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InternalMed_Harrison. FIGURE 345-15 Local staging of gastrointestinal cancers with endoscopic ultrasound. In each example, the white arrowhead marks the primary tumor and the black arrow indicates the muscularis propria of the intestinal wall. A. T1 gastric cancer. The tumor does not invade the mp. B. T2 esophageal cancer. The tumor invades the muscularis propria. C. T3 esophageal cancer. The tumor extends through the muscularis propria into the surrounding tissue and focally abuts the aorta. AO, aorta. FIGURE 345-16 Endoscopic ultrasound (EUS)–guided fine-needle aspiration (FNA). A. Ultrasound image of a 22-gauge needle passed through the duodenal wall and positioned in a hypoechoic pancreatic head mass. B. Micrograph of aspirated malignant cells. (Image B courtesy of Dr. Michael R. Henry; with permission.)


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InternalMed_Harrison. Bedside evaluation also suggests an upper or lower gastrointestinal source of bleeding in most patients. Over 90% of patients with melena are bleeding proximal to the ligament of Treitz, and about 85% of patients with hematochezia are bleeding from the colon. Melena can result from bleeding in the small bowel or right colon, especially in older patients with slow colonic transit. Conversely, some patients with massive hematochezia may be bleeding from an upper gastrointestinal source, such as a gastric Dieulafoy lesion or duodenal ulcer, with rapid intestinal transit. Early upper endoscopy should be considered in such patients.


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InternalMed_Harrison. Endoscopy should be performed after the patient has been resuscitated with intravenous fluids and transfusions, as necessary. Marked coagulopathy or thrombocytopenia is usually treated before endoscopy, since correction of these abnormalities may lead to resolution of bleeding, and techniques for endoscopic hemostasis are limited in such patients. Metabolic derangements should also be addressed. Tracheal intubation for airway protection should be considered before upper endoscopy in patients with repeated recent hematemesis, encephalopathy, and suspected variceal hemorrhage.


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InternalMed_Harrison. Most patients with significant hematochezia can undergo colonoscopy after a rapid colonic purge with a polyethylene glycol solution; the preparation fluid may be administered via a nasogastric tube. Colonoscopy has a higher diagnostic yield than radionuclide bleeding scans or angiography in lower gastrointestinal bleeding, and endoscopic therapy can be applied in some cases. In a minority of cases, endoscopic assessment is hindered by poor visualization due to persistent vigorous bleeding with recurrent hemodynamic instability, and other techniques (such as angiography or emergent subtotal colectomy) must be employed. In such patients, massive bleeding originating from an upper gastrointestinal source should also be considered and excluded by upper endoscopy. The anal and rectal mucosa should be visualized endoscopically early in the course of massive rectal bleeding, because bleeding lesions in or close to the anal canal may be identified that are amenable to endoscopic or surgical


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InternalMed_Harrison. be visualized endoscopically early in the course of massive rectal bleeding, because bleeding lesions in or close to the anal canal may be identified that are amenable to endoscopic or surgical transanal hemostatic techniques.


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InternalMed_Harrison. Peptic Ulcer The endoscopic appearance of peptic ulcers provides useful prognostic information and guides the need for endoscopic therapy in patients with acute hemorrhage (Fig. 345-21). A clean-based ulcer is associated with a low risk (3–5%) of rebleeding; patients with melena and a clean-based ulcer are often discharged home from the emergency FIGURE 345-17 Endoscopic full-thickness resection of a gastrointestinal stromal tumor. A. Subepithelial lesion in the proximal stomach. B. Hypoechoic lesion arising from the fourth layer (muscularis propria) at endoscopic ultrasound. C. Full-thickness resection defect. D. Closure of defect using an over-the-scope clip. FIGURE 345-18 Endoscopic submucosal dissection. A. Large flat distal rectal adenoma with central lobulation. B. Marking the periphery of the lesion with coagulation dots. C. Rectal defect following endoscopic submucosal dissection. D. Specimen resected en bloc.


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InternalMed_Harrison. FIGURE 345-19 Closure of large defect using an endoscopic suturing device. A. Ulcerated inflammatory fibroid polyp in the antrum. B. Large defect following endoscopic submucosal dissection of the lesion. C. Closure of the defect using endoscopic sutures (arrows). D. Resected specimen. FIGURE 345-20 Prevention of stent migration using endoscopic sutures. A. Esophagogastric anastomotic stricture refractory to balloon dilation. B. Temporary placement of covered esophageal stent. C. Endoscopic suturing device to anchor stent to esophageal wall. D. Stent fixation with endoscopic sutures (arrows). Periprocedural Antibiotic Patient Condition Procedure Contemplated Goal of Prophylaxis Prophylaxis All cardiac conditions Any endoscopic procedure Prevention of infective endocarditis Not indicated Bile duct obstruction in the absence ERCP with complete drainage Prevention of cholangitis Not recommended of cholangitis


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InternalMed_Harrison. Bile duct obstruction in the absence ERCP with complete drainage Prevention of cholangitis Not recommended of cholangitis Bile duct obstruction in absence of ERCP with anticipated incomplete Prevention of cholangitis Recommended; continue antibiotics cholangitis drainage (e.g., sclerosing cholangitis, after the procedure hilar strictures) Sterile pancreatic fluid collection (e.g., ERCP Prevention of cyst infection Recommended; continue antibiotics pseudocyst, necrosis), which commu after the procedure nicates with pancreatic duct Sterile pancreatic fluid collection Transmural drainage Prevention of cyst infection Recommended Solid lesion along upper GI tract EUS-FNA Prevention of local infection Not recommendeda Solid lesion along lower GI tract EUS-FNA Prevention of local infection Insufficient data to make firm recommendationb Cystic lesions along GI tract (including EUS-FNA Prevention of cyst infection Recommended mediastinum)


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InternalMed_Harrison. All patients Percutaneous endoscopic feeding Prevention of peristomal infection Recommended tube placement Cirrhosis with acute GI bleeding Required for all such patients, regard-Prevention of infectious complications Recommended, upon admissionc less of endoscopic procedures and reduction of mortality


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InternalMed_Harrison. Synthetic vascular graft and other Any endoscopic procedure Prevention of graft and device Not recommendedd nonvalvular cardiovascular devices infection Prosthetic joints Any endoscopic procedure Prevention of septic arthritis Not recommendede aLow rates of bacteremia and local infection. bEndoscopists may choose on a case-by-case basis. cRisk for bacterial infection associated with cirrhosis and GI bleeding is well established. dNo reported cases of infection associated with endoscopy. eVery low risk of infection. Abbreviations: ERCP, endoscopic retrograde cholangiopancreatography; EUS-FNA, endoscopic ultrasound–fine-needle aspiration; GI, gastrointestinal. Source: Adapted from S Banerjee et al: Gastrointest Endosc 67:719, 2008; with permission from Elsevier.


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InternalMed_Harrison. Interval Between Last Dose Drug of Procedure Management and Procedure Comments aLow-risk endoscopic procedures include esophagogastroduodenoscopy (EGD) or colonoscopy with or without biopsy, endoscopic ultrasound (EUS) without fine-needle aspiration (FNA), and endoscopic retrograde cholangiopancreatography (ERCP) with stent exchange. bHigh-risk endoscopic procedures include EGD or colonoscopy with dilation, polypectomy, or thermal ablation; percutaneous endoscopic gastrostomy; EUS with FNA; and ERCP with sphincterotomy or pseudocyst drainage. cBridging therapy with heparin may be considered for patients discontinuing warfarin who are at high risk for thromboembolism, including those with mitral valve replacement or aortic valve replacement with other risk factors; those with nonvalvular atrial fibrillation with a history of stroke, embolic event, cardiac thrombus, or CHADS2 score ≥4; and those with venous thromboembolism within the past 3 months or severe underlying thrombophilia.


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InternalMed_Harrison. Source: TH Baron et al: N Engl J Med 368:2113, 2013; MA Anderson et al: Gastrointest Endosc 70:1060, 2009; MJ Zuckerman et al: Gastrointest Endosc 61:189, 2005. FIGURE 345-21 Stigmata of hemorrhage in peptic ulcers. A. Gastric antral ulcer with a clean base. B. Duodenal ulcer with flat pigmented spots (arrows). C. Duodenal ulcer with a dense adherent clot. D. Gastric ulcer with a pigmented protuberance/visible vessel. E. Duodenal ulcer with active spurting (arrow). FIGURE 345-22 Endoscopic hemostasis of ulcer bleeding. A. Pyloric channel ulcer with visible vessel (arrow). B. Ulcer hemostasis with placement of an over-the-scope clip.


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InternalMed_Harrison. FIGURE 345-22 Endoscopic hemostasis of ulcer bleeding. A. Pyloric channel ulcer with visible vessel (arrow). B. Ulcer hemostasis with placement of an over-the-scope clip. room or endoscopy suite if they are young, reliable, and otherwise healthy. Flat pigmented spots and adherent clots covering the ulcer base have a 10% and 20% risk of rebleeding, respectively. Endoscopic therapy is often considered for an ulcer with an adherent clot. When a fibrin plug is seen protruding from a vessel wall in the base of an ulcer (so-called sentinel clot or visible vessel), the risk of rebleeding from the ulcer is 40%. This finding generally leads to endoscopic therapy to decrease the rebleeding rate. Occasionally, active spurting from an ulcer is seen, with >90% risk of ongoing bleeding without therapy.


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InternalMed_Harrison. Endoscopic therapy of ulcers with high-risk stigmata typically lowers the rebleeding rate to 5–10%. Several hemostatic techniques are available, including injection of epinephrine or a sclerosant into and around the vessel, “coaptive coagulation” of the vessel in the base of the ulcer using a thermal probe that is pressed against the site of bleeding, placement of hemoclips (Fig. 345-22), or a combination of these modalities (see Video 346e-8). In conjunction with endoscopic therapy, the administration of a proton pump inhibitor decreases the risk of rebleeding and improves patient outcome.


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InternalMed_Harrison. Varices Two complementary strategies guide therapy of bleeding varices: local treatment of the bleeding varices and treatment of the underlying portal hypertension. Local therapies, including endoscopic variceal band ligation, endoscopic variceal sclerotherapy, and balloon tamponade with a Sengstaken-Blakemore tube, effectively control acute hemorrhage in most patients, although therapies that decrease portal pressure (pharmacologic treatment, surgical shunts, or radiologically placed intrahepatic portosystemic shunts) also play an important role. Endoscopic variceal ligation (EVL) is indicated for the prevention of a first bleed (primary prophylaxis) from large esophageal varices (Figs. 345-23 and 24), particularly in patients in whom beta blockers are contraindicated or not tolerated. EVL is also the preferred endoscopic FIGURE 345-23 Esophageal varices.


