting hyperglycemia of usually > 200 mg/dl. If the BG is between 120 - 200 mg/dl, consider stress, post-prandial hyperglycemia, and excess diabetogenic hormones.  Diabetes can be confirmed with the addition of a urinalysis and test for fructosamine levels. 

    Urinalysis should show glucosuria, which occurs when the blood glucose exceeds 180-225 mg/dL. Urine should be routinely evaluated in the diabetic to monitor for urinary tract infection, ketonuria, and glomerular disease. Significant ketonuria in association with systemic illness suggests diabetic ketoacidosis; ketonuria may also occur with anorexia.

    The concentration of fructosamine in serum reflects the average blood sugar concentration over the preceding two to three weeks. As the fructosamine values are not influenced by sudden fluctuations in blood glucose (such as stress in nervous pets or recent food intake), the fructosamine level is a much more reliable indicator in diabetic monitoring than a single glucose determination. The fructosamine assay is based on the ability of ketoamine-linked glucose residues on glycated serum proteins to reduce nitroblue tetrazolium. Other conditions that alter protein metabolic pathways may interfere with the use of fructosamine in diabetic monitoring. In hyperthyroidism, protein turnover is increased; therefore, results of the fructosamine test must be interpreted cautiously in hyperthyroid patients.

    Hemogram results may indicate a stress leukogram and variable increases in WBC’s due to concurrent infection.

    Serum chemistry changes often include elevated liver enzymes (ALT, AST, SAP) secondary to hepatic lipidosis or pancreatitis. Hyperlipidemia and hypercholesterolemia are due to increased lipolysis and decreased lipogenesis. Amylase and lipase may be elevated with concurrent pancreatitis. Electrolytes are often abnormal in the diabetic ketoacidotic patient.

    Treatment/Management/Prevention:

    The goals are to reduce or eliminate the clinical signs of persistent hyperglycemia, avoid insulin-induced hypoglycemia, and prevent or retard the development of cataracts and other diabetic complications.

    For the diabetic dog, the ideal glucose level is between 90 and 200 mg/dl for most of the day with the lowest glucose nadir occurring halfway between the two daily injections of insulin.  A slightly higher glucose level may be acceptable in cats. Stress can elevate blood glucose and the cat is typically more stressed when in the hospital to check glucose levels.

    Treatment for an uncomplicated diabetic:

    In the dog, begin using one of the following intermediate acting (NPH or Lente) insulins at 0.5 U/kg q 12 hours.  In the cat, Lantus at 0.5 mg/kg is the current insulin used.

    NPH (Isophane) Insulins (Humulin N manufactured by Eli Lilly or Novolin N manufactured by Novo Nordisk) are crystalline suspensions of recombinant human insulin with protamine and zinc resulting in intermediate-acting insulin with a slower onset of action and a longer duration of activity than that of regular insulin. Most are available as 100 units/ml (U-100).

    After the first insulin injection, the blood glucose concentrations should be monitored 2 to 3 times within a 4-12 hour period to ensure that hypoglycemia does not occur at the dose used.

    It is important that proper handling of insulin and correct injection techniques are insured.  Inappropriate handling or improper injections can lead to uncontrolled diabetes.

    If hypoglycemia did not develop during the first injection, then give the patient at least one week on this dose before making any adjustments as long as the patient is eating and not showing any signs of hypoglycemia.

    A blood glucose curve should be performed 7–10 days after insulin is started or anytime after the dose is changed. To perform the curve, the pet is brought into the hospital before feeding or insulin is given and an initial glucose sample is taken. Then, the pet is fed its regular food and insulin is given.  Blood samples are then taken at 2-hour intervals for next 12 hours. The disadvantage to this technique is that some dogs won’t eat as they normally would when they are in a clinic environment.

    Thus, an alternative is to feed and give insulin at home in the morning, then bring the animal into the clinic within an hour of the injection and start the curve then. 

    There is a considerable amount of reliable research data showing that diets high in carbohydrates, low in fat, and high in fiber are helpful in regulating diabetic dogs. These types of diets also lowers the average insulin dose, lowers the average blood sugar, lowers the amount of urine being produced, and lowers glycosolated hemoglobins and fructosamine levels. The carbohydrates in these diets are complex carbohydrates. It is important to avoid diets high in simple sugars, which includes any commercial diet semi-moist food, primarily those packaged in foil packets. Diets high in sugar are absorbed very rapidly before the insulin has time to work. The goal in controlling the diabetes with diet is to balance the absorption of sugar with onset of action of the insulin. A high carbohydrate/low fat diet also decreases plasma free fatty acids, increases the number of insulin receptors, increases insulin action at the receptors, and finally, it decreases cholesterol. High fiber diets reduce insulin resistance. The fiber acts to decrease postprandial hyperglycemia, primarily because it delays gastric emptying. A high fiber diet also decreases absorption of glucose and increases insulin action at the receptor.

    The dog needs to be fed the same amount of the same diet at the same times each day. Daily caloric requirements for maintaining ideal body weight should be calculated and fed. Dogs in poor body condition, however, need to be fed more calories. Dogs with recurrent bouts of pancreatitis should avoid high fat diets. Ideally the dog should be fed prior to the insulin injections so that maximal insulin activity is present when maximal post-prandial glucose is being absorbed from the gut. Treats should be avoided during the day. For dogs used to large meals daily, divide the caloric requirements in half and feed in association with the twice daily insulin injection. For dogs used to eating several small meals a day, spread the calculated caloric requirements out over the day similar to what would be done for a cat.

    Cats with type II diabetes should be on a high protein, low carbohydrate diet. Some recent evidence suggests that high protein rather than high fiber diets may be more useful in cats with diabetes. Ongoing studies suggest that such diets (canned kitten diets) result in a decrease in insulin dosage and even remission of the diabetes. This may be due in part to the high protein requirement of cats coupled with the high carbohydrate content of most commercial cat foods.  Unlike dogs, cats can graze throughout the day if that is what they are used to.  The insulin is given the same way as in the dog and at the same frequency, twice daily. 

    Regular dipstick monitoring for urine glucose may help reduce the risk of hypoglycemia because persistent negative results may indicate subclinical hypoglycemia.

    While fructosamine levels provide a useful tool for the evaluation of overall control of diabetes mellitus and long-term glucose regulation, this test is unable to detect short-term or transient abnormalities in blood glucose values. For instance, a patient may have an average blood glucose level within the reference interval over a period of 1-2 weeks preceding the test, but still have transient daily episodes of hypoglycemia and/or hyperglycemia. Serial measurements of blood and/or urine glucose are necessary for the detection of these short-term alterations and are useful in establishing an initial protocol for the feeding and medication of a diabetic patient. Fructosamine levels are more useful for the evaluation of longer-term control, as well as owner compliance with the administration of insulin.

    Special considerations:

    Insulin Overdosage
    Factors that could lead to insulin overdosage include incomplete mixing of insulin suspensions, administration of insulin at irregular intervals, inappetence, excessive exercise, and increased insulin sensitivity associated with the end of diestrus or treatment of concurrent disease such as hyperadrenocorticism.

    Different types of insulin may require different syringes.  Graduations on syringes designed for use with 100 units/ml insulin preparations represent a different volume from graduations on syringes designed for use with 40 units/ml insulin preparations, and this may also lead to dosing errors.

    Insulin Resistance
    Insulin resistance should be suspected if the insulin dosage is > 1.5 U/kg and blood glucose concentration is > 300 mg/dl.  Listed below are concurrent problems that can cause insulin resistance:

    • Hyperadrenocorticism: Either endogenous or exogenous
    • Hypothyroidism and obesity can induce an insulin resistant state
    • Hyperthyroidism 

    • Acromegaly 

    • Severe hyperglycemia
    • Insulin metabolized too quickly 

    • Infection, or concurrent illness 

    • Obesity 

    • Pancreatitis

    • Poor insulin absorption 

    • Antigenic insulin or insulin components 

    • Administration of progestational compounds 

    • Stress

    • Renal disease

    • Hepatic disease
    • Pheochromocytoma
    • Neoplasia

    Diabetes is rarely reversible in dogs, but diabetic cats will sometimes regain the ability to produce their own insulin in the pancreas. Cats that developed diabetes after receiving long term glucocorticoids or hormones are more likely to stop needing insulin after a while compared to cats that developed diabetes without a known cause. 

    Glucometers
    Glucometers should be compared to commercial laboratory results.  Human glucometers register lower glucose levels in order to protect the human diabetic from over dosing with insulin. And using whole blood will yield results that are about 10-15% lower than actual reading because mechanical dilution by the RBCs displaces serum. Thus using serum or plasma gives a more accurate reading. The AlphaTrak by Abbott (Veterinary) is accurate for animals and closer to serum readings than most human glucose meters. Some have noted that serum glucose values are higher than those found at outside laboratories on same sample. And you have to make sure you key in the cat or dog code before you test the sample.

    Urine may also be monitored for both glucose and ketone values. Dip sticks are available in most pharmacies which allow the measurement of both glucose and ketone levels in the urine. Insulin dosages generally are not changed based on urine glucose readings, but persistently high urine glucose values may indicate the need for further evaluation of the pet’s condition.

    Urine ketone levels can also be monitored easily at home. Occasionally, ketones will be detected in the urine and this is normal. However, if ketone levels persist for longer than 3 days, an immediate visit to the veterinarian for further evaluation is in order.

    Various methods are available to diagnose and monitor diabetic dogs and cats, but fructosamine is the best method for confirming a diagnosis, assuming the pet also shows clinical signs of diabetes and displays hyperglycemia.

    Fructosamine and blood glucose curves are probably the two most valuable tools for monitoring diabetic dogs and cats. The number one cause of death in diabetic dogs and cats is not the disease itself; rather, it is the owner’s frustration with the disease. This is an extremely important point to remember when treating diabetic animals. Good communication with the pet owner is perhaps the most important component of managing the disease.

    It is recommended that clinicians schedule a 30-minute appointment with the client at the time of discharge before sending the diabetic patient home for the first time. During this appointment, clinicians should thoroughly discuss the care required for the patient. Include the following instructions in that discussion: how to give the animal injections, how to store insulin, what types of food to feed and how often, how to recognize the signs of hypoglycemia, and how to react to this condition. Also, include information on what clinical signs to look for in terms of monitoring water intake and urine production.

    The client should be given written instructions for use as a reference once they are caring for the patient at home. It is essential that the clinician and veterinary staff strive to educate the caregiver and motivate them to get involved in the care of their diabetic pet. The goals of treatment include elimination of the clinical signs of diabetes, prevention or slowing of cataract formation and resulting blindness, prevention of potentially dangerous hypoglycemia, and prevention and/or treatment of concurrent illness.

    Successful management of diabetes is achievable with insulin therapy, attention to diet, and exercise. Owners of a diabetic cat or dog can restore their pet’s quality of life through effective management of diabetes mellitus.

    Tracheal Collapse in Dogs: Medical and Minimally Invasive Interventional Therapy.

    Tracheal collapse is a progressive, degenerative disease of the cartilaginous rings of predominantly older small and toy-breed dogs (Pomeranian, miniature and toy poodle, Yorkshire Terrier, Chihuahua, Pug) in which hypocellularity, decreased glycosaminoglycan, and calcium contents lead to dynamic airway collapse during respiration. Affected animals present with signs ranging from a mild, intermittent “honking” cough and exercise intolerance to severe respiratory distress from dynamic upper airway obstruction.  Any or all portions of the trachea and bronchi can be affected. Respiration contributes to the collapse. On inspiration the pull of air into the lungs creates negative pressure in the lumen of the cervical trachea and positive pressure opening the tracheal rings of the intra-thoracic trachea and bronchi. During exhalation, the opposite occurs, so the intra-thoracic pressure to push air out results in compression of the intra-thoracic components, while the air moving out serves to open the extra-thoracic trachea in the cervical region.

    Various combinations of anti-inflammatories, anti-tussives, sedatives/tranquilizers, and/or brochodilators are typically effective in alleviating the initial respiratory problems associated with tracheal collapse. In addition, weight loss, restricted exercise, and removal of second hand smoke or inhaled allergens can further palliate clinical signs. Careful regular monitoring of co-morbidities such as cardiac disease or pulmonary disease may help reduce the incidence of respiratory crisis episodes. Those patients that have failed aggressive medical and environmental management and have had other potential causes of respiratory disease either treated or ruled out become candidates for surgical treatment. An owner’s inability to administer medication is not a valid reason to perform surgery as the majority of patients will still require medication following treatment.

    Medical Therapy of Tracheal Collapse

    • Butorphanol tartrate (Torbutrol®)-0.5-1.0 mg/kg; PO; BID to TID
    • Hydrocodone bitartrate (Hycodan®) 0.2 mg/kg; PO; TID to QID
    • Ampicillin-22 mg/kg; IV, IM, SC, PO; TID
    •  Cefazolin (Ancef®, Kefzol®) 20 mg/kg; IV, IM; TID
    • Clindamycin (Antirobe®)-11 mg/kg; PO; BID
    •  Enrofloxacin (Baytril®)-5-10.0 mg/kg; PO or IM; BID
    • Aminophylline
    • Dogs-11 mg/kg; PO, IM, IV; TID
    • Cats-5 mg/kg; PO; BID
    • Oxtriphylline elixir (Choledyl®)-15 mg/kg; PO; TID
    • Dexamethasone (Azium®) 0.2-0.5 mg/kg; IV, IM, SC; BID ; up to 2 mg/kg
    • For emergency treatment
    •  Prednisone-1-2 mg/kg; PO; SID to BID

    Tracheal collapse is suspected with an appropriate signalment, history and eliciting coughing reflexes with simple digital palpation of the trachea. Radiographs and fluoroscopy of the lateral cervical and thoracic trachea in an unanesthetized patient during inspiration and expiration can be diagnostic for tracheal collapse. Radiographs are diagnostic in approximately 60% of patients with moderate to severe tracheal collapse. Special attention should be paid to evaluating the mainstem bronchi because animals with mainstem bronchial collapse are unlikely to benefit from surgical repair of their collapsing cervical trachea. Presently, there is no clinically used method to stent collapsing mainstem bronchi; however, a recent publication investigated intraluminal stents for mainstem bronchial collapse and concluded that such a technique might be useful in affected dogs. In addition to evaluating the trachea on radiographs, thoracic radiographs should also be evaluated for cardiomegaly and pulmonary disease.

    Evaluation of laryngeal function under a light plane of anesthesia should also be performed to rule out laryngeal paralysis or laryngeal collapse. Laryngeal paresis, paralysis, or collapse is present in approximately 30% of dogs with tracheal collapse.  Unfortunately, not all cases can be diagnosed easily, and it may be necessary to elicit a cough while obtaining radiographs to demonstrate tracheal collapse. Endoscopy/tracheoscopy is an excellent technique to evaluate the trachea and bronchi and can be used to grade the degree of collapse. It is also recommended as a procedure to evaluate the trachea prior to surgery in all dogs, regardless of radiographic findings. Cytology and culture of the airway should be obtained to determine if a bacterial component is involved. Recurrent bacterial tracheitis can occur with severe tracheal collapse.


    Classification of collapsing trachea:

    
Grade I - tracheal membrane is slightly pendulous, cartilage maintains normal AC@ shape, lumen reduced approximately 25%


    Grade II - tracheal membrane widened and pendulous, cartilage is partially flattened, lumen reduced approximately 50%


    Grade III - tracheal membrane is almost in contact with dorsal trachea, cartilage is nearly flat, lumen is reduced approximately 75%


    Grade IV - tracheal membrane is lying on dorsal cartilage, cartilage is flattened and may invert, lumen is essentially obliterated


    The result of tracheal collapse is an extremely small cross-sectional area of functional tracheal lumen and high airway resistance.  This increase in resistance along with chronic hypoxia causes increased right ventricular work and can lead to enlargement (hypertrophy) of the right side of the heart.

    Extra-luminal prosthesis techniques were the most widely used technique until 10 years ago. Both ring and spiral prosthesis has been described for this use. Ring prostheses are made by either making individual C-shaped rings or continuous spiral prosthesis. The prosthesis is applied taking great care not to interfere with the vascular or nerve supply of the larynx or trachea. The most common complications associated with extra luminal prosthesis are placement. Complications with this technique include intra-luminal hemorrhage because of suture penetration, peritracheal swelling/inflammation, damage to the recurrent laryngeal nerve resulting in laryngeal paralysis and tracheal necrosis and slough from ischemia if the blood supply to the trachea is severely compromised. If paralysis occurs, surgery (laryngeal tieback) is usually necessary for survival. Coughing usually improves several weeks after surgery; however, this procedure does not usually make these dogs normal.

    Due to the relatively high morbidity associated with surgery and the inability to successfully treat intra-thoracic tracheal collapse, the use of minimally invasive intra-luminal stents has been investigated. A number of stents have been evaluated in the canine trachea, including both balloon-expandable (Palmaz) and self-expanding (Stainless steel, Laser-cut nitinol, Knitted nitinol) stents. The vast superior flexibility makes the use of self-expanding metallic stents particularly appealing for tracheal use in dogs. Clinical improvement rates in 75%-90% of animals treated with self-expanding, intra-luminal stainless steel stents have been reported. 


    Intra-luminal tracheal stents are best reserved for dogs with tracheal collapse that are not good candidates for extra-luminal prosthesis and have failed medical therapy. They can be placed in dogs with intra thoracic tracheal collapse. The main contraindication to their use is in dogs with collapse of the main stem bronchus. They offer the advantages of minimally invasive deployment, short postoperative convalescence, and rapid restoration of airway lumen. When properly sized and appropriately deployed, the short term improvement in respiratory function is truly remarkable. Postoperative coughing is never totally alleviated since the stent interferes with the mucociliary clearance of sputum and predisposes the patient to lower airway infection. Unfortunately, because of their location, they are also subject to severe cycling and bending forces. Consequently, the stent is prone to kinking and the tracheal wall is prone to granuloma formation at the rostral and caudal extents of the stent. Additionally, these stents are very difficult to remove after deployment and adjustment of a broken unit is not possible. Fortunately, fractured stents lend themselves to repair by telescoping of a new stent through the kinked or fractured region. Owners must be advised that tracheal stents should be deployed as late in the animals’ life as possible since few patients live more than 2-3 years without developing one of the previously mentioned significant complications. Unfortunately, medical therapy, surgery, or stenting are not cures for tracheal collapse. When used appropriately in the proper patients, however, stenting can significantly improve the patient’s quality of life when medications alone are no longer adequate.

    There remains some debate with regards to the use of intra-luminal stents in patients with bronchial collapse in addition to tracheal collapse.  Stenting of mainstem bronchi is not currently recommended as secondary and tertiary bronchi will continue to collapse, and therefore the benefit of mainstem bronchial stenting will be minimal and temporary. Certain patients will benefit from tracheal stenting even when concurrent mainstem bronchial collapse is present. Once again, patient evaluation and selection is key in determining the value of stenting in these potential candidates. Tracheal collapse can lead to dyspnea, coughing, or both. Bronchial collapse will usually manifest as a cough, expiratory dyspnea, or both. When both tracheal and bronchial collapse is present, the results following tracheal stent placement becomes less predictable. If dyspnea is the only clinical sign and intra-thoracic tracheal collapse is present, a tracheal stent can help relieve the dynamic obstruction. If the dog’s primary problem is coughing, then it becomes difficult to determine if the coughing is secondary to the tracheal collapse or bronchial collapse.  In the cases in which stents are placed, the bronchial collapse will inevitably continue to progress and continued coughing will be present. Continued coughing will cause repeated cycling of the stent and may increase the risk of subsequent fracture of the implant or predispose to the formation of excessive granulation tissue.

    As mentioned previously, placement of intra-luminal stents is not a cure. Stenting is a palliative procedure, and the vast majority of patients will require continued medical therapy for a good long-term outcome.

    Laryngeal Paralysis in Dogs.

    Laryngeal paralysis (LP) is a common disease process, which results in acute and/or chronic progressive respiratory distress. The clinical signs of LP are due to the paralysis of the cricoarytenoideus dorsalis muscle, which normal is responsible for the abduction of the arytenoid cartilages at each inspiration. The laryngeal recurrent nerve innervates this muscle. Lesions to the laryngeal recurrent nerve or to the cricoarytenoideus dorsalis muscle result in laryngeal paralysis in dogs and cats. Laryngeal paralysis can be unilateral or bilateral and can be either congenital or acquired. Congenital LP is reported in English and Staffordshire, Bull Terriers, Bouvier des Flandres, Siberian Husky and husky-mixes, and in Dalmatians. The mode of inheritance is unknown in all except the Bouvier (autosomal dominant inheritance). Acquired LP in dogs is most often idiopathic. Breeds predisposed to acquire LP include Saint Bernard, Labrador Retriever, Golden Retriever, Newfoundland, Afghan Hound, Standard Poodle, German Shepherd, and many others. Dogs with idiopathic LP are usually middle-aged to elderly. Male dogs are slightly more commonly affected than females. Non-idiopathic LP may be the result of iatrogenic trauma to recurrent laryngeal nerve(s) during cervical surgeries such as thyroidectomy; trauma to the neck from dog fights or penetrating wounds or foreign body; generalized neuropathy or myopathy; central or peripheral lesions of the vagus, recurrent laryngeal, or caudal laryngeal nerves; intrathoracic or extrathoracic neoplastic masses compressing the recurrent laryngeal nerves; or more rarely, hypoadrenocorticism, organophosphate poisoning, or any central nervous system or posterior brain stem disease.

    
The presenting signs are similar for the congenital and acquired forms. Progression of signs is often slow; months to years may pass before an animal develops severe respiratory distress. The early signs of laryngeal paralysis can be quite subtle. Early signs include change in voice, usually a deeper, hoarse or raspy-sounding bark, followed by gagging and coughing, especially during eating or drinking. As the laryngeal paralysis progresses, the dog appears to be working harder to breathe; their facial expression is a bit anxious, eyes are prominent, and their chest is vigorously expanding.  The pet may also look like they are “smiling” when they pant, with their lips pulled way back, and tongue hanging out.  Dogs will seem to tire more easily during activities such as walking. The dog’s endurance decreases and laryngeal stridor (especially inspiratory) increases as the airway occlusion worsen. Because animals use their breathing as a means to cool themselves naturally, laryngeal paralysis patients are more prone to overheating under conditions that would not make a normal dog hot. Episodes of severe dyspnea, cyanosis, or syncope occur in severely affected patients. The extra noise they create with each breath is harsh and easy to hear.  Their tongue may be a darker red or purple in color; they do not want to be touched or restrained.  They are in “respiratory distress” and need medical assistance.  Ironically, the airway compromise gets worse when they breathe harder, similar to asthma.  Fast-moving air will suck the airway shut, while slow moving air will pass more easily.  But the feeling of “air hunger” is a powerful drive and will make an animal try to breathe harder, the airflow will speed up, and a viscous cycle begins.  Additionally, some dogs will trigger their own crisis by simply barking.  The vocal cords are in the larynx; when the dog tries to bark, they contract other neck muscles and narrow their airway.  This smaller airway results in less air getting in during the breaths that follow the bark and may incite a distress episode. Secondary pulmonary edema and atelectasis may worsen their respiratory signs. Male dogs are approximately 3 times more affected than female. Laryngeal paralysis can be accompanied with various degrees of dysphagia, which significantly enhances the probability of aspiration pneumonia. While signs are usually gradual in onset and gradually progressive, many animals with LP are often presented with acute, severe respiratory distress.

    The physical examination of dogs with laryngeal paralysis is fairly unremarkable, unless they are presented in extreme respiratory distress. Dogs have an inspiratory dyspnea that is not alleviated with open mouth breathing. Mild lateral compression of the larynx significantly increases inspiratory dyspnea. Referred upper airway sounds are present during auscultation of the thoracic cavity. Auscultation of the thoracic cavity and the lung field may reveal the presence of pneumonia in the cranial lung lobe due to aspiration. Palpation of the muscle mass may reveal skeletal muscle atrophy in cases of polyneuropathy. A complete neurologic examination is required to evaluate the animal for a polyneuropathy.

    The cranial opening of the larynx is formed by the corniculate processes of the arytenoid cartilage dorsally, the cuneiform processes of the arytenoid cartilages and aryepiglottic folds laterally, and the epiglottis and vocal folds ventrally. The rima glottidis is the narrowest part of the laryngeal airway. It is normally an elongated diamond in shape. The larynx is responsible for three main functions: respiration, deglutition and vocalization. During inspiration, the arytenoids actively abduct, increasing the size of the rima glottidis, resulting in decreased airway resistance. During expiration, the arytenoids passively return to the resting position. During fast exercise, arytenoid abduction is sustained during both inspiration and expiration to maximize airflow and minimize airway resistance. Reflex closure of the larynx during swallowing prevents aspiration of food and fluid into the airway. Voice production is related to movement of air over the vocal and vestibular folds, plus changes in length and thickness of the vocal folds produced by contraction of the laryngeal muscles.

    

As mentioned previously, in cases of LP, the paralysis of the dorsal cricoarytenoid muscles prevents the abduction of the arytenoids and the vocal folds during inspiration. Because the pressure within the glottis is negative, the arytenoids and vocal folds are drawn in to the paramedian position thereby decreasing the size of the glottic lumen and increasing airflow resistance. This narrowing of the glottic lumen causes an increase in airflow velocity, which decreases lateral pressure thus precipitating a further airway narrowing. The airway may narrow so much that airflow actually ceases. This results in an increase in lateral pressure and helps to re-open the glottic lumen. This opening/closing cycle in the larynx causes the vocal folds to oscillate, which produces the characteristic `roaring` or wheeze known as stridor. The loss of laryngeal adduction reduces airway protection and leads to swallowing dysfunction and aspiration pneumonia, as well as altered vocalization as characterized by a hoarse bark.

    The usual diagnostic work-up for a dog suspected of laryngeal paralysis includes CBC, chemistry profile, and standard survey thoracic and cervical radiographs. Blood gas analysis can help determine the degree of respiratory compromise. Hypercholesterolemia, hyperlipidemia, and elevation of liver enzymes activity are present on the chemistry profile for dogs with hypothyroidism. A thyroid profile with endogenous TSH and free T4 is then required to further define the diagnosis. Laryngeal paralysis has inconsistent correlation with hypothyroidism. These tests together with careful physical examination will generally rule out the non-idiopathic causes of LP. Careful assessment of good quality radiographs is critical. In one study, 70% of dogs with confirmed LP had abnormal thoracic radiographs, including 20% with megaesophagus and 15% with aspiration pneumonia. Megaesophagus might be present in dogs with laryngeal paralysis especially if the paralysis is due to polyneuropathy or polymyopathy. Megaesophagus places the animal at more risk for aspiration pneumonia after surgery. Other pathologic conditions to check for on chest films include cardiogenic or noncardiogenic pulmonary edema, mediastinal or thoracic inlet masses, and pulmonary metastases. Lateral cervical films may reveal cervical masses, tracheal collapse or deviation, or intraluminal laryngeal or tracheal masses. The normal larynx is slightly larger than the proximal cervical trachea and is air-filled. Loss of the normal air density in the larynx may indicate laryngeal mass or laryngeal edema. Dystrophic mineralization of the laryngeal cartilages is a common age-related change in dogs and is not clinically significant.

    The definitive diagnosis of laryngeal paralysis, however, is by direct visualization of the larynx under a light plane of anesthesia. If the plane of anesthesia is too deep, then the arytenoids may appear paralyzed (remaining in an adducted or paramedian position) leading to an incorrect diagnosis of laryngeal paralysis. As the anesthetic itself may possibly decrease intrinsic laryngeal function, a recent study confirmed that the use of doxapram hydrochloride (Dopram-V) may be used to stimulate respiratory accentuated intrinsic laryngeal motion. Changes in laryngeal function are therefore more obvious and dramatic in gross appearance after doxapram administration, and the authors propose that it be used routinely as an aid in diagnosing laryngeal paralysis. Doxapram has few detrimental effects, but is contraindicated in patients with hypertension, seizures, severe hypoxia, or increased intracranial pressure. During laryngoscopy, it is useful to have an assistant watch the animal and inform the person performing the procedure each time the animal inspires. The arytenoids and vocal folds should abduct with each inspiration. Sudden expiratory opening of the glottis as with coughing or sighing should not be confused with inspiratory abduction.  The animal should be placed in sternal recumbency and the head elevated to the level that it is normally carried. Animals with LP have an abnormally narrow rima glottidis at rest and absence of abduction of one or both sides of the larynx during inspiration. They often have forced passive movement of the vocal folds during expiration, which mimics active abduction. There is sometimes fluttering or quivering of the arytenoids and/or vocal folds. The laryngeal mucosa is usually edematous and sometimes erythematous. Occasionally, small ulcers or vesicles may be observed on the laryngeal mucosa. 



