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•  Oropharyngeal: inability to propel food from mouth through UES into esophagus

•  Esophageal: difficulty swallowing & passing food from esophagus into stomach

Figure 3-1 Etiologies of and approach to dysphagia (NCP Gastrohep 2008;5:393; Neurogastro 2012;24:57)


•  Etiologies: idiopathic (most common), pseudoachalasia (due to GE jxn tumor), Chagas

•  Sx: dysphagia (solid & liquid), chest pain (1/3 of Pts), regurgitation

•  Dx: barium swallow → dilated esophagus w/ distal “bird’s beak” narrowing; manometry → simultaneous, low amplitude contractions of esophageal body, incomplete relaxation of lower esophageal sphincter (± LES hypertension); EGD → r/o pseudoachalasia (retroflex)

•  Rx: expert pneumatic dilation (≤4% eso perf)  lap Heller myotomy (NEJM 2011;364:1868)

Other esophageal disorders

•  Webs (upper/mid esoph; congenital, GVHD, Fe-defic anemia); Rings (lower; ? due to GERD); Zenker’s diverticulum (pharyngoesoph jxn); dx w/ barium swallow; Rx: endo/surg

•  Infxn esophagitis: odynophagia > dysphagia; often immunosupp w/ Candida, HSV, CMV

•  Pill esophagitis: odynophagia > dysphagia; NSAID, KCl, bisphosp., doxy & tetracycline

•  Eosinophilic esophagitis (Clin Gastro & Hep 2012;10:1066): seen in young or middle-aged, predom . Dx req >15 eos/hpf on bx & exclude GERD (eg, empiric PPI trial). Rx: 3Ds: Diet (elim milk, soy, eggs, wheat, nuts, fish); Drugs (swallow inh steroids), Dilation



•  Excessive transient relaxations of lower esophageal sphincter (LES) or incompetent LES

•  Mucosal damage (esophagitis) due to prolonged contact w/ acid can evolve to stricture

•  Risk factors: hiatal hernia, obesity, gastric hypersecretory states, delayed emptying

•  Precipitants: supine position, fatty foods, caffeine, alcohol, cigarettes, CCB, pregnancy

Clinical manifestations

•  Esophageal: heartburn, atypical chest pain, regurgitation, water brash, dysphagia

•  Extraesophageal: cough, asthma (often poorly controlled), laryngitis, dental erosions

Diagnosis (Gastro 2008;135:1383; Am J Gastro 2010;105:747; Annals 2012;157:808)

•  Based on hx & empiric trial of PPI (Se & Sp: 78% & 54%) (Annals 2004;140:518)

•  EGD if: (1) failure to respond to bid PPI; (2) alarm features: dysphagia, vomiting, wt loss, evid of blood loss; or ? (3)  >50 y w/ sx ≥5 y + nocturnal sx, hiatal hernia, obesity, cigs

•  If dx uncertain & EGD nl → high res manometry w/ 24-h esoph pH monitoring ± impedance

Treatment (NEJM 2008;359:1700)

•  Lifestyle: avoid precipitants, lose weight, avoid large & late meals, elevate head of bed

•  Medical: PPI achieve relief in 80–90% (titrate to lowest dose that achieves sx control)  surgery among Pts who initially respond to acid suppression (JAMA 2011;305:1969)

•  Refractory: confirm w/ pH testing: if acidic or sx correlate w/ reflux episodes → surgical fundoplication (implantation of magnetic esophageal sphincter device being studied; NEJM 2013;368:719); if nl pH or no sx correlation → TCA, SSRI or baclofen (Gastro 2010;139:7.e3)

Complications (NEJM 2009;361:2548; Gastro 2011;140:1084 & e18)

•  Barrett’s esophagus: dx by bx of intestinal metaplasia above GE jxn. Screen for BE if ≥2 of the following risk factors: >50 y, male, white, chronic GERD, hiatal hernia, high BMI.

•  Esophageal adenocarcinoma: risk ~0.12%/y if Barrett’s, ~2.3%/y if low-grade dysplasia, ~6%/y if high-grade dysplasia; ~40% of Pts w/ esoph adenoca report no hx of GERD sx

•  Management: Barrett’s w/o dysplasia: surveillance EGD q3–5 y; low-grade dysplasia: q 6– 12 mo. 4 quadrant bx q 2 cm. Chemopreventive benefit of ASA under study.