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InternalMed_Harrison. FIGURE 345-23 Esophageal varices. therapy for control of active esophageal variceal bleeding and for subsequent eradication of esophageal varices (secondary prophylaxis). During EVL, a varix is suctioned into a cap fitted on the end of the endoscope, and a rubber band is released from the cap, ligating the varix (Fig. 345-24, see Video 346e-9). EVL controls acute hemorrhage in up to 90% of patients. Complications of EVL, such as postbanding ulcer bleeding and esophageal stenosis, are uncommon. Endoscopic variceal sclerotherapy (EVS) involves the injection of a sclerosing, thrombogenic solution into or next to esophageal varices. EVS also controls acute hemorrhage in most patients, but it is generally used as salvage therapy when band ligation fails because of its higher complication rate compared to EVL. These techniques are used when varices are actively bleeding during endoscopy or (more commonly) when FIGURE 345-24 Endoscopic band ligation of esophageal varices.


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InternalMed_Harrison. FIGURE 345-24 Endoscopic band ligation of esophageal varices. A. Large esophageal varices with stigmata of recent bleeding. B. Band ligation of varices. FIGURE 345-25 Gastric varices. A. Large gastric fundal varices. B. Stigmata of recent bleeding from the same gastric varices (arrow). varices are the only identifiable cause of acute hemorrhage. Bleeding from large gastric fundic varices (Fig. 345-25) is best treated with endoscopic cyanoacrylate (“glue”) injection (see Video 346e-10), because EVL or EVS of these varices is associated with a high rebleeding rate. Complications of cyanoacrylate injection include infection and glue embolization to other organs, such as the lungs, brain, and spleen.


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InternalMed_Harrison. After treatment of the acute hemorrhage, an elective course of endoscopic therapy can be undertaken with the goal of eradicating esophageal varices and preventing rebleeding months to years later. However, this chronic therapy is less successful, preventing long-term rebleeding in ~50% of patients. Pharmacologic therapies that Mallory-Weiss Tear A Mallory-Weiss tear is a linear mucosal rent 1891 near or across the gastroesophageal junction that is often associated with retching or vomiting (Fig. 345-27). When the tear disrupts a submucosal arteriole, brisk hemorrhage may result. Endoscopy is the best method of diagnosis, and an actively bleeding tear can be treated endoscopically with epinephrine injection, coaptive coagulation, band ligation, or hemoclips (see Video 346e-12). Unlike peptic ulcer, a Mallory-Weiss tear with a nonbleeding sentinel clot in its base rarely rebleeds and thus does not necessitate endoscopic therapy.


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InternalMed_Harrison. Vascular Ectasias Vascular ectasias are flat mucosal vascular anomalies that are best diagnosed by endoscopy. They usually cause slow intestinal blood loss and occur either in a sporadic fashion or in a well-defined pattern of distribution (e.g., gastric antral vascular ectasia [GAVE] or “watermelon stomach”) (Fig. 345-28). Cecal vascular ectasias, GAVE, and radiation-induced rectal ectasias are often responsive to local endoscopic ablative therapy, such as argon plasma coagulation (see Video 346e-13). Patients with diffuse small-bowel vascular ectasias (associated with chronic renal failure and with hereditary hemor rhagic telangiectasia) may continue to bleed despite endoscopic treatment of easily accessible lesions by conventional endoscopy. These patients may benefit from deep enteroscopy with endoscopic therapy, pharmacologic treatment with octreotide or estrogen/progesterone therapy, or intraoperative enteroscopy.


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InternalMed_Harrison. Colonic Diverticula Diverticula form where nutrient arteries penetrate the muscular wall of the colon en route to the colonic mucosa (Fig. 345-29). The artery found in the base of a diverticulum may bleed, causing painless and impressive hematochezia. Colonoscopy is indicated in patients with hematochezia and suspected diverticular hemorrhage, because other causes of bleeding (such as vascular ectasias, colitis, and colon cancer) must be excluded. In addition, an actively bleeding diverticulum may be seen and treated during colonoscopy (Fig. 345-30, see Video 346e-14). Endoscopy is useful for evaluation and treatment of some forms of gastrointestinal obstruction. An important exception is small-bowel obstruction due to surgical adhesions, which is generally not diagnosed or treated endoscopically. Esophageal, gastroduodenal, and colonic obstruction or pseudoobstruction can all be diagnosed and often managed endoscopically.


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InternalMed_Harrison. Esophageal obstruction by impacted food (Fig. 345-31) or an ingested foreign body is a potentially life-threatening event and represents an endoscopic emergency. Left untreated, the patient may develop esophageal ulceration, ischemia, and perforation. Patients with persistent esophageal obstruction often have hypersalivation and are usually decrease portal pressure have similar efficacy, and the two modalities may be combined.


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InternalMed_Harrison. Dieulafoy’s Lesion This lesion, also called persistent caliber artery, is a large-caliber arteriole that runs immediately beneath the gastrointestinal mucosa and bleeds through a pinpoint mucosal erosion (Fig. 345-26). Dieulafoy’s lesion is seen most commonly on the lesser curvature of the proximal stomach, causes impressive arterial hemorrhage, and may be difficult to diagnose; it is often recognized only after repeated endoscopy for recurrent bleeding. Endoscopic therapy, such as thermal coagulation or band ligation, is typically effective for control of bleeding and ablation of the underlying vessel once the lesion has been identified AB (see Video 346e-11). Rescue therapies, such as angio-FIGURE 345-26 Dieulafoy’s lesion. A. Actively spurting jejunal Dieulafoy’s lesion.


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InternalMed_Harrison. graphic embolization or surgical oversewing, are con-There is no underlying mucosal lesion. B. Histology of a gastric Dieulafoy’s lesion. A sidered in situations where endoscopic therapy has persistent caliber artery (arrows) is present in the gastric submucosa, immediately failed. beneath the mucosa. FIGURE 345-27 Mallory-Weiss tear at the gastroesophageal junction.


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InternalMed_Harrison. FIGURE 345-27 Mallory-Weiss tear at the gastroesophageal junction. unable to swallow water; endoscopy is generally the best initial test in such patients, because endoscopic removal of the obstructing material is usually possible, and the presence of an underlying esophageal pathology can often be determined. Radiographs of the chest and neck should be considered before endoscopy in patients with fever, obstruction for ≥24 h, or ingestion of a sharp object, such as a fishbone. Radiographic contrast studies interfere with subsequent endoscopy and are not advisable in most patients with a clinical picture of esophageal obstruction. Sips of a carbonated beverage, sublingual nifedipine or nitrates, or intravenous glucagon may resolve an esophageal food impaction, but in most patients, an underlying web, ring, or stricture is present and endoscopic removal of the obstructing food bolus is necessary.


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InternalMed_Harrison. Gastric Outlet Obstruction Obstruction of the gastric outlet is commonly caused by gastric, duodenal, or pancreatic malignancy or chronic peptic ulceration with stenosis of the pylorus (Fig. 345-32). Patients vomit partially digested food many hours after eating. Gastric decompression with a nasogastric tube and subsequent lavage for removal of retained material is the first step in treatment. The diagnosis can then be confirmed with a saline load test, if desired. Endoscopy is useful for diagnosis and treatment. Patients with benign pyloric stenosis may be treated with endoscopic balloon dilatation of the pylorus, and a course of endoscopic dilatation results in long-term relief of symptoms in about 50% of patients. Malignant gastric outlet obstruction can be relieved with endoscopically placed expandable stents in patients with inoperable malignancy (Fig. 345-33).


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InternalMed_Harrison. Colonic Obstruction and Pseudoobstruction These both present with abdominal distention and discomfort; tympany; and a dilated, air-filled


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InternalMed_Harrison. FIGURE 345-28 Gastrointestinal vascular ectasias. A. Gastric antral vascular ectasia (“watermelon window of approximately 24 h during stomach”) characterized by stripes of prominent flat or raised vascular ectasias. B. Cecal vascular ectasias. which biliary drainage should be estab-C. Radiation-induced vascular ectasias of the rectum in a patient previously treated for prostate cancer. lished, typically by ERCP. Undue delay jaundice, abdominal pain, and fever is present in about 70% of patients with ascending cholangitis and biliary sepsis. These patients are managed initially with fluid resuscitation and intravenous antibiotics. Abdominal ultrasound is often performed to assess for gallbladder stones and bile duct dilation. However, the bile duct may not be dilated early in the course of acute biliary obstruction. Medical management usually improves the patient’s clinical status, providing a colon on plain abdominal radiography. The radiographic appearance can be characteristic of a


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InternalMed_Harrison. acute biliary obstruction. Medical management usually improves the patient’s clinical status, providing a colon on plain abdominal radiography. The radiographic appearance can be characteristic of a particular condition, such as sigmoid volvulus (Fig. 345-34). Both structural obstruction and pseudoobstruction may lead to colonic perforation if left untreated. Acute colonic pseudoobstruction is a form of colonic ileus that is usually attributable to electrolyte disorders, narcotic and anticholinergic medications, immobility (as after surgery), and retroperitoneal hemorrhage or mass. Multiple causative factors are often present. Colonoscopy, water-soluble contrast enema, or CT may be used to assess for an obstructing lesion and differentiate obstruction from pseudoobstruction. One of these diagnostic studies should be strongly considered if the patient does not have clear risk factors for pseudoobstruction, if radiographs do not show air in the rectum, or if the patient fails to improve


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InternalMed_Harrison. studies should be strongly considered if the patient does not have clear risk factors for pseudoobstruction, if radiographs do not show air in the rectum, or if the patient fails to improve when underlying causes of pseudoobstruction have been addressed. The risk of cecal perforation in pseudoobstruction rises when the cecal diameter exceeds 12 cm, and decompression of the colon may be achieved using intravenous neostigmine or via colonoscopic decompression (Fig. 345-35). Most patients should receive a trial of conservative therapy (with correction of electrolyte disorders, removal of offending medications, and increased mobilization) before undergoing an invasive decompressive procedure for colonic pseudoobstruction.


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InternalMed_Harrison. Colonic obstruction is an indication for urgent intervention. In the past, emergent diverting colostomy was usually performed with a subsequent second operation after bowel preparation to treat the underlying cause of obstruction. Colonoscopic placement of an expandable stent is now a widely used alternative that can relieve malignant colonic obstruction without emergency surgery and permit bowel preparation for an elective one-stage operation (Fig. 345-36, see Video 346e-15).


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InternalMed_Harrison. The steady, severe pain that occurs when a gallstone acutely obstructs the common bile duct often brings patients to a hospital. The diagnosis of a ductal stone is suspected when the patient is jaundiced or when serum liver tests or pancreatic enzyme levels are elevated; it is confirmed by EUS, magnetic resonance cholangiography (MRCP), or direct cholangiography (performed endoscopically, percutaneously, or during surgery). ERCP is currently the primary means of diagnosing and treating common bile duct stones in most hospitals in the United States (Figs. 345-11 and 345-12). Bile Duct Imaging Whereas transabdominal ultrasound diagnoses only a minority of bile duct stones, MRCP and EUS are >90% accurate and have an important role in diagnosis. Examples of these modalities are shown in Fig. 345-37.


