Canadian Association of Gastroenterology Practice ...downloads.hindawi.com/journals/cjgh/1998/303549.pdf · Canadian Association of Gastroenterology Practice Guidelines: Evaluation

Canadian Association ofGastroenterology

Practice Guidelines:Evaluation of dysphagia

Alan W Cockeram ��

DEFINITIONDysphagia may be defined as difficulty in swallowing.Dysphagia may be classified as oropharyngeal or esophageal;oropharyngeal dysphagia arises from a structural or func-tional abnormality in the oropharynx, and esophagealdysphagia occurs as a result of structural or functional abnor-malities in the esophagus.

Esophageal dysphagia may be further subclassified symp-tomatically as dysphagia for solids alone, which usually sug-gests a mechanical problem, versus dysphagia for liquids andsolids, which is more suggestive of a neuromuscular problem.Dysphagia may be described by the patient as a sensation offood ‘sticking’ or as a sensation of food passing slowlythrough the esophagus. True dysphagia always indicates or-ganic disease and always warrants investigation and consul-tation if no cause is found in initial studies. These symptomsshould be distinguished from those of a persistent foreignbody-type sensation or a sensation of a lump, which is moretypical of globus sensation. Odynophagia, defined as painwith swallowing, may occur in association with esophagealdysmotility or as a result of mucosal disease in the esophagus.

PHYSIOLOGY OF SWALLOWINGNormal swallowing is accomplished by a complex series ofinterconnected events. After mechanical crushing of a foodbolus in the mouth, the tongue forces the food bolus to theposterior oropharynx. The upper esophageal sphincter re-laxes, allowing the food bolus to enter the proximal esopha-gus. The food bolus is then propelled down the esophagus byperistaltic contraction. As the food bolus reaches the loweresophageal sphincter, the sphincter relaxes to allow the foodto progress into the stomach.

OROPHARYNGEAL DYSPHAGIAThe majority of cases of oropharyngeal dysphagia occur as aresult of neuromuscular degeneration or damage such as acerebral vascular accident. In addition to strokes, degenera-tive diseases such as amyotrophic lateral sclerosis, myasthe-nia gravis and Parkinson’s disease are the most commonneuromuscular causes. Anatomical causes are less frequentbut include Zenker’s diverticulum, proximal esophagealwebs, strictures, tumour and, less commonly, vertebral os-teophytes. A more complete listing of causes is included inTable 1 (1).

Patients with oropharyngeal dysphagia typically describedifficulty in initiating swallowing. Frequently this may be as-sociated with regurgitation or symptoms of aspiration.Change in speech is often associated. All of these latter fea-

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SPONSORS AND VALIDATION

This practice guideline was developed by Dr Alan WCockeram MD FRCPC and was reviewed by

� Practice Affairs Committee (Chair –Dr A Cockeram): Dr T Devlin, Dr J McHattie,Dr D Petrunia, Dr E Semlacher and Dr V Sharma

� Canadian Association of Gastroenterology (CAG)Endoscopy Committee (Chair – Dr A Barkun)

� Dr N Diamant, Dr N Marcon and Dr W Paterson

� CAG Governing Board

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CAG PRACTICE GUIDELINES

tures suggest neuromuscular degeneration, particularly whenthe symptoms are progressive. Other neurological manifesta-tions should be sought.

ESOPHAGEAL DYSPHAGIAPatients with esophageal dysphagia typically complain ofdysphagia for solids and/or liquids. Gastroesophageal refluxis a frequent cause of esophageal stricture. The majority ofpatients with stricturing secondary to reflux have a history ofheartburn; however, this may be absent or remote in olderpatients and in those with Barrett’s esophagus. Nausea mayindicate reflux with or without gastroparesis. Typicallydysphagia from reflux is slowly progressive. Intermittent dys-phagia for solids suggests a Schatzki’s ring. Esophageal orproximal gastric tumours often produce rapidly progressivedysphagia for solids in the absence of a history of any signifi-cant heartburn. Significant weight loss favours a neoplasticcause although weight loss may occur with esophageal dys-motility, usually at a slower pace. Localization by the patientof the site of dysphagia in the lower retrosternal area usuallyaccurately indicates a more distal esophageal site of obstruc-tion. More proximal localization of the site of dysphagia doesnot predict the true site of obstruction as accurately (2).

