Larynx: Coughing, Dyspnea, Stridor, Surgery
Anjop J. Venker-van Haagen, DVM, PhD, DECVS
Utrecht, The Netherlands

The history and clinical signs in laryngeal disease reflect dysfunction of the larynx in regulating the airflow, in vocalization, in protecting the airway, or the resulting irritation of the "cough receptors". In dysfunction of regulation of the airflow, it is the inability to abduct the vocal folds that causes the predominant signs of dyspnea and stridor on exertion. A dramatic change in vocal ability in dogs and cats is usually a sign of laryngeal tumor rather than of laryngeal paralysis. Irritation of the laryngeal mucosa, as in laryngitis, results in coughing. Without accompanying bronchitis, the cough is loud, dry, and persistent.

Coughing in laryngeal disease is associated with inflammation of the laryngeal mucosa

Acute laryngitis is characterized by edema and hypervascularization of the laryngeal mucosa. The typical clinical signs are repeated bouts of hard, dry coughing and if the irritation is severe, paroxysmal coughing often leads to gagging. The dog's attempt to bark, or the cat's 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. Coughing 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.

Chronic laryngitis is rather common in dogs. It may be mild or severe. Mild laryngitis can persist for years, causing coughing during exertion or straining on the leash, and gagging provoked by severe coughing. There is no laryngeal dysfunction other than mild hoarseness. The laryngeal mucosa is red and thickened. Therapy consists of advice to avoid, if possible, the habits resulting in coughing.

In cats, both herpesvirus and calicivirus can affect the laryngeal mucosa. This can cause a dry cough but more often it results in stridorous breathing due to edema of the laryngeal mucosa. The dominant symptoms in cats are fever, salivation, conjunctivitis, and general distress. The treatment consists of antibiotics and parenteral fluids, together with symptomatic care. The laryngeal edema seldom leads to life-threatening obstruction.

Dyspnea and stridor are associated signs in laryngeal disease

Dyspnea is difficult or labored breathing. It is caused by hypoxemia and hypercapnia, which are detected by the peripheral and central chemoreceptors, respectively. Dyspnea may be caused by insufficient ventilation or insufficient oxygen in the inspired air, or by insufficient circulation, or anemia, or abnormal hemoglobin. Dyspnea in laryngeal disease is caused by insufficient ventilation. Narrowing of the passage through the larynx causes partial obstruction to the airflow. The partial obstruction causes a soft, wheezing sound or a louder stridor. Laryngeal stridor indicates obstruction in the larynx and is always accompanied by some degree of dyspnea. A loud stridor is associated with severe dyspnea. Both the dyspnea and the stridor are caused by narrowing of the passage through the larynx, which may be caused by edema of the laryngeal mucosa, laryngeal hypoplasia, laryngeal paralysis, tumor of the larynx, or trauma to it.

Severe laryngeal edema can be caused by insect bites, but often the cause of acute edema remains obscure. There is a 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 tracheostomy if the dyspnea worsens. Tracheostomy 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 an accumulation of 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.

In cats we are sometimes confronted with chronic edema of the laryngeal mucosa which is refractory to antibiotic therapy. A period of two to three weeks of treatment with a tracheal cannula may be effective. The etiology of the chronic edema is not clear, but viral laryngitis may be the underlying cause. For this reason the use of corticosteroids is not the first choice in these cases.

Prolonged acute laryngitis in dogs may cause laryngeal dysfunction. The laryngeal mucosa is reddened and the vocal folds are thickened. Abduction and adduction are insufficient, resulting in laryngeal dyspnea and stridor. Therapy consist of absolute rest and avoidance anything that causes barking for six weeks, after which laryngoscopy is repeated. Neglect of this form of laryngitis may result in permanent laryngeal dysfunction.

Congenital laryngeal hypoplasia occurs most often in brachycephalic dogs. The inadequate development of the cartilagineous structures of the larynx results in a small and unusually flexible laryngeal skeleton, resulting in a narrow laryngeal opening. In addition, there is inadequate abduction of the vocal folds during inspiration, and eversion of the lateral ventricles occurs as a result of airflow obstruction combined with other malformations. The dogs are dyspneic, and laryngeal stridor indicates the insufficiency of the laryngeal opening. 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.

In dogs and cats, congenital malformations are found occasionally and usually cause laryngeal dysfunction, indicated by stridorous breathing and dyspnea at an early age. When laryngeal function is found to be limited, the prognosis is poor.

Laryngeal paralysis is a complete or partial loss of function of the larynx caused by neurogenic, muscular, neuromuscular, or ankylotic (cricoarytenoid articulation) disease. When the clinical signs and the insufficient movements of the vocal folds revealed by laryngoscopy both indicate laryngeal paralysis, electromyography of the intrinsic laryngeal muscles may be used to confirm the diagnosis. Anesthesia is required for this procedure, but when the detection of normal action potentials is of importance, as in checking the placement of the electrode or to diagnose partial paralysis, a superficial level of anesthesia is necessary.

Laryngeal paralysis of neurogenic origin can be complete or partial. The intrinsic laryngeal muscles are innervated by the recurrent laryngeal nerves. 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 side. Bilateral loss of innervation by the recurrent laryngeal nerves leads to insufficient abduction and adduction and thus dyspnea during exertion. Neurogenic disease can also result in severe dyspnea, namely, adduction during inspiration and sometimes during laryngeal spasm.

Laryngeal paralysis usually occurs as a slowly progressive disease in middle-aged to older dogs. In these cases there is progressive loss of innervation of the intrinsic laryngeal muscles, resulting in partial denervation. 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 intrinsic laryngeal muscles. The disease may progress for a year or longer before serious dyspnea occurs. Laryngeal spasm may be one of the recurrent signs. 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 laterocaudal transposition of the arytenoid cartilage and vocal fold in laryngeal paralysis. This procedure should also be preceded by a tracheostomy and the placement 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 the index finger lateral to the sternohyoid and sternothyroid muscles, the dorsal edge of the thyroid cartilage can be identified by palpation through the thyropharyngeal muscle. By lifting the dorsal edge of the thyroid cartilage with the finger, the caudal part of the cartilage is identified and the thyropharyngeal muscle is opened 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. This should be checked by looking through the mouth. 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.

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 biopsy or removal of laryngeal tumors or inflammatory polyps with a local attachment may be accomplished 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 preceded by a tracheostomy 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. Incision in the ventral midline of the thyroid or cricoid cartilage follows. To prevent webbing, the incision in the thyroid cartilage should be exactly on the midline, in order to avoid damage to the vocal folds. 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 absorbable sutures are placed superficially in the larynx. The wound is closed routinely. In almost all situations it is preferable to place a tracheal cannula in the tracheostoma after surgery.

Trauma to the larynx. 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 tracheostomy, 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. Radiographs do not elucidate details of the traumatic wounds, and the prognosis is more easily determined when the primary wounds are healed. Spontaneous recovery is certainly possible. Perforation of the mucosa, on the other hand, should be repaired surgically in the first days after the trauma. Subcutaneous emphysema indicates mucosal perforation.

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Anjop J. Venker-van Haagen, DVM, PhD, DECVS
The Netherlands


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