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InternalMed_Harrison. If the suspicion for a bile duct stone is high and urgent treatment is required (as in a patient with obstructive jaundice and biliary sepsis), ERCP is the procedure of choice, because it remains the gold standard for diagnosis and allows for immediate treatment (see Video 346e-16). If a persistent bile duct stone is relatively unlikely (as in a patient with gallstone pancreatitis), ERCP may be supplanted by less invasive imaging techniques, such as EUS, MRCP, or intraoperative cholangiography performed during cholecystectomy, sparing patients the risk and discomfort of ERCP. Ascending Cholangitis Charcot’s triad of FIGURE 345-29 Colonic diverticula. FIGURE 345-30 Diverticular hemorrhage. A. Actively bleeding sigmoid diverticulum. B. Hemostasis achieved using endoscopic clips. FIGURE 345-31 Esophageal food (meat) impaction. FIGURE 345-32 Gastric outlet obstruction due to pyloric stenosis.


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InternalMed_Harrison. FIGURE 345-31 Esophageal food (meat) impaction. FIGURE 345-32 Gastric outlet obstruction due to pyloric stenosis. A. Sequela of nonsteroidal anti-inflammatory drug (NSAID)–induced ulcer disease with severe stenosis of the pylorus (arrow). B. Balloon dilation of the stenosis. C. Appearance of pyloric ring after dilation. can result in recrudescence of overt sepsis and increased morbidity and mortality rates. In addition to Charcot’s triad, the additional presence of shock and confusion (Reynolds’s pentad) is associated with high mortality rate and should prompt urgent intervention to restore biliary drainage.


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InternalMed_Harrison. Gallstone Pancreatitis Gallstones may cause acute pancreatitis as they pass through the ampulla of Vater. The occurrence of gallstone pancreatitis usually implies passage of a stone into the duodenum, and only about 20% of patients harbor a persistent stone in the ampulla or the common bile duct. Retained stones are more common in patients with jaundice, rising serum liver tests following hospitalization, severe pancreatitis, or superimposed ascending cholangitis. Urgent ERCP decreases the morbidity rate of gallstone pancreatitis in a subset of patients with retained bile duct stones. It is unclear FIGURE 345-33 Biliary and duodenal self-expanding metal stents (SEMS) for obstruction caused by pancreatic cancer. A. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates a distal bile duct stricture (arrow). B. A biliary SEMS is placed. C. Contrast injection demonstrates a duodenal stricture (arrow). D. Biliary and duodenal SEMS in place.


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InternalMed_Harrison. C. Contrast injection demonstrates a duodenal stricture (arrow). D. Biliary and duodenal SEMS in place. whether the benefit of ERCP is mainly attributable to treatment and prevention of ascending cholangitis or to relief of pancreatic ductal obstruction. ERCP is warranted early in the course of gallstone pancreatitis if ascending cholangitis is suspected, especially in a jaundiced patient. Urgent ERCP may also benefit patients predicted to have severe pancreatitis using a clinical index of severity, such as the Glasgow or Ranson score. Because the benefit of ERCP is limited to patients with a retained bile duct stone, a strategy of initial MRCP or EUS for diagnosis decreases the utilization of ERCP in gallstone pancreatitis and improves clinical outcomes by limiting the occurrence of ERCP-related adverse events. FIGURE 345-34 Sigmoid volvulus with the characteristic radiologic appearance of a “bent inner tube.”


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InternalMed_Harrison. FIGURE 345-34 Sigmoid volvulus with the characteristic radiologic appearance of a “bent inner tube.” FIGURE 345-35 Acute colonic pseudoobstruction. A. Acute colonic dilatation occurring in a patient soon after knee surgery. B. Colonoscopic placement of decompression tube with marked improvement in colonic dilatation.


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InternalMed_Harrison. B. Colonoscopic placement of decompression tube with marked improvement in colonic dilatation. Dyspepsia is a chronic or recurrent burning discomfort or pain in the upper abdomen that may be caused by diverse processes such as gastroesophageal reflux, peptic ulcer disease, and “nonulcer dyspepsia,” a heterogeneous category that includes disorders of motility, sensation, and somatization. Gastric and esophageal malignancies are less common causes of dyspepsia. Careful history-taking allows accurate differential diagnosis of dyspepsia in only about half of patients. In the remainder, endoscopy can be a useful diagnostic tool, especially in patients whose symptoms are not resolved by an empirical trial of symptomatic treatment. Endoscopy should be performed at the outset in patients with dyspepsia and alarm features, such as weight loss or iron-deficiency anemia.


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InternalMed_Harrison. When classic symptoms of gastroesophageal reflux are present, such as water brash and substernal heartburn, presumptive diagnosis and empirical treatment are often sufficient. Endoscopy is a sensitive test for diagnosis of esophagitis (Fig. 345-38), but will miss nonerosive reflux disease (NERD) because some patients have symptomatic reflux without esophagitis. The most sensitive test for diagnosis of GERD is 24-h ambulatory pH monitoring. Endoscopy is indicated in patients with reflux symptoms refractory to antisecretory therapy; in those with alarm symptoms, such as dysphagia, weight loss, or gastrointestinal bleeding; and in those with recurrent dyspepsia after treatment that is not clearly due to reflux on clinical grounds alone. Endoscopy should be considered in patients with long-standing (≥10 years) GERD, because they have a sixfold increased risk of harboring Barrett’s esophagus compared to a patient with <1 year of reflux symptoms. Patients with Barrett’s esophagus (Fig.


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InternalMed_Harrison. (≥10 years) GERD, because they have a sixfold increased risk of harboring Barrett’s esophagus compared to a patient with <1 year of reflux symptoms. Patients with Barrett’s esophagus (Fig. 345-3) generally undergo a surveillance program of periodic endoscopy with biopsies to detect dysplasia or early carcinoma.


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InternalMed_Harrison. Barrett’s Esophagus Barrett’s esophagus is specialized columnar metaplasia that replaces the normal squamous mucosa of the distal esophagus in some persons with GERD. Barrett’s epithelium is a major risk factor for adenocarcinoma of the esophagus and is readily detected endoscopically, due to proximal displacement of the squamocolumnar junction (Fig. 345-3). A screening EGD for Barrett’s esophagus should be considered in patients with a chronic (≥10 year) history of GERD symptoms. Endoscopic biopsy is the gold standard for confirmation of Barrett’s esophagus and for dysplasia or cancer arising in Barrett’s mucosa. FIGURE 345-36 Obstructing colonic carcinoma. A. Colonic adenocarcinoma causing marked luminal narrowing of the distal transverse colon. B. Endoscopic placement of a self-expandable metal stent. C. Radiograph of expanded stent across the obstructing tumor with a residual waist (arrow).


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InternalMed_Harrison. Peptic ulcer classically causes epigastric gnawing or burning, often occurring nocturnally and promptly relieved by food or antacids. Although endoscopy is the most sensitive diagnostic test for peptic ulcer, it is not a cost-effective strategy in young patients with ulcer-like dyspeptic symptoms unless endoscopy is available at low cost. Patients with suspected peptic ulcer should be evaluated for Helicobacter pylori infection. Serology (past or present infection), urea breath testing (current infection), and stool tests are noninvasive and less costly than endoscopy with biopsy. Patients with alarm symptoms and those with persistent symptoms despite treatment should undergo endoscopy to exclude gastric malignancy and other etiologies.


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InternalMed_Harrison. Nonulcer dyspepsia may be associated with bloating and, unlike peptic ulcer, tends not to remit and recur. Most patients describe marginal relief on acid-reducing, prokinetic, or anti-Helicobacter therapy, and are referred for endoscopy to exclude a refractory ulcer and assess for other causes. Although endoscopy is useful for excluding other diagnoses, its impact on the treatment of patients with nonulcer dyspepsia is limited.


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InternalMed_Harrison. About 50% of patients presenting with difficulty swallowing have a mechanical obstruction; the remainder has a motility disorder, such as achalasia or diffuse esophageal spasm. Careful history-taking often points to a presumptive diagnosis and leads to the appropriate use of diagnostic tests. Esophageal strictures (Fig. 345-39) typically cause progressive dysphagia, first for solids, then for liquids; motility disorders often cause intermittent dysphagia for both solids and liquids. Some underlying disorders have characteristic historic features: Schatzki’s ring (Fig. 345-40) causes episodic dysphagia for solids, typically at the beginning of a meal; oropharyngeal motor disorders typically present with difficulty initiating deglutition (transfer dysphagia) and nasal reflux or coughing with swallowing; and achalasia may cause nocturnal regurgitation of undigested food.


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InternalMed_Harrison. When mechanical obstruction is suspected, endoscopy is a useful initial diagnostic test, because it permits immediate biopsy and/or dilatation of strictures, masses, or rings. The presence of linear furrows and multiple corrugated rings throughout a narrowed esophagus (feline esophagus) should raise suspicion for eosinophilic esophagitis, an increasingly recognized cause for recurrent dysphagia and food impaction (Fig. 345-41). Blind or forceful passage of an endoscope may lead to perforation in a patient with stenosis of the cervical esophagus or a Zenker’s diverticulum, but gentle passage of an endoscope under direct visual guidance is reasonably safe. Endoscopy can miss a subtle stricture or ring in some patients. When transfer dysphagia is evident or an esophageal motility disorder is suspected, esophageal radiography and/or a video-swallow study


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InternalMed_Harrison. When transfer dysphagia is evident or an esophageal motility disorder is suspected, esophageal radiography and/or a video-swallow study FIGURE 345-37 Methods of bile duct imaging. Arrows mark bile duct stones. Arrowheads indicate the common bile duct, and the asterisk marks the portal vein. A. Endoscopic ultrasound (EUS). B. Magnetic resonance cholangiopancreatography (MRCP). C. Helical computed tomography (CT).


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InternalMed_Harrison. (see Video 346e-3). In general, endoscopic techniques offer the advantage of a minimally invasive approach to treatment, but rely on other imaging techniques (such as CT, magnetic resonance imaging [MRI], positron emission tomography [PET], and EUS) to exclude distant metastases or locally advanced disease better treated by surgery or other modalities. The decision to treat an early-stage gastrointestinal malignancy endoscopically is often made in collaboration with a surgeon and/or oncologist. Endoscopic palliation of gastrointestinal malignancies relieves symptoms and in many cases prolongs survival. Malignant obstruction can be relieved by endoscopic stent placement (Figs. 345-13, 345-33, and 345-36; see Video 346e-15), and malignant gastrointestinal bleeding can often be palliated endoscopically as well. EUS-guided celiac plexus neurolysis may relieve pancreatic cancer pain.


