General Anatomy And Physiology
The throat is an important, but mosdy ignored, communal area of both the gastrointestinal (GI) and respiratory tracts. Anatomically it is divided into the pharynx and larynx. The pharynx is further divided into the nasopharynx, the oropharynx, and the laryngopharynx. The nasopharynx is located dorsal to the soft palate, between the choanae and the intrapharyngeal opening. It is a functional space that allows the nasal cavity to communicate with the larynx. The oropharynx is ventral to the soft palate and extends from the palatoglossal arches rostrally to the base of the epiglottis caudally. The intrapharyngeal opening and the rostral border of the esophagus create the boundaries of the laryngopharynx, the most caudal part of the pharynx. The laryngopharynx functions as an intersection to both the respiratory and digestive tracts. The larynx consists of three unpaired cartilages (epiglottis, cricoid, and thyroid) and one pair of arytenoid cartilages. The glottis (or cranial opening of the larynx) is composed of the corniculate and cuneiform process of the arytenoid cartilages and the epiglottis. Minor anatomic differences exist between feline and canine larynx. Cats lack the interarytenoid cartilage found in dogs and instead have an interarytenoid ligament in its place. Cats also lack a vestibular ligament. Due to this deficiency the feline arytenoid cartilage is connected to the ventral aspect of the larynx by the vocal ligament. Another important anatomic difference is cats lack the Iaryngeal ventricles that are found between the vestibular and vocal folds in the dog. No dramatic differences exist between feline and canine innervation and muscles of the larynx.
Swallowing, or deglutition, is a complex reflex action that coordinates many structures. Cranial nerves, the swallowing center in the reticular formation of the brain stem, the muscles of mastication, tongue, soft palate, pharynx, larynx, and esophagus are all involved in what appears to be a simple act of allowing transport of material from the mouth to the stomach. As a lesser recognized function, swallowing also allows saliva and debris to be removed from the pharynx. Deglutition begins as a voluntary act but during its execution becomes a reflex. Deglutition is traditionally described as having three phases: (1) oral, (2) pharyngeal, and (3) esophageal. The oral phase begins when mastication is complete. The tongue then moves the food bolus that is organized at the base of the tongue to a position that is on midline between the tongue and the hard palate. Motor fibers to the tongue are supplied by cranial nerve XII. Sensory fibers from the oral cavity and motor fibers to the masticatory muscles and soft palate originate from cranial nerve V. The oral phase is voluntary, but when the food bolus is pushed into the pharynx, receptors are stimulated that initiate the involuntary, or reflex, component of deglutition. Sensory receptors are found in the pharynx, palate, and epiglottis. Impulses from these receptors are transmitted along the glossopharyngeal nerve, recurrent Iaryngeal branch of the vagus nerve, and the maxillary branch of the trigeminal nerve to the swallowing center in the medulla (located in the floor of the fourth ventricle). The efferent arm of the reflex involves the motor nuclei of cranial nerves V, VII, DC, X, and XII. These nerves supply the muscles of mastication, tongue, palate, pharynx, larynx, and esophagus. During the pharyngeal phase the goal is to pass food from the oropharynx into the esophagus and to prevent food from being aspirated into the trachea or moved into the nasopharynx. This is accomplished by elevation of the soft palate and the palatopharyngeal folds moving inward as the vocal cords are pulled together and the larynx is elevated against the epiglottis. The final act during the pharyngeal stage of swallowing occurs when the cricopharyngeal muscle relaxes, the upper esophageal sphincter opens, the bolus moves into the esophagus, the sphincter closes, and the pharyngeal muscles relax. The cricopharyngeal muscle is innervated by the pharyngoesophageal nerve, which is formed by cranial nerves IX and X. The final stage of deglutition, the esophageal stage, transports the bolus from the esophagus, through the gastroesophageal sphincter, and into the stomach, The esophagus is innervated by the vagus nerve.
The larynx has three functions: (1) to act as a conduit for air, (2) to protect the lower airway from aspiration during deglutition, and (3) vocalization. The glottis remains partially open when an animal is at rest. When greater airflow is needed, the glottis is widened by abduction of the arytenoid cartilages and vocal folds (via cricoarytenoid muscles) during inspiration (and the same structures adduct during expiration). The cricoarytenoid muscles are innervated by the caudal laryngeal nerves, which are derived from the recurrent laryngeal nerves. The recurrent laryngeal nerve innervates all the muscles of the larynx except the cricothyroid muscles that are supplied by the cranial laryngeal nerves. During deglutition the larynx is pulled cranially by the geniohyoideus and mylohyoideus muscles. This allows the epiglottis to close over the larynx, protecting the lower airways. The adductor muscles close the glottis concurrently. This creates an additional defense against aspiration.
