Laryngeal paralysis is recognized because of the loss of function in the paired cricoarytenoideus dorsalis (CAD) muscles, which are the only abductors of the arytenoid cartilages. In horses, the condition is usually unilateral (left) and thought to be due to stretching of the left recurrent laryngeal nerve along its longer course around the ligamentum ateriosum. This laryngeal hemiplegia in horses causes stridor that is commonly referred to as roaring and represents more of a performance issue in affected horses than a life-threatening issue.
Laryngeal hemiparesis and hemiplegia probably occur in dogs but are usually not recognized. The clinical entity facing small-animal veterinarians is bilateral laryngeal paralysis. This results in progressively worsening stridor and, ultimately, enough upper airway obstruction that respiratory distress and cyanosis ensue.
Canine laryngeal paralysis may occur as an isolated idiopathic problem, be associated with endocrinopathies (hypothyroidism with axonopathy), result from trauma to the recurrent laryngeal nerves (e.g., bite wounds, iatrogenic surgical injury) or represent one aspect of a more generalized and systemic neurologic or neuromuscular disorder.
The association between laryngeal paralysis and hypothyroidism is the most tenuous. Dogs may be prone to both diseases without any causality between them, and treatment of hypothyroidism usually does not halt or reverse the progression of laryngeal dysfunction. Many dogs with laryngeal paralysis are euthyroid.
The connections between laryngeal paralysis and other neuromuscular diseases are being increasingly recognized and should prompt a careful history gathering and examination to expose other problems that may be concurrent with the more obvious laryngeal signs.
While laryngeal paralysis is seen as a rare congenital problem in some breeds, the clinically significant variant of this disease is that which typically occurs in geriatric sporting dogs, especially Labrador retrievers. Onset of signs is usually after age 10, and many dogs that require treatment are older (12 to 14 years of age).
In addition to stridor (which is usually audible from a distance or can be heard as a loud machinery sound on laryngeal auscultation), affected dogs may also present with a history of coughing, gagging or choking during swallowing. Exercise intolerance is another frequent sign, and its presence should prompt an investigation as to whether it is simply due to hypoxia or whether it might represent signs of appendicular muscle weakness. When dyspnea occurs, it is usually noted more on inspiration.
Once the dog starts becoming sedated, it is helpful to place a rope tie (such as those used for limb restraint on an operating table) around the patient's upper jaw, just behind the canine teeth. This provides an assistant with an easy way to help open the dog's mouth and elevate the head for the examination. The tongue may be grasped with gauze and used to retract the mandible ventrally, exposing the larynx. If there is much resistance to these maneuvers, additional sedation can be administered to just reach the point where such resistance is overcome and the larynx can be observed.
Dogs with end-stage laryngeal paralysis will have arytenoids that are medially displaced and do not abduct during inspiration. This observation can be augmented by administering a bolus of doxapram (2 mg/kg IV) while performing laryngoscopy. Doxapram will induce marked hyperpnea, which in normal dogs will cause increased abduction of the arytenoids. Dogs with laryngeal paralysis will have no such abduction and may have paradoxical motion of the arytenoids such that they adduct during inspiration because of the increased negative airway pressure (Photos 1A and 1B).
In severe cases, dogs may have laryngeal collapse, as the weakened muscles and cartilage succumb to negative pressure even at rest and remain fixed in adduction. In dogs with acute respiratory distress, some elements of laryngitis may be present, secondary to the increased effort expended in trying to breath. However, most affected dogs have little edema and only mild erythema. Dogs with laryngeal tumors may present with identical histories and signs as dogs with paralysis, but this distinction should be immediately evident during laryngeal examination.
Medical management of laryngeal paralysis is at best a stop-gap measure to allow delayed, elective definitive treatment. It is usually predicated on sedation or tranquilization, since stress, anxiety and activity (especially warmer weather) all exacerbate signs. Another strategy that has been reported for attempted medical palliation of signs is the use of tricyclic antidepressants (such as doxepin), although results have not been adequately described, and I have no confidence that any such treatment will forestall the need for surgery in affected dogs. As dogs have an increased demand for oxygen, they increase their tidal volumes and respiratory rates. An inability to reduce airway resistance during such times of peak demand results in further hypoxia, reflexively stimulates further attempts to increase tidal volume and rate and produces a vicious cycle that can quickly proceed to respiratory distress, cyanosis, collapse and death.
Hyperthermia, especially in warmer weather, may become an additional complication that predisposes to patient demise. In severe cases in which tranquilization alone proves insufficient, intubation per os or a temporary tracheotomy may be required to bypass the obstruction produced by the narrow glottis.
Next month, we'll take a look at surgical treatment of laryngeal paralysis in dogs.
Dr. Fingeroth is senior staff surgeon at the Orchard Park Veterinary Medical Center in New York. He is also a consultant to the Veterinary Information Network in the areas of orthopedics and general soft tissue surgery, as well as oncologic, endocrine and neurosurgery. He has been ACVS board-certified since 1988.