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InternalMed_Harrison. Iron-deficiency anemia may be attributed to poor iron absorption (as in celiac sprue) or, more commonly, chronic blood loss. Intestinal bleeding should be strongly suspected in men and postmenopausal women with iron-deficiency anemia, and colonoscopy is indicated in such patients, even in the absence of detectable occult blood in the stool. Approximately 30% will have large colonic polyps, 10% will have colorectal cancer, and a few additional patients will have colonic vascular lesions. When a FIGURE 345-38 Causes of esophagitis. A. Severe reflux esophagitis with mucosal convincing source of blood loss is not found in the colon, ulceration and friability. B. Cytomegalovirus esophagitis. C. Herpes simplex virus esophagitis with target-type shallow ulcerations. D. Candida esophagitis with white plaques adherent to the esophageal mucosa.


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InternalMed_Harrison. are the best initial diagnostic tests. The oropharyngeal swallowing mechanism, esophageal peristalsis, and the lower esophageal sphincter can all be assessed. In some disorders, subsequent esophageal manometry may also be important for diagnosis.


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InternalMed_Harrison. Endoscopy plays an important role in the treatment of gastrointestinal malignancies. Early-stage malignancies limited to the superficial layers of the gastrointestinal mucosa may be resected using the techniques of endoscopic mucosal resection (EMR) (see Video 346e-4) or endoscopic submucosal dissection (ESD) (see Video 346e-5). Photodynamic therapy (PDT) and radiofrequency ablation (RFA) are effective modalities for ablative treatment of high-grade dysplasia and intramucosal cancer in Barrett’s esophagus. Gastrointestinal stromal tumors can be removed en bloc by endoscopic full-thickness resection no lesion is found, duodenal biopsies should be obtained to exclude sprue (Fig. 345-42). Small-bowel evaluation with capsule endoscopy (Fig. 345-43), CT or magnetic resonance (MR) enterography, or balloon-assisted enteroscopy may be appropriate if both EGD and colonoscopy are unrevealing.


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InternalMed_Harrison. Tests for occult blood in the stool detect hemoglobin or the heme moiety and are most sensitive for colonic blood loss, although they will also detect larger amounts of upper gastrointestinal bleeding. Patients over age 50 with occult blood in normal-appearing stool should undergo colonoscopy to diagnose or exclude colorectal neoplasia. The diagnostic yield is lower than in iron-deficiency anemia. Whether upper endoscopy is also indicated depends on the patient’s symptoms.


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InternalMed_Harrison. The small intestine may be the source of chronic intestinal bleeding, especially if colonoscopy and upper endoscopy are not diagnostic. The utility of small-bowel evaluation varies with the clinical setting and is most important in patients in whom bleeding causes chronic or recurrent anemia. In contrast to the low diagnostic yield of small-bowel radiography, positive findings on capsule endoscopy are seen in 50–70% of patients with suspected small intestinal bleeding. The most common finding is mucosal vascular ectasias. CT or MR enterography accurately detects small-bowel masses and inflammation and is also useful for initial small-bowel evaluation. Deep enteroscopy may follow capsule endoscopy for biopsy of lesions or to provide specific therapy, such as argon plasma coagulation of vascular ectasias (Fig. 345-44). FIGURE 345-39 Peptic esophageal stricture associated with esophagitis. FIGURE 345-40 Schatzki’s ring at the gastroesophageal junction.


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InternalMed_Harrison. FIGURE 345-39 Peptic esophageal stricture associated with esophagitis. FIGURE 345-40 Schatzki’s ring at the gastroesophageal junction. FIGURE 345-41 Eosinophilic esophagitis with multiple circular rings of the esophagus creating a corrugated appearance, and an impacted grape at the narrowed esophagogastric junction. The diag-nosis requires biopsy with histologic finding of > 15–20 eosinophils per high-power field. The majority of colon cancers develop from preexisting colonic adenomas, and colorectal cancer can be largely prevented by the detection and removal of adenomatous polyps (see Video 346e-17). The choice of screening strategy for an asymptomatic person depends on personal and family history. Individuals with inflammatory bowel disease, a history of colorectal polyps or cancer, family members with adenomatous polyps or cancer, or certain familial cancer syndromes (Fig. 345-45)


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InternalMed_Harrison. FIGURE 345-43 Capsule endoscopy images of a mildly scalloped jejunal fold (left) and an ileal tumor (right) in a patient with celiac sprue. (Images courtesy of Dr. Elizabeth Rajan; with permission.) FIGURE 345-44 A. Mid-jejunal vascular ectasia identified by double-balloon endoscopy. B. Ablation of vascular ectasia with argon plasma coagulation. FIGURE 345-42 Scalloped duodenal folds in a patient with celiac sprue. FIGURE 345-45 Innumerable colon polyps of various sizes in a patient with familial adenomatous polyposis syndrome. Asymptomatic individuals ≥50 years of age (≥45 Colonoscopy every 10 yearsa Preferred cancer prevention strategy years of age for African Americans) Annual fecal immunochemical test (FIT) or fecal Cancer detection strategy; fails to detect most pol-occult blood test (FOBT), multiple take-home yps; colonoscopy if results are positive specimen cards Computed tomography (CT) colonography every Colonoscopy if results are positive 5 years


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InternalMed_Harrison. Computed tomography (CT) colonography every Colonoscopy if results are positive 5 years Flexible sigmoidoscopy every 5 years Fails to detect proximal colon polyps and cancers Personal History of Polyps or Colorectal Cancer aAssumes good colonic preparation and complete exam to cecum. bHigh-risk adenoma: any adenoma ≥1 cm in size or containing high-grade dysplasia or villous features. Abbreviations: CRC, colorectal cancer; FAP, familial adenomatous polyposis; HNPCC, hereditary nonpolyposis colorectal cancer. Source: Adapted from DA Lieberman et al: Gastroenterology 143:844, 2012; B Levin et al: CA Cancer J Clin 58:130, 2008; American Cancer Society Guidelines (http://www.cancer.org/ cancer/colonandrectumcancer/moreinformation/colonandrectumcancerearlydetection/colorectal-cancer-early-detection-acs-recommendations), accessed November 15, 2013. are at increased risk for colorectal cancer. An individual without these factors is generally considered at average risk.


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InternalMed_Harrison. Screening strategies are summarized in Table 345-3. Although stool tests for occult blood have been shown to decrease mortality rate from colorectal cancer, they do not detect some cancers and many polyps, and direct visualization of the colon is a more effective screening strategy. Either sigmoidoscopy or colonoscopy may be used for cancer screening in asymptomatic average-risk individuals. The use of sigmoidoscopy was based on the historical finding that the majority of colorectal cancers occurred in the rectum and left colon and that patients with right-sided colon cancers had left-sided polyps. Over the past several decades, however, the distribution of colon cancers has changed in the United States, with proportionally fewer rectal and left-sided cancers than in the past. Large American studies of colonoscopy for screening of average-risk individuals show that cancers are roughly equally distributed between left and right colon and half of patients with right-sided lesions have


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InternalMed_Harrison. studies of colonoscopy for screening of average-risk individuals show that cancers are roughly equally distributed between left and right colon and half of patients with right-sided lesions have no polyps in the left colon. Visualization of the entire colon thus appears to be the optimal strategy for colorectal cancer screening and prevention.


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InternalMed_Harrison. Virtual colonoscopy (VC) is a radiologic technique that images the colon with CT following rectal insufflation of the colonic lumen. Computer rendering of CT images generates an electronic display of FIGURE 345-47 Ulcerated ileal carcinoid tumor. FIGURE 345-46 Virtual colonoscopy image of a colon polyp (arrow). (Image courtesy of Dr. Jeff Fidler; with permission.) a virtual “flight” along the colonic lumen, simulating colonoscopy (Fig. 345-46). Comparative studies of virtual and routine colonoscopy have shown conflicting results, but technical refinements have improved the performance characteristics of VC. The use of VC for colorectal cancer screening may become more widespread in the future, particularly at institutions with demonstrated skill with this technique. Findings detected during virtual colonoscopy often require subsequent conventional colonoscopy for confirmation and treatment.


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InternalMed_Harrison. Most cases of diarrhea are acute, self-limited, and due to infections or medication. Chronic diarrhea (lasting >6 weeks) is more often due to a primary inflammatory, malabsorptive, or motility disorder; is less likely to resolve spontaneously; and generally requires diagnostic evaluation. Patients with chronic diarrhea or severe, unexplained acute diarrhea often undergo endoscopy if stool tests for pathogens are unrevealing. The choice of endoscopic testing depends on the clinical setting.


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InternalMed_Harrison. Patients with colonic symptoms and findings such as bloody diarrhea, tenesmus, fever, or leukocytes in stool generally undergo sigmoidoscopy or colonoscopy to assess for colitis (Fig. 345-4). Sigmoidoscopy is an appropriate initial test in most patients. Conversely, patients with symptoms and findings suggesting small-bowel disease, such as large-volume watery stools, substantial weight loss, and malabsorption of iron, calcium, or fat, may undergo upper endoscopy with duodenal aspirates for assessment of bacterial overgrowth and biopsies for assessment of mucosal diseases, such as celiac sprue.


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InternalMed_Harrison. Many patients with chronic diarrhea do not fit either of these patterns. In the setting of a long-standing history of alternating constipation and diarrhea dating to early adulthood, without findings such as blood in the stool or anemia, a diagnosis of irritable bowel syndrome may be made without direct visualization of the bowel. Steatorrhea and upper abdominal pain may prompt evaluation of the pancreas rather than the gut. Patients whose chronic diarrhea is not easily categorized often undergo initial colonoscopy to examine the entire colon and terminal ileum for inflammatory or neoplastic disease (Fig. 345-47).


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InternalMed_Harrison. Bright red blood passed with or on formed brown stool usually has a rectal, anal, or distal sigmoid source (Fig. 345-48). Patients with even trivial amounts of hematochezia should be investigated with flexible sigmoidoscopy and anoscopy to exclude polyps or cancers in the distal colon. Patients reporting red blood on the toilet tissue only, without blood in the toilet or on the stool, are generally bleeding from a lesion in the anal canal. Careful external inspection, digital examination, and proctoscopy with anoscopy are sufficient for diagnosis in most cases.


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InternalMed_Harrison. About 20% of patients with pancreatitis have no identified cause after routine clinical investigation (including a review of medication and alcohol use, measurement of serum triglyceride and calcium levels, abdominal ultrasonography, and CT). Endoscopic assessment leads to a specific diagnosis in the majority of such patients, often altering clinical management. Endoscopic investigation is particularly appropriate if the patient has had more than one episode of pancreatitis.


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InternalMed_Harrison. Microlithiasis, or the presence of microscopic crystals in bile, is a leading cause of previously unexplained acute pancreatitis and is sometimes seen during abdominal ultrasonography as layering sludge or flecks of floating, echogenic material in the gallbladder. Gallbladder bile can be obtained for microscopic analysis by administering a cholecystokinin analogue during endoscopy, causing contraction of the gallbladder. Bile is suctioned from the duodenum as it drains from the papilla, and the darkest fraction is examined for cholesterol crystals or bilirubinate granules. The combination of EUS of the gallbladder and bile microscopy is probably the most sensitive means of diagnosing microlithiasis. FIGURE 345-48 Internal hemorrhoids with bleeding (arrow) as seen on a retroflexed view of the rectum.


