Evaluation of Dysphagia

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Evaluation of Dysphagia CAG PRACTICE GUIDELINES Canadian Association of Gastroenterology Practice Guidelines: Evaluation of dysphagia Alan W Cockeram MD FRCPC DEFINITION Dysphagia may be defined as difficulty in swallowing. SPONSORS AND VALIDATION Dysphagia may be classified as oropharyngeal or esophag- eal; oropharyngeal dysphagia arises from a structural or This practice guideline was developed by Dr Alan W functional abnormality in the oropharynx, and esophageal Cockeram MD FRCPC and was reviewed by dysphagia occurs as a result of structural or functional ab- · normalities in the esophagus. Practice Affairs Committee (Chair – Esophageal dysphagia may be further subclassified Dr A Cockeram): Dr T Devlin, Dr J McHattie, symptomatically as dysphagia for solids alone, which usu- Dr D Petrunia, Dr E Semlacher and Dr V Sharma ally suggests a mechanical problem, versus dysphagia for · Canadian Association of Gastroenterology (CAG) liquids and solids, which is more suggestive of a neuromus- Endoscopy Committee (Chair – Dr A Barkun) cular problem. Dysphagia may be described by the patient as a sensation of food ‘sticking’ or as a sensation of food · Dr N Diamant, Dr N Marcon and Dr W Paterson passing slowly through the esophagus. True dysphagia al- ways indicates organic disease and always warrants inves- · CAG Governing Board tigation and consultation if no cause is found in initial studies. These symptoms should be distinguished from those of a persistent foreign body-type sensation or a sen- reaches the lower esophageal sphincter, the sphincter re- sation of a lump, which is more typical of globus sensation. laxes to allow the food to progress into the stomach. Odynophagia, defined as pain with swallowing, may occur in association with esophageal dysmotility or as a result of OROPHARYNGEAL DYSPHAGIA mucosal disease in the esophagus. The majority of cases of oropharyngeal dysphagia occur as a result of neuromuscular degeneration or damage such as PHYSIOLOGY OF SWALLOWING a cerebral vascular accident. In addition to strokes, degen- Normal swallowing is accomplished by a complex series of erative diseases such as amyotrophic lateral sclerosis, my- interconnected events. After mechanical crushing of a asthenia gravis and Parkinson’s disease are the most food bolus in the mouth, the tongue forces the food bolus common neuromuscular causes. Anatomical causes are to the posterior oropharynx. The upper esophageal sphinc- less frequent but include Zenker’s diverticulum, proximal ter relaxes, allowing the food bolus to enter the proximal esophageal webs, strictures, tumour and, less commonly, esophagus. The food bolus is then propelled down the vertebral osteophytes. A more complete listing of causes is esophagus by peristaltic contraction. As the food bolus included in Table 1 (1). Patients with oropharyngeal dysphagia typically de- Hilyard Place, St John, New Brunswick Correspondence: Dr Alan Cockeram, Hilyard Place, Building A, 270–560 Main Street, St John, New Brunswick E2K 1J5. Telephone 506-634-7742, fax 506-632-1107, e-mail [email protected] Can J Gastroenterol Vol 12 No 6 September 1998 409 Cockeram TABLE 1 scribe difficulty in initiating swallowing. Frequently this Selected causes of oropharyngeal dysphagia may be associated with regurgitation or symptoms of aspi- Structural lesions ration. Change in speech is often associated. All of these Intrinsic pharyngoesophageal lesions latter features suggest neuromuscular degeneration, par- Oropharyngeal carcinoma ticularly when the symptoms are progressive. Other neu- rological manifestations should be sought. Proximal esophageal carcinoma Benign esophageal tumour ESOPHAGEAL DYSPHAGIA Esophageal web Patients with esophageal dysphagia typically complain of Zenker’s diverticulum dysphagia for solids and/or liquids. Gastroesophageal re- High esophageal stricture flux is a frequent cause of esophageal stricture. The major- Inflammatory disease (eg, pharyngitis, tonsillar abscess) ity of patients with stricturing secondary to reflux have a history of heartburn; however, this may be absent or re- Postsurgical change mote in older patients and in those with Barrett’s esopha- Foreign body gus. Nausea may indicate reflux with or without Extrinsic lesions gastroparesis. Typically dysphagia from reflux is slowly Thyroid enlargement or tumour progressive. Intermittent dysphagia for solids suggests a Vertebral spur Schatzki’s ring. Esophageal or proximal gastric tumours Cervical lymphadenopathy often produce rapidly progressive dysphagia for solids in Vascular anomalies the absence of a history of any significant heartburn. Sig- nificant weight loss favours a neoplastic cause although Neuromuscular disease weight loss may occur with esophageal dysmotility, usually Central nervous