The diagnosis of pathologic GERD is determined by combining the results of a number of investigations (Table 2). Inquiry into the patient's primary complaints and clinical history are important first steps in directing subsequent investigation. Often an empiric trial of anti- acid or anti-secretory therapy can be used as a diagnostic maneuver for GERD. This is a legitimate first step for patients with classic symptoms (heartburn, acid regurgitation). This may be all that is necessary if total control of the patient's symptoms results on a standard conservative therapeutic program (lifestyle modification, anti-secretories and prokinetic agents). However, further investigation is warranted if the patient complains of dysphagia, weight loss, or if the patient's symptoms persist in spite of a trial of standard medical therapy. This is particularly important if the patient first presents with these upper gastrointestinal tract symptoms after the age of 50. The obvious concern among such patients is the presence of complicated gastroesophageal reflux disease (e.g., peptic stricture), other benign esophageal pathology (paraesophageal hernia, achalasia, esophageal diverticulum), or esophageal cancer.

Table 2 - Diagnostic work-up of GERD

Careful review of symptoms and the patient's clinical history Esophago-gastro- duodenoscopy with biopsy Barium esophagram and upper GI roentgenograms Esophageal manometry Prolonged (24 hour) esophageal pH testing* Esophago-gastric nuclear scintigraphy* * Not always necessary to make diagnosis but may be important in tailoring surgical approach to patient's pathophysiologic condition.

The next important step in the evaluation of the patient with recalcitrant and/or worrisome esophageal related symptoms is esophago-gastro-duodenoscopy and biopsy. This endoscopic examination can determine the extent of any reflux-related esophageal injury and identify differential pathologic processes that may have been confused for complicated GERD (e.g., achalasia, esophageal cancer, duodeno-gastric ulcer disease). This examination can also determine the presence or absence of any significant hiatal herniation associated with the patient's GERD. The "retroflexed" endoscopic view of the esophago-gastric junction can also discern important anatomic characteristics associated with an incompetent lower esophageal sphincter mechanism. Additionally, the presence of Barrett's metaplasia can be identified by gross endoscopic and/or histologic examination. Its very presence exemplifies significant GERD. Identifying this aberrant esophageal mucosal pattern is important as some histologic forms increase the risk for subsequent development of adenocarcinoma of the esophagus. Close endoscopic surveillance at regular intervals is necessary when Barrett's epithelium is identified.

Barium esophagram and upper GI barium contrast studies can also improve our understanding of the patient's anatomic and physiologic abnormalities which have lead to the GERD state (Figure 2). These radiographic studies are non-invasive and relatively less expensive than endoscopic evaluation. These studies can also identify significant esophageal motor disturbances and evidence of reflux-related mucosal inflammation. They can usually determine the significance of any associated hiatal herniation. Unfortunately, the sensitivity of barium contrast radiographic studies in identifying pathologic GERD (30-40 percent) is less than adequate. Accordingly, we primarily utilize these studies as aids in identifying other pathologic processes (esophageal carcinoma, achalasia, and sclero-derma of the esophagus) in the differential diagnosis of the patient's possible GERD-related symptoms. Contrast studies are also useful in evaluating complex reflux-related pathology. These examinations become particularly important when esophageal shortening associated with esophageal stricture is in question or if a suggestion of paraesophageal herniation is present. Finally, we routinely request these studies prior to surgical intervention so as to provide an anatomic "roadmap" assisting our creation of a tailored anti-reflux repair for the patient.

Figure 2 - Illustration of hiatal hernia and GERD

At this point, most patients who have not been tried on empiric GERD therapy will be placed on an aggressive medical regimen of anti-secretory agents and prokinetic drugs aimed at controlling symptoms and clearing any gastroesophageal acid reflux injury to the esophagus that has been identified. Those patients who have been on standard GERD therapy will usually have their therapies escalated for a short period of time.

Patients who fail to respond to these therapies will require further definition of their esophago-gastric physiology to determine a more precise pathologic diagnosis and to possibly identify those who could benefit from surgical reconstruction of a defective lower esophageal anti-reflux mechanism. The combination of esophageal manometric testing and prolonged esophageal pH monitoring is needed at this point to more clearly objectify the severity of the esophageal physiologic dysfunction and to quantitate the degree of esophageal acid reflux exposure.

Esophageal manometry utilizes a pressure monitoring system introduced transnasally to determine the amplitude and coordination of esophageal muscular contractions (peristalsis). The quality of the lower esophageal "high pressure" zone can also be determined. This lower esophageal high pressure zone is commonly referred to as the physiologic lower esophageal sphincter. The presence and amplitude of effective esophageal peristalsis is also an important consideration affecting medical care options and the nature of any surgical management that may be entertained for the GERD patient. Indeed, it is considered inappropriate under most circumstances to perform "anti-reflux" surgery upon a patient without a pre-operative manometric assessment of esophageal motor function. Absence of esophageal peristalsis or incomplete relaxation of the lower esophageal sphincter zone with swallows should lead the clinical team to suspect a primary diagnosis of esophageal achalasia instead of GERD. Obviously, this is an important diagnostic distinction to make from reflux-related disease as therapeutic options are markedly different for achalasia and GERD. Although a classic clinical history and endoscopic evidence of esophagitis is virtually diagnostic of GERD, 24-hour pH testing is also recommended prior to anti-reflux surgery to objectify the extent and pattern of the reflux acid exposure. Dual esophagogastric pH assessment can assist in determining the contribution of duodeno-gastric reflux in the patient's condition. Similarly, dual pH monitoring of the proximal and distal esophagus can also be useful in diagnosing GERD-induced respiratory disease.

Finally, esophago-gastric nuclear scintigraphy can be helpful in identifying patients with functional impairment in esophago-gastric transit when other tests are equivocal. The information obtained from this assessment, and those previously mentioned, should be used to formulate the best treatment plan and surgical reconstruction for the patient with GERD.

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