Chapter 038. Dysphagia (Part 3)

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Oropharyngeal motor dysphagia results from impairment of the voluntary effort required in bolus preparation or neuromuscular disorders affecting bolus preparation, initiation of the swallowing reflex, timely passage of food through the pharynx, and prevention of entry of food into the nasal and the laryngeal opening. Paralysis of the suprahyoid muscles leads to loss of opening of the UES and severe dysphagia. Because each side of the pharynx is innervated by ipsilateral nerves, a unilateral lesion of motor neurons leads to unilateral pharyngeal paralysis. Neuromuscular disorders causing dysphagia are listed in Table 38-1. They include a variety of cortical and suprabulbar...

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Chapter 038. Dysphagia (Part 3) Oropharyngeal motor dysphagia results from impairment of the voluntary effort required in bolus preparation or neuromuscular disorders affecting bolus preparation, initiation of the swallowing reflex, timely passage of food through the pharynx, and prevention of entry of food into the nasal and the laryngeal opening. Paralysis of the suprahyoid muscles leads to loss of opening of the UES and severe dysphagia. Because each side of the pharynx is innervated by ipsilateral nerves, a unilateral lesion of motor neurons leads to unilateral pharyngeal paralysis. Neuromuscular disorders causing dysphagia are listed in Table 38-1. They include a variety of cortical and suprabulbar disorders, lesions of the cranial nerves in their nuclei in the brain stem or their course to the muscles, defects of
neurotransmission at the motor end plates, and muscular diseases. Some of these disorders also involve laryngeal muscles and vocal cords, causing hoarseness. Since the oropharyngeal phase of swallowing lasts no more than a second, rapid-sequence videofluoroscopy is necessary to permit detection and analysis of abnormalities of oral and pharyngeal function. However, such studies can only be performed in a fully conscious and cooperative patient. A videofluoroscopic swallowing study (VFSS) using barium of different consistencies may reveal difficulties in the oral phase of swallowing. The pharynx is examined to detect stasis of barium in the valleculae and pyriform sinuses and regurgitation of barium into the nose and tracheobronchial tree. Pharyngeal contraction waves and opening of UES with a swallow are carefully monitored. Manometric studies may demonstrate reduced amplitude of pharyngeal contractions and reduced UES pressure without further fall in pressure on swallowing (see Fig. 286-3). General treatment consists of maneuvers to reduce pharyngeal stasis and to enhance airway protection under the direction of a trained swallow therapist. Feeding by a naso- gastric tube or an endoscopically placed gastrostomy tube may be necessary for nutritional support; however, these maneuvers do not provide protection against aspiration of salivary secretions. Gastrostomy tube feeding may actually increase gastroesophageal reflux and lead to more aspiration. Jejunostomy tube feeding may lessen reflux.
Dysphagia resulting from a cerebrovascular accident usually improves with time, although often not completely. Patients with myasthenia gravis (Chap. 381) and polymyositis (Chap. 383) may respond to treatment of the primary disease. Cricopharyngeal myotomy is usually not helpful. Extensive operative procedures to prevent aspiration are rarely needed. Death is often due to pulmonary complications. A cricopharyngeal bar results from failure of the cricopharyngeus to relax but with normal activity of the suprahyoid muscles on swallowing. Barium swallow shows a prominent projection on the posterior wall of the pharynx at the level of the lower part of the cricoid cartilage (see Fig. 286-1). A transient cricopharyngeal bar is seen in up to 5% of individuals without dysphagia undergoing upper gastrointestinal studies; it can be produced in normal individuals during a Valsalva maneuver. A persistent cricopharyngeal bar may be caused by fibrosis in the cricopharyngeus. Cricopharyngeal myotomy may be helpful in severely symptomatic case with functional evidence of obstruction by the cricopharyngeus muscle, but is contraindicated in the presence of gastroesophageal reflux because it may lead to pharyngeal and pulmonary aspiration. Globus pharyngeus mainly occurs in individuals with emotional disorders, particularly in women. Results of barium studies and manometry are normal.
Treatment consists primarily of reassurance. Some patients with globus pharyngeus have associated reflux esophagitis, and they may respond to treatment of the esophagitis. ESOPHAGEAL DYSPHAGIA In an adult, the esophageal lumen can distend up to 4 cm in diameter. When the esophagus cannot dilate beyond 2.5 cm in diameter, dysphagia to normal solid food can occur. Dysphagia is always present when the esophagus cannot distend beyond 1.3 cm. Circumferential lesions produce dysphagia more consistently than do lesions that involve only a portion of circumferences of the esophageal wall, as uninvolved segments retain their distensibility. The esophageal causes of mechanical dysphagia are listed in Table 38-2. Common causes include carcinoma, peptic and other benign strictures, and lower esophageal ring. Esophageal motor dysphagia may result from abnormalities in peristalsis and deglutitive inhibition due to diseases of the esophageal striated or smooth muscle.