Surgical Management of Chronic Aspiration

Before 1972, laryngectomy was routinely chosen to separate the functions of swallowing and respiration in the setting of chronic aspiration. This practice was considered less than ideal because voice and supraglottic respiration are lost. Further, the procedure is irreversible.

In 1972, Habal and Murray described a laryngeal closure procedure in one patient that involved creation of an epiglottic flap to close the larynx. ^[3] In 1975, Lindeman described his experience with a reversible technique in which he diverted the larynx to the esophagus and the trachea to the neck as a stoma in a canine model. ^[4] He subsequently performed this procedure on a patient with a paralyzed larynx. Modifications have been described (eg, laryngotracheal separation [LTS]), including several by Lindeman.

Since then, as diagnostic and therapeutic techniques have become more sophisticated, more specific procedures have been developed to address specific pathology. These procedures included laryngeal-specific techniques, such as vocal cord medialization, total/partial cricoidectomy, and laryngeal suspension. Alimentary procedures, such as feeding gastrostomy and jejunostomy, cricopharyngeal myotomy, and gastric fundoplication, are also useful. Chronic aspiration of excessive oropharyngeal secretions may be controlled via surgical control of salivation.

Chronic aspiration is defined as recurrent episodes of liquid or solid materials that pass below the level of the vocal cords. Surgery is indicated when intractable aspiration with life-threatening sequelae does not respond to conservative medical management.

The etiology of chronic aspiration is multiple and reflective of the functions of the larynx in airway protection, swallowing, phonation, and respiration. A disorder that has an effect on neurologic control, muscular strength, or local anatomy of the upper aerodigestive tract can affect these functions with resultant chronic aspiration.

In the adult population, the most common etiology is neurologic sequelae from a stroke (infarct or hemorrhage). In this circumstance, aspiration is usually secondary to the loss of cough and swallow reflexes. Closed head injuries, anoxic encephalopathy, and CNS depression due to intoxication may also produce aspiration.

Degenerative neurologic diseases (eg, multiple sclerosis, Parkinson disease, amyotrophic lateral sclerosis), neuromuscular diseases (eg, myasthenia gravis, muscular dystrophies), and peripheral neuropathies (eg, cranial nerve disorders, Guillain-Barré syndrome) can result in chronic aspiration. ^[5]

Neurogenic aspiration is commonly differentiated into lower and upper motor neuron etiology. Upper motor neuron pathology presents with aspiration that is characterized as straining or strangling in nature; whereas, lower motor neuron disease is associated with flaccid paralysis and aspiration of liquids. Intracranial complications of infection and/or neoplasms may produce aspiration due to neurologic devastation, either directly or from treatment (ie, radiation, surgery).

Pharyngeal and esophageal disorders, such as laryngopharyngeal and gastroesophageal reflux, cricopharyngeal spasm, strictures, Zenker diverticulum, achalasia, and postradiation/postsurgical changes for neoplastic processes, may result in aspiration. ^[6]

Moreover, the pediatric population may have aspiration as a result of congenital anatomic abnormalities, such as laryngeal clefts and tracheoesophageal fistulas, as well as sialorrhea and many of the previously noted etiologies. ^[7]

A retrospective study by Or et al indicated that spontaneous cerebrospinal fluid (CSF) leaks of the skull base may be an underdiagnosed cause of chronic aspiration pneumonitis. The investigators reported that out of 20 patients with spontaneous CSF rhinorrhea, six had symptomatic chronic pneumonitis. Resolution of the pneumonitis symptoms, as well as of ground-glass opacities seen in the lungs, occurred following fistula repair in all six patients. ^[8]

A retrospective study by Bock et al found that in patients in whom unsensed penetration or aspiration was detected on videofluoroscopic swallowing study, the risk for progression to pulmonary compromise (eg, pneumonia or pneumonitis) or death was associated with the etiology of their dysphagia. For example, the risk for pulmonary events and mortality tended to be greater in patients suffering from generalized, nonspecific dysphagia resulting from deconditioning or frailty. Mortality risk was also increased in postsurgical patients with dysphagia and dysphagia patients with chronic neurologic disease. Moreover, univariate, though not multivariate, analysis showed a relationship between higher Penetration-Aspiration Scale score and reduced time to first pulmonary event. ^[9]

Aspiration is not always a pathologic process. A small amount of aspiration is normal. When the normal mechanisms for airway clearance (ie, coughing, cilia) are present, they protect the airway from complications.

Pathologic aspiration is marked by pulmonary complications (eg, aspiration pneumonitis/pneumonia). A breakdown in airway clearance mechanisms and/or in respiration, phonation, or swallowing mechanisms can result in pathologic aspiration. The pathologic processes responsible for the breakdown of these mechanisms have been previously discussed.