High-grade dysplasia: U/S to r/o invasive cancer; endoscopic mucosal resection of any visible mucosal irregularity + ablation of dysplasia (radiofrequency or photodynamic).



•  Upper abdominal sx: discomfort, pain, fullness, early satiety, bloating, burning


•  Functional (“nonulcer dyspepsia” or NUD ~60%): some combination of visceral afferent hypersensitivity & abnormal gastric motility (Rome III criteria in Gastro 2006;130:1377)

•  Organic (~40%): GERD, PUD, rarely gastric cancer, other (meds, diabetic gastro- paresis, lactose intolerance, biliary pain, chronic pancreatitis, mesenteric ischemia)

•  Alarm features that suggest organic cause & warrant EGD: see list above under GERD

Treatment of functional dyspepsia (Gastro 2005;129:1756; Alim Pharm Ther 2012;36:3)

•  H. pylori eradication → empiric Rx if  serology, NNT = 14 (Cochrane 2006(2) CD002096)

•  PPI effective in some (? misdx GERD), others: TCA, prokinetics, buspirone


Epidemiology & etiologies (Lancet 2009;374:1449)

•  Lifetime prevalence ~10%, but incidence ↓ (H. pylori and potent acid suppression Rx). However, hosp for complic unD’d in general and ↑ in elderly, likely 2° to ↑ NSAID use.

•  H. pylori infection: 80% of duodenal ulcers (DU) and 60% of gastric ulcers (GU) ~50% of population colonized w/ H. pylori, but only 5–10% will develop PUD

•  ASA & NSAIDs: 45% erosions, 15–30% GU, 0.1–4% UGIB

•  Hypersecretory states (often mult. recurrent ulcers): gastrinoma (Zollinger-Ellison syndrome, also p/w diarrhea, <1% of PUD), carcinoid, mastocytosis

•  Malignancy: 5–10% of GU

•  Other: smoking, stress ulcers, XRT, chemo, CMV/HSV (immunosupp), bisphosphonates; steroids alone generally not a risk factor, but may exacerbate NSAID-induced ulceration

Clinical manifestations

•  Epigastric abdominal pain: relieved with food (DU) or worsened by food (GU)

•  Complications: UGIB, perforation & penetration, gastric outlet obstruction

Diagnostic studies

•  Test for H. pylori

Stool antigen or EGD + rapid urease test now dx tests of choice & to confirm erad (4–6 wk post txment); false  if on abx, bismuth, PPI, so stop prior to testing if possible

Serology: ↓ utility, useful only to exclude infection in low prevalence areas (most of U.S.)

•  EGD req to def make dx; consider if fail empiric Rx or alarm features; bx GU to r/o malig; relook in 6–12 wk if apparently benign ulcer >2.5 cm, complicated or sx persist

Treatment (NEJM 2010;362:1597, Gut 2012;61:646)

•  If H. pylori , eradicate:

Triple Rx: clarith+[amox, MNZ or levoflox]+PPI bid × 10–14 d (if clarith resist rate <20%)

Quadruple Rx: MNZ + TCN + bismuth + PPI (if clarith resist rate >15% or amox allergy) erad vs. triple 93 vs. 70%, clarith sens 95 vs. 85%, resist 91 vs. 8% (Lancet 2011;377:905)

Sequential Rx: PPI + amox × 7 d → PPI + clarith + MNZ × 7 d (Lancet 2013;381:205)

Besides PUD, test & Rx if: gastric MALT lymphoma, atrophic gastritis, FHx gastric ca

•  If H. pylori : gastric acid suppression w/ PPI

•  Discontinue ASA and NSAIDs; add PPI

•  Lifestyle changes: d/c smoking and probably EtOH; diet does not seem to play a role

•  Surgery: if refractory to med Rx (1st r/o NSAID use) or for complications (see above)

Prophylaxis if ASA/NSAID required (JACC 2008;52:1502)

•  PPI if (a) h/o PUD/UGIB; (b) also on clopidogrel (although ? ↓ antiplt effect); (c) ≥2 of the following: age >60, steroids or dyspepsia; prior to start test & Rx H. pylori

•  Consider misoprostol; consider H2RA if ASA monotherapy (Lancet 2009;374:119)

•  Consider Δ to COX-2 inhibit (↓ PUD & UGIB but ↑ CV events) if low CV risk & not on ASA

•  Stress ulcer: risk factors = ICU & coagulopathic, mech vent, h/o GIB, steroid use; Rx w/ PPI