Urgent medical care during a breathing crisis often entails supplemental oxygen therapy, external cooling, sedation to take the anxiety of “air hunger” away, and possibly intubation and artificial respiration for a short period to increase their oxygen and decrease the blood carbon dioxide concentration rapidly.  With this brief but effective therapy, most patients will rest comfortably and return rapidly to their pre-crisis state.  Unfortunately, most patients that have reached a crisis point will continue to suffer these breathing episodes because their airway is ineffective. Morphine (0.05-0.1mg/kg IM) is the preferred sedative because it effectively alleviates the anxiety and air-hunger of acute upper airway obstruction. Morphine can be combined with a low dose of Acepromazine (0.01-0.02 mg/kg IM) to reduce anxiety. Rarely, the administration of morphine will worsen the respiratory crisis. Corticosteroids are given intravenously (dexamethasone, 0.2 to 1.0 mg/kg BID) to reduce laryngeal inflammation and edema.  Fluid therapy is administered with caution because some animals with severe upper respiratory tract obstruction develop pulmonary edema. Diuretics are indicated in these patients. Emergency general anesthesia (IV propofol) and endotracheal intubation plus specific surgery or temporary tracheostomy is sometimes required.

    Surgical intervention for laryngeal paralysis is directed at removing or repositioning the laryngeal cartilages that obstruct the rima glottidis. The currently recognized surgical procedures used to correct laryngeal paralysis are unilateral or bilateral arytenoid cartilage lateralization with or without ventricular cordectomy (vocal fold removal), ventricular cordectomy, and partial arytenoidectomy via an oral or ventral laryngotomy approach and permanent tracheostomy. Arytenoid cartilage lateralization is currently the preferred surgical procedure to increase the fixed diameter of the laryngeal airway and provide adequate airflow. Arytenoid lateralization permanently fixes the arytenoid cartilage and vocal fold on one side in abduction, enlarging the airway. The animal is positioned in lateral recumbency for a unilateral lateralization, and a skin incision is made over the larynx just ventral to the jugular groove. The sternohyoid muscle is retracted ventrally to expose the lateral aspect of the thyroid and cricoid cartilages. The larynx is rotated to expose the thyropharyngeal muscle, which is transected at the dorsocaudal edge of the thyroid cartilage. The wing of the thyroid cartilage is retracted laterally, and the cricothyroid junction may be incised. Incision of the cricothyroid joint gives a better exposure, but it is not always needed. Its transection might reduce the diameter of the rima glottidis after arytenoid abduction. The cricoarytenoideus dorsalis muscle or the fibrous tissue left is dissected and transected. The cricoarytenoid articulation is detached from caudal to cranial with scissors. The sesamoid band connecting the arytenoid cartilages dorsally is left intact. However, dorsal displacement of the arytenoid results and creates distortion of the rima glottidis. The disarticulated arytenoid cartilage is only attached to the vocal cord, aryepiglottic fold, and laryngeal mucosa. Invasion through the laryngeal mucosa is avoided. The arytenoid cartilage is sutured to the caudo-dorsal part of the cricoid cartilage. This provides an adequate laryngeal airway with only a unilateral tieback. Placement of the suture on the caudo-dorsal part of the cricoid provides a physiologic position of the suture. One 2-0 non-absorbable suture is placed in a simple interrupted suture pattern from the muscular process of the arytenoid cartilage to the caudo-dorsal edge of the cricoid cartilage and tightened to maintain the arytenoid in position. The amount of tension on the suture should be limited to avoid to over abduct the arytenoids cartilage. The wound is closed by suturing the thyropharyngeal muscle and routinely closing the subcutaneous tissue and skin. At the time of extubation, it is important to observe per os the size of the laryngeal opening achieved to ensure that adequate abduction of the laryngeal cartilages has been obtained. Excessive abduction may lead to aspiration of food or fluid.

    Improvement in inspiratory function is seen in as many as 90 percent of patients. Increased inspiratory sounds usually continue after surgery but are less harsh. Bilateral arytenoid lateralization is possible, but associated with a higher complication rate than the unilateral procedure when performed via a lateral approach.  The incidence of aspiration pneumonia is more common in bilateral laryngeal lateralization compared to unilateral. In a study, 42% of the dogs with bilateral lateralization (via a lateral approach) experienced an episode of aspiration pneumonia. The animal is at risk for aspiration pneumonia for its entire life after surgery. This occurs because when performed via a lateral approach, this type of laryngeal tie-back results in a dorsal enlargement of the rimma glottis. When enlarged dorsally, the epiglottis, being wide at its base and narrow dorsally, is mechanically insufficient as a fail-safe mechanism to prevent aspiration pneumonia as a persistant gap exists between the tip of the epiglottis and the lateralized arytenoid cartilage.  In my experience, bilateral thyroarytenoid cartilage lateralization with bilateral vocal fold excision via a ventral median laryngotomy approach allows for a maximal enlargement of the rimma glottis with minimal incidence of aspiration pneumonia and is the preferred surgical treatment of choice in our facility.

    Partial laryngectomy is associated with a high incidence of postoperative complications including development of laryngeal scar tissue (laryngeal webbing) and development of laryngeal collapse. Partial laryngectomy is not recommended. Permanent tracheostomy bypasses the upper airway obstruction in LP, but is usually not considered the treatment of choice. Permanent tracheostomy is recommended for cases of laryngeal collapse. Laryngeal collapse is most often seen in brachycephalic breeds with long-standing upper airway abnormalities (stenotic nares, elongated soft palate, everted laryngeal saccules, hypoplastic trachea, and tracheal collapse). Fortunately, LP is exceedingly rare in these breeds. Permanent tracheostomy is a surgical option for the treatment of dogs with laryngeal paralysis. The permanent tracheostomy bypasses the upper airway obstruction without inducing any modification in the size of the rima glottidis. This surgical technique is therefore more valuable for dogs at high risk of aspiration pneumonia (myopathy, megaesophagus, hiatal hernia, gastrointestinal disorder). Animals respond well to the treatment and there is a high rate of owner satisfaction. Permanent tracheostomy, however, requires constant attention and maintenance from the owners.

    Postoperative complications are reported in about 1/3 of dogs treated surgically for LP using the various techniques previously mentioned. Minor wound complications are not uncommon. The most significant surgical complication in patients with laryngeal paralysis is the aspiration of liquids into the trachea and lungs. The liquids that can create problems are primarily those that come up from the stomach (either during regurgitation or vomiting), but water is a concern too (typically during swimming, not simply drinking).  It is relatively uncommon for food to be aspirated during eating, but dogs that are very fast eaters can choke and/or gag on food particles. When stomach contents are aspirated, the reaction to gastric acid in the lungs may cause pneumonitis, which may progress to more serious lung infection (pneumonia). Aspiration pneumonia can be life-threatening and can develop slowly or very rapidly. As mentioned previously, the occurrence of aspiration pneumonia is significantly reduced with a ventral laryngotomy approach combined with a ventriculocordectomy. Other potential complications associated with laryngeal lateralization include persistent cough exacerbated after drinking, seroma formation, and breaking of the suture and fragmentation of the arytenoid cartilage. Breaking of the suture and fragmentation of the cartilage may induce recurrence of the clinical signs of laryngeal paralysis. When a bilateral ventral tie-back is performed, the glottis is maximally opened and the likelihood of recurrent clinical signs is diminished as the occurrence of a bilateral breakdown of the surgically placed sutures is extremely unlikely.

    For the majority of animals treated with arytenoid lateralization for laryngeal paralysis, an immediate and significant improvement in respiration is noted. While there may always be a residual change in voice, respiratory distress is alleviated and the majority of dogs return to at least good if not excellent function.

    Acupuncture.

    Acupuncture has been practiced on animals almost as long as it has been practiced on people, with first reports of its utilization for the treatment of certain conditions in animals dating to as early as 3000 years ago in China. Traditional Chinese medicine describes a system of channels or meridians, which control the flow of “chi” or energy. Most illnesses and injuries are either caused by or accompanied by disturbances in the flow and balance of “chi”. Disorders in the function of “chi” can be influenced by treating acupuncture points. The Western, with regards to how acupuncture works, is complicated but involves a bioelectric, humeral, or neurophysiologic theory. Basically, acupuncture points can alter electric fields, release humeral substances such as endorphins and other neurotransmitters such as serotonin and dopamine, and/or effect peripheral nerves, which send a neurologic message which ultimately modifies the mechanisms which ordinarily regulate and control an animal’s physiology. Although many of acupuncture’s physiological effects have been studied, many more are still unknown, and research is being conducted to determine the scientific basis of those effects. The principles behind this art and science of healing aims to correct these imbalances in the body by using needles inserted into specific acupuncture points.

    Before considering acupuncture therapy, patients should have a comprehensive examination and diagnostic work-up including but limited to complete blood work analysis and radiographic evaluation.  The veterinary acupuncturist (who is a licensed veterinarian with additional training/certification in veterinary acupuncture) will usually ask questions regarding your pet’s general health, diet, temperature preferences, current symptoms, and overall energy or activity level.

    Acupuncture is performed with very thin, sterile needles. The acupuncture needles are inserted by the veterinarian into specific points of your pet’s body, which he has decided to use based on his physical examination findings. These points are usually a part of an acupuncture point formula or a collection of individual points chosen to address the imbalances detected during the examination. Insertion of the needles is not usually painful and is tolerated extremely well, but a very sensitive or painful pet may show a mild reaction.

    Depending on the diagnosis, the veterinarian will either leave the inserted needles without touching them or twirl the needles intermittently. Duration of needle insertion is also variable and will be based on you pet’s condition. Additional steps in the treatment could be application of a low voltage electric current (electro-acupuncture) provided by a small device via wires attached to the needles. The needles could also be warmed by the application of heat from a burning Moxa stick (these are herbs rolled into a cigar shape and ignited) or a heat lamp (called a Chi lamp) could be used over the needled areas. Recently we have been using a 12 watt medical laser therapy unit which has acupuncture capabilities.

    Depending on the diagnosis, the veterinarian will either leave the inserted needles without touching them or twirl the needles intermittently. Duration of needle insertion is also variable and will be based on you pet’s condition. Additional steps in the treatment could be application of a low voltage electric current (electro-acupuncture) provided by a small device via wires attached to the needles. The needles could also be warmed by the application of heat from a burning Moxa stick (these are herbs rolled into a cigar shape and ignited) or a heat lamp (called a Chi lamp) could be used over the needled areas. Recently, we have been using a 12 watt medical laser therapy unit which has acupuncture capabilities.

    After a period of time, usually 15 to 30 minutes, the needles are removed. Most animals relax and tolerate acupuncture very well, often falling asleep during treatments; a small number will be panting and restless. Patients usually start with 1-2 treatments per week for 4-6 weeks. A positive response is often noticed within the first 3-6 treatments and sometimes sooner. Once a maximum response is achieved, treatments are tapered off and pets may only need to be seen occasionally.

    Studies have shown that acupuncture has a generally positive effect on the body because it stimulates the release of hormones, pain-killing chemicals, and anti-inflammatory substances. All of these substances have a beneficial effect by promoting tissue repair and improving blood circulation resulting in pain relief and a sense of well-being. Local effects of acupuncture consist of relaxation of muscle spasm or “trigger points” during the acupuncture session.

    Acupuncture has certainly proved to be beneficial for many of the patients in our hospital. While acupuncture is known for having beneficial effects for a wide variety of conditions and diseases, it is most commonly used for alleviation of pain.  We are currently using acupuncture for a variety of conditions including but not limited to degenerative joint disease, muscle soreness, intervertebral disc disease, paralysis, chronic pain syndromes, and even allergies. Additional general conditions that respond to acupuncture include epilepsy, acral lick granulomas, respiratory problems such as asthma, and gastrointestinal imbalances such as diarrhea or constipation. Cancer patients may benefit with pain-relief and a decrease in side-effects from chemotherapy. It’s important to realize that acupuncture is an important adjunctive therapy for supportive therapy and symptomatic relief. Acupuncture is not a cure-all, but rather a therapeutic modality that can be used simultaneously with other more traditional methods of veterinary care.

    Acupuncture is one of the safest therapies utilized in medicine, if practiced by a properly trained and certified veterinarian. Side effects are rare. Some animals may become sleepy or lethargic for 24-48 hours. These circumstances are usually followed by an improvement in the condition and are an indication that the treatment is working. Acupuncture has been recognized as a beneficial treatment modality by world renowned medical associations including the American Medical Association, the American Veterinary Medical Association, and the National Institutes of Health.

    Thymoma.

    Thymoma is an uncommon canine and feline neoplasm of thymic epithelial cells. It is seen in various breeds but may occur more frequently in Labrador Retriever and German Shepherd Dogs. Middle-aged or older dogs (average age of 11 years) can be affected and no sex predilection exists. Affected cats are usually older than 9 years of age. A paraneoplastic syndrome of myasthenia gravis, nonthymic malignant tumors, and/or polymyositis occurs in a significant number of dogs with thymoma. Clinical signs are variable and are related to a space-occupying cranial mediastinal mass and/or manifestations of the paraneoplastic syndrome. Dyspnea is the most common presenting clinical sign. Thoracic radiographs usually show a cranial mediastinal mass. Lymphoma is the main differential diagnosis. A definitive diagnosis may be made by fine needle aspiration of the mass under ultrasound guidance or closed biopsy, but is more likely to be confirmed by thoracotomy. Thymomas may be completely contained within the thymic capsule or may spread by local invasion or metastasis. A staging system allows for an accurate prognosis and a therapeutic plan. Surgical removal of encapsulated thymomas may result in long-term survival or cure. Invasive or metastatic thymomas carry a guarded prognosis. Manifestations of the paraneoplastic syndrome complicate treatment. Adjuvant radiation and chemotherapy may be of value for advanced cases; however, adequate clinical trials have not been done in the dog or cat.

    Most dogs and cats with a cranial mediastinal mass will present with signs of dyspnea, coughing, and/or exercise intolerance. Other signs may include regurgitation, vomiting, or gagging secondary to esophageal compression or paraneoplastic myasthenia gravis. Generalized myasthenia gravis may also occur with a primary complaint by the owner of recurrent weakness or collapse. Precaval syndrome (swelling of the head, neck, and/or thoracic limbs) is possible if the mediastinal mass causes compression of or invades the cranial vena cava. On physical examination, if the cranial mediastinal mass is extremely large, muffled lung sounds will be noted. While most cranial mediastinal masses are usually thymoma or lymphosarcoma, other causes may include ectopic thyroid tissue, branchial cyst, chemodectoma, or thoracic wall tumor. Lymphadenopathy due to infectious or inflammatory causes can also be found in the cranial mediastinum. Fluid within the cranial mediastinum (transudate, exudate, hemorrhage) can occasionally mimic a mediastinal mass. Hypercalcemia may occur in both thymoma and lymphoma. Non-specific azotemia secondary to pre-renal and renal causes may be found. Animals with lymphoma and liver involvement may have variable increases in serum ALP, ALT, and total bilirubin. Hyperphosphatemia can be seen with renal failure, and hypophosphatemia is usually associated with hypercalcemia of malignancy. Two or three thoracic view radiographs (ventrodorsal or dorsoventral and one or two lateral views) are the preferred way to diagnose an intrathoracic mass versus pulmonary, airway, or pleural diseases causing respiratory signs. Tracheal elevation is a consistent sign of a mediastinal mass on the lateral image. Differentiating a pulmonary or thoracic wall mass from a mediastinal mass may be done with the ventrodorsal view. The mediastinum should be twice the width of the spine in the dog. Fat in obese dogs can widen the mediastinum in the absence of a true mass. Pulmonary masses will usually be positioned lateral to the mediastinum, and thoracic wall masses will be peripheral and often cause rib lysis or spreading and cats with a cranial mediastinal mass will present with signs of dyspnea, coughing, and/or exercise intolerance. Other signs may include regurgitation, vomiting, or gagging secondary to esophageal compression or paraneoplastic myasthenia gravis.

    Dogs and cats with thymoma and paraneoplastic myasthenia gravis may also exhibit signs of megaesophagus. Myasthenia gravis is an immune-mediated disorder where autoantibodies directed against nicotinic acetylcholine receptors (ACHRs) on the postsynaptic membrane of the neuromuscular junction cause abnormal neuromuscular transmission. Antibody binding to the ACHRs leads to the loss of functional receptors by complement lysis, accelerated internalization, and degradation of ACHRs; blockage of acetylcholine from the receptors; and decreased synthesis of new receptors. The lack of functional receptors impedes the transfer of the action potential from the neuron to the muscle. There are many presenting clinical signs and 3 clinical syndromes may be present: 1) focal MG with muscle weakness restricted to specific groups of the pharyngeal, esophageal, laryngeal, or facial muscles; 2) generalized MG with exercise induced appendicular muscle weakness and megaesophagus; and 3) acute fulminating MG that involves a rapid onset of appendicular muscle weakness, megaesophagus, and collapse. Due to the striated musculature in the canine esophagus, megaesophagus is present in 85% of canine cases of MG.

    Thymoma combined with MG and megaesophagus has a poor prognosis. Aspiration pneumonia is a common complication. Dogs with acquired MG have a 1-year mortality rate of 60%, and 48% of affected dogs may die within 2 wk of being diagnosed, due to severe respiratory compromise. In a review of thymoma in dogs, 30% to 50% of dogs had MG. The link between thymic disease and MG is complex and may involve the following: general immune dysfunction and loss of self-tolerance, antigenic similarity between the proteins of the neurofilaments of the thymic myoid cells and ACHRs, expression of an ACHR by thymic myoid cells when challenged by a virus or bacterium. Myasthenia gravis associated with thymic disease in dogs is usually generalized and acute.

    The definitive diagnostic test for MG is an ACHR antibody titer obtained with an immunoprecipitation radioimmunoassay. The sensitivity of this test is more than 90% and false positives have not been documented. Electromyographic (EMG) findings and the results of a tensilon response test can support a diagnosis of MG. The initial EMG is normal, but it is followed by a decremental muscular response to a sustained electric nerve stimulus. The tensilon test uses edrophonium chloride, which temporarily prevents the hydrolysis of acetylcholine at the neuromuscular junction by competing with acetylcholine. This increases the acetylcholine concentration and the probability of an action potential at the neuromuscular junction and decreased muscle weakness.

    In cats, a generalized, erythematous, dermatitis with marked, multifocal crusting, and skin thickening is a not uncommon thymoma associated paraneoplastic cutaneous syndrome. This exfoliative dermatosis is characterized by multifocal plaques of inflammatory alopecia, ulceration, easily epilated coat, target lesions, and painful, contracted skin. Histopathology of these lesions is suggestive of erythema multiforme, an immune mediated disease in which lymphocyte mediated attack is directed at epidermal and follicular keratinocytes. Drug reaction, infection, and occult neoplasia are important triggers for EM. Apparently, the abnormal population of mast cells and lymphocytes associated with thymoma is the responsible mechanism by which these characteristic skin changes occur in cats.

    Ultrasound of the cranial mediastinum can be useful in differentiating a cranial mediastinal mass from pleural fluid and may be helpful in determining an aspiration or biopsy site. Ultrasound of the abdomen is indicated in staging of lymphoma, to determine intra-abdominal organ involvement. Because thymomas are rarely metastatic, abdominal ultrasound is not routinely performed in these dogs, except when attempting to differentiate thymoma from lymphoma or in the case of potential intra-abdominal organ dysfunction, based on hematologic or serum chemistry profile abnormalities.

    Aspiration cytology can differentiate thymoma from lymphoma in many instances. Thymomas contain mature lymphocytes, neoplastic epithelial cells, and often mast cells. Lymphomas are usually lymphoblastic with large, immature lymphocytes. A lymphocytic lymphoma or a cystic thymoma may cause cytology to be misleading, and tissue samples may be required. Cytology of pleural effusion can also be diagnostic for lymphoma if there are exfoliated lymphoblasts present.

    Thymomas are invasive or non-invasive. Staging should include thoracic radiography to rule out obvious metastatic disease and further testing based on clinical signs, physical examination, or hematologic and serologic findings.

    Imaging of the thoracic cavity may not indicate the invasiveness of disease, and the presence of effusions should not rule out exploratory surgery. Exploratory surgery is still the best staging procedure to determine resectability.

    The treatment options for thymoma in dogs and cats include thymectomy, chemotherapy, and radiation. Thymectomy is the treatment of choice for noninvasive thymoma without megaesophagus. Dogs undergoing a thymectomy with megaesophagus have poor survival because of aspiration pneumonia, mass recurrence, and worsening of signs. A combination of chemotherapy and radiation therapy may be the most effective treatment for invasive thymoma with megaesophagus. Dogs without signs of megaesophagus that have their mass completely resected usually have prolonged survival times. Animals with megaesophagus often have very short survival times, and surgery may be contraindicated due to the morbidity and mortality associated with the procedure, usually related to aspiration pneumonia. Paraneoplastic syndromes associated with thymoma may or may not resolve with therapy and may occur later in life despite successful therapy. There have been reports of prolonged survivals in some animals with no therapy for their thymomas, which may indicate the slow-growing nature of some tumors.

    As previously mentioned, surgical excision is the treatment of choice. While thymoma tends to be more invasive and difficult to resect in dogs, it is usually less invasive and easier to remove in cats. An intercostal or rib pivot approach is utilized for small masses while median sternotomy is required for removal of large masses.  Non-invasive thymomas do not adhere to intrathoracic structures and are removed using a combination of careful blunt-sharp dissection. The cranial vena cava and phrenic nerves are located along the craniodorsal aspect of most cranial mediastinal masses necessitating careful dissection in this area. Invasive thymomas usually invade vital structures and therefore these animals are difficult surgical candidates, with incomplete removal being much more likely.


    In a recent study involving patients where complete excision was possible (and without the utilization of adjunctive chemo or radiation therapy), the median overall survival time for the cats was 1,825 days with a 1-year survival rate of 89% and a 3-year survival rate of 74%. The median overall survival time for the dogs was 790 days with a 1-year survival rate of 64% and a 3-year survival rate of 42%. Recurrence of thymoma was observed in 2 cats and 1 dog, and a second surgery was performed in each with subsequent survival times of 5, 3, and 4 years following the first surgery. The percentage lymphocyte composition of the mass was the only factor that was significantly correlated with survival time; animals with a high percentage of lymphocytes lived significantly longer. The results of this study indicated that most cats and dogs with thymomas did well after complete excision. Even cats and dogs with invasive masses that survived the surgery and the few cats and dogs with recurrent thymomas or paraneoplastic syndromes had a good long-term outcome. For these reasons, excision should be considered an effective treatment option for dogs and cats with thymomas. Once again, as mentioned previously, radiation and/or chemotherapy may play a role in management of thymoma in dogs and cats, especially in those cases in which complete removal cannot be obtained at surgery. The lymphoid component of the thymoma may determine the completeness of the response to chemo and/or radiation therapy.

    Principles of Tendon Repair.

    A tendon is a dense band of fibrous connective tissue which acts as an intermediary component in the attachment of muscle to bone. When operating within a range of normal physiological forces, tendons exhibit high compliance, great tensile strength and low extensibility. When supraphysiologic forces are placed on tendons, their mechanical characteristics change, and apparently irreversible structural changes take place. Whether or not such changes eventually result in a clinical lesion is dependent upon a number of poorly defined factors. The healing of injured tendons presents the veterinary surgeon with a number of different management decisions as opposite objectives seem to be required in the same wound. Successful restoration of injured tendons requires a rapid gain in tensile strength without adherence to other tissues. For a single scare to provide strength in one area yet not restrict motion in another, a complex series of events must occur. This series of events is dependent upon the anatomy and vascular supply of the tendons and the adjacent tissues.

    A tendon may receive its blood supply from four sources: the muscle or bone to which the tendon is attached (intrinsic vessels), a mesotendon within a synovial sheath, and the paratendon if no sheath exists (extrinsic vessels). Both intrinsic and extrinsic components can be involved in tendon healing. As tendon injuries are often accompanied by injuries to the surrounding soft tissues and/or bone, their healing does not take place in an isolated environment. The gain in tensile strength and adhesions that develop are part of a single healing process, resulting in the tendon and the surrounding tissues healing according to the “one wound-one scar” principle. There is no question that if the wounded tendon could be managed independently of the adjacent soft tissue wound, the problem of tendon repair would be simplified.

    The healing process of tendons can be further divided into healing of sheathed versus non-sheathed tendons. In a non-sheathed tendon, healing depends less on intrinsic blood supply because of the contributions of the wound bed from the paratendon and peritendonous tissues. In sheathed tendons under ideal conditions (i.e., if the primary intrinsic blood supply is not damaged), the potential for primary intrinsic repair exists. Maximization of the intrinsic healing and minimization of extrinsic healing will lead to fewer problems with peritendonous adhesions. Unfortunately, the majority of tendon injuries involves the tendon and tendon sheath and primary intrinsic repair is overshadowed by an extrinsic response by the peritendonous tissues. This response results in adhesion formation in addition to tendon healing and may preclude restoration of normal gliding function.

    In an effort to erect an artificial barrier between the healing tendon and the rest of the wound, numerous materials have been placed around the anastomatic site. In all cases, retardation of the healing process has occurred. This is because in the overwhelming majority of tendon injuries, although numerous intrinsic vessels are present, these vessels are not capable of nourishing the tendon without collateral connections to extrinsic vessels. In addition, tendon healing is dependent upon migration of cells from outside the tendon into the defect between tendon ends. Therefore, successful isolation of a tendon anastomosis from the extrinsic tissues invariably results in failed healing. The best approach to minimizing adhesion formation and subsequent restricted gliding function is to use proper surgical technique and postoperative care.

    Obviously, the importance of adhesions in tendon surgery depends upon the necessity for restoration of normal gliding function. The return of sufficient tensile strength may be more important than restoration of normal gliding function in a number of instances. For example, in treating injuries involving large weight-bearing tendons, provision of tensile strength adequate to prevent distraction during weight-bearing, rather than prevention of adhesions, should be the primary concern of the surgeon. This is because the formation of adhesions which would restrict the motion of these structure is rare, and a successful clinical outcome depends primarily on the maintenance of close opposition of the sutured tendon ends throughout healing.

    The goals of tendon repair are apposition of the severed tendon ends with minimal disruption of blood flow, minimal suture bulk, and maximum strength of the overall repair. As is true with any surgical technique, suture materials and tendon suture patterns have been developed and recommended in an attempt to optimize results. These patterns have evolved in an attempt to maximize both tensile strength and normal gliding function.

    Monofilament suture material is recommended for tendon repair because of its ability to glide within tissue and may be less likely to initiate tearing or separating of the tendon. While synthetic, monofilament, non-absorbable suture material has been the preferred suture material in the past, polydioxanone (PDS*) is absorbed slowly and loses its strength slowly. Therefore, enough strength would remain until the tendon begins to acquire intrinsic tensile strength. In addition, PDS* is less likely than non-absorbable suture materials to create a suture sinus in a contaminated environment.

    As mentioned previously, several suture patterns have been designed for the surgical repair of severed tendons, including the Bunnell, Bunnell-Mayer, locking loop or modified Kessler, and three lopp pulley techniques. In the immediate postoperative healing period the sutures are relied upon to maintain tendon apposition and resist gap formation. They provide mechanical support and serve as a scaffold for initial cellular migration. The suture pattern should not restrict blood flow within the tendon or enhance scar formation by irritating the surrounding tissues. In light of these criteria, the locking loop and three loop pulley techniques are favored, as they are less restrictive of the intrinsic blood supply and provide greater tensile strength than do Bunnell sutures. The three loop pulley pattern has been shown to provide more tensile strength and resistance to gap formation than the locking loop pattern; however, it may compromise gliding function because of the quantity of suture material on the surface of the tendon. With this in mind, the locking loop pattern would seem best suited for use in situations where maximum gliding function is necessary, while the three loop pulley pattern may be used advantageously in high-load situations where provision of early tensile strength rather than restoration of normal gliding function is of primary concern.

