A.J. Venker-van Haagen, DVM, PhD, DECVS
Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, University Utrecht
Utrecht, The Netherlands
What is the function of the larynx?
The larynx acts as a sphincter at the cranial end of the tracheobronchial tree. In order of priority, its functions are to protect the lower airway, to regulate the respiratory airflow, and to vocalize. The cartilages of the larynx (cricoid, thyroid, arytenoid, corniculate, and cuneiform cartilages) and the epiglottis interact under influence of the neuromuscular system of the larynx to perform these functions. The cartilages of the larynx both support and respond to the activity of the extrinsic and intrinsic laryngeal muscles. These muscles move the larynx in swallowing and they open and close the vocal folds in order to protect the larynx and for respiration and vocalization.
Some knowledge of the neurophysiology of laryngeal innervation is necessary for understanding of laryngeal dysfunction. The glottic closure reflex that enables the larynx to protect the lower airway from aspiration of solids or liquids is a polysynaptic reflex. The mucosal receptors respond to stimuli such as touch and liquids. The afferent (sensory) innervation of the laryngeal mucosa is carried by the internal branch of the ipsilateral cranial laryngeal nerve. The afferent impulses generated are delivered to the solitary tract and nucleus (NTS) in the brainstem. The cells of the NTS project to the thalamus and to the nucleus ambiguus, which is located in the brainstem and contains the motoneurons of the efferent (motor) innervation to the laryngeal intrinsic muscles. The axons of these motoneurons form the later ipsilateral recurrent laryngeal nerve. The left recurrent laryngeal nerve passes through the thoracic inlet with the vagus nerve fibers and then returns cranially to the larynx and innervates the left intrinsic laryngeal muscles. The right recurrent laryngeal nerve also runs caudally with the vagus but without entering the thoracic inlet it turns cranially to the larynx to innervate the right intrinsic laryngeal muscles. The regulation of the respiratory movement of the glottis--opening for inspiration and closing after expiration--is regulated in the respiratory center in the brainstem and higher central nervous systems. Vocalization requires not only laryngeal reflexes, but also coordination of respiration and deglutition.
Laryngeal paralysis of neurological origin can be complete or partial. Trauma in the region dorsolateral to the trachea on one or both sides can cause unilateral or bilateral laryngeal paralysis. Unilateral laryngeal paralysis caused by interruption of one recurrent laryngeal nerve usually does not lead to clinical signs, because of the compensatory activity of the contralateral innervation. Bilateral loss of innervation by the recurrent laryngeal nerves results in insufficient abduction and adduction and thus dyspnea during exertion. Neurogenic disease can also result in severe distress, namely, adduction during inspiration and laryngeal spasm. Laryngeal paralysis is usually a slowly-progressive disease in middle-aged to older dogs. There is progressive loss of innervation of the intrinsic laryngeal muscles, resulting in partial denervation.
The clinical signs of laryngeal paralysis are stridor (a wheeze) during inspiration or during both inspiration and expiration, caused by insufficient opening of the glottis. There is dyspnea during exertion or excitement and, since respiratory cooling is also hindered by the too narrow laryngeal opening, hyperthermia may occur. Laryngeal spasm may be one of the recurrent signs. Direct inspection of the larynx via the oropharyngeal cavity is the most informative procedure. Sedation is needed and when care is taken in the choice of anesthesia and the dose, the respiratory movements of the arytenoid cartilages and the vocal folds can be assessed. Electromyographic recordings are most useful to diagnose this type of disease because there are normal motor unit potentials together with denervation potentials (fibrillations and complex repetitive discharges), usually in all of the intrinsic laryngeal muscles. The disease may progress for a year or longer before serious dyspnea occurs. Laryngeal surgery aiming at widening of the laryngeal opening is the treatment of choice.
A lateral approach to the arytenoid cartilage is the method of choice for caudolateral transposition of the arytenoid cartilage and vocal fold in laryngeal paralysis. This procedure should be preceded by a tracheotomy and the insertion of an intratracheal tube through the stoma. With the dog in dorsal recumbency, a paramedian skin incision is made, 1 cm from the ventral midline. By passing lateral to the sternohyoid and sternothyroid muscles, the dorsal edge of the thyroid cartilage is identified by palpation through the thyropharyngeal muscle. By lifting the dorsal edge of the thyroid cartilage with the index finger, the caudal part of the cartilage is identified and the fibers of the thyropharyngeal muscle are separated bluntly to facilitate the approach to the cricothyroid articulation. This articulation is separated, giving a clear view of the intrinsic laryngeal muscles when the thyroid cartilage is lifted. The muscular process of the arytenoid cartilage is separated from the cricoid cartilage after transection of the dorsal cricoarytenoid muscle. The arytenoid cartilage is then freed from the cricoarytenoid ligament and the interarytenoid tissues. The arytenoid cartilage is now free to move to a more lateral and caudal position. An assistant looking through the dog's mouth should check that adequate opening of the glottis is achieved. The muscular process of the arytenoid cartilage is then attached to the most caudal point of the dorsal edge of the thyroid cartilage. A second suture prevents pivoting of the arytenoid cartilage. It is necessary to examine the result again through the mouth. After suturing of the thyropharyngeal muscle the wound is closed routinely.
