Laryngeal paralysis is a condition that results from loss of normal arytenoid abduction.  The disease can be unilateral (hemiparalysis) or bilateral (complete paralysis).  Cricoarytenoid articulation (abduction) is controlled exclusively by the cricoarytenoideus dorsalis muscle innervated by the recurrent laryngeal nerve (a branch of the vagus nerve.)

Most commonly, it is a slowly progressive disease but will frequently show up clinically as acute respiratory distress.  The disease may be associated with generalized muscular, neurologic, neuromuscular conditions, tumors, trauma, or chronic tracheitis / laryngitis.  In cats it is fairly rare, but has been associated with FeLV infection.  Although the condition can occur at an early age as a congenital lesion (Bouvier des Flanders and Siberian Huskys), it typically shows up in middle age to older large breed dogs.  Clinical impression suggests Labrador and Golden Retrievers are over represented.  Presentation will vary with the severity of disease.  With a slow insidious onset, owners may only note a change in the sound of the dog’s bark.  Acute exacerbation of the problem can lead to respiratory distress, cyanosis, and death.  The condition in this form can be difficult to distinguish from an animal in congestive heart failure, as both will show respiratory distress and cyanosis.  Also, ventricular arrhythmias (VPC’s) can occur with laryngeal paralysis due to hypoxia (low blood oxygen levels).  The dog with laryngeal paralysis does, however, have a very characteristic breathing pattern.  The respiratory distress is typically localized to the inspiratory phase only, and is accompanied by louder stridor (very noisy inspiratory sounds).  These dogs will have open mouth breathing , and their tongues can become swollen or enlarged (as seen with heat stroke).  A lot of dogs will present with an elevated temperature (102 – 104) as the problem can be exacerbated by the Texas sun and overheating.

The panting and respiratory effort associated with overheating causes laryngeal edema, worsening the obstructive process.  On auscultation, lung sounds can be very harsh, but these are typically dry and referred upper airway sounds.  Auscultation at the thoracic inlet and trachea reveal the same harsh sounds, only louder than in the lungs.

History and physical exam is usually enough to reach a tentative diagnosis and begin emergency treatment.  Sedation and corticosteroids (to help reduce the edema) can be employed in a crisis.  Oxygen can be supplemented as needed.  Definitive diagnosis requires direct visualization of the larynx under light sedation.  Direct visualization also permits one to rule out other obstructive processes (masses, abscesses, etc.) in the oropharynx (back of the throat).  EMG studies of the arytenoid muscles can also be done.  Long term control can be either medical or surgical.  Several surgical procedures have been described.  Medical treatment involves keeping the pet at a lean, healthy weight, inside in the air conditioning, avoiding collars (harnesses are much better), restricting exercise, and periodic use of steroids (anti-inflamatories) and acepromazine (or other tranquilizers).  Also, any underlying condition (metabolic, tumors…) should be addressed.