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InternalMed_Harrison. FIGURE 345-48 Internal hemorrhoids with bleeding (arrow) as seen on a retroflexed view of the rectum. 1900 Previously undetected chronic pancreatitis, pancreatic malignancy, or pancreas divisum may be diagnosed by either ERCP or EUS. Sphincter of Oddi dysfunction or stenosis is a potential cause for pancreatitis and can be diagnosed by manometric studies performed during ERCP. Autoimmune pancreatitis may require EUS-guided pancreatic biopsy for histologic diagnosis. Severe pancreatitis often results in pancreatic fluid collections. Both pseudocysts and areas of walled-off pancreatic necrosis can be drained into the stomach or duodenum endoscopically, using transpapillary and transmural endoscopic techniques. Pancreatic necrosis can be treated by direct endoscopic necrosectomy (see Video 346e-2).


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InternalMed_Harrison. Local staging of esophageal, gastric, pancreatic, bile duct, and rectal cancers can be obtained with EUS (Fig. 345-15). EUS with fine-needle aspiration (Fig. 345-16) currently provides the most accurate preoperative assessment of local tumor and nodal staging, but it does not detect most distant metastases. Details of the local tumor stage can guide treatment decisions including resectability and need for neoadjuvant therapy. EUS with transesophageal needle biopsy may also be used to assess the presence of non-small-cell lung cancer in mediastinal nodes. Direct scheduling of endoscopic procedures by primary care physicians without preceding gastroenterology consultation, or open-access endoscopy, is common. When the indications for endoscopy are clear-cut and appropriate, the procedural risks are low, and the patient understands what to expect, open-access endoscopy streamlines patient care and decreases costs.


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InternalMed_Harrison. Patients referred for open-access endoscopy should have a recent history, physical examination, and medication review. A copy of such an evaluation should be available when the patient comes to the endoscopy suite. Patients with unstable cardiovascular or respiratory conditions should not be referred directly for open-access endoscopy. Patients with particular conditions and undergoing certain procedures should be prescribed prophylactic antibiotics prior to endoscopy (Table 345-1). In addition, patients taking anticoagulants and/or anti-platelet drugs may require adjustment of these agents before endoscopy based on the procedure risk for bleeding and condition risk for a thromboembolic event (Table 345-2).


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InternalMed_Harrison. Common indications for open-access EGD include dyspepsia resistant to a trial of appropriate therapy; dysphagia; gastrointestinal bleeding; and persistent anorexia or early satiety. Open-access colonoscopy is often requested in men or postmenopausal women with iron-deficiency anemia, in patients over age 50 with occult blood in the stool, in patients with a previous history of colorectal adenomatous polyps or cancer, and for colorectal cancer screening. Flexible sigmoidoscopy is commonly performed as an open-access procedure.


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InternalMed_Harrison. When patients are referred for open-access colonoscopy, the primary care provider may need to choose a colonic preparation. Commonly used oral preparations include polyethylene glycol lavage solution, with or without citric acid. A “split-dose” regimen improves the quality of colonic preparation. Sodium phosphate purgatives may cause fluid and electrolyte abnormalities and renal toxicity, especially in patients with renal failure or congestive heart failure and those over 70 years of age.


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InternalMed_Harrison. Video Atlas of Gastrointestinal Endoscopy Louis Michel Wong Kee Song, Mark Topazian Gastrointestinal endoscopy is an increasingly important method for diagnosis and treatment of disease. This atlas demonstrates endoscopic 346e findings in a variety of gastrointestinal infectious, inflammatory, vascular, and neoplastic conditions. Cancer screening and prevention are common indications for gastrointestinal endoscopy, and the premalignant conditions of Barrett’s esophagus and colonic polyps are illustrated. Endoscopic treatment modalities for gastrointestinal bleeding, polyps, and biliary stones are demonstrated in video clips. The images shown in this atlas are also found in Chap. 345 of the book. Video 346e-1 Methods of deep enteroscopy. (Animations courtesy of Dr. Mark Stark and Dr. Jonathan Leighton; with permission.)


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InternalMed_Harrison. Video 346e-1 Methods of deep enteroscopy. (Animations courtesy of Dr. Mark Stark and Dr. Jonathan Leighton; with permission.) Video 346e-2 Pancreatic necrosis treated by transduodenal endoscopic drainage and necrosectomy. Video 346e-3 Endoscopic full-thickness resection of a gastric subepithelial lesion. Video 346e-4 Endoscopic submucosal dissection of a large rectal adenoma. Video 346e-5 Over-the-scope clip closure of a spontaneous 346e-1 esophageal perforation. Video 346e-6 Endoscopic suturing for stent fixation. Video 346e-7 Actively bleeding duodenal ulcer treated with dilute epinephrine injection, thermal probe application, and hemoclips. (Video courtesy of Dr. Navtej Buttar; with permission.)


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InternalMed_Harrison. (Video courtesy of Dr. Navtej Buttar; with permission.) Video 346e-8 Actively bleeding esophageal varices treated with endoscopic band ligation. Video 346e-9 Large, bleeding gastric varix treated with endoscopic cyanoacrylate injection. Video 346e-10 Dieulafoy’s lesion treated endoscopically. Video 346e-11 Bleeding Mallory-Weiss tear treated with hemoclip placement. Video 346e-12 Radiation proctopathy treated with argon plasma coagulation. Video 346e-13 Actively bleeding colonic diverticulum treated with dilute epinephrine injection and band ligation. Video 346e-14 Stent placement for palliation of malignant colonic obstruction. Video 346e-15 Bile duct stones removed after endoscopic sphincterotomy. Video 346e-16 Barrett’s esophagus with high-grade dysplasia treated with endoscopic mucosal resection. Video 346e-17 Pedunculated and sessile colonic polyps removed with snare cautery during colonoscopy. CHAPTER 346e Video Atlas of Gastrointestinal Endoscopy


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InternalMed_Harrison. CHAPTER 346e Video Atlas of Gastrointestinal Endoscopy Diseases of the Esophagus Peter J. Kahrilas, Ikuo Hirano ESOPHAGEAL STRUCTURE AND FUNCTION The esophagus is a hollow, muscular tube coursing through the pos-terior mediastinum joining the hypopharynx to the stomach with a 347 sphincter at each end. It functions to transport food and fluid between these ends, otherwise remaining empty. The physiology of swallowing, esophageal motility, and oral and pharyngeal dysphagia are described in Chap. 53. Esophageal diseases can be manifested by impaired function or pain. Key functional impairments are swallowing disorders and excessive gastroesophageal reflux. Pain, sometimes indistinguishable from cardiac chest pain, can result from inflammation, infection, dysmotility, or neoplasm.


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InternalMed_Harrison. The clinical history remains central to the evaluation of esophageal symptoms. A thoughtfully obtained history will often expedite management. Important details include weight gain or loss, gastrointestinal bleeding, dietary habits including the timing of meals, smoking, and alcohol consumption. The major esophageal symptoms are heartburn, regurgitation, chest pain, dysphagia, odynophagia, and globus sensation.


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InternalMed_Harrison. Heartburn (pyrosis), the most common esophageal symptom, is characterized by a discomfort or burning sensation behind the sternum that arises from the epigastrium and may radiate toward the neck. Heartburn is an intermittent symptom, most commonly experienced after eating, during exercise, and while lying recumbent. The discomfort is relieved with drinking water or antacid but can occur frequently interfering with normal activities including sleep. The association between heartburn and gastroesophageal reflux disease (GERD) is so strong that empirical therapy for GERD has become accepted management. However, the term “heartburn” is often misused and/or referred to with other terms such as “indigestion” or “repeating,” making it important to clarify the intended meaning.


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InternalMed_Harrison. Regurgitation is the effortless return of food or fluid into the pharynx without nausea or retching. Patients report a sour or burning fluid in the throat or mouth that may also contain undigested food particles. Bending, belching, or maneuvers that increase intraabdominal pressure can provoke regurgitation. A clinician needs to discriminate among regurgitation, vomiting, and rumination. Vomiting is preceded by nausea and accompanied by retching. Rumination is a behavior in which recently swallowed food is regurgitated and then reswallowed repetitively for up to an hour. Although there is some linkage between rumination and mental deficiency, the behavior is also exhibited by unimpaired individuals who sometimes even find it pleasurable.


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InternalMed_Harrison. Chest pain is a common esophageal symptom with characteristics similar to cardiac pain, sometimes making this distinction difficult. Esophageal pain is usually experienced as a pressure type sensation in the mid chest, radiating to the mid back, arms, or jaws. The similarity to cardiac pain is likely because the two organs share a nerve plexus and the nerve endings in the esophageal wall have poor discriminative ability among stimuli. Esophageal distention or even chemostimulation (e.g., with acid) will often be perceived as chest pain. Gastroesophageal reflux is the most common cause of esophageal chest pain.


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InternalMed_Harrison. Esophageal dysphagia (Chap. 53) is often described as a feeling of food “sticking” or even lodging in the chest. Important distinctions are between uniquely solid food dysphagia as opposed to liquid and solid, episodic versus constant dysphagia, and progressive versus static dysphagia. If the dysphagia is for liquids as well as solid food, it suggests a motility disorder such as achalasia. Conversely, uniquely solid food dysphagia is suggestive of a stricture, ring, or tumor. Of note, a patient’s localization of food hang-up in the esophagus is notoriously imprecise. Approximately 30% of distal esophageal obstructions are perceived as cervical dysphagia. In such instances, the absence of concomitant symptoms generally associated with oropharyngeal dysphagia such as aspiration, nasopharyngeal regurgitation, cough, drooling, or obvious neuromuscular compromise should suggest an esophageal etiology.


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InternalMed_Harrison. Odynophagia is pain either caused by or exacerbated by swallowing. Although typically considered distinct from dysphagia, odynophagia may manifest concurrently with dysphagia. Odynophagia is more common with pill or infectious esophagitis than with reflux esophagi-tis and should prompt a search for these entities. When odynophagia does occur in GERD, it is likely related to an esophageal ulcer or deep erosion. Globus sensation, alternatively labeled “globus hystericus,” is the perception of a lump or fullness in the throat that is felt irrespective of swallowing. Although such patients are frequently referred for an evaluation of dysphagia, globus sensation is often relieved by the act of swallowing. As implied by its alternative name (globus hystericus), globus sensation often occurs in the setting of anxiety or obsessive-compulsive disorders. Clinical experience teaches that it is often attributable to GERD.


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InternalMed_Harrison. Water brash is excessive salivation resulting from a vagal reflex triggered by acidification of the esophageal mucosa. This is not a common symptom. Afflicted individuals will describe the unpleasant sensation of the mouth rapidly filling with salty thin fluid, often in the setting of concomitant heartburn.


