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.
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