    Postoperative management of a surgical repair of a tendon rupture should consist of external support and immobilization for three weeks, followed by an additional three to four week period of restricted activity as the intrinsic tensile strength of the healing tendon increase. There should then be a gradual return to normal activity. Recent evidence indicates that limited passive motion aids in the longitudinal orientation of tendon fibrils in tendon repair while active motion will inhibit early repair of the tendon. When controlled passive motion is utilized, tendons heal more rapidly than in immobilized repairs. The difficulty encountered in veterinary surgery is how to conveniently implement limited passive motion without placing too much stress on the healing tendon too soon in a potentially uncooperative patient. Hopefully, additional advances will be made in the near future to help overcome these difficulties and to optimize the healing of tendon injuries in general.

    Principles of External Skeletal Fixation.

    Numerous methods of fracture fixation are available to the veterinary surgeon. External skeletal fixation is an effective method of fracture repair, which has experienced a resurgence in popularity in the last few years. Several types of external skeletal fixation devices are commonly utilized, including the Kirshner-Ehmer apparatus and the Synthes and Hoffman external fixators. Many configurations and various modifications have been described for the application of external fixators. A review of apparatus design has resulted in classification of external skeletal fixators into three types, each possessing separate attributes and indications for use. Type 1 for unilateral splints uses fixation pins, which are inserted through both bone cortices, but penetrate only on skin surface. Type 2 or bilateral splints use fixation pins, which are inserted through both cortices and both skin surfaces. Type 3 or biplanar splints are a combination of unilateral and bilateral splintage employed in a three dimensional configuration.

    An external skeletal fixator (ESF) can be used as the primary method of fracture fixation or can be used to enhance the stability provided by another primary fixation modality. External fixators may be used in a variety of clinical situations including simple fractures, open or compound fractures, delayed and non-unions, highly comminuted fractures, fractures in which there are extensive soft tissue damage, and infected fractures. They are also frequently recommended in cases requiring transarticular stabilization and for stabilization of corrective osteotomies. When used properly, application of an ESF results in a number of advantages over other techniques of fracture repair, including minimal disruption of soft tissues attachments to bone and minimal disturbance of the blood supply to the bone. When used in difficult fracture situations involving open or compound wounds, osteomylitis and/or extensive soft tissue injury, the contaminated fracture sites are not disturbed by the presence of the fixation device and dissemination of the contamination is minimized.

    As with any surgical technique, the use of an ESF is not without some disadvantages or potential complications. Disadvantages of an ESF include delayed healing under certain condition, ideal reduction is not always possible, the fixation may fail in cases of osteoporosis, and the ESF may catch on an object thereby ruining the fixation. Complications associated with the use of an ESF include pin tract drainage and infection, pin loosening, pin breakage, iatrogenic fractures, damage to vessels and nerves, and disturbed muscle function due to pin placement. The disadvantages and complications must be taken into consideration when deciding whether to use external fixation. The majority of the disadvantages and complications associated with an ESF can be alleviated if the important principles of application are followed carefully.

    Historically, the major limitation for the use of external skeletal fixation has been its ability to adequately stabilize fracture fragments until healing has occurred. It is absolutely essential to maintain the holding power of the pins the bone and the stiffness of the fixation pins if rigid immobilization is to be maintained. Maximum stress of the fixation pins occurs at the pin-bone interface. Stress transfer from bone to metal and, over time, stress concentration at these sites can eventually lead to pin loosening, drainage, infection, or breakage. Information gathered from numerous studies and clinical experience indicates that stiffness, bone holding power, and clinical performance of an ESF is dependent upon numerous factors including configuration, diameter and number of connecting bars, pin diameter, number of pins, type of pin, angle and location of pins in cortical bone, length of pins from the connecting bars to the bone, method of pin insertion, and inherent stability at the fracture site. Each of these factors must be critically assessed by the surgeon to decrease the likelihood of pin loosening and loss of fixator stiffness and associated morbidity.

    The method of fixation pin insertion used should avoid generating mechanical damage and bone necrosis. High speed power insertion of pins results in thermal necrosis of bone, while insertion by a hang drill results in excessive mechanical damage. Both techniques are associated with a decreased force required for axial extraction of the fixation pins. Current recommendations include predrilling with a smaller drill bit and either low speed power or hand chuck insertion of fixation pins to decrease the incidence of mechanical or thermal necrosis and subsequent premature pin loosening.

    The type of pin used influences greatly the stability of the pin-bone interface, as well as fixators stiffness. While nonthreaded pins exhibit decreased bone holding power, they are stiffer, stronger, and more resistant to bending and breaking than threaded pins. A recent study indicated that single cortex partially threaded pins compare favorable to pins with threads engaging both cortices with regard to holding power. In addition, these pins provided more resistance to bending at the pin-bone interface than fully threaded pins. Essentially, the single cortex partially threaded pin combines the increased holding power of threaded pins with the stiffness of the nonthreaded pins. The use of partially threaded pins, either exclusively or in combination with nonthreaded pins, should be considered in clinical cases where prolonged external skeletal fixation is required. Other studies have indicated that morbidity decreased significantly with the exclusive use of threaded pins or a combination of threaded and smooth pins as compared to the exclusive use of the smooth pins. Prolonged stability of the pin-bone interface was considered to be the reason.

    Numerous recommendations have been made with regard to the angle and location of fixation pin placement in cortical bone. Information gathered from many studies indicates that an angle of approximately 70 degrees to the long axis of the bone and inward (central) angling of the pins improves fixation stiffness. It may also reduce pin loosening, because nonparallel pins will tend to restrict the motion of their neighbor. The appropriate number of pins per fragment has not been objectively determined; however, a minimum of 2 and perhaps 3 or 4 pins per fragment should be used as increasing the number of fixation pins per fragment reduces the incidence of premature loosening. Each pin should be inserted through a separate stab incision in intact skin and avoid penetration of large muscles masses. This practice will help alleviate problems with incision or wound management, decrease the incidence of pin tract infection and make incision closure easier.

    Bone-connecting bar distance should be minimized while avoiding interference with the skin. Doubling the bone-clamp distance reduces the fixator stiffness by 25%. Increasing the diameter of the fixation pins or the diameter and number of the connecting bars will increase fixator stiffness. The configuration of the fixators will also affect fixator stiffness, with Type 3, or biplanar splints, being the strongest configuration.

    In conclusion, since fractures vary widely in type, stability, condition of the soft tissues, and activity and size of the patient, it is obvious that no one configuration is best suited for all fractures. Providing that the proper principles of application are followed, external skeletal fixation can provide the stable fixation necessary for fracture healing and good to excellent post-operative limb function. The information presented should hopefully enable the surgeon in choosing the best ESF design for the fracture type under consideration.

    Stifle Luxation in the Dog and Cat.

    Total derangement or dislocation of the stifle joint is a serious injury usually caused by severe direct or indirect trauma to the knee. The type of dislocation observed depends upon the direction and location of the inciting trauma. Luxation of the stifle joint is not a very common injury because of the many soft tissue structures that interact to provide stability for the joint. These structures include the cranial and caudal cruciate ligaments along with the medial and lateral collateral ligaments. In addition, some support may also be derived from the quadriceps muscle and patella tendon cranially and the oblique poplitcal muscle, hamstring muscles, and the gastroenemius muscle, caudally. In many cases, fractures may accompany dislocations. Other structures are also likely to be injured including the menisci, joint capsule, popliteal artery, and peroneal nerve. Vascular integrity and neurologic function must be carefully evaluated as these complications usually are the limiting factor in the outcome of the injury.

    Successful treatment of a stifle joint luxation must allow the animal to regain functional use of the limb. Good results achieved by a variety of methods support the notion that various techniques, which maintain reduction and stability, can be successful clinically. Initial maintenance of reduction and stability encourages well-organized periarticular collagen formation to provide long term joint stability. Closed reduction maintained with external coaptation, open reduction with extraarticular or intraarticular ligament reconstruction with transarticular external skeletal fixation and open reduction with transarticular pinning have been successful methods of treatment for stifle joint luxations. Although successful return to function has been reported following use of these techniques, some authors recommend stifle joint arthrodesis as the primary surgical treatment because of the severe general disruption sustained by the periarticular soft tissues at the time of injury. Based upon my experience, the results of surgical reduction and stabilization are generally good to excellent, and primary arthrodesis should only be attempted after attempts at reconstruction fail.

    Because of the relatively infrequent occurrence of stifle joint luxation, only a few articles have appeared over the last several years comparing the results of various techniques of surgical intervention. It is generally agreed that it is difficult to accurately achieve and maintain reduction by closed methods alone. To provide a stable environment for healing of the soft tissues leading to well organized collagen formation and long term joint stability, surgical intervention is recommended.

    A standard lateral parapatella approach and lateral arthrotomy is used to gain access to the stifle joint and allow inspection of the intraarticular and periarticular soft tissue damage. Because ligaments can appear to be grossly intact while having lost any load carrying ability, all ligaments should be inspected while undergoing stress palpation. Numerous different combinations of ligament damage have been reported with rupture of both cruciate ligaments and one of the collateral ligaments occurring most frequently. Interestingly, despite severe ligamentous and soft tissue damage, there is usually minimal, if any, gross articular damage observed at surgery. Remnants of the damaged cruciate ligament or ligaments should be removed and partial meniscectomy performed in animals with meniscal tears or avulsions. It is at this point that the various options available to this surgeon to achieve and maintain reduction and stability come into play.

    In one technique, although the collateral ligaments are assessed for damage, they are not repaired; and reduction is achieved and maintained by placement of a transarticular pin while the stifle joint is held in a functional angle of approximately 135-140 degrees. While the technique is generally effective in cats and small dogs, transarticular pinning is not an especially rigid fixation. Distal pin migration and bending of the pin where it crosses the joint occur frequently, and failure of the technique may be due to reliance upon the transarticular pin to provide most of the stability of the fixation. It is quick, inexpensive, and easy to perform compared to other techniques, however, and may be the technique of choice in debilitate or muli-trauma patient in which anesthesia time should be limited. The authors of the technique conclude, however, by mentioning that better success would be achieved when the pin is used to maintain reduction while additional fixation in the form of a transarticular external skeletal fixators is used to provide sufficient rigidity to allow adequate healing of periarticular soft tissues. Such additional fixation would absolutely be necessary when repairing stifle luxations with this technique in medium and large sized dogs.

    In another technique, the stifle luxation is maintained in reduction with multiple extraarticular sutures while transarticular external skeletal fixation is used to provide rigid fixation. In this technique, damaged collateral ligaments are repaired and extraarticular suture stabilization is performed for the damaged cruciate ligaments. Extraarticular stabilization is considered technically easier and may avoid further soft tissue disruption and instability of the joint when compared to intraarticular ligament reconstruction techniques. Transarticular external skeletal fixation augments joint stability while the tissues progress through the stages of inflammation and repair. Consistently, good to excellent functional results have been achieved in cats and all sizes of dogs with this surgical protocol.

    My own personal preference is to use extraarticular stabilizing sutures and transarticular external skeletal fixation for medium and large sized dogs. In small dogs and cats, extraarticular stabilization and external coaptation consisting of a modified Bobby Jones bandage has consistently resulted in good to excellent results. While the majority of animals experience a loss of stifle joint range of motion in extreme flexion, the loss of flexion does not seem to interfere with clinical limb function. The development of mild to moderate degenerative joint changes have been observed radiographically. However, there does not appear to be a correlation between radiographic changes and functional limb use. The periarticular bone formation observed may be induced by the inciting trauma and not by post-operative instability or abnormal joint mechanics.

    In conclusion, stifle joint luxation is an uncommon injury resulting from severe trauma. With proper surgical treatment, good to excellent clinical results and a return to normal or near normal function can be expected in the majority of patients.

    The Medical and Legal Implications of Veterinary Cosmetic Surgical Procedures.

    While at first it might seem odd that pets are the recipients of cosmetic surgical procedures, upon further consideration it makes perfect sense. The problem is the accepted definition of cosmetic or plastic surgery. In the human field, the term cosmetic surgery is usually reserved for those procedures which are beautifying, nonessential, and non-medical.  In the veterinary field, an ethical veterinarian would not subject his patients to such procedures. There is always the attendant risk of anesthesia and surgical complication (as there is in the human field) with any procedure, let alone cosmetic ones. A veterinary surgeon weighs those risks every time he contemplates a surgical procedure, and it is a judgment call of whether to proceed with surgery or not depending upon the risks versus the gain to each individual patient. It is more than a matter of semantics to consider essential veterinary plastic surgical procedures more appropriately as reconstructive dermatologic surgery rather than cosmetic surgery.

    The non-pet owning public finds it fascinating that dogs are even mentioned in the same breath as plastic surgery. Pet owners, however, are well aware of the myriad number of procedures that dogs have routinely and maybe not so routinely undergone to improve their health and welfare. Among those procedures which are “cosmetic” by nature but are truly reconstructive in nature are entropion and ectropion surgery (“eye lift or tuck”), nasal alar fold and deviated septum surgery (“nosejob”), cheiloplasty (“facelift”), facial fold reductions, orthodontic and maxillofacial surgery,  breast reduction, vaginal fold and tail fold pyoderma surgery,  skin grafting and myocutaneous flap surgeries, and the placement of prosthetic implants for limb salvage procedures.

    Anybody familiar with Chows and Sharpeis is familiar with their ocular problems. These breeds are consistently afflicted with congenital and hereditary tendencies, which result in the eyelids rolling in toward the eyeball and predisposing the cornea to persistent pain, discomfort, infection, and injury, which may progress to vision loss or blindness.  Saint Bernards, Newfoundlands,  Great Pyrenees, Mastiffs, and others suffer from the opposite congenital tendency, which is to have the eyelids droop outwardly predisposing these breeds to similar ocular injury. No one in their right mind would contest the necessity of reconstructive procedures to alleviate the constant ocular pain and attendant complications these congenital tendencies provoke.  The corrective procedures, however, are “cosmetic” in origin as the surgeon is basically performing an eyelift or tuck. It’s just that the procedure is being performed for a truly medical and not a cosmetic result.  No one performs an eyelift surgery to make a 10-years-old dog look likes she’s 6-years-old. All that the dog understands is that he is more comfortable and is able to see again without pain.

    Nose job surgeries are similarly indicated for those breeds with inherent upper respiratory distress syndromes. Boston Terriers, Pugs, Boxers, Bulldogs, and other chondrodystrophic breeds (ie., “smushed in faces”) are compromised by narrowed nostrils. The inability to breathe through their nose and the resultant obligatory mouth-breathing leads to and exacerbates a variety of upper respiratory problems. Surgically opening these narrowed nostrils is a simple, easy, and minimally invasive surgery, which tremendously improves the quality of life for these animals. Once again, no one is performing nose surgery because the owner doesn’t like the shape of their pet’s nose. It’s nice to be able to breathe without having to consistently make a coordinated effort to do so.

    Everybody who spends their time around dogs has been “slimed” at one time or another by flying saliva. Mastiffs are the poster child for droopy lips and excessive, uncontrolled salivation. In the old days, veterinarians actually removed the sub-mandibular salivary glands to decrease the amount of saliva formed and secreted in an attempt to prevent a consistently wet skin fold and resultant chronic bacterial and yeast infection in the skin below the lips. In many cases, these skin infections spread systemically causing urinary tract infection, heart valve infections, and dental disease. Rather than remove the salivary glands, a “facelift” or cheiloplasty effectively alleviates the problem. The lips are alternately pulled up and back and rolled in to prevent salivary leakage. The majority of the procedure is performed within the oral cavity to be more cosmetic, but no one can deny the medical benefits to be gained by that portion of the canine population with chronic lip fold infections. It’s also much less invasive a surgery than removing the salivary glands.

    As you can see, many of the “cosmetic” surgical procedures performed on dogs are performed because of the complications associated with abnormal skin folds. It is for this reason that breast reductions and some vaginal, facial, and tail surgeries are carried out. While I am a Board certified Veterinary Surgeon, my practice is not limited to veterinary surgery. I operate a full service veterinary facility open 24 hours a day 7 days a week. As such, I see a tremendous amount of general practice cases. Many clients have recently adopted dogs from the shelters, pounds, and/or rescue groups which need to be spayed. A good proportion of these intact females have had multiple pregnancies. As a result of these pregnancies, there is a tendency for pendulous breast tissue and secondary intra-mammary skin fold infections. It makes sense to reduce the pendulous and cystic breast tissue under the same anesthetic that a spay procedure is performed to eliminate the chronic maintenance that would otherwise be required of the new owner to prevent consistent skin infections in the area. As a result of multiple pregnancies as well as for a variety of other congenital and/or hereditary reasons, many female dogs have chronic irritation of the vaginal area and secondary ascending urinary tract infections because of excessive vaginal skin folds. The removal of these folds prevents excessive vaginal licking and irritation and urine scalding, resulting in a much more comfortable pet. The same is true for tail and facial fold infections commonly observed in Bulldogs and other chondrodystrophoid breeds. Cosmetic removal of the kinked tail effectively eliminates an area of chronic irritation and infection. By the same token, cosmetic removal of excessive and deep facial skin folds removes a source of chronic irritation from persistent fungal and bacterial infection.

    Many animals that have suffered through a significant trauma or cancer may require skin grafts or the movement of large flaps of skin and the attached underlying musculature, a procedure known as myocutaneous flap transfer. Once again, while cosmetic in nature, these procedures obviously are medically beneficial to the patient. Recently, advancements in prosthetic surgery are making it possible to consider osseointegrated prosthetic limb implants for limb salvage. In these procedures, a stainless steel or titanium implant is placed within the bone of a limb to act as a scaffold for placement of a prosthesis that mimics both cosmetically and functionally a normal limb. The potential benefit to dogs, which would otherwise have lost a limb to amputation, is enormous.

    The question comes down to where does an ethical veterinarian cross the line with regard to the procedures that some clients would consider frivolous and other clients would consider a necessity? All of the procedures that have been previously mentioned are medically beneficial and help tremendously improve a patient’s quality of life when applied intelligently and with discretion. I have been asked to perform botox, collagen, and restylane injections as well as testicular implant surgery.  My answer, whenever I have been asked, is a resounding “No!!” In my opinion, these procedures serve no known medical benefit for the patient. The pet owners that ask for such procedures to be performed on their pets would be better off spending their money on psychotherapy in order to understand why anthropomorphization of their pets is flat out crazy.

    Pain Management.

    Animals and people have similar neural pathways for the development, conduction, and modulation of pain. This biological similarity makes the expression of both acute and chronic pain comparable. Like humans, dogs and cats develop myopathies and neuropathies that lead to muscle and neurological pain and discomfort. Other painful conditions, which may be similarly expressed include ear infections, dental conditions, sinus pain, skin lesions, and the pain of acute and chronic, repetitive trauma. Untreated pain decreases quality of life in all patients and prolongs recovery from surgery, injury, or illness. Today, with a better understanding on how pain develops and is perpetuated, pain management has become an essential part of high quality and compassionate patient care in the veterinary field. Providing adequate pain management helps pets recover faster, improving the human-animal bond and the pet’s overall well-being.

    Different kinds of pain

    When a negative, painful insult is encountered, the body’s endocrine system produces substances such as cortisol, catecholamine, and other inflammatory mediators that alter normal physiologic parameters. As a result of the release of these substances into the general circulation, substantial changes occur at the tissue level including decreased oxygen delivery to tissues, increased cellular metabolic demands, impaired immune function, increased risk of infections, delayed wound healing, prolonged convalescence, and cardiovascular stress.

    In the past, pain was most commonly classified either as acute or chronic. Recently, a newer approach has been to consider pain as adaptive or maladaptive.

    Adaptive pain is a normal response to tissue damage. It includes all types of pain involving the release of inflammatory mediators that will cause heat, redness, swelling, pain, and loss of function of the injured area. Inflammation is a major component of pain and can be present both in postoperative/trauma patients and in chronic pain states such as osteoarthritis.

    If adaptive pain is not properly managed, it will eventually result in physical changes in the spinal cord and brain, which will lead to maladaptive pain. In maladaptive pain, the central nervous system becomes more sensitive and the thalamus, which serves as a relay station for nerve impulses from the periphery to the cortex, becomes a spontaneous pain generator. The adjustment from thinking of pain as either acute or chronic to adaptive or maladaptive makes it easier to understand why pain can be so difficult to control in certain patients.

    How do I know my pet is in pain?

    There are numerous signs that an animal can exhibit while experiencing pain:

    • They can fail to exhibit normal behavior, as evidenced by being more lethargic, with perhaps a decreased appetite or decreased grooming tendencies, especially in cats.
    • They may express an abnormal behavior, such as an increase in vocalization, aggression, altered posture and/or facial expression, hiding (cats especially), restlessness, and inappropriate elimination.
    • An increase in body tension and reaction to touch, or hyperpathia, is also consistent with an animal experiencing pain in a specific injured body area or region. A distinct change in physiologic parameters such as an elevated heart rate, respiratory rate, blood pressure, and/or pupilary dilation is also indicative of pain.
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      What can I do to help my pet?

      Understanding the circumstances that can lead to the development of pain may help anticipate and properly manage the emergence of pain as a clinical condition. Attention must be paid to the development or presence of unusual bumps, scrapes, bruises, or sensitivities. Any change in an animal’s desire or ability to run, jump, play, or otherwise ambulate normally must be evaluated.

      Simple basic lifestyle changes such as controlled exercise regimes and weight management can help reduce joint pain and stress.

      Providing favorable environmental conditions to help prevent or alleviate pain and discomfort such as ensuring easy access to litter boxes, soft bedding, non slippery surfaces, limited access to stairs, and “warming up” your pet appropriately prior to exercise will help reduce the need for pharmacologic intervention in many cases.

      How do we manage pain?

      At our hospital, we utilize both pharmacological and a non-pharmacological treatments for pain management. Your doctor will recommend the best way to individually manage your pet’s painful condition.

      Pharmacological intervention:

      Prior to an elective surgical procedure, appropriate opioids will be administered. Based upon the type of procedure performed, the addition of local anesthetics, epidurals, and steroidal or non-steroidal anti-inflammatory will provide pre and intra-operative comfort and a better postoperative recovery period. Throughout the anesthetic recovery period, hospitalization and the immediate post-operative recovery period at home, additional non- steroidal anti-inflammatory drugs (NSAIDs), opioids or opioid patches will be provided to your pet.

      For maladaptive types of pain not associated with an elective procedure, numerous different options may be chosen by your veterinarian.

      NSAID’s and Corticosteroids are the drugs of choice for many of the inflammatory conditions resulting in pain, acting by inhibiting substances released at multiple levels along the biochemical pain pathway.

      Topical anesthetics are useful to manage well-delineated painful areas such as small burns or urine scalding.
      When aberrant pain is refractory to traditional analgesics, specific drugs like Gabapentin, which acts on the central nervous system, may be required to restore normal central nervous system transmission and control pain and discomfort.

      However, many patients with long term chronic, intermittent pain often benefit from the combination of pharmacological as well as non pharmacological therapy.

      Non-Pharmacological intervention:

      The newly developed high power Class IV lasers generate visible and invisible light beams that are absorbed as light energy by cells (photobiostimulation). This results in the activation of biological reactions, which have been shown to result in an increase in circulation to the damaged area thus creating an optimal healing environment.

      Acupuncture has long been recognized by renowned medical associations for its analgesic properties. One of the ways acupuncture works is by slowly releasing an animal’s own opioid-like substances (endorphins) from the brain, spinal cord, and peripheral nerves to help alleviate pain at its source.

      Rehabilitation therapy is crucial to help the patient return to normal function or to help improve overall body condition. Rehabilitative techniques include heat and cold therapy, passive range of motion exercises, stretching, balancing exercises, massage, joint mobility, and controlled walking exercises.

      Nutrition or “food therapy” is a science that selects food or herbs customized to each individual based upon their inborn tendencies, age, species, personality, and disease process. A specifically formulated diet can help prevent or help in the management of many painful conditions including but not limited to certain skin diseases, osteoarthritis, cancer, and gastrointestinal problems.

      Nutraceuticals (glucosamine, chondroitin, msm, creatine) may decrease joint inflammation and assist in cartilage repair. Additional products, which have demonstrated to be of help by decreasing inflammation and modifying the progression of osteoarthritis and therefore pain,  include the omega-3 and omega-6 fatty acids and chondroprotective agents such as polysulfated glycosaminoglycans (Adequan).

      Platelet Rich Plasma Therapy.

      The usual protocol for the initial treatment of muscle and tendon injuries includes rest, ice, compression, and elevation of the injured area. This combination prevents further injury, reduces pain, inflammation, and swelling and thereby encourages healing. Not exactly an easy task when dealing with dogs and cats. Physical therapy is usually applied when the acute stage of injury has subsided. It usually involves massage, stretching, and exercises, many times augmented with ultrasound and acupuncture therapy.  Non-steroidal and steroidal anti-inflammatory drugs are also commonly used. Surgery is reserved for the more severe and intractable injuries. However a novel approach, very different from the usual methods and involving blood platelets, shows much promise and is causing much excitement in the orthopedic and sports injury world.


      When tissue is injured, the inflammatory response is triggered. This is necessary even though the heat and swelling are unpleasant. Inflammation stops the spread of infection and clears away damaged tissue. However, healing of the tissues cannot take place until the inflammation process is switched off. The fact that platelets play a role in the control of both of these processes forms the rationale behind PRP treatment. Most everyone thinks of blood platelets as being responsible for blood clotting after injury, which is true. What many people do not know is that blood platelets serve two other important functions. Blood platelets are responsible for bringing the white blood cells to the injured area to clean up the remains of dead and injured cells. Most importantly to this discussion, blood platelets release growth factors that are directly responsible for tissue regeneration. These substances are called cytokins and include platelet derived growth factor, epithelial growth factor, transforming growth factor, insulin growth factor, and other important growth factors. By ultimately inhibiting inflammation, platelets form part of the mechanism that switches the process off, and stimulates healing by producing the various tissue growth factors mentioned above which stimulate new blood vessel growth. It is for these reasons that PRP treatment has been promoted for tendon, ligament, muscle, and joint injuries, which have been historically normally slow to heal.

      Platelet-rich plasma, or PRP, is derived from blood that is drawn from the patient and run through a special centrifuge, which separates the blood’s less dense components from its heavier ones. This process distills a portion of the blood to a platelet concentration level that is much richer than regular blood. At the same time, it helps to remove both red and white blood cells from the platelet rich part of the plasma.

      Plasma containing this concentrated level of platelets provides an abundance of the previously mentioned growth factors, which are the proteins in the body that stimulate cells in the tendon, ligament, muscle, or joint to start the healing process. When PRP is injected into damaged tendons or ligaments, cells in the tissue—along with new cells circulating in the blood—are stimulated to bring even more new cells to the injured site. Therefore, the growth factors derived from platelets initiate connective tissue healing, bone regeneration and repair, promote development of new blood vessels, and generally stimulate the wound healing process by accelerating epithelial and epidermal regeneration. Because the patient’s own blood is used to make the specialized plasma—this is known as an autologous process—there is no risk of the treatment being rejected, as it might be if the blood had been provided by a donor.

      
Although PRP technology is considered cutting edge technology, it was initially developed 20 years ago for heart surgery to aid with wound healing and blood loss. Its benefits are now being applied towards the facilitating of healing of muscle, tendons, ligaments, articular and meniscal injuries. PRP has also been utilized for bone repair; it can be added to harvested autogenous bone or to a mixture of autogenous bone and freeze-dried bone/alloplastic material to improve the consistency for handling during surgery and minimizing particulate migration as well as to add increased platelets (i.e. increased growth factors) into the area to stimulate healing.

      In our practice, the utilization of PRP has been directed towards Achilles tendon injuries, cruciate ligament injuries, complicated orthopedic fractures and delayed bone healing,  and degenerative joint disease of the shoulder, elbow, hip, knee, and ankle. The number of injections performed depends upon the severity and type of condition being treated. The use of certain anti-inflammatory drugs is not recommended during PRP therapy as they may diminish the success of the procedure by interfering with the initial inflammatory reaction induced by the platelets. The use of omega 3 and 6 essential fatty acid fish oil supplements and other natural anti-inflammatory agents do not seem to work the same way as the non-steroidal anti-inflammatory agents and are therefore not restricted in use throughout the platelet facilitated natural healing process. Depending upon the condition being treated, the pet may require nothing more than a local anesthetic for the administration of PRP or may require a ‘twilight’ anesthetic.  A real advantage to PRP therapy is that it may not only facilitate the healing process, it may in certain cases provide an alternative to surgery.

      While platelet rich plasma therapy offers a promising solution to accelerate the healing of bone, muscle, tendon, ligament, and joint conditions naturally without subjecting the patient to invasive surgical procedures and significant risks, there is no one, standard protocol . Frequently, chronic injuries require more than one injection. In both acute and chronic injuries, injections may be combined with an exercise or physical therapy program, acupuncture and/or Class IV laser therapy to enhance the success of the treatment.

