10
Upper and Lower Esophageal Spasm
Dysphagia, or impaired swallowing ability, is a very common disorder that can have adverse effects on quality of life and overall health. Although over 20% of the adult population experiences dysphagia several times a month,1 the impact on overall health and quality of life can range from minimal, in the case of mild dysphagia, to severe and life-threatening, in the case of severe dysphagia. Dysphagia may result from dysfunction of any of the components involved in the complex neuromuscular interaction of swallowing. There are two major categories of dysphagia: (1) oropharyngeal, which refers to difficulty in the passage of a food bolus from the oropharynx into the esophagus; and (2) esophageal, which refers to disturbances of the passage of the food bolus within the esophagus itself.2 Hyperfunction of any of the muscles involved in swallowing is a frequent cause of dysphagia, although in most cases of moderate or severe dysphagia, there are multiple, significant deficits related to muscle strength, coordination, and sensation. With regard to isolated hyperfunctional dysphagia, dysfunction of the cricopharyngeal (CP) muscles (failure to relax) is the most common cause of oropharyngeal dysphagia, and hypertonicity of the lower sphincter is associated with esophageal dyshagia.3,4
Treatment of these disorders depends on the etiology of the dysphagia (stroke, neurodegenerative disease, congenital disorders, high vagal lesions, postlaryngectomy, etc.), and may include surgery, medications, or swallowing therapy, or some combination of them. When the main cause of dysphagia is hyperfunctional muscles, chemodenervation with botulinum neurotoxin (BoNT) is a reasonable treatment option. This chapter reviews the anatomy, physiology, and management of hyperfunctional swallowing disorders that may affect the pharyngoesophageal phase of swallowing.
Failure of the upper esophageal sphincter (UES) to relax, termed cricopharyngeal achalasia (CA), can cause severe dysphagia. CA is a characteristic symptom in a variety of neurologic disorders including lesions of the skull base and stroke. UES hypertonicity is also associated with distal esophageal reflux,5 so in mildly symptomatic patients, treatment with proton pump inhibitors may be effective. Clinical symptoms of CA include globus sensation and dysphagia. In laryngectomized patients, CA will also reliably cause difficulty with tracheoesophageal puncture (TEP) phonation. For this reason, most surgeons now perform CP myotomy at the time of the laryngectomy. In newborns, an esophagram confirms the diagnosis. In adults, however, the diagnosis is best aided by manometry or electromyography (EMG). However, equivocal findings with these testing modalities, which have significant technical aspects, do not rule out CA.
Cricopharyngeal achalasia can be managed with a variety of treatments, including mechanical dilatation, pharyngeal plexus neurectomy, and CP myotomy. The definitive treatment of CA remains CP myotomy, via either an endoscopic or open transcervical approach.6 Injection of BoNT into the cricopharyngeus muscle, either percutaneously or endoscopically under general anesthesia, has shown benefit in 70 to 100% of patients in noncontrolled series.7 The effects of the injection lasted between 4 months and 1 year. Therefore, BoNT injection is not only an attractive nonsurgical alternative treatment for CA but also a useful tool to identify which patients could be expected to experience benefit from CP myotomy. An important exception is patients with fibrosis of the CP, who will not experience benefit from BoNT, but may benefit from dilation or myotomy.
Lower esophageal sphincter (LES) spasm, referred to as achalasia, esophageal achalasia, and cardiospasm, is a primary esophageal motility disorder characterized by failure of a hypertensive LES to relax and the absence of esophageal peristalsis. These abnormalities cause a functional obstruction at the gastroesophageal junction, leading to dysphagia, regurgitation, weight loss, and occasionally chest pain. These symptoms may also be mimicked by neoplasm and infection (Chagas disease). Treatments for achalasia include medications, balloon dilation, and myotomy. Calcium channel blockers and nitrates have shown short-term efficacy, but their use is limited by side effects, including headache, dizziness, hypotension, and peripheral edema.8 Although the durability of response in patients undergoing myotomy or balloon dilation techniques is superior that in patients who undergo BoNT injection, intrasphincteric injection of BoNT has been demonstrated to be an extremely safe and effective treatment for those patients who are not good surgical candidates, or who prefer to avoid surgical risks.9
Workup
Evaluation of dysphagia requires a thorough history and physical examination, often including fiberoptic evaluation of the oropharynx, endolarynx, and hypopharynx, and of the esophagus and stomach. Additional studies are listed in Table 10.1.
Upper Esophageal Sphincter
The radiographic hallmark of CP achalasia, the “cricopharyngeal bar,” represents the protrusion of the CP muscle into the digestive tract as the bolus of radiopaque material passes through the UES. However, the absence of a CP bar does not rule out the possibility of UES hyperfunction if the history and physical examination findings are suggestive (Fig. 10.1). Fiberoptic pharyngoscopy may reveal pooling of secretions with the pyriform sinus region on the affected side. Electromyography (EMG) studies may reveal the lack of cessation of electrical activity, although a decrease in signal is usually noted during swallowing, even in patients with CP achalasia.
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