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InternalMed_Harrison. Endoscopy, also known as esophagogastroduodenoscopy (EGD), is the most useful test for the evaluation of the proximal gastrointestinal tract. Modern instruments produce high-quality, color images of the esophageal, gastric, and duodenal lumen. Endoscopes also have an instrumentation channel through which biopsy forceps, injection catheters for local delivery of therapeutic agents, balloon dilators, or hemostatic devices can be used. The key advantages of endoscopy over barium radiography are: (1) increased sensitivity for the detection of mucosal lesions, (2) vastly increased sensitivity 1901 for the detection of abnormalities mainly identifiable by color such as Barrett’s metaplasia or vascular lesions, (3) the ability to obtain biopsy specimens for histologic examination of suspected abnormalities, and (4) the ability to dilate strictures during the examination. The main disadvantages of endoscopy are cost and the utilization of sedatives or anesthetics.


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InternalMed_Harrison. Contrast radiography of the esophagus, stomach, and duodenum can demonstrate reflux of the contrast media, hiatal hernia, mucosal granularity, erosions, ulcerations, and strictures. The sensitivity of radiography compared with endoscopy for detecting reflux esophagitis reportedly ranges from 22–95%, with higher grades of esophagitis (i.e., ulceration or stricture) exhibiting greater detection rates. Conversely, the sensitivity of barium radiography for detecting esophageal strictures is greater than that of endoscopy, especially when the study is done in conjunction with barium-soaked bread or a 13-mm barium tablet. Barium studies also provide an assessment of esophageal function and morphology that may be undetected on endoscopy. Tracheoesophageal fistula, altered postsurgical anatomy, and extrinsic esophageal compression are conditions where radiographic imaging complements endoscopic assessment. Hypopharyngeal pathology and disorders of the cricopharyngeus muscle are better


InternalMed_Harrison

InternalMed_Harrison. and extrinsic esophageal compression are conditions where radiographic imaging complements endoscopic assessment. Hypopharyngeal pathology and disorders of the cricopharyngeus muscle are better appreciated on radiographic examination than with endoscopy, particularly with rapid sequence or video fluoroscopic recording. The major shortcoming of barium radiography is that it rarely obviates the need for endoscopy. Either a positive or a negative study is usually followed by an endoscopic evaluation either to obtain biopsies, provide therapy, or clarify findings in the case of a positive examination or to add a level of certainty in the case of a negative one.


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InternalMed_Harrison. Endoscopic ultrasound (EUS) instruments combine an endoscope with an ultrasound transducer to create a transmural image of the tissue surrounding the endoscope tip. The key advantage of EUS over alternative radiologic imaging techniques is much greater resolution attributable to the proximity of the ultrasound transducer to the area being examined. Available devices can provide either radial imaging (360-degree, cross-sectional) or a curved linear image that can guide fine-needle aspiration of imaged structures such as lymph nodes or tumors. Major esophageal applications of EUS are to stage esophageal cancer, to evaluate dysplasia in Barrett’s esophagus, and to assess submucosal lesions.


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InternalMed_Harrison. Esophageal manometry, or motility testing, entails positioning a pressure-sensing catheter within the esophagus and then observing the contractility following test swallows. The upper and lower esophageal sphincters appear as zones of high pressure that relax on swallowing, while the intersphincteric esophagus exhibits peristaltic contractions. Manometry is used to diagnose motility disorders (achalasia, diffuse esophageal spasm) and to assess peristaltic integrity prior to the surgery for reflux disease. Technologic advances have enhanced esophageal manometry as high-resolution esophageal pressure topography (Fig. 347-1). Manometry can also be combined with intraluminal impedance monitoring. Impedance recordings use a catheter with a series of paired electrodes. Esophageal luminal contents in contact with the electrodes decrease (liquid) or increase (air) the impedance signal, allowing detection of anterograde or retrograde esophageal bolus transit.


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InternalMed_Harrison. GERD is often diagnosed in the absence of endoscopic esophagitis, which would otherwise define the disease. This occurs in the settings of partially treated disease, an abnormally sensitive esophageal mucosa, or without obvious explanation. In such instances, reflux


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InternalMed_Harrison. Diseases of the Esophagus testing can demonstrate excessive esophageal exposure to refluxed gastric juice, the physiologic abnormality of GERD. This can be done by ambulatory 24to 48-h esophageal pH recording using either a wireless pH-sensitive transmitter that is anchored to the esophageal mucosa or a transnasally positioned wire electrode with the tip stationed in the distal esophagus. Either way, the outcome is expressed as the percentage of the day that the pH was less than 4 (indicative of recent acid reflux), with values exceeding 5% indicative of GERD. Reflux testing is useful with atypical symptoms or an inexplicably poor response to therapy. Intraluminal impedance monitoring can be added to pH monitoring to detect reflux events irrespective of whether or not they are acidic, potentially increasing the sensitivity of the study. Hiatus hernia is a herniation of viscera, most commonly the stomach,


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InternalMed_Harrison. Hiatus hernia is a herniation of viscera, most commonly the stomach, FIGURE 347-1 High-resolution esophageal pressure topography (right) and conventional manometry (left) of a normal swallow. E, esophageal body; LES, lower esophageal sphincter; UES, upper esophageal sphincter.


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InternalMed_Harrison. E, esophageal body; LES, lower esophageal sphincter; UES, upper esophageal sphincter. A lower esophageal mucosal ring, also called a B ring, is a thin membranous narrowing at the squamocolumnar mucosal junction (Fig. 347-2). Its origin is unknown, but B rings are demonstrable in about 10–15% of the general population and are usually asymptomatic. When the lumen diameter is less than 13 mm, distal rings are usually associated with episodic solid food dysphagia and are called Schatzki rings. Patients typically present older than 40 years, consistent with an acquired rather than congenital origin. Schatzki ring is one of the most common causes of intermittent food impaction, also known as “steakhouse syndrome” because meat is a typical instigator. Symptomatic rings are easily treated by dilation.


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InternalMed_Harrison. Web-like constrictions higher in the esophagus can be of congenital or inflammatory origin. Asymptomatic cervical esophageal webs are demonstrated in about 10% of people and typically originate along the anterior aspect of the esophagus. When circumferential, they can into the mediastinum through the esophageal hiatus of the diaphragm. esophagusFour types of hiatus hernia are distinguished with type I, or sliding hiatal hernia, comprising at least 95% of the overall total. A sliding hiatal hernia is one in which the gastroesophageal junction and gastric cardia translocate cephalad as a result of weakening of the phrenoesophageal ligament attaching the gastroesophageal junction to the diaphragm at the hiatus and dilatation of the diaphragmatic hiatus. The incidence of sliding hernia increases with age. True to its name, sliding hernias enlarge with increased intraabdominal pressure, swallowing, and respiration. Conceptually, sliding hernias are the result of wear and tear: increased


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InternalMed_Harrison. with age. True to its name, sliding hernias enlarge with increased intraabdominal pressure, swallowing, and respiration. Conceptually, sliding hernias are the result of wear and tear: increased intraabdominal pressure from abdominal obesity, pregnancy, etc., along with hereditary factors predisposing to the condition. The main significance of sliding hernias is the propensity of affected individuals to have GERD.


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InternalMed_Harrison. Types II, III, and IV hiatal hernias are all subtypes of paraesophageal hernia in which the herniation into the mediastinum includes a visceral structure other than the gastric cardia. With type II and III paraesophageal hernias, the gastric fundus also herniates with the distinction being that in type II, the gastroesophageal junction remains fixed at the hiatus, whereas type III is a combined sliding and paraesophageal hernia. With type IV hiatal hernias, viscera other than the stomach herniate into the mediastinum, most commonly the colon. With type II and III paraesophageal hernias, the stomach inverts as it herniates and large paraesophageal hernias can lead to an upside down stomach, gastric volvulus, and even strangulation of the stomach. Because of this risk, surgical repair is often advocated for large paraesophageal hernias. FIGURE 347-2 Radiographic anatomy of the gastroesophageal junction.


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InternalMed_Harrison. FIGURE 347-2 Radiographic anatomy of the gastroesophageal junction. FIGURE 347-3 Examples of small (A) and large (B, C) Zenker’s diverticula arising from Killian’s triangle in the distal hypopharynx. Smaller diverticula are evident only during the swallow, whereas larger ones retain food and fluid. cause intermittent dysphagia to solids similar to Schatzki rings and are similarly treated with dilatation. The combination of symptomatic proximal esophageal webs and iron-deficiency anemia in middle-aged women constitutes Plummer-Vinson syndrome.


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InternalMed_Harrison. Esophageal diverticula are categorized by location with the most common being epiphrenic, hypopharyngeal (Zenker’s), and midesophageal. Epiphrenic and Zenker’s diverticula are false diverticula involving herniation of the mucosa and submucosa through the muscular layer of the esophagus. These lesions result from increased intraluminal pressure associated with distal obstruction. In the case of Zenker’s, the obstruction is a stenotic cricopharyngeus muscle (upper esophageal sphincter), and the hypopharyngeal herniation most commonly occurs in an area of natural weakness proximal to the cricopharyngeus known as Killian’s triangle (Fig. 347-3). Small Zenker’s diverticula are usually asymptomatic, but when they enlarge sufficiently to retain food and saliva they can be associated with dysphagia, halitosis, and aspiration. Treatment is by surgical diverticulectomy and cricopharyngeal myotomy or a marsupialization procedure in which an endoscopic stapling device is used to divide the


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InternalMed_Harrison. halitosis, and aspiration. Treatment is by surgical diverticulectomy and cricopharyngeal myotomy or a marsupialization procedure in which an endoscopic stapling device is used to divide the cricopharyngeus.


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InternalMed_Harrison. Epiphrenic diverticula are usually associated with achalasia or a distal esophageal stricture. Midesophageal diverticula may be caused by traction from adjacent inflammation (classically tuberculosis) in which case they are true diverticula involving all layers of the esophageal wall, or by pulsion associated with esophageal motor disorders. Midesophageal and epiphrenic diverticula are usually asymptomatic until they enlarge sufficiently to retain food and cause dysphagia and regurgitation. Symptoms attributable to the diverticula tend to correlate more with the underlying esophageal disorder than the size of the diverticula. Large diverticula can be removed surgically, usually in conjunction with a myotomy if the underlying cause is achalasia. Diffuse intramural esophageal diverticulosis is a rare entity that results from dilatation of the excretory ducts of submucosal esophageal glands (Fig. 347-4). Esophageal candidiasis and proximal esophageal strictures are commonly found in


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InternalMed_Harrison. is a rare entity that results from dilatation of the excretory ducts of submucosal esophageal glands (Fig. 347-4). Esophageal candidiasis and proximal esophageal strictures are commonly found in association with this disorder.


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InternalMed_Harrison. FIGURE 347-4 Intramural esophageal pseudodiverticulosis associ-ated with chronic obstruction. Invaginations of contrast into the esophageal wall outline deep esophageal glands.