      Euthanasia.

      It’s never an easy decision to make, but perhaps the kindest thing you can do for a pet that is extremely ill or so severely injured that it will never be able to resume a life of good quality is to have your veterinarian induce its death quietly and humanely through euthanasia.

      A decision concerning euthanasia may be one of the most difficult decisions you will ever make for your pet. Although it is a personal decision, it doesn’t need to be a solitary one. Your veterinarian, your family, and close friends can help you make the right decision and can support you as you grieve the loss of your pet.

      What should I do?

      Eventually, many owners are faced with making life-or-death decisions for their pets. Such a decision may become necessary for the welfare of the pet and your family. Consider not only what is best for your pet, but also what is best for you and your family. For example, if your pet has an injury or disease that requires more care than you and your family can give to make sure it has a good quality of life, euthanasia may be the right decision. Quality of life is important for pets and people alike.

      Once the decision for euthanasia has been made, it is sometimes easier to discuss what you want done with the remains of your pet’s body before your pet is euthanized—by making arrangements prior to euthanasia; it can bring some degree of comfort to know what will be done with your pet’s body, and you will not have to focus on these decisions while you are grieving the recent loss of your beloved pet. Your veterinarian can provide information about burial, cremation, and other alternatives.


      How will I know when?

      If your pet can no longer experience the things it once enjoyed, cannot respond to you in its usual ways, or appears to be experiencing more pain than pleasure, you may need to consider euthanasia. Likewise, if your pet is terminally ill or critically injured, or if the financial or emotional cost of treatment is beyond your means, euthanasia may be a valid option. Sometimes asking yourself the question, “Does my pet have more bad days than good days?” can help you make the decision. Euthanasia might be necessary if a pet has become vicious, dangerous, or unmanageable. Some undesirable and abnormal behavior can be changed, so it is important to discuss these situations with your veterinarian. You and your family’s safety should always be taken into consideration.

      Your veterinarian understands your bond with your pet and can examine and evaluate your pet’s condition, estimate its chances for recovery, and discuss any potential disabilities, special needs, and long-term problems. He or she can explain medical and surgical options as well as risks and possible outcomes. Because your veterinarian cannot make the euthanasia decision for you, it is important that you fully understand your pet’s condition. If there is any part of the diagnosis or the possible effects on your pet’s future that you don’t understand, ask questions that will help you understand. Although there are times when the decision needs to be made immediately, you usually will have some time to review the facts and discuss it with your family and friends before making the decision.

      How do I tell my family?

      Family members usually are already aware of a pet’s problems. However, you should review with them the information you have received from your veterinarian. Long-term medical care can be a burden that you and your family may be unable to bear emotionally or financially, and this should be discussed openly and honestly. Encourage family members to express their thoughts and feelings. Even if you have reached a decision, it is important that family members, especially children, have their thoughts and feelings considered.

      Children have special relationships with their pets and should not be excluded from the decision-making process because they might seem too young to understand. Preventing children from participating in the process may only complicate and prolong their grief process. Children respect straightforward, truthful, and simple answers. If they are prepared adequately, children usually are able to accept a pet’s death.

      Will it be painless?

      Euthanasia is most often accomplished for pets by injection of a death-inducing drug. Your veterinarian may administer a tranquilizer first to relax your pet. Following injection of the euthanasia drug, your pet will immediately become deeply and irreversibly unconscious as the drug stops brain function. Death is quick and painless. Your pet may move its legs or head or breathe deeply several ties after the drug is given, but these are reflexes and don’t mean that your pet is in pain or is suffering.

      How can I say goodbye?

      The act of saying goodbye is an important step in managing the natural and healthy feelings of grief and sorrow following the loss of a beloved friend and companion.

      Once the euthanasia decision has been made, you and other family members may want to say goodbye to your pet. A last evening with your pet at home or a visit to the pet at the hospital may be appropriate. Family members who want to be alone with the pet should be allowed to do so. Some pet owners choose to be present during their pet’s euthanasia, but others choose to say goodbye beforehand and not be present during euthanasia. This is a very personal decision and you should do what feels right for you. Do not let others pressure you into making a choice that makes you uncomfortable.

      How can I face the loss?

      After your pet has died, it is natural and normal to feel grief and sorrow. For some people, spending some time with their pet after euthanasia is helpful. The grieving process includes accepting the reality of your loss, accepting that the loss and accompanying feelings are painful, and adjusting to your new life that no longer includes your pet. By understanding the grieving process, you will be better prepared to manage your grief and to help others in the family who share this loss.

      Sometimes well-meaning family and friends may not realize how important your pet was to you or the intensity of your grief. Comments that make may seem cruel and uncaring although they were not meant to be taken that way. Be honest with yourself and others about how you feel. If you feel despair, talk to someone who will listen to your feelings about the loss of your pet. Talk about your sorrow, but also about the fun times you and your pet spent together, the activities you enjoyed, and the memories that are meaningful to you.

      The stages of grief

      There are many stages of grief, but not everyone experiences them all or in the same order. The stages include denial, anger, guilt, depression, acceptance, and resolution. The grief can seem to come in waves, may be brought on more intensely by a sight or sound that sparks your memory, and may seem overwhelming at times.

      Your first reaction may be denial—an unwillingness to accept the fact that your pet has died or that death is unavoidable. Denial may begin when you first learn the seriousness of your pet’s illness or injuries. Often, the more sudden the death, the more difficult the loss is to accept and the stronger the denial.

      Anger and guilt often follow denial. Your anger may be directed toward people you normally love and respect, including your family, friends, or your veterinarian. People coping with death will often say things that they do not really mean, unintentionally hurting those whom they do not mean to hurt. You may feel guilty or blame others for not recognizing the illness earlier, for not doing something sooner, for not being able to afford other types of or further treatment, or for being careless and allowing your pet to be injured.

      Depression is a common experience after the death of a special pet. The tears flow, there are knots in your stomach, and you feel drained of all your energy. Day-to-day tasks can seem impossible to perform and you may feel isolated and alone. Many depressed people will avoid the company of friends and family. It might be hard to get out of bed in the morning, especially if your morning routine involved caring for your pet’s needs. Sometimes you may even wonder if you can go on without your pet. The answer is yes, but there are times when special assistance may be helpful in dealing with your loss. If you are suffering from profound depression, seek professional assistance.

      Eventually, you will come to terms with your feelings. You can begin to accept your pet’s death. Resolution has occurred when you can remember your pet and your time with them without feeling the intense grief and emotional pain you previously felt. Acceptance and resolution do not mean that you no longer feel a sense of loss, just that you have come to terms with the fact that your pet has died.

      Even when you have reached resolution and acceptance, feelings of anger, denial, guilt, and depression may reappear. If this does happen, these feelings will usually be less intense, and with time, they will be replaced with fond memories.

      Although everyone experiences the stages of grief, grieving is always a very personal process. Some people take longer than others to come to terms with denial, anger, guilt, and depression, and each loss is different. If you understand that these are normal reactions, you will be better prepared to cope with your feelings and to help others face theirs. Family and friends should be reassured that sorrow and grief are normal and natural responses to death.

      If you or a family member have great difficulty in accepting your pet’s death and cannot resolve feelings of grief and sorrow, you may want to discuss these feelings with a person who is trained to understand the grieving process and can support and help you as you mourn your loss. Your veterinarian certainly understands the relationship you have lost and may be able to suggest support groups and hot lines, grief counselors, clergymen, social workers, physicians, or psychologists who can help.

      Remembering your pet

      The period from birth to old age is much shorter for most domestic animals than for people, and death is a normal part of the lifecycle. It cannot be avoided, but understanding and compassion can help you, your family, and your friends manage the grief associated with it.

      For some people, a memorial service or ritual (such as releasing balloons or spreading cremated remains) can be therapeutic. You may choose to keep and display reminders of your beloved pet. Such as photos or mementos or anything that helps you recall and treasure the good times you spent with them. You may also wish to make a memorial contribution to a charity in honor of your pet and the deep bond you shared. Just as the grieving process varies from person to person, so does the method of remembering the pet that shared your life.

      Should I get another pet?

      The death of a beloved pet can upset you emotionally, especially when euthanasia is involved. Some people may feel they would never want another pet. For some, the thought having—and eventually losing—another pet may seem unbearable. These feelings may pass with time. For others, a new pet may help them recover from their loss more quickly. Just as grief is a personal experience, the decision of when, if ever, to bring a new pet into your life is a personal one.

      If a family member is having difficulty accepting the pet’s death, getting a new pet before that person has resolved his or her grief may make them feel that you think the life of the deceased pet was unworthy of the grief that is still being felt. Family members should agree on the appropriate time to bring a new pet in to their lives. Although you can never replace the pet you lost, you can find another to share your life.

      Heartworm Disease.

      Heartworm disease is caused by Dirofilaria immitis, a parasitic worm that lives as an adult in the right side of the dog’s heart and large blood vessels leading to the lungs. Heartworms do most of the damage in the adult stage. Dogs are considered the definitive host for heartworms, however, heartworms may infect more than 30 species of animals (e.g., coyotes, foxes, wolves and other wild canids, domestic cats and wild felids, ferrets, sea lions, etc.) and humans as well. When a mosquito carrying infective heartworm larvae bites a dog and transmits the infection, the larvae grow, develop and migrate in the body over a period of several months to become sexually mature male and female worms. These reside in the heart, lungs and associated blood vessels. As mature adults, the worms mate and the females release their offspring (microfilariae) into the blood stream. Offspring can be detected in the blood (pre-patent period) about six to seven months after the infective larvae from the mosquito enter the dog. The male heartworms (four to six inches in length) and the females (10-12 inches) become fully grown about one year after infection, and their life span in dogs appears to average up to five to seven years.

      The onset and severity of disease in the dog is mainly a reflection of the number of adult heartworms present, the age of the infection and the level of activity of the dog. Dogs with higher numbers of worms are generally found to have more severe heart and lung disease changes. Until the number of mature heartworms exceeds 50 in a 25-kg dog, nearly all of the heartworms reside in the lower caudal pulmonary arteries. Higher numbers of heartworms result in their presence in the right chambers of the heart. In such infections, the most common early pathological changes caused by heartworms are due to inflammatory processes that occur in and around the arteries of the lower portion of the lungs in response to the presence of heartworms. Later, the heart may enlarge and become weakened due to an increased workload and congestive heart failure may occur. A very active dog (e.g., working dog) is more likely to develop severe disease with a relatively small number of heartworms than an inactive one (e.g., a lap dog or couch potato). Occasionally, a dog with a large number of heartworms may not only have worms in the heart, but also in the caudal vena cava between the liver and the heart. If the heartworms are not removed surgically, this syndrome causes sudden collapse and death within two to three days.

      Canine heartworm infection is widely distributed throughout the United States. Heartworm infection has been found in dogs native to all 50 states. All dogs, regardless of their age, sex, or habitat, are susceptible to heartworm infection. The highest infection rates (up to 45%) in dogs (not maintained on heartworm preventive) are observed within 150 miles of the Atlantic and Gulf coasts from the Gulf of Mexico to New Jersey and along the Mississippi River and its major tributaries. Other areas of the United States may have lower incidence rates (5% or less) of canine heartworm disease, while some regions have environmental, mosquito population and dog population factors that allow a higher local incidence of heartworm infection. Regions where heartworm disease is common have diagnosed infections in dogs as young as one year of age, with most areas diagnosing infections primarily between the ages of three and eight years. Although there are differences in frequency of infection for various groups of dogs, all dogs in all regions should be considered at risk, placed on prevention programs and frequently examined by a veterinarian.
      Heartworm disease may cause a combination of medical problems in the same dog including dysfunction of the lungs, heart, liver and kidneys. Signs of heartworm disease may occur within 6 months of infection or may not appear at all depending upon the number of adult worms that are present. In most cases, signs will begin within 1-2 years after infection. Typical signs include coughing, labored breathing, weakness, and tiring with exercise. Since the signs vary, the disease may be well advanced before the dog begins to show any problems, or signs may be mistaken for another problem. In advanced stages, the heart and lungs can be severely damaged. Eventually, heart failure can occur and the dog can die from damage cause by heartworms unless appropriate treatment is instituted. The disease may have an acute onset but usually begins with barely detectable signs resulting from a chronic infection and a combination of physiologic changes. Dogs with a low number of adult worms in the body that are not exercised strenuously may never have apparent signs of heartworm disease. However, in most dogs, the heart and lungs are the major organs affected by heartworms with varying degrees of clinical signs.

      Clinical Signs Associated with Canine Heartworm Disease:
          Early Infection- No abnormal clinical signs observed
          Mild Disease -Cough
          Moderate Disease -Cough, exercise intolerance, abnormal lung sounds
          Severe Disease- Cough, exercise intolerance, dyspnea (difficulty breathing), abnormal lung sounds, hepatomegaly (enlargement of the liver), syncope   (temporary loss of consciousness due to poor blood flow to the brain), ascites (fluid accumulation in the abdominal cavity), abnormal heart sounds, death

      DISEASE TRANSMISSION

      Heartworms are transmitted from dog to dog by mosquitoes. There are three stages in the development of heartworms in the dog.

      1. The adult female, living in the right side of the heart and/or major vessels to the lungs, produces immature worms called “microfilariae” that circulate in the blood stream. The microscopic microfilariae can live for up to 3 years.

      2. When a mosquito bites an infected dog, it takes in blood containing microfilariae. The microfilariae mature in the mosquito over a period of two weeks to become infective larvae.

      3. The mosquito, carrying infective larvae, deposits them in other dogs during blood meals. Larvae develop over 3-6 months and migrate to the right heart. Within 6 months, the larvae develop into adult heartworms that are responsible for the disease process in the heart and lungs. The adult heartworms can live up to 7 years. The adults produce microfilariae, hence completing the life cycle.

      To identify heartworm infection, a blood sample is taken from the dog. This test detects specific antigens primarily found in adult female heartworms and are used with much success to detect canine heartworm infection. Currently, tests are available as in-clinic tests as well as at many veterinary reference laboratories. Most commercial tests will accurately detect infections with one or more mature female heartworms that are at least seven or eight months old, but the tests generally do not detect infections of less than five months duration. The identification of the offspring (microfilaria) of heartworms from a blood sample indicates infection with adult heartworms. Identifying offspring can also be accomplished through either one of two concentration tests: the modified Knott’s test (a technique requiring spinning the blood sample in a mechanical device called a centrifuge) or a filter test. Practitioners will often do a quick examination of a blood smear to look for the presence of the offspring (microfilaria), but this procedure is not sensitive enough to rule out heartworms and only verifies the presence of an infection. Another parasitic infection of dogs that is capable of producing circulating microfilariae, detectable upon examination of the blood, is called Acanthocheilonema (Dipetalonema) reconditum. A reconditum is a non-disease-causing parasite that matures in the tissues beneath the skin of dogs. Its offspring can be differentiated from those produced by heartworms through microscopic examination evaluating size, shape and their movement.

      Radiographic abnormalities develop early in the course of the disease. Radiographs of the heart and lungs are the best tool available to evaluate the severity of the disease. Typical changes observed are enlargement of the following structures: right-side of the heart, main pulmonary artery, and pulmonary arteries in the lobes of the lung. Blunting and thickening of pulmonary arteries, along with tortuosity is often noted. Evidence of inflammation in the lung tissue that surrounds the pulmonary arteries is often found.

      The elimination of heartworms from your dog requires medication to kill the adult heartworms and microfilariae. Most dogs infected with heartworm can be successfully treated. The goal of treatment is to kill all adult worms with an adulticide and all microfilariae with a microfilaricide. It is important to try to accomplish this goal with a minimum of harmful effects from drugs and a tolerable degree of complications created by the dying heartworms. Heartworm infected dogs showing no signs or mild signs have a high success rate with treatment. Patients with evidence of more severe heartworm disease can be successfully treated, but the possibility of complications and mortality is greater. The presence of severe heartworm disease within a patient in addition to the presence of other life-threatening diseases may prevent treatment for heartworm infection.

      There is currently one drug approved by the FDA for use in dogs for the elimination of adult heartworms. This drug is an organic arsenical compound. Dogs receiving this drug therapy will typically have had a thorough pretreatment evaluation of its condition and will then be hospitalized during the administration of the drug. Melarsomine dihydrochloride (Immiticide®, Merial) has demonstrated a higher level of effectiveness and safety than any other adult heartworm treatment previously available. It is administered by deep intramuscular injection into the lumbar muscles. One injection is administered intramuscularly and then the dog returns for an additional injection 30 days later. Following treatment with an arsenical compound, the dog must be rested for 4-6 weeks, during which time the dead adult heartworms will slowly be reabsorbed. The primary post-adulticide complication is the development of severe pulmonary thromboembolism. Pulmonary thromboembolism results from the obstruction of blood flow through pulmonary arteries due to the presence of dead heartworms and lesions in the arteries and capillaries of the lungs. If heartworm adulticide treatment is effective, some degree of pulmonary thromboembolism will occur. When dead worms are numerous and arterial injury is severe, widespread obstruction of arteries can occur. Clinical signs most commonly observed include fever, cough, hemoptysis (blood in the sputum) and potentially sudden death. It is extremely important to not allow exercise in any dog being treated for heartworms. Often dogs with severe infections will also require the administration of anti-inflammatory doses of corticosteroids.

      The microfilariae must also be eliminated so the dog will not be a source of infection for other dogs. Elimination of the microfilariae is monitored by using blood tests that can easily identify microfilariae in the blood. The most effective drugs for this purpose are the macrocyclic lactone (ML) anthelmintics, i.e.,milbemycin oxime, selamectin, moxidectin and ivermectin. These drugs are the active ingredients in commonly used heartworm preventives. Although their usage as microfilaricides has not been approved by the FDA, they are widely used by veterinarians as there are no approved microfilaricidal drugs currently available. It is recommended that microfilariae positive dogs being treated with these macrocyclic lactones be hospitalized for at least eight hours following treatment for observation of possible adverse reactions, including those resulting from rapid death of the microfilariae. Circulating microfilariae usually can be eliminated within a few weeks by the administration of the ML-type drugs mentioned above. Today however, the most widely used microfilaricidal treatment is to simply administer ML preventives as usual, and the microfilariae will be cleared slowly over a period of about six to nine months. In some cases, not all microfilariae can be eliminated and the veterinarian may recommend retreatment of your dog for adult heartworms and microfilariae.

      While treatment of canine heartworm disease is usually successful, prevention of the disease is much safer and more economical. There are a variety of options for preventing heartworm infection, including daily and monthly tablets and chewables and/or monthly topicals. These products are extremely effective and when administered properly on a timely schedule, heartworm infection can be prevented. The American Heartworm Society is now recommending year-round prevention, even in seasonal areas. One reason for this is compliance – to make sure the medicine has been given properly by the pet owner. In addition, most monthly heartworm preventives have activity against intestinal parasites. Many of these same intestinal parasites that infect dogs can also infect people, with estimated infections occurring in three to six million people every year. So this added benefit of monthly deworming makes great sense.

      The products listed below are intended to be given on a monthly basis and are highly effective in preventing heartworm disease if given as directed.

      Ivermectin
      Ivermectin (Heartgard® & Heartgard® Plus by Merial, Iverhart® Plus & Iverhart MAX™ by Virbac and Tri-Heart® Plus by Schering-Plough) was the first in this family of drugs to be approved for preventing heartworm infection. An infection with larvae as long as two months prior to the initiation of ivermectin treatment will be blocked from development.

      Milbemycin
      Milbemycin oxime (Interceptor® & Sentinel® by Novartis) has benefits, which are similar to ivermectin.

      Selamectin
      Selamectin (Revolution® by Pfizer) is applied topically to prevent heartworm disease.

      Moxidectin
      Moxidectin (Advantage Multi™ by Bayer) is available in a topical formulation, in combination with a flea control product, imidacloprid. Moxidectin is also available as a six-month injectable product for dogs (ProHeart®6 (moxidectin) Sustained Release Injectable for Dogs, by Fort Dodge Animal Health).

      Flexural Tendon Contracture (Flexural Deformity) In Kittens.

      This condition is commonly called tendon contracture even though the tendons don’t actually contract. Rather, it is generally a soft tissue problem that involves the flexure tendons, the muscles, ligaments and joint capsules of the distal extremities.  If caught early, preferably at birth or within a day or two, there is a reasonable to excellent chance that the condition can be rectified with a combination of massage, physiotherapy (stretching/flexing the limb), warm compresses (to ease muscles which have locked into position) and by splinting (or very rarely pinning) the leg into the proper position. One thing that is certain is that the longer the elapsed time between birth and treatment of a twisted contracted limb, the less likely it is that the kitten will fully recover due to atrophy of nerves and muscles. This is particularly important in rescue work where a litter may not be found until the kittens are several weeks old or older. By that stage the twisted limbs may be beyond correction, or at the very least, require more extensive treatment and time to recover.

      Clinically, the kittens present as healthy animals with an inability to walk normally because their feet are twisted and contracted. In some longer standing cases the kittens are walking on the front of their ankles or wrists as their toes are pointed straight back. In this case, Oliver (“Twist”) presented as an older kitten with a long standing history of deformity. After a few months of physical therapy and corrective splinting (with a very patient, understanding and attentive mom) Oliver’s bilateral rear limb deformities were corrected and he has returned to normal function, as can be seen in the before and after photos as well as the video where he can be seen running and jumping and playing with his bro. With appropriate and consistent care and time, many of these kittens will do very well with physical therapy and splinting and can live out a normal happy and healthy life as fully active cats.

       

       

      TOXOPLASMOSIS AND PREGNANCY.

      Toxoplasmosis is an infection caused by the protozoan parasite Toxoplasma gondii that can threaten the health of an unborn child if a woman becomes infected with Toxoplasma for the first time while she is pregnant. The infection is usually contracted from handling soil or cat litter that contains cat feces infected with the parasite. Cats generally pick up these organisms when they hunt and eat infected prey. Healthy cats rarely get sick themselves from the parasite, but when they are infected for the first time, they can shed it in their feces. It can also be contracted from eating undercooked meat from animals infected with the parasite or from uncooked foods that have come in contact with contaminated meat. Cats excrete the pathogen in their feces for a number of weeks after contracting the disease, generally by eating an infected rodent. Even then, cat feces are not generally contagious for the first 1-3 days after excretion, after which the cyst matures and becomes potentially pathogenic. Studies have shown that only about 2% of cats are shedding oocysts at any one time, and that oocyst shedding does not recur even after repeated exposure to the parasite.

      With rare exception, women who have been infected at least 6 to 9 months before conception develop immunity to and do not pass it on to their baby. If you have been infected with Toxoplasma once, you usually will not become infected again.A positive antibody titer indicates previous exposure and immunity and largely ensures the unborn baby’s safety. A simple blood draw at the first pre-natal doctor visit can determine whether or not a woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to toxoplasmosis while pregnant, the baby is at particular risk. According to the Organization of Teratology Information Services (OTIS), when the mother gets infected between weeks 10-24 of pregnancy, the risk for severe problems in the newborn is about 5-6%. Effects on the baby include: premature birth, low birth weight, fever, jaundice, abnormalities of the retina, mental retardation, abnormal head size, convulsions, and brain calcification. During the 3rd trimester, a fetus has an increased risk of becoming infected, but the risk of damage to the fetus is decreased since most of the important development has already occurred.

      Now that you have an understanding of the risks involved if a pregnant woman is exposed to and subsequently contracts toxoplasmosis during the initial stages of her pregnancy, you can understand why I have a problem with the recommendations made by OB/GYNE doctors to their pregnant patients. Many of my clients schedule an office visit after learning of their pregnancy because they are scared to death that the family cat will cause the death or disfigurement of their unborn child and that they need to get rid of their cats while they were pregnant, or at the very least have their cat tested for toxoplasmosis. These recommendations drive me absolutely crazy! To recommend that a pregnant woman get rid of her cat(s) is taking the easy way out. It might take a bit of effort and time for a doctor to explain the real risks of toxoplasmosis and how to reduce them, but that is exactly what needs to be done to protect babies as well as prevent unnecessary suffering for mothers, families, and family pets.

      These are the facts:
      1. People become infected with toxoplasmosis when they inadvertently eat the parasite. The risk of contracting toxoplasmosis from ingesting cat feces is much lower than it is from handling and eating undercooked pork. So if doctors are going to counsel that pregnant women “get rid” of anything, it should actually be pork, not their pet cats.

      2. If anybody is going to be tested for toxoplasmosis, it should be the pregnant woman, not the cat. A cat will come up positive if it has been exposed to the parasite at any point in its life, but it only poses a risk if it is shedding the parasite in its feces, which generally occurs for a very short period. Therefore, a positive feline test is meaningless in this situation. Testing a pregnant woman, on the other hand, can be helpful. If her test is positive already, perfect. She has been infected in the past and even if she is exposed again during her pregnancy her unborn child will not be affected. If she is negative, then she should take precautions.Pregnant women can protect themselves and their babies from toxoplasmosis by following these simple rules:

      • Cook foods at safe temperatures and use a food thermometer to ensure that meat is cooked thoroughly.

      • Peel or thoroughly wash fruits and vegetables before eating.

      • Wash cutting boards, dishes, counters, utensils and hands with hot, soapy water after they have come in contact with raw foods.
      • Wear gloves when gardening and during any contact with soil or sand because it might contain cat feces. Wash hands thoroughly after coming in contact with soil or sand.


      • Avoid changing cat litter if possible. Better yet, get someone else in the household to change the litter box. If a pregnant woman does have to clean out the litter boxes, she should scoop them at least once daily. The parasite must spend 24 to 48 hours outside of the cat’s body before it is capable of causing an infection, so frequently cleaning the box will virtually eliminate the chances of disease transmission. If you must do it, wear gloves and wash your hands thoroughly afterward. Keep your cat inside and do not handle stray or adopted cats. Do not feed your cat raw or undercooked meats.

      In my experience, I have never had a client contract toxoplasmosis, let alone pass it on to their unborn child. In fact, I have never known a female veterinarian that tested positive for exposure to toxoplasmosis. These women have subsequently become pregnant and all have given birth to happy, healthy children, all the while continuing to work in a veterinary practice throughout the majority of their pregnancies. The risk of toxoplasmosis causing birth defects in an unborn child because there is a cat in the household is, therefore, tremendously overblown. While there is always a potential risk, following simple precautions and employing common sense should eliminate the fear that your pet cat is a danger to your unborn child.

       

      Prevention and Treatment of Rattlesnake Bites in Dogs.

      Rattlesnakes live in a variety of habitats, ranging from wetlands, deserts and forests, and from sea level to mountain elevations. Rattlesnakes are most active in warmer seasons, from Spring to Autumn. In southern latitudes (and here in Southern California) they are occasionally found year-round. Dogs are at risk for rattlesnake bites; in fact dogs are about 20 times more likely to be bitten by venomous snakes than people and are about 25 times more likely to die if bitten. Snake bites are life threatening, extremely painful, expensive to treat, and can cause permanent damage even when the dogs survive. Dogs can encounter a rattlesnake anytime they are in rattlesnake habitat. You and your dog may live in rattlesnake habitat, or perhaps you travel through or frequently visit places where rattlesnakes are found. Maybe rattlesnakes are around when you take your dog hiking, camping or hunting. Like people, dogs may stumble over the location of a snake by accident. Curiosity or a protective instinct can place your dog at risk. When dogs encounter snakes during play or work in the snake’s natural habitat, most bites tend to occur on the face or extremities. The rattlesnake bite is generally “hemotoxic” which means that it exerts its toxin by disrupting the integrity of the blood vessels. The swelling is often dramatic with up to 1/3 of the total blood circulation being lost into the tissues in a matter of hours. The toxin further disrupts normal blood clotting mechanisms leading to uncontrolled bleeding. This kind of blood loss induces shock and finally death. Facial bites are often more lethal as the swelling may occlude the throat or impair ability to breathe. Less than a decade ago, a dog unfortunate enough to be bitten by a large Western Diamondback rattlesnake and injected with a full load of venom faced a grim fate, particularly if it was more than a couple of hours away from medical help. Since its availability in 2003, the Red Rock Biologics rattlesnake vaccine has helped provide the best protection against poisonous snakes and has become the standard of preventive veterinary care for dogs at high risk for rattlesnake bites.