The clinical presentation of chronic aspiration is variable and nonspecific. Clinical symptoms suggestive of chronic aspiration include choking, coughing, fever, dyspnea, dysphonia, frequent throat clearing, chest pain, dysphagia, odynophagia, tachypnea, wheezing, rales, and emesis. The pediatric population may have many of these symptoms as well as stridor, failure to thrive, apneic episodes, and regurgitation of feedings. Further, the presentation of chronic aspiration may be so-called silent aspiration, with no presenting symptoms or signs until complications develop. See the image below.

Base of tongue thyroglossal duct cyst in infant presenting with dysphagia and aspiration without associated stridor or airway obstruction.

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Surgical intervention for intractable aspiration is indicated when life-threatening complications ensue and conservative measures do not adequately control episodes of aspiration.

The upper aerodigestive tract (from the oropharynx to the larynx) allows for separating the various functions of these areas while also coordinating them. These functions are respiration, phonation, swallowing, and airway protection via cough reflexes/ciliary clearance.

The pertinent anatomy and physiology of the oropharynx is related to its function in speech and swallowing. The borders of the cheeks and lips define the mouth. The interior of the mouth contains the dentition, mucosa, salivary gland apertures, and tongue. The hard and soft palate forms the roof of the mouth. The most posterior portion of the soft palate or velum is extremely important in preventing the nasopharyngeal reflux during swallowing. The anterior and posterior muscular pillars formed by the palatoglossus and palatopharyngeus muscles (which form the tonsillar fossa) are important functional and anatomic landmarks.

The pharynx is bordered by mucosa that covers the constrictor muscles of the oropharynx and the hypopharynx. The larynx is bounded superiorly by the upper tip of the epiglottis and inferiorly at the lower border of the cricoid cartilage. The laryngeal mucosa is draped over a cartilaginous framework, which includes the epiglottis, the aryepiglottic folds, the false vocal folds, the cuneiform, corniculate and arytenoid cartilages, and the true vocal folds (which include the vocalis muscles and membranous coverings). The major cartilaginous framework, from superiorly to inferiorly, is the thyroid cartilage (which houses the glottis proper) and the cricoid cartilage. The hyoid bone also serves as an attachment to which the larynx is suspended.

Deglutition is a complex act that is under both voluntary and involuntary neural controls. Swallowing is typically divided into 4 stages. The first 2 stages are under voluntary control, except in the newborn period when the swallowing reflex is regulated at the level of the brain stem. The second 2 stages are reflex actions. The afferent limb of this reflexive action consists of sensory and proprioceptive fibers in the glossopharyngeal, trigeminal, and superior laryngeal nerves that supply the laryngeal and pharyngeal mucosa. Impulses are transmitted to the swallowing center in the floor of the fourth ventricle. The efferent limb consists of general visceral efferent fibers that begin in the nucleus ambiguous and descend through the vagus nerve to supply the laryngeal and pharyngeal musculature.

The preparatory phase consists of the ingestion of food into the mouth and the formation of a food bolus after chewing and salivary mixing. The bolus is held between the hard palate and anterior two thirds of the tongue, while the tongue base and soft palate act to close the pharynx until the bolus is fully prepared.

The oral phase begins with the elevation of the anterior tongue as it meets the hard palate and the food bolus is pushed posteriorly into the pharynx. The preparatory and oral phases are under voluntary control. Once the anterior tonsillar pillar is met, the pharyngeal phase is initiated. The pharyngeal constrictors, the palatopharyngeus, and the closed velum interact to essentially squeeze the bolus down the pharynx and the hypopharynx toward the esophagus.

Once the esophageal phase begins, respiration ceases with laryngeal closure; the epiglottis, aryepiglottic folds, false vocal folds, and true vocal folds close. Concomitantly, the soft palate meets the posterior pharyngeal wall in the nasopharynx, thus closing the nasopharynx during the swallow. The cricopharyngeus muscle relaxes, and esophageal peristalsis completes the swallow.

The cough reflex is mediated via the sensory receptors of the airway located within the respiratory epithelium from the larynx to the terminal bronchioles. The medullary cough centers control the reflex with afferent and efferent limbs of the reflex via cranial nerve X and, to a lesser extent, cranial nerves V and IX.

Cough can be voluntarily initiated without stimulation from other afferent pathways. The efferent fibers of the cough reflex leave the medullary cough center through the phrenic and spinal motor nerves to the diaphragm and intercostal muscles, respectively. The abdominal and pelvic muscles also participate in the efferent limb. The cough mechanism is initiated with a rapid, high-volume inspiration via maximally abducted vocal cords and intrathoracic expansion. This results in a high-pressure gradient once the vocal cords adduct, the supraglottic larynx closes, and the expiratory muscle contracts. This compressive coughing is primarily mediated through the closure action of the false vocal folds, which act as a sphincter. Finally, the glottis opens, accompanied by expiration of a high-pressure air column that carries expectorated materials from the airway. ^[10]

Contraindications to surgical intervention for chronic aspiration are procedure specific and are discussed with each procedure. Generalized surgical contraindications include bleeding diatheses, anesthetic contraindications, poor pulmonary reserve, and/or expectation of return of normal function.