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InternalMed_Harrison. Esophageal cancer occurs in about 4.5:100,000 people in the United emphasize both the rarity and lethality of esophageal cancer. OneStates with the associated mortality being only slightly less at notable trend is the shift of dominant esophageal cancer type from 4.4:100,000. It is about 10 times less common than colorectal can-squamous cell to adenocarcinoma, strongly linked to reflux disease cer but kills about one-quarter as many patients. These statistics and Barrett’s metaplasia. Other distinctions between cell types are the 1904 predilection for adenocarcinoma to affect the distal esophagus in white males and squamous cell to affect the more proximal esophagus in black males with the added risk factors of smoking, alcohol consumption, caustic injury, and human papilloma virus infection (Chap. 109). The typical presentation of esophageal cancer is of progressive solid food dysphagia and weight loss. Associated symptoms may include odynophagia, iron deficiency, and, with


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InternalMed_Harrison. infection (Chap. 109). The typical presentation of esophageal cancer is of progressive solid food dysphagia and weight loss. Associated symptoms may include odynophagia, iron deficiency, and, with midesophageal tumors, hoarseness from left recurrent laryngeal nerve injury. Generally, these are indications of locally invasive or even metastatic disease manifest by tracheoesophageal fistulas and vocal cord paralysis. Even when detected as a small lesion, esophageal cancer has poor survival because of the abundant esophageal lymphatics leading to regional lymph node metastases. Benign esophageal tumors are uncommon and usually discovered incidentally. In decreasing frequency of occurrence, cell types include leiomyoma, fibrovascular polyps, squamous papilloma, granular cell tumors, lipomas, neurofibromas, and inflammatory fibroid polyps. These generally become symptomatic only when they are associated with dysphagia and merit removal only under the same circumstances.


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InternalMed_Harrison. The most common congenital esophageal anomaly is esophageal atresia, occurring in about 1 in 5000 live births. Atresia can occur in several permutations, the common denominator being developmental failure of fusion between the proximal and distal esophagus associated with a tracheoesophageal fistula, most commonly with the distal segment excluded. Alternatively, there can be an H-type configuration in which esophageal fusion has occurred, but with a tracheoesophageal fistula. Esophageal atresia is usually recognized and corrected surgically within the first few days of life. Later life complications include dysphagia from anastomotic strictures or absent peristalsis and reflux, which can be severe. Less common developmental anomalies include congenital esophageal stenosis, webs, and duplications.


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InternalMed_Harrison. Dysphagia can also result from congenital abnormalities that cause extrinsic compression of the esophagus. In dysphagia lusoria, the esophagus is compressed by an aberrant right subclavian artery arising from the descending aorta and passing behind the esophagus. Alternatively vascular rings may surround and constrict the esophagus. Heterotopic gastric mucosa, also known as an esophageal inlet patch, is a focus of gastric type epithelium in the proximal cervical esophagus; the estimated prevalence is 4.5%. The inlet patch is thought to result from incomplete replacement of embryonic columnar epithelium with squamous epithelium. The majority of inlet patches are asymptomatic, but acid production can occur as most contain fundic type gastric epithelium with parietal cells.


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InternalMed_Harrison. Esophageal motility disorders are diseases attributable to esophageal neuromuscular dysfunction commonly associated with dysphagia, chest pain, or heartburn. The major entities are achalasia, diffuse esophageal spasm (DES), and GERD. Motility disorders can also be secondary to broader disease processes as is the case with pseudoachalasia, Chagas’ disease, and scleroderma. Not included in this discussion are diseases affecting the pharynx and proximal esophagus, the impairment of which is almost always part of a more global neuromuscular disease process.


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InternalMed_Harrison. Achalasia is a rare disease caused by loss of ganglion cells within the esophageal myenteric plexus with a population incidence of about 1:100,000 and usually presenting between age 25 and 60. With longstanding disease, aganglionosis is noted. The disease involves both excitatory (cholinergic) and inhibitory (nitric oxide) ganglionic neurons. Functionally, inhibitory neurons mediate deglutitive lower esophageal sphincter (LES) relaxation and the sequential propagation of peristalsis. Their absence leads to impaired deglutitive LES relaxation and absent peristalsis. Increasing evidence suggests that the ultimate cause of ganglion cell degeneration in achalasia is an autoimmune process attributable to a latent infection with human herpes simplex virus 1 combined with genetic susceptibility.


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InternalMed_Harrison. Long-standing achalasia is characterized by progressive dilatation and sigmoid deformity of the esophagus with hypertrophy of the LES. Clinical manifestations may include dysphagia, regurgitation, chest pain, and weight loss. Most patients report solid and liquid food dysphagia. Regurgitation occurs when food, fluid, and secretions are retained in the dilated esophagus. Patients with advanced achalasia are at risk for bronchitis, pneumonia, or lung abscess from chronic regurgitation and aspiration. Chest pain is frequent early in the course of achalasia, thought to result from esophageal spasm. Patients describe a squeezing, pressure-like retrosternal pain, sometimes radiating to the neck, arms, jaw, and back. Paradoxically, some patients complain of heartburn that may be a chest pain equivalent. Treatment of achalasia is less effective in relieving chest pain than it is in relieving dysphagia or regurgitation.


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InternalMed_Harrison. The differential diagnosis of achalasia includes DES, Chagas’ disease, and pseudoachalasia. Chagas’ disease is endemic in areas of central Brazil, Venezuela, and northern Argentina and spread by the bite of the reduviid (kissing) bug that transmits the protozoan, Trypanosoma cruzi. The chronic phase of the disease develops years after infection and results from destruction of autonomic ganglion cells throughout the body, including the heart, gut, urinary tract, and respiratory tract. Tumor infiltration, most commonly seen with carcinoma in the gastric fundus or distal esophagus, can mimic idiopathic achalasia. The resultant “pseudoachalasia” accounts for up to 5% of suspected cases and is more likely with advanced age, abrupt onset of symptoms (<1 year), and weight loss. Hence, endoscopy is a necessary part of the evaluation of achalasia. When the clinical suspicion for pseudoachalasia is high and endoscopy nondiagnostic, computed tomography (CT) scanning or EUS may be of value.


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InternalMed_Harrison. is a necessary part of the evaluation of achalasia. When the clinical suspicion for pseudoachalasia is high and endoscopy nondiagnostic, computed tomography (CT) scanning or EUS may be of value. Rarely, pseudoachalasia can result from a paraneoplastic syndrome with circulating antineuronal antibodies.


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InternalMed_Harrison. Achalasia is diagnosed by barium swallow x-ray and/or esophageal manometry; endoscopy has a relatively minor role other than to exclude pseudoachalasia. The barium swallow x-ray appearance is of a dilated esophagus with poor emptying, an air-fluid level, and tapering at the LES giving it a beak-like appearance (Fig. 347-5). Occasionally, an epiphrenic diverticulum is observed. In long-standing achalasia, the esophagus may assume a sigmoid configuration. The diagnostic criteria for achalasia with esophageal manometry are impaired LES relaxation and absent peristalsis. High-resolution manometry has somewhat advanced this diagnosis; three subtypes of achalasia are differentiated based on the pattern of pressurization in the nonperistaltic esophagus (Fig. 347-6). Because manometry identifies early disease before esophageal dilatation and food retention, it is the most sensitive diagnostic test.


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InternalMed_Harrison. There is no known way of preventing or reversing achalasia. Therapy is directed at reducing LES pressure so that gravity and esophageal pressurization promote esophageal emptying. Peristalsis rarely, if ever, recovers. However, in many instances, remnants of peristalsis masked by esophageal pressurization and dilatation prior to therapy are demonstrable following effective treatment. LES pressure can be reduced by pharmacologic therapy, pneumatic balloon dilatation, or surgical myotomy. No large, controlled trials of the therapeutic alternatives exist, and the optimal approach is debated. Pharmacologic therapies are relatively ineffective but are often used as temporizing therapies. Nitrates or calcium channel blockers are administered before eating, advising caution because of their effects on blood pressure. Botulinum toxin, injected into the LES under endoscopic guidance, inhibits acetylcholine release from nerve endings and improves dysphagia in about 66% of cases for at least 6


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InternalMed_Harrison. on blood pressure. Botulinum toxin, injected into the LES under endoscopic guidance, inhibits acetylcholine release from nerve endings and improves dysphagia in about 66% of cases for at least 6 months. Sildenafil and alternative phosphodiesterase inhibitors effectively decrease LES pressure, but practicalities limit their clinical use in achalasia.


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InternalMed_Harrison. FIGURE 347-5 Achalasia with esophageal dilatation, tapering at the gastroesophageal junction, and an air-fluid level within the esophagus. The example on the left shows sigmoid deformity with very advanced disease.


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InternalMed_Harrison. The only durable therapies for achalasia are pneumatic dilatation and Heller myotomy. Pneumatic dilatation, with a reported efficacy ranging from 32–98%, is an endoscopic technique using a noncompliant, cylindrical balloon dilator positioned across the LES and inflated to a diameter of 3–4 cm. The major complication is perforation with a reported incidence of 0.5–5%. The most common surgical procedure for achalasia is laparoscopic Heller myotomy, usually performed in conjunction with an antireflux procedure (partial fundoplication); good to excellent results are reported in 62–100% of cases. A European randomized controlled trial demonstrated an equivalent response rate of approximately 90% for both pneumatic dilation and laparoscopic Heller myotomy at 2-year follow-up. Occasionally, patients with advanced disease fail to respond to pneumatic dilatation or Heller myotomy. In such refractory cases, esophageal resection with gastric pull-up or interposition of a segment of transverse


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InternalMed_Harrison. with advanced disease fail to respond to pneumatic dilatation or Heller myotomy. In such refractory cases, esophageal resection with gastric pull-up or interposition of a segment of transverse colon may be the only option other than gastrostomy feeding.


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InternalMed_Harrison. An endoscopic approach to LES myotomy has been introduced, referred to as per oral esophageal myotomy. This technique involves the creation of a tunnel within the esophageal wall through which the circular muscle of the LES and distal esophagus are transected with electrocautery. Short-term studies of efficacy have been favorable. Potential advantages over the conventional laparoscopic approach include avoidance of surgical disruption of the diaphragmatic hiatus and more rapid recovery. In untreated or inadequately treated achalasia, esophageal dilatation predisposes to stasis esophagitis. Prolonged stasis esophagitis is the likely explanation for the association between achalasia and esophageal squamous cell cancer. Tumors develop after years of achalasia, usually in the setting of a greatly dilated esophagus with the overall squamous cell cancer risk increased 17-fold compared to controls.


