Geriatric dogs suspected of having laryngeal paralysis should receive a comprehensive evaluation that includes a complete
blood count, a serum chemistry profile, a urinalysis, electrocardiography and thoracic radiography. The latter is of particular
significance as the association between laryngeal paralysis and systemic neuromuscular diseases results in significant numbers
of affected dogs also having or developing megaesophagus, and possibly aspiration pneumonia. Thyroid testing may also be conducted
if the dog has other signs that suggest this disease, but the relationship between the two is dubious as noted above.
Photo 1A: The appearance of a normal larynx in an unaffected dog during inspiration at rest (no doxapram stimulation given).
(Photo courtesy of Dr. Brendan McKiernan.)
The sine qua non of diagnosis is direct laryngeal examination awake or under light sedation. A flexible endoscope (properly
protected from patient-induced trauma) can be used, while a gross examination per os, using a laryngoscope to depress the
epiglottis and help visualize the larynx, is more typical. It is important that drug selection for sedation and dosing be
carefully chosen, since certain drugs or oversedation can diminish laryngeal function and lead to false positive results.
The most commonly used drugs include thiopental, propofol and ketamine-diazepam or similar combinations. Thiopental and propofol
have been shown to result in better jaw relaxation and laryngeal exposure and may be easier to titrate to a proper level of
Photo 1B: A dog with bilateral laryngeal paralysis demonstrating paradoxical motion (adduction) of the arytenoids and vocal
folds during inspiration, caused by increased negative airway pressure. Intravenous doxapram may be used to increase inspiratory
effort and more clearly demonstrate this paradoxical motion, confirming the diagnosis. The adducted arytenoids and vocal folds
explain the audible noise (stridor) heard when dogs with laryngeal paralysis breathe and the severe respiratory compromise
and distress they can have as a consequence. (Photo courtesy of Dr. Brendan McKiernan.)
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.