Congenital laryngeal hypoplasia occurs most often in brachycephalic dogs. The inadequate development of the cartilaginous structures of the larynx results in a small and unusually flexible laryngeal skeleton and thus a narrow laryngeal opening. In addition, there is inadequate abduction of the vocal folds during inspiration, and the lateral ventricles are everted as a result of airflow obstruction combined with other malformations. Surgical correction of the malformed larynx in brachycephalic dogs has been mentioned in the literature, but the risk of inducing further collapse and contraction by scar tissue, resulting in a more severe obstruction, is very high.
Acute laryngitis is characterized by edema and hypervascularization of the laryngeal mucosa. This leads to repeated bouts of hard, dry coughing. When the irritation is severe, paroxysmal coughing often leads to gagging. The dog's attempt to bark, or the cat's attempt to purr, may also elicit the characteristic dry cough. The cause of the disease determines the progression of the clinical signs.
The most common cause of acute laryngitis in dogs is infectious tracheobronchitis (kennel cough). There is usually no fever or other sign of systemic illness. The signs can persist for three weeks or longer. Therapy consists of rest and avoidance of excitement. Pediatric cough syrups are usually very effective. A moist environment and additional oral administration of water diminish the irritation of the mucosa and hence the coughing. There is no indication for corticosteroids. If there is no fever, there is no indication for antibiotics. In cats, viral rhinotracheitis (herpesvirus) and calicivirus infection may affect the laryngeal mucosa. This seldom results in a dry cough but rather in stridorous breathing caused by edema of the laryngeal mucosa. The dominant symptoms in cats are fever, salivation, conjunctivitis, and general distress. The treatment consists of antibiotic therapy, parenteral fluids, and symptomatic therapy. The laryngeal edema seldom leads to life-threatening obstruction that necessitates tracheotomy.
Severe laryngeal edema can be caused by insect bites, but often the cause of acute laryngeal edema remains obscure. There is rapidly increasing inspiratory and expiratory dyspnea and stridor. The progression is unpredictable and may be life threatening. Administration of corticosteroids, preferably intravenously, is the first step. Preparations should be made for intubation and tracheotomy if the dyspnea worsens. Tracheotomy provides relief to the patient and should be considered at an early stage. Prolonged strenuous breathing can lead to the development of lung edema, after which cumulative complications can lead to death. In most cases the tube can be removed in three to five days, after inspection of the larynx ensures that the airway is patent.
Chronic laryngitis is rather common in dogs. According to the clinical manifestations, a mild and a severe form can be distinguished. The mild form may exist for years, causing coughing during exertion or straining on the leash, and gagging in association with coughing. There is no laryngeal dysfunction other than a mild hoarseness. The laryngeal mucosa is red and thickened.
In cats we are sometimes confronted with chronic edema of the laryngeal mucosa that is resistant to corticosteroid therapy. A period of two to three weeks of treatment with a trachea cannula may be effective. The etiology of the chronic edema remains obscure.
Primary laryngeal tumors occur occasionally in dogs and cats. Squamous cell carcinomas often invade the laryngeal tissues rapidly and are usually inoperable short of removal of a large part or the entire larynx. Fine needle aspiration biopsy is the technique of choice for diagnosis. Surgical removal of tumors or inflammatory polyps having a local attachment may be approached successfully via a ventral midline incision through the thyroid cartilage to the laryngeal lumen.
The ventral midline approach to the vocal folds or subglottic area is indicated to expose intraluminal processes, for diagnosis as well as surgical treatment. The procedure is preceded by a tracheotomy and the introduction of an intratracheal tube through the stoma. The larynx is approached via a ventral midline skin incision over the thyroid and cricoid cartilages. The sternohyoid muscles are separated and the thyroid and cricoid cartilages are freed. The thyroid or cricoid cartilage is then incised on the ventral midline. To prevent webbing, the incision in the thyroid cartilage should be exactly on the midline, so that the vocal folds are not damaged. For subsequent stability of the thyroid cartilage, the cranial 2 mm of the cartilage should be left intact. Use of a small retractor to separate the halves of the thyroid or cricoid cartilages provides an opening for inspection and eventual surgical removal of proliferated tissue. After this procedure, the thyroid or cricoid cartilage is closed with superficially placed absorbable sutures. The subcutis and skin are then closed routinely. In almost all situations it is preferable to place a tracheal cannula in the tracheostoma after surgery.
Accidental trauma to the larynx may cause a life threatening situation when hemorrhage and edema prevent the normal airflow. Immediate intratracheal intubation under anesthesia, followed by tracheotomy, is the best approach in the management of these cases. The damage to the larynx is difficult to evaluate during the first few days after trauma. Spontaneous recovery is certainly possible. Perforation of the mucosa, on the other hand, should be repaired surgically. Subcutaneous emphysema indicates mucosal perforation.