Dysphagia for liquids as well as solids is more suggestive ofan esophageal motility disorder but solid-only dysphagia mayalso occur with motor disorders, often in a sporadic pattern(versus the more predictable pattern noted with mechanicalcauses). Patients with dysmotility may note aggravation ofdysphagia with colder foods. Odynophagia may occur withesophageal dysmotility. A history of heartburn in addition todysphagia for both solids and liquids may suggest reflux-induced dysmotility, or a disease process such as sclerodermawith reflux superimposed upon esophageal dysmotility.

An alternative approach is to classify motility disorders ashypomotile versus spastic. Hypomotile disorders with de-creased activity in the body and/or sphincter include sclero-derma and other collagen vascular disorders. These oftenresult in gastroesophageal reflux. Spastic motor disorderswith increased contraction in the body and/or sphincter in-clude achalasia and other motor disorders listed in the pri-mary category in Table 2 (3). These may result in functionalobstruction leading to dysphagia and/or pain.

CLINICAL EVALUATIONPatient history is critically important in evaluating dys-phagia (4). The pertinent details of the history are alluded toabove. Historical features that should be sought include thefollowing:

� difficulty in initiating versus completing swallowing;

� timing of symptoms after initiating swallowing;

� other neurological symptoms, ie, voice change, drooling,aspiration and/or weakness;

� dysphagia for solids versus liquids;

� intermittent versus progressive dysphagia;

� sporadic versus predictable dysphagia;

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� history of remote or recent heartburn;

� weight loss;

� odynophagia;

� foreign body sensation; and

� prior history of any caustic ingestion.

Figure 1 provides a diagnostic algorithm for symptom-based diagnosis (5).

PHYSICAL EXAMINATIONIn patients with oropharyngeal dysphagia, the physicianshould make particular note of other neurological manifesta-tions, such as abnormal speech pattern, drooling, other cra-nial nerve lesions or other more generalized motor abnor-malities, eg, weakness or gait disturbance. The chest shouldbe examined to rule out the possibility of aspiration pneu-monia.

The patient with esophageal dysphagia should be care-fully examined for any cervical lymphadenopathy, organo-

megaly, abdominal mass and evidence of weight loss, all ofwhich may suggest a neoplasm. Skin lesions such as telang-iectasia, sclerodactyly or calcinosis may occur in associationwith scleroderma and esophageal dysmotility. Occasionally asuccussion splash may be heard in the chest in patients withachalasia.

APPROACH TO INVESTIGATIONThe screening procedures of choice classically have been anesophagram and upper gastrointestinal series, and many fam-ily physicians follow this route. However, upper gastrointes-tinal series can miss significant lesions, especially in earlydisease and particularly if the esophageal lumen is not welldistended during filming. Specialized techniques may im-prove the sensitivity of the examination. Video studies maybe more useful in evaluating esophageal dysmotility, particu-larly in cases of oropharyngeal dysphagia where the x-ray istruly the only way to evaluate this area. Slow motion view-ing may help to identify more minor discoordination or aspi-ration. After objective clinical evaluation the speechpathologist may assist the clinician in the evaluation of oro-pharyngeal dysphagia. Modified barium swallow using bar-ium impregnated marshmallows or pudding may be useful.Upper gastrointestinal series is not always required first ifendoscopy is to be undertaken. Certainly a negative esopha-

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gram should not be considered sufficient to rule out organicdisease nor should it be a reason to cease investigation of thepatient with persisting dysphagia.

In the patient with a significant history suggesting me-chanical obstruction, endoscopy is more likely to be helpfulin establishing a diagnosis because it is more sensitive in de-tecting mucosal lesions such as minor ulcerations and less se-vere changes of reflux. In addition, endoscopy offers theadded benefit of biopsy and/or brushings, and offers the pos-sibility of therapy in conjunction with the diagnostic test. Ifsignificant mechanical narrowing is identified one may pro-ceed with dilation at the same setting. Endoscopy is quitesensitive at detecting strictures less than 10 mm in diameterbut slightly less sensitive for wider strictures (6). Endoscopymay not detect tapered narrowing of the esophagus when thelumen is wider than the endoscope and there is no associatedmucosal abnormality.

Neither endoscopy nor radiography are totally accurate inall situations and they are not interchangeable. Often thetwo are complementary and both are operator-dependent.