      The canine rattlesnake vaccine comprises venom components from Crotalus atrox (western diamondback). This vaccine is meant for use in healthy dogs to help decrease the severity of rattlesnake bites. The vaccine is produced from inactivated Crotalus atrox venom with an adjuvant and preservatives added. Dogs develop neutralizing antibody titers to C. atrox venom; the vaccine is specifically for the toxin of the Western Diamondback rattlesnake and provides the best protection against the venom of that particular rattlesnake, however the vaccine has been shown to provide cross protection against the venom of other types of rattlesnakes and copperheads since the venom of pit vipers share some of the same toxic components. In fact, most of the 15 species of rattlesnakes in the United States have fairly similar venom.  This is how one antivenin is able to cross-protect against so many rattlesnake species.  The protection afforded by the vaccine depends on the similarity of snake venoms to the Western Diamondback.

      The vaccine however does not provide protection against the Mojave rattlesnake, Eastern Diamondback rattlesnake, cottonmouths or coral snakes.

      The vaccine works by stimulating the dog’s immune system to produce antibodies against rattlesnake toxin. Initially, a dog should receive two subcutaneous doses about 30 days apart.  It is best to give vaccination boosters about 30 days before beginning of exposure to rattlesnakes. Protection peaks about 30 to 45 days after boosters and lasts about six months.  As the antibodies are short lived and the vaccine typically only provides protection for six months, a booster shot is necessary either once a year one month before “snake season” or twice a year in areas where rattlesnakes are year-round risks. The protection level that a dog receives from the vaccine depends upon how well that individual dog produces these specific antibodies and may vary. Protective antibodies made by your dog in response to the vaccine start neutralizing venom immediately. On average, antibody levels in recently vaccinated dogs are comparable to treatment with three vials of antivenin. Almost no vaccine is effective 100% of the time.  There are undoubtedly some dogs whose immune systems just won’t produce as many antibodies necessary for maximum protection but the partial protection they receive may still be enough to save their lives or help them recover more quickly. Therefore, this vaccine should not be used solely as a means of protection against rattlesnake bites. It is meant to provide some protection and to reduce the severity of the snakebite.  Adverse events are reported in far less than one percent of all vaccinated dogs.  Most of these side effects are mild and need no veterinary care.  The most common side effect is the development of an injection site cellulitis; these vaccine site reactions can be treated with hot, moist compresses, antibiotics, and pain relief medication if necessary.  Systemic reactions (typically flu like symptoms) are reported in fewer than one in 3,000 vaccinates and usually self-resolve in two to three days.

      Even good antibody protection can be overcome in special snakebite circumstances. A vaccinated dog’s resistance to rattlesnake venom can be overcome with enough venom or special circumstances.  But what are those circumstances?  Special snakebite circumstances include smaller dogs, larger snakes, multiple snake bites to the same dog, and bites near vital organs.  Smaller dogs are always going to have a harder time fighting off the same amount of venom as larger dogs.  Larger snakes can produce and deliver larger doses of venom in a single bite.  Multiple snake bites to the same dog can naturally deliver larger quantities of venom.  Bites near vital organs allow the venom to start destroying those organs before the antibodies in the dog’s blood plasma have time to find and neutralize the harmful proteins in the rattlesnake venom.  Other special circumstances may include some dogs whose immune systems just don’t produce enough antibodies, intravenous bites, and some snake species that the vaccine has little or no protection against.

      The reported benefits of vaccination include a delay in onset of symptoms, fewer symptoms, less severe symptoms, a decrease in mortality rate, faster recovery times, and little or no tissue necrosis.  In addition, most veterinarians also report less painful dogs, less lethargy, less swelling, that the swelling progression typically reversed within the first 1 to 2 hours, and that dogs had full recoveries in about 24 to 48 hours. As mentioned previously, according to Red Rock Biologics, the manufacturers of the rattlesnake vaccine, the antibody levels in recently vaccinated dogs are comparable to treatment with three vials of antivenin. So, although canines still need emergency veterinary treatment, they should experience less pain and a reduced risk of permanent injury from the rattlesnake bite. Snakebites are always an emergency. Even if your dog is vaccinated against rattlesnake venom, always get the pet to a veterinarian as soon as possible following any snakebite. Even non-venomous snake bites can lead to serious infections and antibiotic treatment may be needed. A veterinarian can determine what additional treatment is needed.

      Since the most common mechanism of death from rattlesnake bite is circulatory collapse, intravenous fluid support, antibiotic therapy, cardiac and blood pressure monitoring, antihistamine administration and pain management are very important.  Fluids may be started at a relatively slow rate if the patient is stable but should signs of impending trouble occur, circulatory volume replacement and treatment for shock is indicated. Blood transfusion may be necessary if life-threatening blood loss has occurred. A minimum of twenty four hours of post-bite observation and hospitalization is prudent. In addition, treatment of snakebite should include antivenin administration. There are numerous misconceptions about antivenin. The first is simply the name of the product. It is not “anti-venom.” It is not a single injection that provides the antidote to snake bite venom. Antivenin is a biological product consisting of antibodies made in response to exposure to four common Crotaline venoms. The antibody serum is reconstituted into an intravenous drip that is run into the patient over at least 30 minutes or so. Antivenin is expensive (at least $600-$800 per vial) and a large dog with a severe bite is likely to require several vials. Antivenin is very helpful in the inactivation of snake venom but there is a narrow window during which it must be used. After about 4 hours post-bite, antivenin is less effective in countering the effects of snake venom.

      In summary, rattlesnake envenomation is a serious life threatening injury and immediate veterinary care is warranted for the best success rates in surviving the ordeal. The benefits of prophylactic vaccination include more time to get to a veterinary hospital, the reduction in the amount of pain and swelling experienced, faster recovery times, and a decrease in the mortality rate. It is not meant as a sole means of protection. Emergency treatment consisting of intravenous fluid support, antibiotic administration, antihistamines, pain management and antivenin will result in the best chance of successfully surviving a rattlesnake bite.

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      FLEA CONTROL.

      Anyone who has ever battled fleas knows how difficult they are to eradicate. Once a home becomes infested, control can be difficult, time-consuming and expensive. A flea-infested dog or cat can introduce hundreds of new flea eggs into the home each day. By mid- to late summer, pet owners often find themselves fighting a losing battle against established flea populations that are enormous. In Southern California, where I practice, it is a year-round concern.

      To effectively control fleas, it is necessary to understand their life cycle and habits. The best way to manage fleas is through prevention. By taking action before fleas are abundant, pet owners can avoid severe infestations later in the season. Preventive flea control has been made possible by new product innovations and insights into flea biology. We now know that adult fleas (the biting stage) spend virtually their entire life on the pet, not in the carpet. Eggs are laid on the fur and fall off into carpeting, beneath furniture cushions, and wherever else the pet lays, sleeps or spends time. After hatching, the eggs transform into larvae, pupae, and eventually adults to renew the cycle. Pet owners can break the cycle of flea development and prevent future generations by killing the eggs as they are laid on the pet, or by eliminating the egg-laying adults. The easiest way to do this is to take action before flea problems get out of control. Below is a quick summary of the most important aspects of the flea lifecycle.

      •  Adult flea—lives on the host animal (dog or cat), where the female lays her eggs

      •  Egg—flea eggs are laid on the host animal but fall off into the bedding, carpeting, and elsewhere in the animal’s environment. These pearly white eggs are barely visible to the naked eye and are usually impossible to find without a magnifying lens. Flea eggs hatch into larvae in 1–10 days, depending on the temperature and humidity; the warmer and more humid, the more rapidly the eggs hatch

      •  Larva—flea larvae feed on organic material in the environment and on the droppings from adult fleas. They are sensitive to sunlight and to drying, so inside the house the larvae prefer deep carpet, bedding, and cracks in the floor boards. Outside the house, the larvae prefer shaded areas that have plenty of organic material (grass, leaves, etc.) or moist, sheltered soil. As the larvae feed on adult flea droppings, they are found in highest numbers in areas where flea-infested animals spend much of their time

      •  Pupa—after 5–11 days, the larvae produce a fine cocoon in which they complete their development. During this stage of their life cycle, fleas are resistant to insecticides. In ideal conditions, adult fleas hatch from their cocoon in as little as 5 days, although fleas can survive in the pupated form for up to 5 months. Hatching is stimulated by vibration, physical pressure, heat, and carbon dioxide; in other words, the presence of a potential host animal.


      Immediately after hatching from its cocoon, the adult flea seeks out a host animal. It must have a meal of blood within a few days in order to survive and produce eggs. Within 2 days of her first blood meal, the female flea begins producing eggs. Fleas can continue to produce eggs for up to 100 days. A single flea can produce thousands of eggs.

      Fleas feeding on your dog can cause several problems.  Most dogs will itch and scratch at the flea bite—in most dogs, the itching is mild and temporary, however, some dogs become allergic to flea saliva and develop severe itching, hair loss, and skin damage from scratching and biting at the site and the body in general. If left untreated, significant skin infections can develop. As fleas are an essential part of the tapeworm’s life cycle, dogs are commonly infested with tapeworms when they swallow fleas that contain the immature tapeworm stages. Finally, flea bite anemia can occur with severe flea infestations because of the significant blood loss associated with large numbers of fleas feeding on the host. This usually occurs only in young, sick, debilitated, or neglected animals.  It is easy to tell when a dog is heavily infested with fleas, as you can see the fleas crawling over the dog’s skin and through the hair. If your dog has only a light infestation, you may not see any fleas unless you look for them. A common place to see fleas is on your dog’s belly and the inside of the thighs, where the hair is thin or the skin is bare. Another place to look is in the dense hair over your dog’s rump, especially near the base of the tail. Part the hair and inspect the skin for either fleas or flea dirt. Flea dirt is actually flea droppings. It looks like black grains of sand or cracked pepper on the dog’s skin. If you place a few particles of flea dirt on a white surface (e.g. a piece of paper) and wet them, you will see a reddish brown stain form. This is because the flea droppings contain digested blood from the flea’s blood meal. You may also notice tiny areas of dried blood on the dog’s bedding from moistened flea dirt that has since dried.


      Going by the common precautionary statements on many readily available dog flea and tick treatment products, it sure seems that these products would be or could be harmful to us. So it may make you wonder what these products will do to your dog when you apply it to them. There are countless stories of dogs or cats that have suffered some ill effects from the use of these products which further add to the controversy as to whether it is indeed safe to use them on pets. That’s also precisely the reason why more dog owners are looking towards natural flea control for their dog. Unfortunately, natural remedies are universally unsuccessful in eradicating significant flea populations.  They’re free of hormones and insecticides. They’re reasonably priced. They’re guaranteed. They’re safe. THEY’RE INEFFECTIVE AND A WASTE OF TIME AND MONEY. I’ve been a veterinarian for over thirty years and I’ve heard all the stories of how natural remedies such as garlic, tea tree oil, eucalyptus, fennel, rosemary, rue, wormwood, lemon grass, citronella, neem, lavender, yellow dock etc protect your dogs from fleas. I’ve dealt with numerous clients who convinced themselves that these products helped control their pet’s flea related problems and who were in total denial.  I’ve seen the utilization of flea baths, flea dips, flea powder and flea collars result in toxic reactions or the death of pets because they were used without the guidance of a veterinarian’s advice. The most common mistake regarding these products is all too often the “more is better” approach that some people take when using flea products. More is NOT better when it comes to chemicals or
      medications!  I remember going to The World’s Fair in NYC in 1964 and visiting the DuPont exhibit. Their slogan was “Better Living Through Chemistry.” Probably a bit of
      an over statement. Now, before you think I believe in the utilization of chemical warfare, since the availability of topical flea products such as Advantage, Frontline, Revolution, and Vectra, severe, relentless flea related problems have almost become a thing of the past.


      Personally, I have not seen one animal get sick let alone die from the appropriate utilization of these products. I have, however, seen more patients die from flea infestation than from all of the above flea control products combined. Fleas cause skin disease and contribute to autoimmune disease in cats and dogs. They spread tapeworms and are vectors for infectious maladies ranging from cat scratch fever to bubonic plague.


      Flea Control Recommendations

      For the flea allergic patient, continuous excellent flea control is required to remain symptom free. Even very minimal exposure may be sufficient to perpetuate itching in a hypersensitive patient. In the past, veterinarians and pet owners always had to try to control fleas by treating the environment of the animal for the immature stages of the flea. This approach, although effective when properly instituted, is labor intensive and requires frequent repetitive applications. Also, some of the older products made for killing fleas on our pets do not kill fleas instantly or are not long lasting enough to really help flea allergy patients, because the female fleas survived long enough to lay a few eggs and perpetuate the life cycle.

      Today’s Flea Control Products
      Today, veterinarians have great flea control products that are highly efficacious, long lasting and very safe to choose from amongst. Many of these products treat more than just fleas so that there are products that can be utilized for any one of a number of situations depending upon your pet’s exposure risks. Several products are available which are convenient and effective. 

      Sentinel® (Lufenuron) from Novartis
      These prescription drugs are available as a once a month flavored chewable (soy and pork) pill or oral liquid suspension to be given with a full meal. Female fleas that feed on pets treated with lufenuron produce sterile eggs. The product does not kill adult fleas. It is a very easy way to break the life cycle but pets remain fully susceptible to the emergence of any fleas from pupa already present in the environment. Therefore, 4 to 7 months may pass before the flea free state is reached. In order to stop the life cycle, every animal in the patient’s environment must receive lufenuron or another insect growth regulator.

      Nylar® (Pyriproxifen)
      This is a relatively new insect growth regulator that is extremely effective against flea eggs. It remains 100% effective for 150 days after a single spray application! It is presently available as a spray on and as a drip on in combination with permethrin for dogs and a spray with pyrethrins for cats and is included in the new product line, Vectra®. Environmental foggers and sprays are also being marketed and many professionals use this chemical for home treatments.

      Advantage® (imidacloprid), K9 Advantix® (with permethrin), Advantage Multi® (with moxidectin) from Bayer
      These products are available as topicals for either dogs or cats. Advantage Multi® is a prescription drug that also is a heartworm preventive. Advantage® seems to be very well tolerated by sensitive cats. It provides flea knockdown in about 8 hours. 100% killing can be maintained for at least two weeks. It is susceptible to wash off, therefore outdoor active dogs and dogs that swim or that must be bathed because of dermatitis must be re treated frequently. (Weekly re treatment is allowed with Advantage only®). Imidacloprid has no efficacy against ticks, but K-9Advantix®, with permethrin does. K9 Advantix is only labeled for once a month, and ONLY FOR DOGS.

      Frontline® Spray, Frontline Plus® and Frontline Top Spot® (fipronil) from Merial

      Fipronil is a broad spectrum insecticide available as a spray or a drip-on. Fipronil binds chemically to the hair and is absorbed through the hair follicle by the sebaceous glands. In spray formulation fipronil may kill fleas at 95% for up to 30 days after application on dogs and stands up to biweekly bathing. It is labeled for puppies and kittens of 8 weeks (10 weeks for Top Spot®). It is also affective against ticks. The major problem with the spray is the high volume of alcohol based product that must be applied. Many cats will show minor adverse reactions with this application technique. The product is labeled to be applied no more than once a month. Frontline Plus® contains the insect growth regulator, S-methoprene and so provides control of eggs and adult fleas.

      Revolution® (selamectin) from Pfizer
      This prescription drug is designed as a once-a-month heartworm preventive and flea preventive for dogs and cats as young as 6 weeks old.  It also kills adult fleas and can be used to treat sarcoptic mange, ear mites and ticks.  It also helps control roundworms and hookworms in cats. The product is placed on the skin at the back of the neck, but is absorbed into the body to have its effect when female fleas ingest it with a blood meal.  Adult fleas will die slowly, but more importantly, female fleas stop egg production as soon as they are exposed. It is most useful as a preventive for flea infestation and in the presence of a flea problem in an allergic pet, but it is an excellent flea control product for cats.

      Capstar® (nitenpyram) from Novartis
      This is a prescription tablet for dogs and cats as young as 4 weeks of age.  It offers extremely rapid and complete killing of adult fleas on the pets after administration.  It is safe enough that the tablets may be used as needed, as often as once per day, whenever you see fleas on your pet.  This is designed to be used in combination with an insect growth regulator to knock out fleas when these slower products are being used for long-term control.  It can also be used when the pet has visited a flea-infested environment for rapid protection. When given every-other-day, it is a useful flea control for single cat households.


      Comfortis ®for Dogs (spinosad) from Elanco Animal Health Division of Eli Lilly

      This monthly prescription tablet for fleas represents a completely new class of drugs in flea control.  It is available for use on puppies and dogs 14 weeks of age or older and is available in 5 different sized flavored (soy and pork) chewable tablets. It is meant to be used once a month and preliminary results show it will be very useful for flea allergic pets as it has a rapid kill rate.

      Vectra 3-D for Dogs® (dinotefuran, permethrin, pyriproxifen) from Summit Vet Pharm
      This product is a monthly topical application for flea, tick and mosquito control with an insect growth regulator.  It provides long-lasting repellent, and is a fast acting adult flea killer that also provides control for the egg stage of the flea for at least 30 days. 

      Permethrin is added to provide tick control and as a repellant. Pyriproxifen (Nylar) is added for flea egg control (See above.)  Water and shampooing lowers efficacy after 14 days. Do not use on cats (because of the high concentration of permethrin). This product is fast-acting and should be very useful for households with flea allergy patients.

      Vectra for Cats® (dinotefuran, pyriproxifen) from Summit Vet Pharm

      This product is not on market currently, but soon to be introduced.


      As you can see, there are numerous products that are available to very effectively prevent and/or control your pet’s flea problem. These products differ in their ability to also control ticks, mosquitoes, heartworm disease, sarcoptic mange, ear mites, and internal parasites such as hookworms and roundworms. For these reasons, there is no one “best” product for every pet. Which one is best for you and your pet depends upon the region of the country in which you reside as this has a profound effect of your pet’s risk of exposure to these parasites. Similarly, it is important as to whether or not your pet spends significant amounts of time outdoors, goes to the dog park or doggie daycare, or is boarded frequently. In these situations, your pet is at greater risk for communicable parasitic problems. Speaking with your veterinarian and telling him or her what type of exposure risks your pet may have will enable you to decide which of these excellent products is most appropriate to not only control fleas, but to also control a variety of other parasitic issues.

       

      Spay/Neuter.

      As a veterinary specialist practicing in Los Angeles for the last twenty-five years, I have had a tremendous opportunity to work with the overwhelming majority of rescue groups here in the Los Angeles area.  I have consistently donated time and effort to rehabilitating animals saved from the shelters for these groups in order for them to be rehabilitated and placed with new families.

      The ability to save an animal from certain death and place them in a loving home is extremely rewarding.  Working with these groups to provide tremendously discounted services to achieve these results is a way of giving back to the community.  It affords me the opportunity to provide top quality veterinary medical and surgical care to animals that would otherwise be unable to take advantage of the fact that such veterinary care now exists in the majority of our communities.

      While certainly a rewarding experience, I believe that every veterinarian would love to see the day when their services were no longer called upon to help save unwanted pets as a result of the pet over-population problem.  California State bill AB1634 tries to address the problem with pet over-population in an attempt to decrease the influx of animals into our shelter system.

      While well intentioned – this bill as it currently stands is not without its flaws and is controversial and divisive.  The past twenty-five years of my practice experience indicates that there is no one simple and easy answer to the elimination of pets being relinquished at our shelters.  Certainly, the appropriate spaying and neutering of pets is a great place to start.  It is just that it is not the complete answer for the elimination of our shelter over-crowding.

      The issue to how best to solve the pet over population problem is an extremely controversial topic.  The controversy stems from the fact that there are hundreds of thousands to millions of animals euthanized in the State of California alone during the course of one year. A controversial bill known as AB1634 is set for hearing in the California State Assembly Committee on business and professions and is designed to cut the numbers of animals entering the California shelter system on a yearly basis. 

      The question is whether or not government forced mandatory spay and neutering of dogs and cats older than four months of age will actually solve the pet over population problem.  In order to successfully understand why mandatory spay and neuter is not necessarily the answer to the current pet over population problem – one needs to have a detailed understanding of the factors which led to pets arriving at the shelter system in the first place.

      The reality of the situation is that an extraordinary number of pet owners are extremely responsible with regards to the welfare of their pets.  Their pets are being cared for emotionally and medically and are not breeding indiscriminately if they’re even breeding at all.  That’s because the overwhelming majority of pet owners already spay and neuter their pets without undue government interference. 

      It is a small proportion of pet owners predominantly the indigents that do not avail themselves to even appropriately priced spay and neuter procedures from licensed veterinarians.  These owners don’t even pretend to be responsible enough to bring their animals in for even the most routine of veterinary services (i.e. routine physical examinations, deworming, vaccinations, spay and neuter etc.)  As such – the veterinary community has limited ability to educate this portion of the pet owning public, because of a lack of contact at any point in time with their pets.  The great majority of animals that end up in our shelter system, unfortunately, are derived from this small portion of the pet owning public. 

      If simply spaying or neutering your pet was the solution to the over-crowding of the pet shelter system – it would have worked already!  The top ten reasons dogs are relinquished to shelters in the United States are: moving, landlord issues, cost of pet maintenance, no time for the pet, inadequate facilities, too many pets in the home, pet illness, personal problems, biting or no homes for the litter-mates.  Of these top ten reasons, only two (i.e. too may pets in the home and no homes for litter-mates) would be directly influenced by a mandatory spay/neuter provision. These reasons rank sixth and tenth respectively on the top ten list.

      It would appear that the overwhelming majority of the time that pets are relinquished to the shelters is because of the owners inability’s to properly care for their pet – not primarily because they have too many.  While decreasing the amount of pets these people own will certainly have an impact, by no means is mandatory spay/neuter alone going to impact tremendously the amount of animals being relinquished to the shelter.

      In Los Angeles, one could already feel the effects of low cost spay/neuter programs aimed at indigent owners having an effect. There have been a tremendous decrease in the amount of puppies being presented to the shelter because of the success at these out-reach programs going into areas of the city requiring assistance and spaying and neutering pets for free.  An expansion of these services would play an enormous role in decreasing an unwanted pet population entering the shelter system, but as we can see from the top ten list of why these animals end up in the shelter – it is not going to even come close to eliminating animals being relinquished and still crowding our shelter system.

      As we have seen in Los Angeles over the last few years, the number of puppies entering the system decrease – we have also seen a tremendous rise in the number of animals entering the system that have already been spayed and neutered for just these reasons. Unfortunately, whether spayed or neutered, the majority of animals enter the shelter system because a certain portion of the pet owning population considers their pets to be disposable!

      I see multiple cases every week where people adopt animals from the shelter and bring them in when they’re sick or injured.  As soon as they realize that they are financially responsible for taking care of the injury or illness – they relinquish the pet.  Instead of humanely putting the animal down, we have the owners sign over ownership to our facility so that we could rehabilitate them medically and surgically and working with the rescue groups here in Los Angeles, adopt them out to proper owners who will see to these animals emotional and medical needs. These people turn right around and go back to the shelter to adopt yet another animal!  It makes the shelter adoption records look great, because they’re moving that many more animals through their system successfully rather then humanely euthanizing them. 

      However, the reality is that animals are consistently being given out to a portion of the population that does not have the financial or emotional capacity to properly take care of the pets that have been relinquished to them.  It has nothing to do with whether or not the animal was spayed or neutered – it has to do with the mindset of the person that adopted the animal in the first place.

      I firmly believe that pet ownership is a privilege and no longer an inherent right in the United States.  While extraordinarily difficult to legislate let alone enforce responsible pet ownership is the only way to diminish or eliminate the relinquishment of animals into our shelter system.  The enactment of a mandatory spay/neuter provision will enable those low cost to no cost spay/neuter clinics operating in the portions of our city that produce the overwhelming majority of unwanted pets to reach a greater population of indigent owners than previously thought possible. 

      Because it will be the law – these clinics should be afforded a much better opportunity to convince these owners that their animals have to be spayed and neutered.  This should certainly decrease the amount of animals in these areas that would eventually for the multitude of reasons already mentioned eventually ending up in our shelter system.  However, it is not enough of an answer to stop the relinquishment of pets into our shelter system.  This bill should not be looked at as the answer to pet over-population, but merely as a first step in helping to prevent unwanted pets from being relinquished.

      Much more work needs to be done with enforcing animal welfare guidelines that are already in place with respect to the care and treatment that animals receive.  If the already pre-existing animal welfare statutes were actually enforced rather than giving violators a mere slap on the wrist – the number of inappropriate pet owners would be substantially slashed leading to a much greater reduction in the amount of animals entering our shelter system than could possibly be accomplished by spay and neuter alone.

      I certainly have my concerns with regards to undue government influence regarding decisions that have always been within the domain of the pet owner.  What the majority of pet owners must understand, however, is that because they are responsible, the passage of this bill should have virtually zero impact on their ability to own animals appropriately. 

      The plain fact is that if all people acted responsibly – we wouldn’t need laws.  One could make an analogy with regards to laws regarding rape, child molestation and shooting a police officer.  Ninety-nine percent of the population doesn’t really need these laws in place because nobody in their right mind would think of raping somebody, molesting a child or shooting a police officer.  Unfortunately,  a very small percentage does not act responsibly and for that reason laws are required in order to be able to enforce the standards that society has deemed appropriate.  It’s the same thing with the passage of this mandatory spay/neuter bill.  The overwhelming majority of pet owners are already in compliance, it is the very small percentage that is responsible for a portion of the reason why animals are relinquished to the shelters.

      I do have a problem with responsible pet owners being forced by government decree to spay and neuter their pet, considering that they are truly not a part of the problem.  In its present form this bill needs to be tweaked to reflect this concern.  Currently, the legislative language bans California State residents from owning an intact dog or cat more than four months old without a permit.  While early age spay and neuter certainly results in a decrease in the pet population, it also results in a number of unnecessary risks to your pet and I have a hard time reconciling the fact that responsible pet owners should subject their animals to any risk, whatsoever, considering they are not a part of the pet over-population problem. 

      Exemptions would be offered to breeders who would pay a permit fee to continue to be able to keep intact animals and breed them.  Certainly, the concern is that breeders who have intact animals should somehow be responsible for funding animal control.  A situation which many feel is extremely unfair.

      The truth of the matter also is that very, very few purebred animals end up in the shelter in the first place.  The majority of the purebreds that end up in the shelter are of a very few and specific breed types and the majority if not almost all of these purebreds are being bred indiscriminately by inappropriate backyard breeders.  Very few purebred Labrador and Golden Retrievers costing upwards of twenty-five hundred to three thousand dollars end up being relinquished to the shelter.  If they end up there at all, they do so because they temporarily escaped from their owner.  These owners are usually scouring the shelter for their animals immediately and very few if any ever getting euthanized or burdening our shelter system for more than a short period of time.

      Ask any shelter rescue group in Los Angeles and they will tell you that the majority of purebred animals crowding our shelter system are Pitbulls, Shar-peis, Chows and Rottweilers.  Most of which were given away or sold for incredibly small amounts of money at local backyard breeders in the area.  As deplorable as puppy mills are – it is not even these animals that are entering the shelter system.  The granting of permits at a price to appropriate reputable breeders to continue to breed animals will certainly generate revenue for the State, but will probably not result in any type of substantial decrease of animals being relinquished to the shelter, because these animals are not the ones crowding the shelters in the first place.

      Considering the overwhelming majority of responsible pet owners already spay and neuter their pets – the likelihood of there being substantial revenue of fines for violating the spay/neuter provision is not that great.  The sad truth of the matter is that the overwhelming majority of the violators of the spay/neuter provision are the poor and indigent pet owners who cannot afford to take care of their pets appropriately in the first place.

      An increased effort must be made to allow an expansion of the already existing low or no cost spay/neuter clinics to operate in these areas more effectively, in order to make sure that the population of pet owners is in compliance.  As mentioned previously, this will certainly have an impact on the number of animals presented to the shelter for euthanasia, but by no means will this eliminate the vast majority of animals presented to the shelters for relinquishment. 

      Once again, there is almost a national absence of puppies in the shelter systems at present, this has been accomplished through education and low and no cost spay/neuter clinics going to the areas of greatest concern and operating without the government being involved.  Until a certain portion of the population could be convinced that it is inappropriate for them to own animals in the first place – we will never empty our shelter system.  As long as this bill could be tweaked to protect the rights of responsible pet owners – the advantages far out-weight the disadvantages of its passage.

      Urogenital Surgery.

      Article coming soon.

      Arthrodesis.

      Article coming soon.

      Gallbladder Surgery.

      Article coming soon.

      Gastro-intestinal Surgery.

      Article coming soon.