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InternalMed_Harrison. DES is manifested by episodes of dysphagia and chest pain attributable to abnormal esophageal contractions with normal deglutitive LES relaxation. Beyond that, there is little consensus. The pathophysiology and natural history of DES are ill defined. Radiographically, DES has been characterized by tertiary contractions or a “corkscrew esophagus” (Fig. 347-7), but in many instances, these abnormalities are actually indicative of achalasia. Manometrically, a variety of defining features have been proposed including uncoordinated (“spastic”) activity in the distal esophagus, spontaneous and repetitive contractions, or high-amplitude and prolonged contractions. The current consensus, derived from high-resolution manometry studies, is to define spasm by the occurrence of contractions in the distal esophagus with short latency relative to the time of the pharyngeal contraction, a dysfunction indicative of impairment of inhibitory myenteric plexus neurons. A. Classic achalasia 1905


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InternalMed_Harrison. A. Classic achalasia 1905 B. Achalasia with compression C. Spastic achalasia FIGURE 347-6 Three subtypes of achalasia: classic (A), with esophageal compression (B), and spastic achalasia (C) imaged with pressure topography. All are characterized by impaired lower esophageal sphincter (LES) relaxation and absent peristalsis. However, classic achalasia has minimal pressurization of the esophageal body, whereas substantial fluid pressurization is observed in achalasia with esophageal compression, and spastic esophageal contractions are observed with spastic achalasia. When defined in this restrictive fashion (Fig. 347-8), DES is actually much less common than achalasia.


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InternalMed_Harrison. When defined in this restrictive fashion (Fig. 347-8), DES is actually much less common than achalasia. Esophageal chest pain closely mimics angina pectoris. Features suggesting esophageal pain include pain that is nonexertional, prolonged, interrupts sleep, meal-related, relieved with antacids, and accompanied by heartburn, dysphagia, or regurgitation. However, all of these features exhibit overlap with cardiac pain, which still must be the primary consideration. Furthermore, even within the spectrum of esophageal diseases, both chest pain and dysphagia are also characteristic of peptic or infectious esophagitis. Only after these more common entities have been excluded by evaluation and/or treatment should a diagnosis of DES be pursued.


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InternalMed_Harrison. Diseases of the Esophagus 1906 peristalsis, hypertensive LES) that are insufficient to diagnose either achalasia or DES. These findings are of unclear significance. Reflux and psychiatric diagnoses, particularly anxiety and depression, are common among such individuals. A lower visceral pain threshold and symptoms of irritable bowel syndrome are noted in more than half of such patients. Consequently, therapy for these individuals should either target the most common esophageal disorder, GERD, or more global conditions such as depression or somatization neurosis that are found to be coexistent.


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InternalMed_Harrison. The current conception of GERD is to encompass a family of conditions with the commonality that they are caused by gastroesophageal reflux resulting in either troublesome symptoms or an array of potential esophageal and extraesophageal manifestations. It is estimated that 15% of adults in the United States are affected by GERD, although such estimates are based only on population studies of self-reported chronic heartburn. With respect to the esophagus, the spectrum of injury includes esophagitis, stricture, Barrett’s esophagus, and adenocarcinoma (Fig. 347-9). Of particular concern is the rising incidence of esophageal adenocarcinoma, an epidemiologic trend that parallels the increasing incidence of GERD. There were about 8000 incident cases of esophageal adenocarcinoma in the United States in 2013 (half of all esophageal cancers); it is estimated that this disease burden has increased twoto sixfold in the last 20 years.


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InternalMed_Harrison. Although the defining criteria are in flux, DES is diagnosed by manom- etry. Endoscopy is useful to identify alternative structural and inflamma-The best-defined subset of GERD patients, albeit a minority overall,tory lesions that may cause chest pain. Radiographically, a “corkscrew have esophagitis. Esophagitis occurs when refluxed gastric acid andesophagus,” “rosary bead esophagus,” pseudodiverticula, or curling can pepsin cause necrosis of the esophageal mucosa causing erosions andbe indicative of DES, but these are also found with spastic achalasia.


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InternalMed_Harrison. ulcers. Note that some degree of gastroesophageal reflux is normal,Given these vagaries of defining DES, and the resultant heterogeneity of physiologically intertwined with the mechanism of belching (tranpatients identified for inclusion in therapeutic trials, it is not surprising sient LES relaxation), but esophagitis results from excessive reflux,that trial results have been disappointing. Only small, uncontrolled trials often accompanied by impaired clearance of the refluxed gastric juice.


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InternalMed_Harrison. exist, reporting response to nitrates, calcium channel blockers, hydrala-Restricting reflux to that which is physiologically intended depends on zine, botulinum toxin, and anxiolytics. The only controlled trial showing the anatomic and physiologic integrity of the esophagogastric junction,efficacy was with an anxiolytic. Surgical therapy (long myotomy or even a complex sphincter comprised of both the LES and the surroundingesophagectomy) should be considered only with severe weight loss or crural diaphragm. Three dominant mechanisms of esophagogastricunbearable pain. These indications are extremely rare.


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InternalMed_Harrison. junction incompetence are recognized: (1) transient LES relaxations NONSPECIFIC MANOMETRIC FINDINGS (a vagovagal reflex in which LES relaxation is elicited by gastric dis-Manometric studies done to evaluate chest pain and/or dysphagia tention), (2) LES hypotension, or (3) anatomic distortion of the often report minor abnormalities (e.g., hypertensive or hypotensive esophagogastric junction inclusive of hiatus hernia. Of note, the third factor, esophagogastric junction anatomic disruption, is both significant unto itself mmHg and also because it interacts with the first two mechanisms. Transient LES relaxations


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InternalMed_Harrison. Jackhammer esophagus Diffuse esophageal spasm account for about 90% of reflux in normal subjects or GERD patients without hiatus hernia, but patients with hiatus hernia have a more heterogeneous mechanistic profile. Factors tending to exacerbate reflux regardless of mechanism are abdominal obesity, pregnancy, gastric hypersecretory states, delayed gastric emptying, disruption of esophageal peristalsis, and gluttony. After acid reflux, peristalsis returns the refluxed fluid to the stomach and acid clearance is completed by titration of the residual acid by bicarbonate contained in swallowed saliva. Consequently, two causes of prolonged acid clearance are impaired


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InternalMed_Harrison. Normal latency with hypercontractility Short latency, premature contraction peristalsis and reduced salivation. Impaired FIGURE 347-8 Esophageal pressure topography of the two major variants of esophageal peristaltic emptying can be attributable spasm: jackhammer esophagus (left) and diffuse esophageal spasm (right). Jackhammer to disrupted peristalsis or superimposed esophagus is defined by the extraordinarily vigorous and repetitive contractions with normal reflux associated with a hiatal hernia. With peristaltic onset and normal latency of the contraction. Diffuse esophageal spasm is similar but superimposed reflux, fluid retained within primarily defined by a short latency (premature) contraction. a sliding hiatal hernia refluxes back into the


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InternalMed_Harrison. FIGURE 347-7 Diffuse esophageal spasm. The characteristic “cork-screw” esophagus results from spastic contraction of the circular muscle in the esophageal wall; more precisely, this is actually a helical array of muscle. These findings are also seen with spastic achalasia. Latency= 3.5 s a peptic stricture or adenocarcinoma, each of which 1907 benefits from early detection and/or specific therapy.


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InternalMed_Harrison. Latency= 3.5 s a peptic stricture or adenocarcinoma, each of which 1907 benefits from early detection and/or specific therapy. Extraesophageal syndromes with an established association to GERD include chronic cough, laryngitis, asthma, and dental erosions. A multitude of other conditions including pharyngitis, chronic bronchitis, pulmonary fibrosis, chronic sinusitis, cardiac arrhythmias, sleep apnea, and recurrent aspiration pneumonia have proposed associations with GERD. However, in both cases, it is important to emphasize the word association as opposed to causation. In many instances, the disorders likely coexist because of shared pathogenetic mechanisms rather than strict causality. Potential mechanisms for extraesophageal Erosive esophagitis Esophageal stricture with chronic


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InternalMed_Harrison. Erosive esophagitis Esophageal stricture with chronic GERD manifestations are either regurgitation with direct contact between the refluxate and supraesophageal structures or via a vagovagal reflex wherein reflux activation of esophageal afferent nerves triggers efferent vagal reflexes such as bronchospasm, cough, or arrhythmias.


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InternalMed_Harrison. Although generally quite characteristic, symptoms from GERD need to be distinguished from symptoms related to infectious, pill, or eosinophilic esophagitis, peptic ulcer disease, dyspepsia, biliary colic, coronary artery disease, and esophageal motility disorders. It is especially important that coronary artery disease be given early consideration because of its potentially lethal implications. The remaining elements of the CD differential diagnosis can be addressed by endoscopy, upper gastrointestinal series, or biliary tract ultraso-FIGURE 347-9 Endoscopic appearance of (A) peptic esophagitis, (B) a peptic stricture, nography as appropriate. The distinction among eti (C) Barrett’s metaplasia, and (D) adenocarcinoma developing within an area of Barrett’s ologies of esophagitis is usually easily made by endos- Diseases of the Esophagus esophagus. esophagus during swallow-related LES relaxation, a phenomenon that does not normally occur.


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InternalMed_Harrison. Inherent in the pathophysiologic model of GERD is that gastric juice is harmful to the esophageal epithelium. However, gastric acid hypersecretion is usually not a dominant factor in the development of esophagitis. An obvious exception is with Zollinger-Ellison syndrome, which is associated with severe esophagitis in about 50% of patients. Another caveat is with chronic Helicobacter pylori gastritis, which may have a protective effect by inducing atrophic gastritis with concomitant hypoacidity. Pepsin, bile, and pancreatic enzymes within gastric secretions can also injure the esophageal epithelium, but their noxious properties are either lessened without an acidic environment or dependent on acidity for activation. Bile warrants attention because it persists in refluxate despite acid-suppressing medications. Bile can transverse the cell membrane, imparting severe cellular injury in a weakly acidic environment, and has also been invoked as a cofactor in the pathogenesis of Barrett’s


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InternalMed_Harrison. medications. Bile can transverse the cell membrane, imparting severe cellular injury in a weakly acidic environment, and has also been invoked as a cofactor in the pathogenesis of Barrett’s metaplasia and adenocarcinoma. Hence, the causticity of gastric refluxate extends beyond hydrochloric acid.


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InternalMed_Harrison. Heartburn and regurgitation are the typical symptoms of GERD. Somewhat less common are dysphagia and chest pain. In each case, multiple potential mechanisms for symptom genesis operate that extend beyond the basic concepts of mucosal erosion and activation of afferent sensory nerves. Specifically, hypersensitivity and functional pain are increasingly recognized as cofactors. Nonetheless, the dominant clinical strategy is empirical treatment with acid inhibitors, reserving further evaluation for those who fail to respond. Important exceptions to this are patients with chest pain or persistent dysphagia, each of which may be indicative of more morbid conditions. With chest pain, cardiac disease must be carefully considered. In the case of persistent dysphagia, chronic reflux can lead to the development of copy with mucosal biopsies, which are necessary tion. In terms of endoscopic appearance, infectious esophagitis is diffuse and tends to involve the proximal esophagus far more