If patient history or barium studies suggest esophagealdysmotility one may choose to proceed directly with eso-phageal manometry, but in most cases it is preferable to pro-ceed with endoscopy before manometry to ensure that nomechanical lesion is present. In some cases dysmotility maybe related to unsuspected reflux esophagitis. Rarely esophag-

eal dysmotility may arise as a result of lesions in the cardiawhich may be poorly identified by upper gastrointestinal se-ries. After mechanical obstruction has been excluded onemay then proceed with esophageal manometry. Severalrecording systems are available; discussion of the relativemerits of each is outside the scope of this Practice Guideline.The typical manometric features of the major causes of mo-tility disturbances of the esophagus are outlined in Table 3.

THERAPYThe outcome of the diagnostic procedures dictates the thera-peutic approach.

Patients with oropharyngeal dysphagia may be helped byconsultations with speech pathologists and dieticians and bydietary changes including predominantly soft, puréed or jel-lied foods and avoidance of liquids that may be aspirated. Asa short term measure in patients with oropharyngealdysphagia, nasoenteric feeding may be useful. Oropharyn-geal dysphagia from cerebrovascular accidents may graduallyimprove with time; however, if there is no improvement af-ter more than a month or in cases where neuromuscular de-generative disease has caused oropharyngeal dysphagia, thenmanagement with gastrostomy is indicated. Gastrostomymay be performed using several different techniques.

Patients with mechanical dysphagia arising from eso-phageal lesions require appropriate dilation. Benign diseaseusually responds to single or repeated dilations. Surgery israrely indicated to treat the obstruction per se, although pa-tients with severe reflux with or without a stricture may beconsidered for antireflux surgery. The majority of patients re-spond well to medical management with dilation as neces-sary. There is evidence that treatment with a proton pumpinhibitor lessens stricture recurrence (7,8).

Patients with neoplastic lesions causing stricturing re-quire appropriate investigation to stage the disease. Surgicalresection offers the only possibility of cure. If resection is notconsidered feasible, internal and/or external radiotherapymay be considered for squamous cell neoplasms. Chemother-apy may also be considered. Patients with unresectable dis-ease who require frequent dilation benefit from endopros-thesis. While there is a significant risk with placement ofrigid esophageal endoprosthesis, such modalities offer goodpalliation of symptoms. Newer expendable stents can beplaced with less risk. Laser or thermal ablation of tumoursare other alternatives.

Patients with esophageal dysmotility may respond topharmacotherapy using nitrates or calcium channel antago-nists, although there are no controlled trials demonstrating abenefit in motor disorders other than achalasia. Esophagealdilation is sometimes helpful. In patients with achalasia,treatment with pneumatic dilation remains the standardtherapy, but in patients who would not tolerate a complica-tion of dilation, the recent advent of botulinum toxin mayoffer an alternative. Current evidence suggests that the re-sponse may not be sustained. Patients failing to respond topharmacological or endoscopic therapy may be consideredfor myotomy or rarely for esophagectomy.

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Canadian Association of Gastroenterology Practice Guideline Disclaimer

This clinical practice guideline has been developed by theauthor on behalf of the Canadian Association ofGastroenterology (CAG) in order to outline the clinicalapproach to management problems or training issues. Afterpreparation by the author, based on a review of theliterature, each guideline is extensively reviewed by theCAG Practice Affairs Committee, composed of practitionersfrom across Canada. Changes are made, and once theguideline is felt to be appropriate, it is then circulated forfurther review by recognized Canadian experts and thenamended further. Finally, the guideline is presented to theCAG Governing Board for further review and final approval.

Practice guidelines are intended to give an understanding ofa clinical problem and outline one or more preferredapproaches to investigation and management of theproblem. While practice guidelines are intended to be

useful to all physicians, it is recognized that specialists mayrely less on practice guidelines than those in more generalpractice. These guidelines are intended to give a practicalapproach to a problem based on the current literature, butare not intended to be state-of-the-art reviews withextensive references.

Practice guidelines are developed to be of assistance topractising clinicians and are not intended to be the onlyapproach to the management of clinical problems, nor arethey intended to be considered as a ‘standard of care’. TheCAG Practice Affairs Committee recognizes that clinicalcircumstances may at times justify an approach differentfrom that outlined in a practice guideline. It is alsorecognized that new developments in medical research andclinical practice may require subsequent changes to thepractice guideline.

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