      Using the Power of Positive Control.

      Your puppy may start off playful and easygoing, but as she matures she may become more difficult to control. Since dog breeds have been selected over many generations for specific characteristics (physical and behavioral), and since much of a dog’s behavior comes from the genes of the parents, researching the breed and meeting the parents or siblings can help you to get a better idea of what your dog might be like as an adult. While genetics plays an important role, how you handle, train, and communicate with your puppy is also critical in shaping adult behavior.

      It is important to learn how to communicate with your new puppy and meet all of her behavioral needs. Training should start as soon as you bring your puppy home. Begin by rewarding your dog only for behaviors that are desirable while preventing behaviors that are undesirable. Consistency is critical, so make sure all family members are on the same page. Otherwise, you may soon find that you are losing control as your dog becomes increasingly unruly and no longer responds to your commands. Early experiences should include learning positive ways to make handling enjoyable and teaching your dog to give up food and toys for even more valuable rewards in order to eliminate possessive and guarding behavior. This should help to prevent problems with handling and possessive aggression.

      Taking Control, Ensuring Success

      Set up your household to ensure success. When you cannot watch your puppy, house her in a safe area where she cannot do harm to herself or to your household. When you are with your puppy, training and control can be achieved by rewarding behaviors or interrupting those that are undesirable. Keeping your puppy on a leash will help prevent her from getting into trouble and will also provide you with a means of controlling unruly and undesirable behaviors and guiding her to what is desirable. For better head control, you can attach the leash to a head halter

      Reward-based techniques, such as giving your puppy food, favored toys, and praise when she displays good behavior, are the best ways to train. By giving rewards consistently, immediately, and predictably, your puppy can quickly learn which behaviors are acceptable and which are not. Avoid physical punishment, scolding, leash corrections, or pinning the dog down, as they can lead to fearful, defensive, and even aggressive reactions. Visit http://www.avsabonline.org for the American Veterinary Society of Animal Behavior’s position statements on punishment and training.

      Problems often begin with normal behaviors that get out of control. Examples are pulling against the leash on walks, jumping up during greetings, play biting, and barking for attention. As soon as your puppy begins to exhibit undesirable, demanding, or overly exuberant behavior, you should ignore her so you do not encourage the behavior. For dogs that jump on you to greet you, try a verbal command such as “quit” or “off,” but do not give your puppy any attention until the behavior ceases. If your dog has been trained, an even better choice is to use one of the commands such as “sit,” “down,” or “go to your bed” (or crate or room) to teach your dog a more desirable greeting behavior, which you can then reward. Keeping a leash and head halter attached anytime problems might arise is an effective means of immediately interrupting undesirable behavior and teaching your puppy how to act appropriately.

      Handling Your Hound

      Throughout your dog’s life, you will need to handle or lift her, bather or groom her, brush her teeth, clean in or around her ears and eyes, and trim her nails. These interactions can elicit fear and possibly aggression from some dogs that are not used to them. Gentle, positive handling exercises can prevent these types of problems from emerging. Begin at times when your puppy is calmest, such as after a walk or dinner, starting at a level she will accept. Give your dog tasty treats while gently handling her. Puppies that are headstrong or fearful may struggle and resist. Should this happen, you will need to gradually overcome any resistance by proceeding slowly and using rewards such as food to turn the situation into one that is enjoyable. Always end the session on a positive note and use this as a starting point for your next session. Never force the puppy to a point where you cause fear, struggling, or aggression. If you identify resistance or threats, seek the guidance of your veterinarian.

      “Drop it”

      Possessive behavior or guarding of food, toys, or stolen items is related to how strongly your dog wants to keep what she has. It is not related to how she feels about you. Should your puppy display any aggression, seek immediate guidance from your veterinarian. To help prevent guarding, the first step is to teach the puppy to give up objects for rewards of higher value. Begin with a toy that is of minimal appeal and teach your dog to give it you by trading it for a tasty piece of kibble. Initially, you should present the food and say “drop it” while the dog has the object in his mouth. Each time thereafter, do not show the food when you say “drop it,” and give it to your dog only after she drops the object. Once she reliably drops objects on command for food, switch to intermittent food reinforcement (offer praise each time and food only occasionally). After the pet willingly gives up toys of minimal appeal, progress to practicing the “drop” command with toys that are more attractive to her and tastier treats as rewards. Clicker training (a clicking sound is associated with a food reward) can also be a very effective way to reward your dog for dropping. Simply monitor your dog closely until she drops the object and then immediately click and reward the behavior.


      Mealtime

      Although it’s best not to bother a dog during meals, it is important that the dog does not feel threatened when family members are around. To this end, have your dog site while you prepare her food and place it on the floor. Then call your dog to come and eat. During feeding approach your dog once or twice, interrupt her with a “sit” or “come” command, then lift up the food bowl, put a special treat in the bowl, and give it back. Another exercise is to have your dog sit, place about 10 percent of her meal in her bowl, and have her come and eat. As soon as she is finished, have your dog sit, then pick up the bowl and add another 10 percent. Repeat, and occasionally add a special treat, until your pup eats all the food. To reduce any threat the dog might feel when people come near her while she is eating, occasionally drop a special treat into the bowl as you walk by. If your dog shows any threat, consult your veterinarian. Never punish a puppy for growling while at her dinner bowl.

      Who’s Tugging Whom?

      Tug can be a fun game to play, but only if it does not escalate into unruly or aggressive behavior. Teach your dog to sit or lie down before the game begins and be certain that you can stop the game without problems. Practice a “drop” or “give” command during the tug game, then give a treat and resume play. When the game is done, either take the toy away and give a final treat or leave the toy with the dog (as long as she doesn’t damage the toy or become aggressive).

      Even with the best of efforts, problems may arise. If you are having difficulty training your puppy or controlling unruly behavior or aggression, contract your veterinarian.

      Understanding Behavior Changes in Aging Pets.

      As pets get older, they may develop new, undesirable behaviors. This can be caused by changes in the household, stress, or the effects of disease and aging on virtually any organ of the body, including the brain. Changes in eating, elimination habits, sleep habits, and activity levels might be the first signs of an emerging health problem. In fact, behavioral changes may be the first or only sign of medical conditions such as pain, a decline in sensory or organ function, endocrine diseases, or brain aging. Based on AAHA (American Animal Hospital Association) and AAFP (American Association of Feline Practitioners) senior care guidelines, most dogs are considered middle-aged or mature at 7 to 8 years of age (perhaps 4 years for large breeds), and senior at 10 to 11 years of age (perhaps 6 years for large breeds); cats are middle-aged at 7 to 10 years and senior at 11 to 14 years.

      Health Care for Older Pets

      Giving a little extra attention to senior pets’ health care may help them live longer, healthier lives. It is critical to identify and report any changes in the health or behavior of senior pets to your veterinarian immediately. Your veterinarian will also work to detect any emerging problems during health-care visits, through a physical examination and blood and urine screening tests, which can help detect abnormalities even before there are noticeable physical signs of disease. Since pets age much more quickly than humans, senior pets require more frequent health-care visits.

      The good news is that a wide range of therapeutic options are now available—from special diets that can slow the decline of problems such as renal failure or brain aging, to drugs that control medical problems such as thyroid disease, diabetes, and arthritis. Early diagnosis and intervention allow your veterinarian to treat these diseases before there are serious complications, and perhaps even slow the progress of disease.

      Medical Problems that Might Affect Behavior

      The behavioral effects of disease and aging can be manifested in the way pets eat, drink, or sleep and in their activity level and personalities. For example, pets that are in pain from arthritis or dental disease may be more irritable, more aggressive, more fearful, less active, or less hungry. Pets that begin to lose their hearing or sight may be less attentive, sleep more soundly, and startle when approached. Diseases that affect the nervous system, such as brain tumors and brain aging, can have a wide variety of effects on behavior, including personality changes and disorientation. Endocrine imbalances, disease, and deterioration of virtually any organ (e.g., heart, liver, kidneys, lungs, brain) can have a wide variety of effects on pets’ behavior.

      Brain Aging

      As the body ages, so does the brain. Changes in the brains of older dogs and cats are similar to changes in elderly people. Recent studies of dogs indicate that, as in humans, the effects of aging on the brain range from none at all to severe dementia. Older pets may become less aware of their environments, develop signs of memory loss, and exhibit a decline in learning ability. This can occur as early as 8 to 9 years of age in some dogs, while others retain healthy brain function throughout their lives. In cats, signs associated with brain aging generally emerge at a slightly older age.

      There is a wide range of signs associated with brain aging, including the following.

      • Disorientation: pets might be disoriented if they get lost in familiar places, get stuck behind furniture, or show decreased responsiveness to sights and sounds
      • Activity changes: Pets may begin to sleep more and play less. As cognitive function declines, there may be an increase in activities such as restless pacing, licking, or repetitive barking
      • Sleep cycle alterations: Pets may experience restless, unsettled sleep, or waking at nights.
      • Changes in social interaction: Pets may become less interested in greeting or social play with familiar people or pets. Some pets may become more irritable.
      • Apathy and depression: Pets may have less interest in people, other animals, toys, eating, and grooming.
      • Anxiety: Signs of anxiety include fear of sounds, people, or environments; clinging to family members; and an increase in irritable aggression.
      • Learning and memory problems: The ability to adapt to new environments and learn new tasks may be greatly impaired. Dogs may no longer respond to some of their previously learned commands, be less able to perform tasks learned in agility or obedience training, or be less able to function in the work for which they were trained (e.g., drug-sniffing dogs, seeing-eye dogs). House soiling may also be a sign of declining memory in both dogs and cats. Your veterinarian can determine the cause of these physical signs by completing a physical examination, a neurological examination, and diagnostic tests. Depending on the findings, more specialized testing, such as ultrasound or brain imaging, may also be needed.

      Treating Behavior Problems in Older Pets

      Fortunately, treatments for cognitive problems are now available. These include a prescription diet, natural supplements, and a drug, available through your veterinarian that have been shown to improve behavioral signs and might even slow the progress of cognitive dysfunction disease in dogs. Currently, there is no treatment for signs of brain aging in cats, but research continues in this area.

      In addition to medical therapy and diet, there are other things you can do to help your pet. For example, recent data suggest that keeping pets physically and mentally active improves cognitive function. Exercise your pet daily, play games frequently, review simple obedience commands during daily walks and play, and occasionally provide new toys. The type of toy with a compartment for food or treats that makes your dog actively work for food is especially effective. If your dog has renal failure or diabetes, she may need to make more frequent trips outdoors or need a doggie door. Your cat might need to have his litter box cleaned more frequently, need a larger litter box, or require a little box that is more accessible if he has failing sight or arthritis. And, of course, be sure to give your pet lots of love and attention during his or her golden years.

      Training Your Dog for Baby’s Arrival.

      Growing up with a dog can add a special dimension to your child’s life. You can help build the best possible relationship by taking some simple steps. These include socializing and training your puppy early, adequately preparing the pert for the new baby, and shaping safe interactions between your pet and young child. By doing this, you can help build a wonderful, lasting relationship between your child and your best friend.

      Thinking Ahead, Part 1: Training Your Pup

      If you are thinking of starting a family and have just gotten a puppy, you can do some simple things immediately to begin the socialization process to children. Enroll the puppy in a socialization and obedience class at eight to ten weeks of age. Once the pup learns to sit, ask children you know to request a sit for a small treat in calm situations. This teaches the puppy to look forward to being around children and having hands close by. Always supervise your dog around any children to ensure that no unpleasant experiences occur.

      Teach your pup to be relaxed while eating. As he eats, sit on the floor next to the bowl and gently pet and talk to him. Occasionally give you puppy a small treat. This teaches him to enjoy having someone nearby at mealtimes. Also teach the pup to accept all types of handling. Touch his ears, paws, tail, collar, and so on while offering him a small treat.

      Thinking Ahead, Part 2: Planning for Baby

      Before your baby arrives, be sure your pet is up-to-date on veterinary visits and free of pain. If he has exhibited aggressive behavior or has shown any fear toward babies or children, get a referral from your veterinarian to a behaviorist. Also address other behaviors that could lead to dangerous situations, such as jumping on people or furniture, pawing for attention, and acting boisterously. If you dog will need a leash and head halter or muzzle for safety reasons, you should train him to wear these products before the baby arrives. Also, practice basic obedience commands with your dogs so you have the control you need.

      Because you will be caring for your baby, your pet will no longer be able to get attention upon request. Therefore, teach your pet that exhibiting calm behavior like sitting and staying is the only way to get attention. If your dog does not have a regular routine, you should develop a schedule so he learns that there are predictable times for play and attention. Provide your pet with a confined resting area (such as a crate or room), so he has a place to rest or play with toys when you are busy with the baby. If at all possible, plan for a dog walker after the baby arrives.

      Prepare your dog for the changes to come by carrying a doll around. Put it in the crib, lift it out of the crib, sit on the sofa with it, pass it between family and friends, and pretend to feed it. Recordings of baby sounds are also available. Whenever your pet approaches the doll gently or responds calmly to the recording, ask him to sit or stay for a treat. After your baby is born, bring home a blanket with the baby’s scent on it, wrap it around the doll, and continue the exercises.

      Bringing Home Baby


      Your pet will be excited to see the new mother when she returns home, so have someone else bring the baby into the house. Delay the introduction of the dog to the baby until the pet is calm. You can allow the dog to approach and sniff the baby (swaddled in a light blanket), but use the leash and head halter (or muzzle, if necessary).

      Give your dog lots of praise and even a small treat whenever the baby is present, especially when the baby moves or vocalizes and the pet responds calmly. You can also distract and satisfy the dog with a food-stuffed toy when you are tending to the baby.

      Working with a Crawling Baby and a Toddler

      Your pet needs to learn that a crawling baby is not something to be feared. Try the following exercise. Start the pet on a short lead securely held by an adult. A second adult places the baby on the floor approximately fifteen feet away and allows the child to crawl about three feet toward the dog. Then ask your dog to sit or stay and give the dog a treat for remaining calm. Repeat the exercise, gradually allowing our baby to crawl closer to your dog, but not close enough to put the baby in danger. You can also use this type of exercise when your child begins toddling.

      As soon as your child begins talking, you can involve the child in training using the following simple exercise. Begin with the child sitting in the lap of one adult and the other adult sitting across the room. Each adult takes turns calling the pet back and forth to sit for a treat. Coach the child to say “come” and “sit” with the grown-up and toss the treat to the pet. As the child learns the words, the adult’s voice can be phased out.

      Keeping Things Safe

      Babies and young children should never be left alone with any dog and must be closely supervised when a dog is present. When you cannot supervise, you can use a room or crate in a quiet spot to keep the child and dog separated. Even friendly dogs and family dogs can pose a danger to small children.

      Teach your child safe behaviors around dogs. Tell the child to avoid dogs that are resting, eating, or playing, or dogs that seem hurt. Discourage the child from hugging dogs and petting their faces. Also instruct children not to run when playing with or near dogs. Tell your child to always say the family dog’s name before a pat so the dog isn’t caught off guard.

      You must teach by example because kids typically mimic their parent’s behavior. If you are ever concerned about your pet’s proximity to your child, use a happy tone to call the dog out of the situation, and when you cannot properly supervise their interaction, confine your dog. Never use physical punishment or harsh words to correct the pet. When your child and pet are next to each other, never scold either one.

      Teaching Your Puppy to Mind Her Manners.

      Puppy training should begin from the moment you bring your new pet home—it will go much faster and smoother when your pet is young. Early training can help in such important areas as communicating with your pet, training your pet to respond to signals and commands, socializing, and preventing unruly behavior. A great way to get started is to enroll her in a puppy class, many of which begin for dogs as young as eight weeks. Positive training methods are important for successful training. Using punishment during a puppy’s formative months can ruin the bond with your pet. Use positive reinforcement to facilitate—rather than force—the training process. The best reinforcers for training and shaping desirable behavior are food, a favored toy, affection, and social attention.

      Getting Started

      The healthiest choice for a reward is the puppy’s own food, combined with praise. Training just prior to the puppy’s mealtime can help increase her interest in the food. Special treats may be needed if your pet has a picky appetite.

      Initially, the food reward should be given immediately following every correct response. As the pup learns the behavior, stop giving a food reward for less than exact responses, and reward only quick, well-performed responses. Once you reach you goal, continue to give praise for every correct response but begin to provide the food reward on a more intermittent, random basis. This will result in the longest retention of learning.

      “Come”

      Hold a piece of dry food between your thumb and forefinger, extend it toward the pup, and say her name. As she approaches you, repeatedly wave your hand toward your chest and say “come.” This gives your pet both a verbal and a visual cue. When she reaches you, give her the food. As she eats, quickly take a few steps back and repeat the procedure. An alternate way to teach this command is to toss the first piece of food six to eight feet away for the pup to chase. After the pup eats it, say “come” to call her back to you for another piece of food.

      “Sit”

      Start with the pup in the standing position. Hold a piece of food between you thumb and forefinger, place it directly in front of her nose, and say her name. Slowly move the food over her head so her nose points straight up and her rear end is leveraged into the sitting position. Say “sit” as she assumes the position and give her the food. Be careful not to hold the food lure too high above her head or she will jump for the food. After some practice, your puppy should automatically sit with an upward sweep of the hand or when you say the word “sit,” even without showing the food. Also use this lure technique to train your dog to sit up from a lying-down position by simply holding the food in front of her nose and sweeping it up over her head so she rises to the sitting position.

      “Lie Down”

      Teaching your dog to lie down on command is easier if you being on a smooth surface with the puppy in the sitting position. Hold a piece of dry food directly in front of her nose. Say her name and, with a swift movement, move the food down to the floor directly next to her front paws. As your dog slides into the down position, say “down” and give the food reward. This command usually takes a little more patience than the first two. Be careful to move the food to the floor right next to the paws. If the food is too far in front of the pup, she may stand and walk to the food. With time, the downward sweep of your hand or the word “down” will cause the pup to go into the down position.

      “Stay”

      The “stay” command will be the most difficult command for your puppy to learn. Young puppies don;t like to sit still for every long and love to follow people around. Keep this in mind when you begin training. Train when your puppy is calm, possibly after a long walk or play session. Have her sit by using a hand and a verbal signal, but do not give a food reward. As soon as the puppy is sitting, lean toward he, look her in the eye, and extend the palm of your hand toward her. In a calm, firm voice say “stay.” Wait only one second, then lean down, calmly praise her, and give the food reward while she is still sitting. Then say “okay” to release her. Repeat the exercise. Gradually request that the pup stay for longer periods. If your puppy’s eyes wander from yours, calmly repeat “stay” in a serious tone as you lean toward her. Increase your distance, beginning with one step away. Once your pet understands the concept, progress slowly to longer stays and greater distances.

      Additional Tips

      Here are some additional tips to make great progress during basic training. Patience, consistency, and repetition are key!

      Start training in a quiet area. When the puppy’s responses to your commands become dependable, move the training to environments with more distractions.

      Be sure the pet knows one command before proceeding to the next. Tone of voice is important. When teaching “come,” “sit,” and “down,” use a calm, positive, and consistent tone of voice to command the behavior and a high-pitched happy tone as a reward. “Stay” works better with a slow, deep-toned command.

      Avoid repeating commands. If you do not teach your puppy to respond to the first command, she will learn that it’s not necessary to obey until multiple commands are given. If she doesn’t respond, you can gently guide her into the requested position, then be sure to have a few more training sessions before making the command in a non-training situation.

      Praise your puppy and say “good dog” whenever you give a food reward. This will reinforce desired behavior and help maintain a strong response, even as the food reward is gradually withdrawn.

      A dog is more likely to respond if you use both hand and verbal signals rather than only a verbal command.
      Enroll in a puppy class so you can get guidance from the instructors and your puppy can learn in the presence of other dogs.

      When your puppy seems fidgety and has a shorter attention span, keep the training session short and stop before the pup begins ignoring commands.

      If you have difficulty getting your puppy to be calm and focused, a head halter should be considered to more immediately—but gently—guide her into the desired response.

      Taming the Kitten with an Attitude.

      Play helps prepare kittens to become great hunters and develops their social skills with other cats. But this behavior is not fun when the pet treats people like big mice or when a playful pounce punctures skin. Although play bites are usually inhibited and swatting is often done with retracted claws, sharp teeth and nails can damage clothing or cause injury. The risk of injury increases when the behavior is directed toward the face, a person with fragile skin, or someone with an immune deficiency disorder.

      Cat play is typically seen in young, active cats and involves elements of hunting, including stalking, chasing, attacking, and biting. The attacks escalate when people encourage the behavior because they think it’s cute. Most kittens play with other kittens in a rough-and-tumble way. When a feline playmate is not available, a family member may become the next best target. However, while you may be an appealing target for your cat’s play, you don’t have the fur, mobility, or defensive skills of a cat, which increases the likelihood of injuries.

      Teasing a small kitten with your fingers and toes may seem like fun, but this can escalate to harder bites as your pet grows up. If you want to be more to your cat than a big toy, never encourage this behavior. While some of these little guys can seem quite bloodthirsty and relentless, their behavior can usually be controlled.

      Controlling the Little Beast

      Since play is normal, you will first need to focus on engaging your cat in acceptable ways to play. Providing a feline playmate of the same age and temperament will usually draw the play attacks away from you and toward the new buddy. Consider this option only if you are prepared to care for two cats, however. Discuss with your veterinarian whether another cat seems right for your home and how to introduce the new cat. If adding a cat is out of the question, then you must take the responsibility for providing the proper type of ply and shaping your pet’s behavior.

      Always maintain control at playtime. Play that is initiated by the cat should be ignored or interrupted. If you can use a few commands, such as “playtime,” before each play session and “come” and “sit” for food and treats, you may be able to interrupt the cat and change his focus with a command before play attacks begin.

      
Play interaction with the cat should involve tossing or dangling toys for him to chase and catch to direct the play away form you. The more vigorous the interaction with the toys, the better. Keep your kitten so busy and worn-out that he doesn’t even think about going after you. Stock up on all types of fun, tempting toys for your cat to chase, pounce upon, and even sink his teeth into. Use toys that are the size and texture that your cat would most want to hunt. A short wand or fishing rod can be used to dangle small plastic, leather, or feather toys in front of your cat. Coasting or even stuffing a toy with food or catnip can increase its appeal. Consider feeding multiple smaller meals. Placing your cat’s food inside toys that require manipulation such as batting, rolling, or chewing to dispense the food can provide a good alternative to hunting. Motion-activated toys can amuse your cat when you are not around. Or give your cat Ping-Pong balls or unshelled walnuts for swatting. Also provide objects for exploration (e.g., cardboard boxes, paper bags, kitty condos) and perching (e.g., on windowsills).

      To Swat or Not to Swat

      Avoid all physical punishment, such as swatting your pet or thumping him on the nose to stop rough play. It may cause your cat to fear you, become aggressive, or even play more roughly. A blast of air from a compressed air can (obtained from a photography store) and a squirt from a water gun are safe ways to discourage the behavior. This approach is likely to work only when you can anticipate an attack and are prepared to interrupt your kitten as he begins the assault. However, this is not always easy since attacks are most likely to occur when you are busy or unprepared. Vigilance is a necessary ingredient for being consistent in teaching your kitten not to attack, and a bell on the collar may help to keep track of his whereabouts. Do not use these techniques if they are not immediately effective or if they cause fear.

      Up All Night

      Nighttime attacks are more difficult to handle and, in most cases, the simple solution is to keep the cat out of the bedroom when you sleep. Often this behavior will decrease and finally stop as the pet grows older. If the kitten has the annoying habit of waking you up by sucking on earlobes or elbows, try applying a light coat of underarm deodorant to those areas to discourage him. Or keep a can of compressed air nearby to discourage those surprise attacks. Increasing daytime play should also help to decrease nighttime activity.

      Family Feuds

      Problems with other cats in the home can occur when the play target is another cat that is weak, fearful, or old and cannot tolerate the young cat’s playful behavior. The pets should be kept separate unless supervised. Before play gets too rough, use a command to encourage the rambunctious cat to come and take a treat or play with his toys. You can also discourage the behavior with a water gun. Do not yell at the kitten during play attacks because this can make both cats more nervous. Sometimes the cat being attacked can become so stressed that veterinary counseling should be sought regarding the possible use of pheromones or medication.

      Nail Trimming-An Ounce of Prevention

      Since young kittens tend to use their paws in play, it’s a good idea to keep those nails trimmed to prevent them from snagging sensitive skin. It’s easy to condition your cat to accept nail trimming, but you must have patience and pick the right time. The worst time to attempt nail trimming is when the pet is alert and active. All kittens occasionally nap, so take advantage of downtime to trim nails. Handle the paw very gently, use a sharp pair of trimmers, and quickly take off the tip of one nail. If the pet continues to snooze, take the tip off another nail or two. If your cat stirs, give him a small treat. Never force the pet to hold still for a nail trim, and always cease before he squirms and resists.

      Solving Separation Anxiety Problems.

      Most dogs cope well when left alone, but some show distress, anxiety, or panic when separated from the family. Generally, pets with separation anxiety may stay near family members and spend little time outdoors on their own. They may become anxious as the family prepares to leave, not eat when alone, and be overly excited during homecomings. The most common signs of separation anxiety are vocalization when the family departs and destructiveness and elimination problems during their absence. Dogs behave in these ways because of uncontrollable anxiety and not spit or anger. Dogs with separation anxiety usually display destructiveness at exits and windows, and the vocalization often includes howling, whining, or repetitive barking. If dogs target food or garbage, this may be scavenging or exploratory behavior rather than separation anxiety. Often, dogs with separation anxiety display other signs of anxiety (such as trembling, restlessness, and salivation) that may be evident as you depart or upon your arrival home. They may also vomit or have diarrhea while you are gone. If you note destructiveness, vocalization, or elimination problems while you are home, you and your veterinarian should first rule out other possible causes.

      Causes of Separation Anxiety

      Genetics, early experience, and maternal behavior may all play a role in causing this problem. Some dogs develop separation anxiety after a change in their routine or after a traumatic experience that occurred when they were alone. Dogs that have noise phobias are more likely to be anxious if left alone. You might prevent separation anxiety if you teach your puppy to spend time away from family members in a resting area, bed, or crate, either for napping or playing with toys.

      Treating the Problem

      Start with a veterinary visit to rule out any medical problems. Ask your veterinarian to confirm that the problem actually is separation anxiety and then to help you develop a treatment plan designed specifically for your dog and your home.

      Preparing for Future Departures

      The following training program will take some time and effort to implement, but if you work at it, your dog should begin to accept your departures.

      To start, provide your dog with a predictable daily routine and enough physical and mental enrichment to meet the dog’s needs. After exercise, play, or training sessions, schedule times with no interaction so your pet learns to spend time alone in the resting area. Focus all training on rewarding your pet for behaviors that you want the dog to learn, such as relaxed stays, and not on punishing your pet for behaviors that you want to stop.

      Never punish the dog for destructive behavior done in your absence. Some dogs see mild correction as a form of attention, while others will become increasingly conflicted and anxious about whether to greet you or avoid you. Most important, punishment does not reduce your dog’s anxiety about being left alone and is likely to make the problem worse.

      Take the following steps to implement a training program geared toward reducing separation anxiety:
      Start your training program by identifying everything that your dog enjoys (affection, play, walks, treats, toys, and food). Use these rewards to train your dog to perform a relaxed “sit”, “down”, and “stay,” especially in the resting area. Gradually encourage your dog to stay and relax for longer sessions before giving a reward. Stop rewarding attention-seeking behaviors (such a barking, whining, or pawing), and teach your dog that sitting or lying calmly is the only way to earn affection. Also, avoid indiscriminate petting and attention, and instead use exercise and reward-based obedience training to provide social interaction.

      Train your dog to go to the resting area after an exercise, play, or training session. You can train her to go to and stay in the resting place by leaving toys and chews in the area. You may want to try using a head halter or crate to teach the dog to stay in the area for longer periods of times. Try using a dog-appeasing pheromone spray or diffuser or aromatherapy in the area, giving the dog a piece of clothing that belongs to a family member and/or playing music or turning on the television to further relax your dog while in the resting area.

      As practice, put on your coat, grab your keys, and walk out of the home or open the garage door while your dog is relaxed or playing with toys. Frequently repeat these pre-departure actions until your dog becomes accustomed to them and they no longer trigger any anxiety. Ignore your dog for a few minutes, and while the dog is calm and occupied, leave for a very short period (one minute or less) and return while your pet is still calm. Gradually increase the length of your absence.