system diseases at a slower pace. Localization by the patient of the site of Cerebrovascular accident dysphagia in the lower retrosternal area usually accurately Parkinson’s disease indicates a more distal esophageal site of obstruction. More Brain stem tumour proximal localization of the site of dysphagia does not pre- Amyotrophic lateral sclerosis and other motor neuron diseases dict the true site of obstruction as accurately (2). Dysphagia for liquids as well as solids is more suggestive Congenital and degenerative disorders of an esophageal motility disorder but solid-only dysphagia Huntington’s chorea may also occur with motor disorders, often in a sporadic Multiple sclerosis pattern (versus the more predictable pattern noted with Tabes dorsalis mechanical causes). Patients with dysmotility may note Poliomyelitis aggravation of dysphagia with colder foods. Odynophagia Cranial nerve diseases may occur with esophageal dysmotility. A history of heart- Diabetes mellitus burn in addition to dysphagia for both solids and liquids may suggest reflux-induced dysmotility, or a disease pro- Recurrent laryngeal nerve palsy (eg, mediastinal tumour, postsurgical onset) cess such as scleroderma with reflux superimposed upon esophageal dysmotility. Transection or injury An alternative approach is to classify motility disorders Skeletal muscle diseases as hypomotile versus spastic. Hypomotile disorders with Inflammatory myopathies decreased activity in the body and/or sphincter include Polymyositis/dermatomyositis scleroderma and other collagen vascular disorders. These Scleroderma and mixed connective tissue disease often result in gastroesophageal reflux. Spastic motor dis- Inclusion body myositis orders with increased contraction in the body and/or Muscular dystrophies sphincter include achalasia and other motor disorders listed in the primary category in Table 2 (3). These may Oculopharyngeal muscular dystrophy result in functional obstruction leading to dysphagia Myotonia dystrophica and/or pain. Other muscular disorders Thyroid disease CLINICAL EVALUATION Cricopharyngeal dysfunction Patient history is critically important in evaluating dys- Other neuromuscular disorders phagia (4). The pertinent details of the history are alluded Myasthenia gravis to above. Historical features that should be sought include the following: Amyloidosis · Botulism difficulty in initiating versus completing swallowing; · Modified from reference 1 timing of symptoms after initiating swallowing; 410 Can J Gastroenterol Vol 12 No 6 September 1998 CAG Practice Guidelines TABLE 2 Etiologies of esophageal dysphagia Dysphagia Neuromuscular (motility) disorders Difficulty initiating swallows Food stops or ‘sticks’ after Primary (includes coughing, choking swallowing Achalasia and nasal regurgitation) Other primary motility disorders OROPHARYNGEAL ESOPHAGEAL Diffuse esophageal spasm DYSPHAGIA DYSPHAGIA Nutcracker esophagus (hypertensive peristalsis) Hypertensive lower esophageal sphincter Solid food only Solid or liquid food Nonspecific esophageal dysmotility Mechanical obstruction Neuromuscular disorder Secondary Motor disorder secondary to reflux esophagitis Intermittent Progressive Intermittent Progressive Scleroderma Other collagen disorders Chagas’ disease Chronic heartburn Chronic heartburn Mechanical lesions – intrinsic No weight loss Most common Peptic stricture Bread/ Age >50 Chest Bland regurgitation Lower esophageal (Schatzki’s) ring steak Weight loss pain Weight loss Carcinoma Other Lower Peptic Carcinoma Diffuse Sclero- Achalasia Esophageal webs esophageal stricture esophageal derma Esophageal diverticula (often with an associated esophageal ring spasm motor disorder) Benign tumours Figure 1) Algorithm for symptomatic assessment of the patient with dyspepsia. Important differentiating symptoms are within Foreign bodies boxes. Modified and reproduced with permission from reference 5 Medication-induced injury Mechanical lesions – extrinsic Vascular compression cranial nerve lesions or other more generalized motor ab- Mediastinal abnormalities normalities, eg, weakness or gait disturbance. The chest Cervical osteoarthritis should be examined to rule out the possibility of aspira- Modified from reference 3 tion pneumonia. The patient with esophageal dysphagia should be care- · other neurological symptoms, ie, voice change, fully examined for any cervical lymphadenopathy, organo- drooling, aspiration and/or weakness; megaly, abdominal mass and evidence of weight loss, all of which may suggest a neoplasm. Skin lesions such as telang- · dysphagia for solids versus liquids; iectasia, sclerodactyly or calcinosis may occur in associa- · intermittent versus progressive dysphagia; tion with scleroderma and esophageal dysmotility. · sporadic versus predictable dysphagia;
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