History And Physical Examination
Animals with diseases of the throat can have a variety of historical complaints. Pharyngeal diseases can be confusing because historical findings can be related to swallowing difficulties or the upper respiratory tract (URT). Historical findings secondary to laryngeal dysfunction are usually related to either inability to regulate airflow and protect the airway, or they are related to changes in vocalization. Respiratory sounds can be extremely useful in localizing the disease, whether it is pharyngeal or laryngeal, but they are not helpful if one tries to attribute a specific respiratory sound to a specific condition. Coughing, dyspnea, and nasal discharge are common clinical complaints. Stertor, a snoring sound heard on inspiration, is usually due to an intermittent obstruction such as an elongated soft palate. Stridor, an inspiratory high-pitch wheeze, is most commonly associated with laryngeal lesions. Stridor is created by air turbulence through a narrowed laryngeal opening. Any changes in vocalization would suggest a laryngeal disorder. Reverse sneezing, which is described as short periods of forceful inspiratory nasal effort with the head pulled back, indicates irritation to the dorsal nasopharyngeal mucosa. Dysphagia cases can be confusing because ineffective swallowing may not be obvious to the owner and may not be the primary historical complaint. Other signs such as coughing, gagging, regurgitation, and nasal discharge may be reported in animals with either oropharyngeal dysphagia or other diseases of the throat.
A complete physical examination (including a neurologic examination) is important when evaluating animals with pharyngeal or laryngeal disease because dysfunction may be indicative of systemic disease (i.e. myopathy, neuropathy) or there may be secondary complications from the disorder (e.g. aspiration pneumonia). If laryngeal disease is suspected, the larynx should be palpated for pain or structural abnormalities. The area over the larynx should be ausculted for abnormal sounds secondary to turbulence. Part of this complete physical examination may include exercising the patient, because occasionally manifestation of the disease only occurs after physical exertion. Many animals will have dyspnea, and a thorough physical examination may not be possible until the animal is stable. Significant airway compromise may be overlooked. It is important to assess the degree of respiratory compromise by evaluating the patient’s attitude, posture, mucous membrane color, and both respiratory rate and pattern. Precluding the emergency situation, once the general examination is complete one may concentrate on examining the oral cavity. It is extremely difficult, if not impossible, to adequately evaluate the larynx and pharyngeal areas without heavy sedation or general anesthesia. In most cases it is easier for the examiner, and safer for the animal, if tracheal intubation is performed. A standard method of evaluating the oral cavity should be established so that one does not miss an important abnormality. The larynx is evaluated both for structural problems and functional abnormalities; the pharynx is evaluated for physical abnormalities. Pharyngeal function cannot be evaluated when the patient is sedated; rather, video fluoroscopy is recommended when critically assessing pharyngeal function.
Inflammatory laryngeal disease is common in both the dog and the cat. The most common cause of acute inflammation of the larynx is infectious agents such as canine infectious tra-cheobronchitis (ITB), commonly called kennel cough, or the feline upper respiratory agents (i.e. FHV-1, FCV). ITB is a result of coinfection of Bordetella bronchiseptica with either canine parainfluenza virus or canine adenovirus-2 (CAV-2). With most cases of lib, the only clinical sign is paroxysmal coughing in an otherwise healthy dog. Due to inflammation of the larynx the cough is a loud, high-pitched, “goose honk” cough. Occasionally a dog may be febrile, lethargic, and inappetent. ITB is usually self-limiting, but the severity of the cough, combined with the possibility of pneumonia complicating the disease, warrants treatment. Doxycycline at 5 to 10 mg/kg orally once daily is the antimicrobial of choice for B. bronchiseptica. Short-term administration of an anti-inflammatory dose of glucocorticoids can be effective in decreasing laryngeal edema. Antitussives, such as butorphanol tartrate or hydrocodone bitartrate, are effective in minimizing the severity of the cough but should not be used if pneumonia is suspected. Other causes of inflammatory laryngeal disease include endotracheal intubation, insect bites, foreign body penetration, or trauma from bite wounds, leash and choke chain injuries, or being hit by cars. Frequently no cause for acute laryngeal inflammation is found. Acute inflammatory laryngeal disease is usually self-limiting, and no specific treatment is indicated if the animal has only mild signs. However, if moderate to severe signs exist, a short course with an anti-inflammatory dose of glucocorticosteroids can be initiated to decrease laryngeal edema. Respiratory obstruction secondary to laryngeal inflammation is an uncommon clinical presentation but can occur in severe instances such as in laryngeal trauma. A tracheostomy is indicated if the patient is dyspneic, cyanotic, or extremely anxious due to laryngeal inflammation.
Obstructive Inflammatory Disease
An obstructive inflammatory laryngeal disease has been described in cats and dogs. Although rare, it is a disease worth noting because the gross appearance can mimic laryngeal neoplasia. The underlying cause of inflammation is unknown. Feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) have not been found to be associated with this disease. In the feline reports, dyspnea secondary to upper airway obstruction was reported in all cats; retching, coughing, and dysphonia were also common. Stridor and dysphonia was reported in dogs. Direct visualization of the larynx reveals a laryngeal mass that cannot be distinguished from neoplasia or severe swelling and edema (). Histopathology is imperative to distinguish between neoplasia and obstructive inflammatory disease.
Histopathology reveals either granulomatous or nongranulomatous laryngitis (neutrophilic and lymphoplasmacytic). Most patients with obstructive inflammatory laryngeal disease need to be stabilized. This is accomplished by establishing an airway through tracheostomy tube placement. Treatment with corticosteroids (dexamethasone, prednisone, or prednisolone) has variable success, and occasionally surgical resection of the proliferative tissue is indicated. The prognosis is guarded, with a high mortality rate during the initial diagnostic and treatment period.