      Moving Toward Successful Departures

      When you are actually going somewhere, try the following tips:
      Restrict your dog to the designated resting area during periods of absence, but only if she has learned to play with toys, relax, or sleep in this area. A dog that is not used to confinement may become more anxious when confined. In this case, you may need to find a dog-sitter or doggy day care when you go out for long periods of time until the separation anxiety is under control.

      Before each departure, provide your dog with play and exercise, and then encourage her to go to the resting place.
      Use your dog’s favorite chewy treats or chew toys. Some dogs might be sufficiently interested in treat-filled toys and chews that you an leave while she is occupied with them. Also consider consulting with your veterinarian about anti-=anxiety medication. Anti-anxiety drugs may help reduce your dog’s anxiety and greatly improve the success of the behavior program. They can take one or more weeks to begin working and are more effective if combined with a behavior program that teaches your dog to cope with being home alone.

      Solving Housesoiling Problems.

      While most cats are very clean and dependable in using a litter box, they may eliminate in undesirable locations for a number of different reasons.

      Two Types of Elimination Problems

      Marking is when urine is sprayed on vertical objects such as furniture, plants, or walls. Cats spray in a standing posture with their tail raised ant heir backside facing the object. In rare cases, cats may mark with urine or stools on horizontal surfaces. Marking may be a territorial signal or can be brought on by stress.

      Housesoiling is when voiding of stool and/or urine occurs in places other than the litter box. The cat will assume a squatting posture and eliminate on a horizontal surface. Cats may soil to avoid the litter, the box, or the location, or because they prefer to use a different surface or location.

      Rule Out medical Causes First

      These might include diseases that increase the frequency of urination (such as kidney disease or diabetes) and diseases that make urination painful (such as bladder disease or arthritis), or those that increase the frequency of bowel movements (such as diarrhea) or cause discomfort (such as constipation or anal sac problems). Hormonal conditions (such as thyroid disease) and diseases that affect the nervous system (such as tumors or senility) can also lead to Housesoiling. Therefore, solving any Housesoiling problem should begin with a veterinary visit.

      If the problem is not medical, the next step is an in-depth evaluation to determine the behavioral cause and design a treatment plan that will best suit your cat and your household.

      Here are some general things that may cause elimination problems:

      • Environmental or social changes that occurred just prior to the onset of the problem
      • Changes in the litter, box location, box type, and/or frequency of cleaning
      • Availability of more desirable locations and surfaces to eliminate
      • Problems in the relationship between the pet and other pets or people in the home

      Causes of Marking

      Marking may occur as a response to the introduction of new pets, objects (like new plants or furniture), or odors into the home (like fireplace logs or a visitor’s purse or boots), people moving into or out of the home, or moving to a new home. Cats that spray near doors and windows may be marking in response to other cats coming onto the property. Any changes in the environment that lead to an increase in anxiety or conflict can also cause marking (like remodeling, redecorating, or getting a new roommate).

      Causes of Housesoiling

      Cats may avoid the litter box, or prefer locations or surfaces other than the litter box, for these or other reasons:

      • Medical problems
      • Unclean litter box
      • Not enough litter boxes
      • Being confronted in the litter box by a family dog, cat, or human (some owners try to give a cat medication or trim his/her nails while eliminating)
      • Undesirable litter box location (insufficient privacy or near a noisy appliance or furnace)
      • Preferred feel or comfort of a surface or location other than the litter box

      What to Do: Basic Tips

      Scoop all litter boxes daily and replace the litter weekly. Provide at least one litter box per cat plus one extra. Clean soiled areas with an effective odor remover. To determine which litter type your cat prefers, offer two or three different options side by side to see which one he uses use most (clay, clumping, recycled paper, scented, unscented, different brands, sand or soil, different depths). Then place the preferred litter into different boxes to determine which type he prefers (different heights, different openings, with or without a litter liner, covered or uncovered, self-cleaning). Also try the preferred litter and box in a different location that your cat might prefer.

      Marking Solutions

      Cats that have not been castrated or spayed are most likely to spray, so neutering is the first step in the treatment for marking. If the problem is due to an unhealthy relationship with other cats or people in the home, seek additional guidance from a behavioral specialist. If your cat is spraying when other cats come onto your property, move anything that might attract stray cats (garbage cans, feeding stations, or bird feeders). Try cat repellents, motion-activated alarms, or motion-activated sprinklers to keep strays out of the yard. Keep your cat away from doors and windows, put up blinds or shutters on the windows, or place booby traps in the area where your cat hears or sees the other cats. Safe, effective booby traps include upside-down carpet runners with nubs up, double-sided tape, unpleasant odors (potpourri, citrus, menthol), a stack of empty soda cans, and motion detectors that set off an alarm or a spray of air. Synthetic feline pheromones can be effective at reducing anxiety and marking. No drugs are license for the treatment of feline urine marking; however, a number of human and dog medications might be effective. Your veterinarian can explain their benefits and risks.

      Housesoiling Solutions

      Most cats can be prevented from soiling when supervised. When the owners are unable to watch the cat, it may help to confine him with his litter box in a small area of the home where he does not soil. Understanding your cat’s daily elimination routine can help you determine when he will need to be confined or supervised.

      Preventing access to the soiling area may be the easiest solution: Close doors, put up barricades such as child gates, move furniture over the spot, or use booby traps. Try placing the pet’s food bowl, toys, or bed in the soiled areas. If you see your cat soiling, interrupt him with a water sprayer or noise device, but do not physically punish him, rub his nose in the mess, or yell at him.

      Evaluate the litter box location, litter type, cleaning schedule, and any other factors that might deter litter use. IF the pet is soiling in one or two specific areas, it might be preferable to move the litter box to that area or a similar area. If the cat is using a particular surface, such as a tile floor or carpet, you might make his litter box similar by giving him an empty litter box or placing a carpet remnant in the box. Gradually add small amounts of litter to the box until your cat feels comfortable using a box with litter.

      If these steps do not solve the problem, consult your veterinarian for further guidance.

      Solving Digging and Chewing Problems.

      Most puppies have a strong natural desire to investigate and chew. But this desire can be a major problem if your puppy digs up your roses or destroys your new shoes. Many families focus on punishment to correct the problem, but you’ll find that reinforcing good behavior works better and keeps your dog happier. Be sure to puppy-proof your home so your puppy ca safely explore and investigate without getting into trouble. Just as children enjoy playing with new and novel items, you may find that your puppy prefers to lay with your possessions over her own toys. When all else fails, remember that unwanted chewing or digging is never cause by your dog’s desire to get even with you.

      Chew and Feeding Toys

      It’s important to provide a supply of safe and interesting toys so your dog can entertain herself when she’s on her own. When selecting chew and feeding toys, begin with a variety of toys to determine which type your pup prefers. Rotate different toys in and out every few days to keep them interesting. When you see your pup chewing her toys, reward her with affection or a bit of puppy food. Toys made of durable rubber, beef-hide chews, and dental treats are generally good options. Some toys are designed so you can stuff food into the openings. Others can be covered or filled with a small amount of food spread. This will increase your puppy’s interest in the toys and will extend the length of time she stays occupied. Other toys that might capture your pup’s interest are ones that must be moved or manipulated to release small pieces of food or kibble. They come in a variety of shapes and sizes and provide great mental stimulation. In fact, by feeding most of your dog’s food, along with a few treats, in these toys, feeding times can be longer, more challenging, and more enriching than eating from a food bowl.

      Preventing Problems

      Even with an excellent selection of appealing chew toys, many household items may still be more inviting to your pup. Never give items to your puppy to chew that are similar to household items you don’t want destroyed. For example your puppy may not be able to distinguish between old and new shoes. Sessions of play and exercise are a must, since unused energy contributes to her desire to search and destroy,

      Until you can trust you pet, supervise her constantly or confine her to a safe area, such as her dog crate or exercise pen, where she can nap or play with one of her chew or feeding toys. A good way to prevent your puppy from chewing undesirable objects in your presence is to leave a long leash attached to your dog so you can easily guide her away. Leaving the leash attached to a head halter can provide more immediate control of the muzzle.

      As your puppy grows older and is allowed more freedom around the home, she may slip up and attempt to munch on items you want her to avoid. Some puppies can be taught to avoid this if the items taste bad. Use commercial anti-chew sprays, mentholated products, or a small amount of cayenne pepper mixed with water as deterrents.

      Punishment for chewing is not a good solution because it can cause your puppy to fear you. At best, it may only teach her not to chew the items when you’re watching. If you do catch your dog in the act of chewing, just make a sharp noise or give a gentle tug on a leash (if attached) to interrupt her, then provide a chew toy.

      Anxiety

      Destructive behavior may be due to anxiety. Extreme anxiety and destructiveness during your absence may be due to separation anxiety, which may require a more in-depth consultation with your veterinarian or a behaviorist. You might lessen her anxiety by teaching her that she cannot receive attention on demand. Train her to rest or play with her toys in her own bed or crate rather than constantly lying near you. Exercise your dog before you leave home, and try to leave when she is resting or occupied with her toys. Practice short departures, then gradually increase the length of time that your dog is alone.

      Digging

      Dogs dig for a number of reasons: to get to deeper soil to cool off, to chase rodents, to bury and retrieve bones, to escape confinement, or just for the fun of it. Digging commonly occurs when pets are left alone with insufficient stimulation. Provide your dog with increased play and exercise before leaving her some stimulating toys for chewing and play. For some dogs, the most practical option is to provide a digging area. Build an eight-inch-deep wood frame and sink it into the ground. Mix the soil with sand and partially bury toys (smear a small amount of cheese or meat juice on the exposed ends). Occasionally give your dog food treats to reinforce appropriate digging.

      Sometimes having a second dog for companionship and play can reduce chewing and digging. However, give some serious thought to adding a second pet, since you could end up with two destructive dogs instead of one.

      As with chewing, punishment should not be used to stop your dog’s digging. If you do not identify and address the cause, the digging will continue in your absence. You might try to interrupt the behavior while remaining out of sight by turning on a sprinkler, using a remote spray collar, or tossing a noise device such as a shake can filled with pebbles or a few coins. Alternatively, you might cover the surface by placing chicken wire or stones over the area, or confine your dog to a pen or run that is paved or covered with stones. If your dog continues to dig, the best solution may be to keep her indoors when you are not around to supervise until she is older and less likely to dig.

      Solving Chewing and Scratching Problems.

      Most cats, especially young kittens, have a strong natural desire to play and explore. But this desire can lead to major problems when your cat claws your sofa or destroys your houseplants. The best way to prevent destructive chewing and scratching is by providing an environment that meets all of your cat’s needs.

      Exploration and Play

      The first consideration is that environment be stimulating but safe. Cat-proof your home and build or purchase a play center where your cat can climb, perch, and scratch. Provide toys your cat can bat around, such as spring-mounted, dangling, or bouncy toys. Some cats enjoy climbing into empty cardboard boxes or cat carriers, especially if food treats have been left inside. Ping-Pong balls and unshelled walnuts make inexpensive toys that many cats love.

      One of the best ways to provide additional stimulation is to make feeding more like the natural feeding behavior of cats by providing numerous small meals each day and by encouraging play that includes batting, chasing, and pouncing. This can be accomplished by placing some or all of the cat’s food inside toys that require rolling, batting, or pawing to release the food. There are also feeders that can be timed to open every few hours.

      Another great way to stimulate your cat and provide an outlet for hunting is to engage in a number of interactive play sessions during the day. These might include throwing or rolling toys (which can be filled with catnip or food) or the use of toys that attached to wands or sticks that are the right size and texture to entice your cat to chase and bite the toys and not the human hand. Avoid tempting your kitten into play by teasing him with your fingers—you may end up with a play-biting cat.

      Preventing Chewing Problems

      Indoor cats with little access to grass or other vegetable matter may chew houseplants. Offer lettuce, catnip, or a kitty herb garden in exchange. Then keep your plants out of the cat’s reach unless you are around to supervise.

      Some cats enjoy sucking or chewing on material such as rugs, clothing, cables, and electrical cords. Others may chew or even swallow items such as string, wool, rubber bands, or baby bottle nipples, which can be dangerous. You can correct many of these problems by following the previous exploration and play suggestions and by keeping these objects away from your cat. In addition, try providing alternative opportunities for chewing, such as changing to foods with higher bulk or a dental diet, or offering dental treats or even a dog chew toy to provide greater oral stimulation. Some breeds, such as Siamese and Burmese, seem to have a genetic tendency to suck and chew excessively, especially on wool. If problems persist, see your veterinarian.

      To keep your cat away from problem areas, first try child locks, barricades, or closed doors. For persistent problems or areas that cannot be barricaded, you might consider remote punishment, taste and odor aversion, or booby traps as deterrents. Never use physical punishment or yelling—it may cause your cat to fear you and to avoid the problem area only when you are around.

      If you remain out of sight and remotely punish your cat with a device such as a water gun or loud noise, he may cease without fearing you. Destructive chewing can also be discouraged by using commercial anti-chew sprays, mentholated products, vinegar, or a little cayenne pepper mixed with water. Other options are aversive odors (deodorant soap, citrus oil), hiding exposed wires or cables inside metal or plastic piping, booby traps such as motion-activated alarms or spray devices, and a stack of plastic cups set to topple when the cat enters the area or begins to chew or scratch.

      Preventing Scratching Problems

      Scratching is a normal behavior that allows your cat to condition his claws and mark his territory. It also provides a nice stretch. Of course, when your cat’s scratching is on furniture or your favorite stereo speakers, it quickly becomes intolerable. The goal of treatment is to direct scratching away from targets that are unacceptable and toward a designated scratching area that is acceptable to you and your cat.

      Encourage your cat to use a scratching post by placing one near his favorite sleeping area and perhaps a second post in the area where he is most likely to scratch. It is important to select surface textures that are both practical and appealing to cats—carpet, sisal, a nubby fabric, or even bare wood. Attract your cat to the scratching post by attaching a few toys, rubbing a little catnip into the surface, or providing a more elaborate structure with climbing and perching areas. Give your cat food rewards for approaching and scratching the post. If you prefer to build your own scratching post, ensure that the post is tall enough for your cat to scratch with his legs fully extended and is sturdy enough to support his weight without toppling. You can leave the wood bare or cover it with a suitable surface. You can also construct an inexpensive scratching post by securely attaching a fireplace log to a plywood base.

      Persistent Scratching Problems

      If your cat continues to scratch in an inappropriate area, put a post there. Food rewards for scratching post should keep your cat more interested in the post than in your furniture. If destructive scratching persists, cover the scratched area with plastic, a loosely draped piece of material, short strips of double-sided tape, or one of the booby traps previously discussed. Keeping the nails trimmed may minimize damage. Another option is to use plastic coverings available from your veterinarian that fit over your cat’s claws.

      Since scratching can be a form of marking, a feline cheek-gland pheromone might be helpful for stopping this behavior when used in your home. You may want to discuss this option with your veterinarian.

      One important thing to keep in mind is that before you try to prevent or stop undesirable scratching behavior, first make sure that you have provided enough outlets for play, places to climb, and appropriate items to scratch.

      Solving Barking Problems.

      Most dogs get noisy when exposed to anything new or unusual. The stimuli that trigger a dog to vocalize can vary from dog to dog and from household to household. Vocalization can be in the form of barking, whining, growling, or howling.

      Why All The racket?
      Many situations can lead to barking:

      • Strangers or other animals entering the dog’s property
      • Slight of prey, such as a squirrel running through the yard
      • Separation from the pack, mother, or other family members
      • Unfamiliar sounds, such as a smoke detector alarm
      • Need for attention, food, or affection
      • Other anxieties or high states of arousal
      • Growling is associated with fearful or assertive displays. Whenever growling achieves the dog’s goals (for example, a person stops approaching or moves away), the behavior is reinforced because the threat has been successfully removed. Subsequently, the growling will likely become more frequent or intense. Some medical problems can contribute to vocalization, and senility in particular may b lead to barking problems in older pets. If barking becomes intense, repetitive, and difficult to interrupt, it may be deemed compulsive. Pets with medical, geriatric, or compulsive disorders should begin with a veterinary visit to determine if medical treatment might be needed to complement the behavior therapy.

        Prevention Starts Early

        Socializing a puppy with a variety of new people, animals, environments, and noises can reduce anxieties as the dog grows up. Provide regular sessions of play and exercise. After these sessions, be sure to give your puppy some times to play with her toys or rest on a bed or mat, so she gets used to spending time on her own, too.

        You can reinforce barking by giving in to you puppy’s demands. For example, if you allow a barking dog to come indoors, or if you feed, praise, play with, or even approach the pet to quiet her, it may encourage barking. Focus on rewarding your dog only when she is behaving appropriately and quietly.

        Correcting Bad Habits

        Correcting the problem requires an understanding of what causes the barking. If you can remove the cause, the barking will decrease and may ultimately stop.

        You’ll also need to review basic obedience training. Once you can achieve quiet and relaxed “sit” and “down” commands, you can begin to use these commands when barking begins. Focus on teaching your dog desirable behaviors that can be rewarded rather than trying to punish or correct undesirable barking. Commands and lure reward training can be used to quiet the dog as barking begins. Training dogs to be quiet on command allows them to bark when needed but stop at your request.

        Training with the aid of a head halter can be particularly effective, since it provides a physical aid for making eye contact and quieting the dog with a pull on the leash. It also provides reinforcement by releasing tension, which can be followed by giving a favored treat or toy for remaining quiet.

        Begin training sessions with situations that are easily controlled (a family member knocking at the door) before proceeding to more difficult situations (a stranger coming to the door). Ask the dog to be quiet on command and give her a reward for quiet behavior. At each subsequent training session the dog should remain quiet a little longer before the reward is given. Teaching a dog to stop all barking in the presence of a very strong stimulus can be difficult and may be impractical. Barking must be interrupted immediately after it begins, and the process should be repeated until the dog does not bark at the stimulus anymore (at which time she can be rewarded).

        Punishment is generally ineffective in the control and correction of barking. It may actually increase your dog’s fear and anxiety, and in turn the barking may increase or change to aggression when situation is repeated (like meeting new people). In fact, when barking is due to fear, treatment should focus on remaining calm and making the situation positive. In addition, when you punish your pet, you can cause an increase in fear or aggression toward you. Finally, even when punishment is effective, it may stop the barking when you are there, but it will do little to nothing to affect the barking when you are not present. In some cases, a diversion device, such as a whistle, can be used to interrupt barking, which would then provide an opportunity to reward your dog when she quiets down.

        Practical Products

        There are several products that may interrupt barking. Devices include ultrasonic trainers, audible alarms, water sprayers, and shake cans (an empty tin can with coins or pebbles sealed inside). If these products interrupt the barking, you can then reward your dog when she is quiet.

        When you are not present, some barking is likely to persist. If it is excessive, you might want to try to keep your dog away from the sounds and sights that stimulate barking. Alternatively, a bark-activated product might occasionally be useful. However, unless the dog is also trained to be quiet in the presence of the stimulus, devices will only temporarily disrupt—not eliminate—barking habits.

        Bark-activated products may be the most practical means of deterring inappropriate barking and may be a better choice than owner-activated devices since they ensure immediate and accurate training. Some bark-activated products are designed to be placed in an area where the dog might bark, while bark-activated collars may be more useful for dogs that do not bark in a specific location. Audible and ultrasonic collars may work for some dogs. Collars that spray compressed air may be somewhat more effective without causing any physical harm. These products work best if the owner is present o monitor the dog and to reward her with praise, play, or a treat as soon as the barking ceases. Following these guidelines, your dog’s barking problem should diminish over time.

        Keeping Mouthing and Biting Under Control.

        It’s normal for a puppy to use her mouth during play and social interaction, but it’s certainly no fun having those sharp teeth embedded in your ankle or arm. It’s important to teach your puppy how to use her mouth in an acceptable manner. Strategies for controlling the little piranha include encouraging acceptable play, providing sufficient stimulation to meet her needs, teaching her basic commands such as “sit” and “down,” and ignoring or interrupting undesirable biting behavior.

        When play biting becomes too intense or persists into adulthood, seek the advice of a behavior specialist so you can determine the best courts of action.

        Don’t Make Things Worse

        Do not encourage your puppy’s pesky behavior. Don’t get you pup all fired up with rough play, teasing, or a game of tug-of-war if these lead to biting. Avoid games that encourage your puppy to attack any part of your body, and don’t wear gloves during play to allow your puppy to bite.

        Be careful not to inadvertently reward the behavior. If biting works to get your attention, the behavior will continue. Petting your dog, picking her up, talking to her, or even giving her a mild shove or a light scolding can actually reward biting behavior. Therefore, any hard contact between you puppy’s teeth and the human body should be a signal for you to cease giving any attention to your dog. Immediately stopping play and ignoring your puppy or walking away will teach your puppy that attention and play stop when biting begins. Similarly, do not begin to play if your puppy is displaying “demanding” behaviors such as pawing, jumping up, barking, or mouthing.

        When biting begins during play, or if you can anticipate biting, try to change her focus to a toy or some other form of play that does not involve biting. Another option is to use a training command, such as “sit” or “down,” and reward her with a treat or toy if she settles down. A loud “ouch” when your dog bites can also be used to interrupt the behavior and mark the stopping of play. Play should begin again only if biting does not recur.

        There will likely be times when your puppy becomes overly aroused and you cannot effectively deal with the problem. In these situations, one option is to immediately leave the room and shut the door (as long as it’s safe to leave your puppy alone) and return only when the puppy is settled. Otherwise take her to her safe area (such as a crate or pen) and give her a feeding or chew toy to keep her (and her mouth) occupied.

        Avoid harsh corrections and physical punishment. Never hit or slap your pet, thump her nose, squeeze her lips against her teeth, shake her by the scruff of the neck, roll her onto her back, or force your fingers into her mouth. This kind of correction is likely to make the biting problem worse, ruin the bond with your pet, and lead to more serious problems, such as fear and aggression. On the other hand, some puppies may actually find these harsh corrections to be a big game, which only encourages them to bite an play more toughly.

        Channel That Energy

        If your puppy is constantly demanding attention by mouthing or biting or is playing too rough, then you will need to provide other ways to keep her brain and body active. Schedule regular play and exercise throughout the day in ways that do not involve mouthing, such as walking and running, playing fetch, chasing a ball, practicing some of her training exercises, or even playing tug games as long as your puppy’s teeth remain on the toy and do not touch your body.

        Another way to channel your puppy’s energy is to provide frequent opportunities for playing with other friendly dogs. Giving your puppy dental treats, toys that are designed to be manipulated to release a treat, or those that promote prolonged chewing also provide opportunities to use the mouth and teeth in an acceptable and health way. The more energy the pup uses for these other activities, the less she will use for mouthy biting behavior. Remember the training mantra, “A tired puppy is a good puppy.”

        Communicating with Your Puppy

        Enroll your pet in puppy socialization and training classes as soon as possible. Teach her a few simple commands so you can communicate with her when she begins to engage in undesirable behaviors. Training sessions combine social time, mental stimulation, and learning new skills, while keeping your puppy focused on behaviors other than play biting.

        Teach your puppy what behaviors you expect of her before she gets any rewards. For example, ask her to sit before giving her things she wants, and occasionally command her to stay for a second or two before following you around the home or going through a doorway. Be consistent.

        You may want to permit soft mouthing and inhibited bites during play if you have a home in which there are no children or elderly family members who might be at risk. You can teach soft contact by placing your hand in the pet’s mouth when she is very calm and praising her when she mouths softly. However, if she bites with enough pressure that it is uncomfortable for you, say “ouch” and stop the play.

        Training Aids

        A dragline can be a helpful tool for managing your pup’s biting behavior. Attach a long line (ten feet indoors and twenty feet or longer outdoors) to your pet’s collar so you can quickly grab the line when you need to stop the biting. Be sure that the pet is closely supervised when she is wearing a dragline. With a gentle pull on the leash you can immediately stop mouthing and biting. Release tension as soon as the dog settles down. If the puppy will not focus, gets easily distracted, or uses her mouth excessively, more effective control of the head and muzzle can be achieved by using the dragline with a head halter. Head halters can give all family members, even young children, a considerable amount of control over the pet.

        Enough is Enough: Using a “Stop” Command


        If biting begins during play, it is important that the pet learn to stop on command. This can be done by giving an “enough” command when she is biting. Begin training when the pet is very calm. Hand the puppy a small piece of dry food as you say “okay” in a relaxed tone. Next, hold another piece of food in front of her and firmly say “enough” without raising your voice or yelling. If the puppy doesn’t attempt to make contact with your hand or the food for two seconds, say “okay” and give her the food. IF she touches you hand before two seconds pass and before you say “okay,” immediately say “enough” with sufficient force to make her back away but not frighten her. Be dramatic, lean toward the pup, and make eye contact when you give the instructive reprimand. Gradually increase the time the puppy has to wait. Once she learns to leave the food alone on command, practice the exercise without food by using only your hand. Later, repeat the exercise when the puppy is more keyed up

        The goral is to get to the point that the puppy will not take food or touch your hand once you have said “enough,” no matter how tasty the treat or how interesting your hand. For this technique to work, the whole family must be very consistent, have precise timing, and practice every day. If necessary, a leash and head halter can be used to teach the “enough” command. Whenever the puppy ignores the command to stop biting, a gentle pull on the leash will closer her mouth. Eventually the puppy will stop biting when you give the command.

        Introducing your Puppy to the World.

        Puppies don’t come into our world with ready knowledge about humans or the world in which we live. They need to learn about everything and everyone while they are young and sociable. This is very important, because dogs can become fearful or antisocial toward new people and animals if they have limited early exposure. They may also become fearful or anxious about places, situations, sounds, sights, and odors with which they are unfamiliar. Therefore it is important that you expose your young puppy to as many new people, animals, and experiences as possible, especially those that are different from your home and family.

        What is Socialization?

        Socialization is the process of developing relationship with other living beings. The most important time for socializing puppies is during their first three months of life. If this time passes without your puppy making sufficient social contact, irreparable damage may result, leading to fear, timidity, or aggression. During the first seven weeks the puppy’s most important contacts should be with her mother and littermates to establish social relationships and communication with other dogs. However, social interactions with people should not be neglected at this important stage of development. After seven weeks, it’s important for the puppy to learn about her new family and home, so this is a good time to adopt. The more people and other animals to which your puppy is exposed during this socialization period, the less likely she will fear similar situations later in life. Although the first twelve weeks are the most important, socialization should continue into adulthood.

        Socializing Your Puppy

        Start with simples, calm introductions over the first few days, with one person at a time. As long as the puppy doesn’t display any fear, begin to include more people, noises, and activities. Invite friends, relatives, and their pets to come to your home to meet, greet, and play with your puppy. To make new introductions special, give a small food treat to your puppy whenever she meets someone. However, do not give the treat if she is lunging or jumping up. Teach her to sit before giving treats or attention. When your veterinarian says your puppy is adequately vaccinated, taker her on as many walks and outings as possible but be careful to avoid areas where stray dogs (that may carry diseases) roam.

        It is important that your puppy meet and receive treats from a wide variety of people, of all ages and appearances. A puppy that grows up in a restricted social group, such as all adults or all females, may show fear and aggression when later exposed to children or men. Some pups seem to consider children a completely different species since they walk, act, and talk much differently than adults. If there are no children living at home, it is likely your puppy will encounter them at some time. Therefore, you may need to go out of your way to provide your puppy with plenty of positive interactions with children during her early months. The same is true for anything else that is not normally found in your home, such as men with beards or people wearing hats or uniforms.

        What is Habituation?

        Habituation describes how a pet can adapt to new environments through repeated exposure. As your puppy matures, new situations can lead to fear and anxiety. Begin habituation at an early age by frequently exposing your puppy to different sights, sounds, odors, surfaces, and situations. For example, repeated short car rides can minimize car ride anxiety—provided that nothing unpleasant occurs during the ride. Expose your puppy to a variety of stimuli, such as traffic sounds, sirens, airplanes, water, elevators, and alarm clocks. If your puppy seems to be exceptionally cautious when first introduced, start with mild exposure and give food rewards for non-fearful responses. Your puppy can then be gradually “built up” to more intense exposure. Recordings of sounds are available if it’s difficult for you to expose your puppy to these sounds in your own neighborhood.

