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Laryngeal Paralysis

Geriatric Onset Laryngeal Paralysis Polyneuropathy (GOLPP) aka Laryngeal Paralysis
Mary Ann Nieves, DVM, DACVS

We are all familiar with the canine patient that presents with harsh breathing or in respiratory collapse due to laryngeal paralysis. These patients have long been diagnosed as having idiopathic laryngeal paralysis, a condition of unknown etiology. Historically, acquired laryngeal paralysis is a condition of older middle to large purebred and mixed breed dogs; the Labrador retriever is well represented in this group. While most cases of laryngeal paralysis are acquired, a congenital form has been identified in many breeds including the Bouvier de Flanders, Siberian husky, Siberian husky mixed breed, and Alaskan sled dog. Hereditary laryngeal paralysis has also been noted in the dalmatian, Rottweiler, Pyrenean mountain dog, Leonberger and white-coated German shepherd dog with which polyneuropathies are often associated. Congenital laryngeal paralysis typically presents in dogs less than two years of age. Although much less common, laryngeal paralysis can also be seen in cats.

Today, we now know that laryngeal paralysis is a single manifestation of a much more generalized disease known as geriatric onset laryngeal paralysis polyneuropathy (GOLPP). A thorough understanding of GOLPP will help us to educate clients on the complexity and progressiveness of this disease. Other clinical manifestations of this condition include esophageal dysfunction and progressive neurodegeneration often mistaken to be secondary to orthopedic disease. The disease process is progressive in dogs with some patients taking years to progress, while others progress rapidly.

A prospective study was conducted evaluating esophageal function in canine patients with idiopathic laryngeal paralysis as compared with breed and age matched controls. Patients with idiopathic laryngeal paralysis were found to have esophageal dysfunction, especially with liquids, and more pronounced in the cervical and cranial thoracic esophagus. The study found that patients with esophageal dysfunction were more likely to have developed aspiration pneumonia. Ten of the 32 dogs with idiopathic laryngeal paralysis had generalized neurologic signs when enrolled in the study, and all dogs by one year had developed generalized neurologic disease.1 Current recommendations are to assess esophageal and neurologic function in these patients to be able to help them and their families as they progress through this disease.

Laryngeal paralysis anatomy and diagnosis

Abduction and adduction of the paired arytenoid cartilages and tensing of the ventral vocal cord control airflow into the trachea through the rima glottidis. Abduction of the arytenoid is controlled by the cricoarytenoideus dorsalis muscle innervated though the caudal laryngeal nerve of the recurrent laryngeal nerves. The recurrent laryngeal nerves arise from the vagus in the thorax, and course cranially alongside the trachea. The thoracic and cervical esophagus is innervated by the pararecurrent laryngeal nerves, which arise from the recurrent laryngeal nerves. Loss of nervous control to the paired arytenoid cartilages results in a mechanical upper airway obstruction that inhibits normal airflow through the larynx and into the lower respiratory tract. The degree of compromise to the opening of the rima glottidis determines the severity of clinical signs noted.

The activities and panting that accompany the warmer and humid temperatures exacerbate clinical signs of laryngeal paralysis. Subtle signs associated with neurologic dysfunction include change in bark, exercise intolerance, stridor, coughing, throat-clearing or gagging generally when drinking or eating.

We are generally faced with two clinical presentations, a patient who is stable with a change in bark and progressive exercise intolerance or one that is acutely unstable, in respiratory distress with collapse, cyanosis and hyperthermia. Cases presenting in distress are stabilized with sedatives, oxygen by face mask or temporary intubation, intravenous fluids and steroids. Respiratory distress in some patients cannot be alleviated with temporary intubation and oxygen therapy, and repeated attempts to arouse the patients while on intranasal oxygen support results in a repeat of respiratory distress and anxiety. These patients generally require immediate surgical intervention. Stable patients or patients with early signs of laryngeal paralysis should be assessed for esophageal function and electrodiagnostic testing to evaluate for general neurologic dysfunction. This information can provide valuable information in determining which patients may be at increased risk for aspiration pneumonia and generalized weakness.

Diagnosis is based on history, a “characteristic” upper airway stridor and on oral examination of the larynx. Light sedation is required to examine the larynx adequately. Several protocols for light sedation have been proposed. Propofol is an excellent choice as long as it is not provided too quickly which can cause apnea. Dopram is extremely helpful in determining function and is generally used during our laryngeal function assessment. Ultra-short acting thiobarbiturates are also adequate. Drugs such as ketamine or mixtures thereof should be avoided.

Differential diagnoses for upper respiratory stridor include oral or cervical masses, upper respiratory inflammation or foreign bodies. Initial assessment of these patients should include a complete blood count, chemistry profile and abbreviated thyroid profile. Thoracic and cervical radiographs are recommended to evaluate for possible laryngeal or tracheal intraluminal or extraluminal masses or signs of aspiration pneumonia. Occasionally, tracheoscopy may be recommended if clinical signs and results of imaging are ambiguous.

Surgical intervention

While there are several methods to surgically address laryngeal paralysis, the technique of choice is a unilateral arytenoid lateralization (i.e. laryngeal tie-back procedure or laryngoplasty). This procedure has the highest rate of success with the lowest rate of complications. The primary complication encountered is aspiration pneumonia. This can occur preoperatively due to concurrent esophageal dysfunction with esophageal reflux and regurgitation. Most patients generally do very well postoperatively and are often sent home the day after surgery. The use of postoperative medications to control pain must take into account the potential for regurgitation. Hydromorphone should be avoided. Preoperative anti-emetics, metoclopramide and cisapride should be considered. Our choice of postoperative analgesic is a torbugesic constant rate infusion. Postoperative regurgitation is monitored carefully and opioid medications are discontinued if patients are showing sensitivity to these agents.

Postoperative considerations and care

Surgical intervention, in our experience, results in markedly improved respiratory function and exercise tolerance, allowing patients to return to family life. Short-term postoperative management includes halter leads instead of neck leashes, hand feeding of canned food or dry diet and small amounts of water although allowing them to drink as much as required for the first postoperative week. Regular diet and water depth in the bowl is allowed over the second postoperative week, allowing patients to become accustomed to their “new “ airway. Some coughing and gagging with drinking will likely continue for life.

Esophageal dysfunction should be evaluated by an esophagram study either pre- or postoperatively depending on the presentation of the patient, stable versus emergent in respiratory distress. Based on Dr. Stanley’s study, patients should be fed at a 30° incline plane in a sitting position and post-prandially maintained in this position for 10 minutes. Some patients may benefit from metoclopramide and cisapride long term. There is anecdotal evidence that some patients may benefit from treatment before feeding and before bedtime. Clinical signs of aspiration pneumonia should be discussed with owners to aid in early detection and treatment.1

Physical therapy using an underwater treadmill, balancing and coordination exercises are also recommended for patients showing hind limb weakness with the goal of maintaining muscle mass and strength as progressive proprioceptive loss occurs. Daily activities such as short walks on cool days should be encouraged. Reduced activity particularly during hot or humid weather is a lifelong restriction.

Please feel free to call the surgery team at BluePearl Veterinary Partners if you have a patient with progressive upper respiratory stridor or suspected laryngeal paralysis.