        Additional Help

        An excellent way to promote early socialization and habituation is to enroll your pet in a puppy class. These classes offer a great opportunity for socialization and an early start in training at a time when puppies learn rapidly and before bad habits are picked up. Many communities now have classes where puppies can be admitted as early as eight weeks of age. Puppy classes should provide a variety of exposure opportunities that might not be available tin your home. These should include meeting and playing with a variety of people and dogs, as well as fun opportunities to habituate to different surfaces, obstacles, sounds, and moving objects such as skateboards, seesaws, wheelchairs, or even vacuum cleaners. Some puppy classes also have a costume-and-uniform night. By exposing your puppy to these experiences in a controlled and fun environment, she will less likely be fearful of later experiences and be well prepared should you wish to progress to agility training or hospital visitation programs. Ask your veterinarian about what classes are available in your area. A commercial collar or diffuser with pheromones that simulate those produced by a nursing mother dog may also help reduce fear and improve sociability.

        Punishment can negatively influence your puppy’s relationship with people. Therefore, avoid training methods and classes that use physical punishment or that recommend the use of physical confrontation such as rolling over, pinning down, or showing your dog’s face in a mess. These methods could make your dog fearful of the human hand or even cause her to snap at you in fear. During the early months of your puppy’s life, stay positive and minimize interactions that might make your pet anxious. Even veterinary visits can be made positive by keeping upbeat and bringing along your puppy’s favorite treats.

        Properly socializing and shaping your puppy’s temperament requires an investment in time and patience. But your efforts will all be worthwhile when you become the proud parent of a social, friendly, well-adjusted dog.

        Housetraining Your Puppy.

        Your home has just been blessed with a new puppy who arrived cuddly, warm, and ready to be loved. Unfortunately, she did not arrive housetrained.

        Housetraining your new puppy can be easy and successful if you dedicate the necessary time and patience. A simple housetraining plan includes using rewards to teach your puppy where to eliminate, constant supervision, and preventive confinement when you are not able to supervise. With these elements, most pups can be trained in a relatively short period of time.

        Getting the Message Across

        If you want your puppy to eliminate outside, it’s helpful to know what events might stimulate elimination. These include eating, drinking, playing, and waking from naps. If you watch your puppy carefully, especially after these activities, you will soon be able to notice signs that she needs to eliminate.

        The first and most important step is to teach your puppy where you want her to eliminate. To accomplish this, you must accompany her every time she goes outdoors. Choose a specific location with easy access. The area will soon become a familiar spot as the pup recognizes the odor from previous excursions. Mildly praise any sniffing or other pre-elimination behaviors. When she eliminates, praise her heartily, offer a tasty food reward, or start playing. Rewards help the puppy quickly learn what is expected whenever she goes outside. Many dogs can learn to eliminate on command if you add a unique word or phrase such as “potty time” or “hurry up” just as they begin to eliminate.

        As you begin housetraining, try to take your puppy outdoors every one to two hours. As she grows older and gets the hang of things, you can wait gradually longer between outings.

        Scheduling Puppy’s Dinnertime

        Controlling your puppy’s feeding schedule provides some control over her elimination schedule. Offer food a few times a day at the same times, and make it available for no longer than thirty minutes. Most will eliminate within a predictable time after eating, usually within the first hour. This way, you can plan your schedule so that your puppy eats, eliminates, and plays before you confine her or leave her alone. If your puppy tends to eliminate overnight, you may want to give her her last meal at least three to five hours prior to bedtime.

        Preventing Mistakes

        The most challenging part of the housetraining process is preventing your pup from eliminating indoors. Do not consider your puppy housetrained until she has gone for at least four to eight consecutive weeks without eliminating anywhere in the home. Until she accomplishes this, keep her within eyesight of a family member at all times. A leash is a handy tool to keep your puppy nearby.

        When you are unable to provide supervision because you are busy, sleeping, or away from home, confine your pup to a relatively small, safe area. Always take her out to eliminate and make sure that she ahs sufficient play and exercise before confinement.

        A wire or plastic crate provides an excellent area in which to confine your puppy when you cannot observe her. Most puppies will quickly adapt to the crate. Be sure to associate good things with the area, rather than using it for punishment. Feeding in the crate, tossing toys inside for the pup to chase, and hiding treats in there should all encourage your puppy to look forward to being in the crate. Do not use the crate for longer than your puppy can physically control elimination, or for more than four hours during the day on a daily basis.

        If your puppy will be home for longer periods, you should arrange to have someone walk her every few hours. Alternatively, you will need to confine your puppy to a larger area, such as a small room or exercise pen, with enough space to rest and play and a spot to eliminate if necessary. For easier cleaning, place paper or puppy elimination pads at the sites where she eliminates.

        Returning to the Scene of the Crime

        To help prevent your puppy from returning to previously soiled areas, remove urine and fecal odor with an effective commercial product. Saturate the areas—spraying the surface is seldom sufficient. If your puppy begins eliminating in areas of the home, prevent access to these areas by closing doors to the rooms, using baby gates, or moving furniture over the soiled areas. Motion-activated sprays or alarms can teach your puppy to avoid an area. Since most dogs avoid eliminating in areas where they eat or play, placing food, water bowls, bedding or toys at the pots where the puppy soils may discourage elimination in these areas.

        Keeping Your Cool

        No puppy has ever been housetrained without making a mistake or two. Be prepared for the inevitable. It does not help to become frustrated and harshly discipline your puppy. Punishment is the least effective and most overused approach to housetraining. Your goal is to teach your puppy where to eliminate, since trying to punish a puppy for every place she might soil is a fruitless task. The only time that it makes any sense to try to stop undesirable soiling is when you see it occurring. A quick stomp of the foot, loud clap, tug on the leash, or abrupt “no” should be all that is necessary to stop the behavior. Immediately take your pup outdoors to finish. A correction that occurs after your puppy has finished eliminating is useless because she will not understand why she is being corrected. If the punishment is too harsh, she may learn not to eliminate in front of you, even outdoors, and you run the risk of ruining the bond with your puppy. Under no circumstance should you rub her nose in a mess. She will learn absolutely nothing from this, except to be afraid of you.

        Some pets will squat and urinate as they greet family members. Never scold them. This problem is due to either nervousness or excitement, and scolding will make the problem worse. Avoid any type of greeting that triggers this behavior. The problem should eventually improve if you ignore your puppy during greeting until she is calm, or teach her to sit calmly for a treat.

        With a little patience and a consistent approach, your puppy will be as housetrained as the rest of your family.

        Housetraining Your Kitty.

        While most cats can be trained to use a litter box, it’s important that you help your kitten get off to a good start. If possible, obtain a kitten that has already bee litter box trained in his previous home.

        The Right Stuff

        When you get your kitten, find out what type of litter was used in his previous home. Use the same type of litter at first, then gradually introduce a new brand if necessary. A plastic box is the most practical and easy to clean. The sides should be low enough that your kitten can easily climb in and out. Place the box in a relatively quiet area with minimal traffic that is easily accessible. Kittens are creatures of habit. Once you find a litter, litter box, and location that the cat likes, stick with it.

        Some kittens dislike certain scents or litter liners, so it is usually best to start with an unscented clay or clumping litter in a clean, dry litter box. If you already have cats at home, provide at least one additional box for each new cat. Most kittens will use kitty litter in preference to other surfaces, except perhaps the soil of a potted plant. To prevent mishaps, keep plants out of your kitten’s reach or cover the soil with pinecones or decorative rocks.

        To ensure that your kitten uses his litter box, keep him within sight at all times. If he stops playing and begins sniffing around, gently carry him back to the litter box. Praise any sniffing or scratching and give him loads of praise or a small food treat for eliminating. Whenever you are unable to watch your kitten, restrict him to a small, cat-proofed room with his litter box. Continue this for at least the first two weeks, until he is using his box regularly.

        Using a covered litter box can help control the odor in your home and can be helpful for kittens with poor aim. If your cat is reluctant to use a covered box, you might first try using a large cardboard box with the entry end left open and then switch to a covered box if successful.

        It’s a Dirty Job but You’ve Got to Do It

        You must keep the box clean so your kitten will return to use it. To start, it is better to err on the side of being too fastidious about the cleaning. Scoop the box at lest once daily and more often if you have the time. Replace litter regularly so the depth remains constant. Clean the box once a week, unless you are using a clumping litter (which might only need a complete cleaning every two to four weeks). To clean the box, empty the contents, use soap and hot water, then rinse well to remove all soap odor.

        Changes

        Once you find the litter, type of box, and location your kitten likes, avoid making sudden changes. If you need to change the litter box location, place a separate box in a new location but do not take away the old litter box until your kitten is using the new location. If you decide to switch brands of litter, gradually replace the old litter with the new over a couple of weeks. Alternatively, add a second box with the new litter but do not remove the old litter until the cat is using the new one.

        Since it is important that your kitten feel comfortable where is eliminates, try to prevent anything unpleasant from happening when he is near his litter box. Don’t give your cat medicine or scold him when he’s near the box. Locate the box in an area free of startling noises, such as a washing machine, radiator, or furnace. To keep your kitten’s litter box away form children or dogs, use a baby gate or a cat door to give him some privacy.

        Causes of Housesoiling

        If your kitten eliminates outside his box, it won’t take long for him to develop a habit of using this undesirable area. Therefore, it is essential that you immediately identify and correct the cause.

        These are some common causes of litter box problems:

        • The brand of litter was changed.
        • The litter has scented additives or the odor of cleanser/deodorants.
        • The litter box is not cleaned frequently enough.
        • The litter box was changed or moved to a new area.
        • The kitten was frightened or something frightening happened in or near the box.
        • The kitten has medical problems.
        • The kitten has found a more appealing area or surface.

        When Mistakes Occur

        When mistakes occur, thoroughly clean all soiled areas with a commercial odor neutralizer. Many cats will not soil where they eat or play, so you can place the pet’s food bowl or toys in the area that has been soiled. To decrease the appeal of the soiled area, place a sheet of plastic carpet runner (nubs up), two-sided tape, an aversive odor (perfume, citrus, commercial spray), or a motion-detector alarm in the area. Never punish your kitten for making a mess outside his litter box. Punishment can make the problem worse and might cause the kitten to fear you, especially if you swat him or rub his nose in the mess.

        If your kitten continues to eliminate out of the litter box, take him to your veterinarian. A physical exam and lab tests can determine whether there are medical problems. For example, bladder disease, diarrhea, and constipation can irritate your kitten when he eliminates and cause him to avoid the box.

        Spraying

        Spraying is a form of territorial marking that may begin around six months of age. The cat will back up to a vertical surface, such as a wall or sofa, and spray urine against it. Although neutering eliminates most spraying, some neutered cats do spray. If the problem persists after neutering, seek advice from your veterinarian.

        Helping Your Dog Overcome the Fear of People.

        Dogs can become fearful of people because of inadequate handling and socialization during the first few months of life, previous unpleasant experiences with people, medical problems, or genetics. No matter what the cause, the goal is to teach your dog to be relaxed around people and enjoy their company. You can do this by carefully controlling interactions with unfamiliar people so your dog is less likely to feel threatened and more likely to relax and have a positive experience.

        What Not to Do

        Don’t make the mistake of forcing your dog into social situations. He needs to gradually learn to feel comfortable around people. Encouraging visitors to approach or reach for a pet that is fearful only makes matters worse. Even if your dog allows strangers to pet him, it doesn’t mean he enjoys it. If your dog feels trapped because he is on a tight leash or can’t escape when someone approaches, he might become aggressive. If you try to console him when he growls, you may inadvertently reinforce the aggressive behavior.

        Since the goal is to change the association from ear to something that is positive (known as “counter-conditioning”), any unpleasant encounter can worsen the problem. Don’t raise your voice or yell and never use physical punishment or harsh corrections such as pinning, using a pinch or prong collar, popping a choke collar, or hitting. Although punishment may temporarily stop the undesirable behavior, it will only heighten your pet’s fear and anxiety.

        During the initial stages of training, keep your pet away from situations that might make him anxious. For example, avoid crowded areas during walks and confine him to a quiet room during noisy social gatherings in your home.

        Control Social Situations

        The first thing you can do to make your dog feel more comfortable is to instruct visitors how to act around him. The less threatening the person appears, the better. Most dogs are more comfortable if visitors squat, avoid eye contact, and keep hands to their side. A quiet tone of voice and slow body movements are also important.

        Your dog may also feel less threatened if he can avoid the situation. Too much tension on the leash or holding the pet tightly will likely make him more nervous. Be sure you have adequate control and keep enough distance between your pet and unfamiliar people to ensure safety and keep your dog calm. Your dog also takes his cues from you, so if you are anxious or nervous, you should avoid stressful situations until you are comfortable and able to calm your pet.

        Help Your Dog Relax with People

        To lessen your pet’s anxiety, you need to repeatedly associated something very positive with the presence of people. Special food treats can help you dog warm up to people. Be sure to select treats or bits of food that he thinks are absolutely fabulous. Small pieces of chicken meat, cheese, freeze-dried liver, or semi-moist dog treats are good choices for most dogs. To really enhance the association between food and unfamiliar people, these special treats should be given only when introducing him to unfamiliar people.

        Getting Started

        If your pet is extremely anxious around people, begin where he is most comfortable—perhaps in your home or yard. Be certain that he is reward-trained to sit and relax immediately on command. Next, begin exposure training by setting up a greeting with a friend or relative with whom your dog is unfamiliar. Have the person stand at a far enough distance that your dog is relaxed and shows no sign of anxiety. Ask your dog to sit when he first notices the person and give him the special treat. Then have the person move a step closer. Give your pet another treat if he stays relaxed.

        The person should gradually approach while you continue giving treats. If your dog begins to show any sign of tension (for example, if he won’t take his eyes off the person, seems agitated, shows less interest in the treats, or responds more slowly to the command), the person can move sideways instead of forward; if your pet takes the food and settles down, the person can then move forward again. The exercise should go so slowly that the pet should show no sign of anxiety, such as trembling, pulling away, or whining anxiously. Be prepared to stop the session before you reach your pet’s limits. The goal is to end on a positive note and begin the next session at a distance that elicits no sign of anxiety in your dog, until eventually he relaxes and takes treats from the visitor.

        Improving Control and Safety

        Consider the use of a head halter and leash if you need more control, especially if your dog shows signs of aggression. Head halters are a quick and effective way to turn the dog’s eyes and head away from the person, close his mouth, or make eye contact. You should release the tension when he is calm. Confine your pet to a room or crate in that room before your company arrives. You can then bring the dog out wearing the head halter to begin the introduction process. Once the dog is comfortable with the exposure exercises in your home, practice at the homes of various friends, and then in a wide variety of situations.

        Making Progress Step by Step

        Once your dog learns to accept unfamiliar people who move slowly and calmly, he should gradually be introduced to similar but progressively stronger stimuli, including quicker movements and various tones of voice used by the person who is approaching. If there is risk of aggression, seek the assistance of a behaviorist before starting these exercises.

        Specific things about a person may make a pet anxious, such as beards, glasses, hats, carried objects, uniforms, vanes, wheelchairs, and tone of voice. Pay attention to what makes your pet most anxious and avoid these stimuli in your initial training sessions. For example, if your dog is especially afraid of beards and glasses, wait until he is comfortable with people without beards and glasses before including them in the conditioning sessions. Slowly add accessories such as hats, large purses, sunglasses, and backpacks, and gradually change the type of person (for example, from a man with a beard to a woman with a walker).

        If your pet is overly fearful or anxious, anti-anxiety medications, natural supplements, or pheromones may help to calm him and improve treatment success. Discuss these options with your veterinarian.

        Preventing the Fear of People

        In most cases, dogs will not become fearful of people if they have ample opportunities to socialize with a wide variety of people during the first few months of life, are frequently handled in a gentle manner, and are raised without harsh training techniques or physical punishment. Enrolling in puppy classes at eight to ten weeks of age can be an excellent way to ensure socialization with a variety of people, dogs, and environments.

        Helping Cats and Kittens with Fear.

        Cats and kittens may exhibit fearful behavior for a number of reasons. For some, the tendency to be anxious and fearful is inherited, especially from the father. Others may exhibit fear because of insufficient social or environmental experience. Even though cats are domestic animals, they need frequent and pleasant social handling from people during the early weeks of life to be comfortable with humans. Lack of environmental experience during the early months can also cause problems. Kittens that are raised in a rural environment may have difficulty adjusting to the hustle and bustle of city life. Traumatic experiences such as rough handling, punishment, or scary events may also cause fearful behavior. Some cats become more anxious when moved to a new home or when there are changes in the home. And last, pain or chronic discomfort can affect a cat’s temperament and lead to fear and avoidance behaviors. For that reason it is important to take a fearful cat, especially a newly fearful cat, to the veterinarian for a checkup before beginning behavior modification.

        No matter what the cause, the goal is to change the negative association with unfamiliar people and fearful situations to one that is positive. This can be accomplished by repeatedly introducing your cat to a person—from a distance—when he is relaxed and gradually decreasing the distance between him and the person. This process of repeated exposure that results in less anxiety is called desensitization. By combing introductions with something the pet likes, such as food or play, you can change the emotional response; this is known as counter-conditioning.

        Patience Is the Key

        You must go slowly and not make the mistake of pushing your at into uncomfortable situations. For example, allowing people to come up and reach for a pet that is nervous and distressed will usually make matters worse. Some cats may even become aggressive when frightened.

        Anything you do that your cat construes as unpleasant may worsen this fear and anxiety. Do not raise your voice, act anxious, or use punishment of any type. During the training period, your pet should be protected from any overwhelming situations. For example, you might confine your cat to a quiet room during noisy social gatherings or when active children are in the home. Keep in mind that most cats adapt more quickly to social situations if they have some freedom and control, and holding pets tightly when someone approaches usually makes them more nervous. However, make sure visitors are safe by confining your cat if he appears aggressive.

        Pay attention to what makes your pet most anxious. Cats hide, vocalize, arch their back, hiss, and hold their ears back when anxious, so when you see these reactions try to identify the cause. Once you recognize things that make your cat anxious, avoid them in your initial training sessions. Your goal is to slowly raise your cat’s tolerance to people and situations that currently make him nervous and fearful.

        Fear of People

        The first thing you can do to make your cat more comfortable with unfamiliar people is to instruct visitors how to act around him. The less threatening a person appears to your pet, the better. Ask visitors to sit or squat low to the floor, making little or no eye contact. They should speak quietly, move slowly, avoid initiating touch, and allow your cat to approach when ready.

        You may have noticed that certain things about a person make your pet exceptionally anxious, such as gender, facial hair, eyeglasses, hats, tone of voice, or simply the proximity to your cat. Avoid those characteristics during your initial training sessions. For example, if your cat is more afraid of men, begin counter-conditioning sessions with women. If your cat dislikes children, start with adults. Slowly add accessories such as hats, large purses, sunglasses, and backpacks. Over time, introduce your cat to stronger stimuli, including more eye contact, faster movement, various tones of voice, and closer distances.

        To lessen your pet’s anxiety, you need to associate something exceptionally special with the presence of people. The aim is to replace your pet’s feelings of fear with a happy anticipation of good things. Special food treats can be very helpful. Be sure to select treats or bits of food that your cat thinks are absolutely fabulous—small pieces of chicken, meat, tuna, cheese, shrimp, and freeze-dried fish are good choices. To fully enhance the association, these treats should be given only during conditioning sessions. At first, give the treats when your cat enters the room with the visitor there. Next, have the visitor calmly flip treats to your pet with minimum hand movement. Gradually have the visitor flip them closer so your cat has to approach the person to retrieve the treat. Without reaching toward your pet, the visitor can allow your cat to come up and sniff or take food from an open hand. For cats who really enjoy playing, toys may be another alternative for making a positive association with a stranger.

        Fear of Objects

        Desensitization and counter-conditioning also can be helpful for reducing fear of inanimate things, such as objects and noises. For example, if your kitten becomes frightened when a kitchen timer beeps, cover the timer with a towel to produce a sound so quiet that your pet looks toward it without fear. Then toss your pet a treat. Repeat this again and again, uncovering the timer little by little. Eventually your cat will look forward to the noise because he ahs become conditioned to expect something good after hearing it.

        A similar approach can be taken with a pet that becomes afraid when you carry objects, such as large garbage bags. Take several bags that are so small they do not make the cat anxious and place them in locations around the home next to containers of tasty treats. Whenever you walk by, pick up a bad and toss a treat to your cat. When you can tell that your cat gets excited whenever you pick up a bag, increase the size of the bags and repeat.

        Additional Help

        Commercial pheromone products are safe and may effectively help relieve anxiety in some cats. For severe cases, anti-anxiety medication can be helpful. You may want to discuss these options with your veterinarian.

        Some fearful cats will display intense aggression instead of avoidance. If this is the case with your pet, your veterinarian may suggest referral to a specialist who can develop a treatment plan for these more serious problems.

        Crate Training.

        We all need a special place to call our own-a sanctuary of sorts. Your pet is no different. Part of raising a healthy dog is providing her with her own “safe haven,” and crates are a perfect solution. Most dogs can be easily trained to enjoy spending time in their crates.

        Crate training is neither cruel nor unfair, provided your puppy has sufficient social interaction, exercise, and an opportunity to eliminate before she is placed in the crate. In fact, allowing your dog to wander through the home unsupervised to investigate, chew, and eliminate is unwise and potentially dangerous.

        There are numerous benefits to crate training your dog:
        • Safety for your dog
        • Prevention of household damage (chewing, elimination, etc.)
        • Help with house training
        • Preparation for travel, boarding, and spending time alone
        • Improved relationships (fewer problems mean less frustration and discipline)

        How to Choose a Crate

        Two basic styles of crates exist: metal collapsible crates with tray floors and plastic traveling crates. Look for one that is large enough for your dog to stand up and turn around in–even when she is full-grown. Provide the type of bedding on which your dog likes to nap, but keep in mind that your pup might be less likely to chew flat, tightly woven carpet samples or remnants that she is blankets or towels. If your dog must be left alone for more than four hours at a time, consider a pen or dog-proofed room for confinement rather than a crate. Another option is an exercise pen that allows a little more room to move about. Also consider a midday visit from a dog walker.

        Because dogs are social, the ideal location for the crate is in a room where your family spends a lot of time, such as the kitchen, den, or bedroom, rather than an isolated laundry or furnace room. A radio, television, or CD may help calm your dog and mask noises that may trigger barking. Finally, for the crate to remain a positive, enjoyable retreat, never use it for punishment.

        Training Puppies

        Introduce your puppy to the crate as soon as possible. Place treats, toys, chews, or food in the crate to motivate her to enter voluntarily. You can teach her to go into the crate on command at feeding time or when given a chew toy. Practice frequently by tossing pieces of kibble in the crate. Each time she runs inside, say “Go to your crate.” Eventually she will learn to enter when you give the command and point to the crate.

        The first confinement session should be after a period of play, exercise, and elimination (when she is ready to take a nap or quietyly play with a toy). Place your puppy in her crate with a treat and a toy and close the door. Leave the room but remain close enough to hear her. You can expect some distress the first few times your puppy is separatef from family members, but she should soon settle down if she is tired. Never reward the pup by letting her out when she cries or whines. Instead, ignore her until the crying stops and release her before it starts again. If your puppy won’t settle in her crate, make sure that you choose a time when she has had sufficient play and exercise and that she has recently eliminated so she is ready to relax or nap.

        As the crate training continues, be sure to give her a favored chew toy or food-dispensing toy when placing her in the crate so she has something to keep her occupied. Gradually increase the amount of time your pet spends in her crate. However, be certain to return and release your pet before she needs to eliminate.

        If you have a regular routine for when your dog goes in her crate, she may soon begin to enter voluntarily when it’s time to rest or to chew on a toy. Crating your dog is really not much different from placing a baby in a crib or playpen. You can use the crate in a similar manner, allowing your dog to take a nap or play with toys in the crate when you can’t supervise her directly.

        Remember to wait until your dog is quiet before you release her from the crate. If she continues to vocalize, try the following:

        • Interrupt the behavior with a firm “no” command through an intercom placed near the crate.
        • Gently throw an aluminum can containing a few pennies onto the floor near the crate.
        • Use a device that emits a sound or spray of air each time your dog barks.

        These disruptions should be strong enough to stop the barking, but do not repeat them if they are not immediately successful or cause excessive fear.

        Training Adult Dogs

        Training adult dogs is similar to training puppies, except that the introduction period should be much longer. Introduce your dog to the crate by setting it up in the feeding or sleeping area with the door open. Close the door to the room or use a baby gate to keep the pet in the room. Place food, treats, and toys in the crate so your dog is encouraged to enter on her own. Add comfortable bedding so she is likely to stay inside and rest. Once she enters the crate freely, you can begin to close the door for short periods of time. Some dogs may adapt more quickly if you have crates available in more than one area of the home where the family spends time.

        Some dogs do not deal well with confinement. These are usually pets who have not been properly crate trained, older pets that are used to more freedom, or pets with anxiety disorders. If your pet panics each time she is placed in her crate with signs of drooling, destructive escape behavior, biting the crate (hard enough to break teeth), anxious vocalizations, or elimination, stop using the crate and consult your veterinarian.

        Busy Dogs are Good Dogs.

        Every dog—and every animal, in fact—has social, mental, and physical needs that must be met to ensure a healthy and happy life. Over the 13,000 years or more of domestication, dogs have been bred into a wide variety of sizes and shapes and for a wide range of tasks, such as hunting, retrieving, herding, and pulling sleds. The type and amount of mental and physical stimulation required by any dog will depend on age, breed, health, and even individual differences.

        Building a Positive Relationship

        Dogs make wonderful family pets because of their social nature. Social times with your pet not only are important to meet mental and physical needs, but also can make your dog more content, improve your relationship, and help your dog learn what you want to communicate during training. When these needs are not me, a dog may exhibit destructive behaviors, such as raiding the garbage, digging, soiling inside the house, seeking attention, biting, and jumping on people.

        To help build a good relationship between you and your dog, always focus on rewarding what is desirable rather than punishing what is undesirable. If you focus only on trying to stop undesirable behavior, you might instead contribute to mental distress, abnormal behavior (such as excessive grooming and spinning), and stress-induced diseases. Reward-based obedience training, fetching, and agility training are activities that have benefits on many different levels.

        Keeping the Brain Busy

        Keeping the body busy is essential for maintaining good physical health and lean body weight, as well as providing an outlet for the daily activities in which your dog would otherwise engage. Choose games and activities that are fun and practical for you but also designed for your dog to use the natural instincts of her breed. For example, herding dogs may be most suited to games that involve running and chasing, or even herding trials; hunting dogs may benefit from retrieving games; terriers may enjoy having a pit in which to dig; and sled dogs may enjoy activities such as pulling a cart. Agility training, flyball, herding trials, and Frisbee competitions are also fun and positive ways to provide physical and mental stimulation. But also keep in mind that because of health or age some dogs may be less able to perform strenuous physical activities; in these cases, medication or diet for any underlying pain and some alternate activities such as shorter walks, tug toys, and food puzzles may be more feasible ways to keep the brain and body enriched.

        Play and exercise also provide important social time together and can be used to improve training. Walks, jogging, chase games, retrieving, playing with food, hide-and-seek with pieces of food, and even tug toys (provided that the dog will drop them voluntarily without aggression) are just a few examples of interactive games. Dogs can also expend energy and improve their social skills by playing with other pets.

        Alone Time

        There are times when your dog will need to spend time on her own. Pets that have a regular and appropriate social enrichment program may use these times to nap and rest. It’s often most comforting and safest for both the pet and the family to use a consistent location (a room, create, dog bed, or pen) for resting and napping when you are not there. Feeding and chew toys can also be left in this area to keep your dog occupied.

        Some dogs may still be energetic and want to engage in further play at times when they need to be left alone. These dogs can be given an opportunity to occupy their alone time by playing with toys. Multiple meals and feeding toys are an excellent way to have your dog focus on desirable activities when you are no around to supervise. Many toys are designed to be stuffed, coated, or filled with food, treats, or chews and require some form of manipulation to dispense the food. Other options are foods that promote dental health by requiring more time to chew and timing devices that deliver food or tos throughout the day. Your pet’s interest in these and all toys can be maintained if most of your dog’s daily ration is fed from them, special treats are added, and the toys are novel. Therefore, it may be best to rotate the toys to maintain interest rather than making the same ones constantly available. Again, your pet should be confined to a safe, stimulating, dog-proof area so destructive behavior and soiling in other parts of the home can be prevented.

        Dietary Concerns

        Working for food requires mental and physical activity. While working for food means that your pet will expend time and energy in food acquisition, the amount of calories given in feeding toys must be counted as part of your dog’s daily total. After you add up all the calories from training treats, food toys, and chews, you can give your dog a small bowl of food with her remaining calories and nutrition at the end of the day. After eliminating one last time before bedtime, your dog should be ready to settle down for a night of sleep.

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