Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (37 page)

• 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).

DYSPEPSIA (“INDIGESTION”)

Definition

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

•
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

PEPTIC ULCER DISEASE (PUD)

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

GASTROINTESTINAL BLEEDING

Definition

• Intraluminal blood loss anywhere from the oropharynx to the anus • Classification:
upper
= above the ligament of Treitz;
lower
= below the ligament of Treitz • Signs:
hematemesis
= blood in vomitus (UGIB);
hematochezia
= bloody stools (LGIB or rapid UGIB);
melena
= black, tarry stools from digested blood (usually UGIB, but can be anywhere above and including the right colon)
Etiologies of upper GI bleed (UGIB)

•
Peptic ulcer disease
(50%):
H. pylori
, NSAIDs, gastric hypersecretory states •
Varices
(10–30%): esophageal ± gastric, 2° to portal HTN. If isolated gastric → r/o splenic vein thrombosis.

•
Gastropathy/gastritis/duodenitis
(15%): NSAIDs, ASA, alcohol, stress, portal hypertensive •
Erosive esophagitis/ulcer
(10%): GERD, XRT, infectious (CMV, HSV or
Candida
if immunosuppressed), pill esophagitis (bisphosphonate, NSAIDs; ± odynophagia) •
Mallory-Weiss tear
(10%): GE junction tear due to retching against closed glottis •
Vascular lesions
(5%)

Dieulafoy’s lesion: superficial ectatic artery usually in cardia → sudden, massive UGIB

AVMs, angioectasias, hered. hemor. telangiectasia: submucosal, anywhere in GI tract

Gastric antral vascular ectasia (GAVE):  “watermelon stomach,” tortuous, dilated vessels; a/w cirrhosis, atrophic gastritis, CREST syndrome

Aortoenteric fistula: AAA or aortic graft erodes into 3rd portion of duodenum; p/w “herald bleed”; if suspected, diagnose by endoscopy or CT

• Neoplastic disease: esophageal or gastric carcinoma, GIST

• Oropharyngeal bleeding and epistaxis → swallowed blood
Etiologies of lower GI bleed (LGIB)

• Diverticular hemorrhage (33%): 60% of diverticular bleeding localized to right colon • Neoplastic disease (19%): usually occult bleeding, rarely severe • Colitis (18%): infectious, ischemic, radiation, inflammatory bowel disease (UC >> CD) • Angiodysplasia (8%): most commonly located in ascending colon and cecum • Anorectal (4%): hemorrhoids, anal fissure, rectal ulcer • Other: postpolypectomy, vasculitis
Clinical manifestations

• UGIB > LGIB: N/V, hematemesis, coffee-ground emesis, epigastric pain, vasovagal, melena • LGIB > UGIB: diarrhea, tenesmus, BRBPR, hematochezia (11% UGIB;
Gastro
1988;95:1569)
Initial management

•
Assess severity
: tachycardia (can be masked by bB use) suggests 10% volume loss, orthostatic hypotension 20% loss, shock >30% loss •
Resuscitation
: placement of 2 large-bore (18-gauge or larger) intravenous lines Volume replacement: NS or LR to achieve normal VS, UOP, & mental status •
Transfuse
: blood bank sample for type & cross; use O-neg if emerg; transfuse as needed; for UGIB (esp. w/ portal HTN) use more restrictive Hb goal (eg, 7 g/dL) (
NEJM
2013;368:11) •
Reverse coagulopathy
: FFP & vit K to normalize PT; plts to keep count >50,000

•
Triage
: consider ICU if unstable VS or poor end organ perfusion

Intubation for emergent EGD, if ongoing hematemesis, shock, poor resp status, Δ MS

? OutPt management if SBP ≥110, HR <100, Hb ≥13 (
) or ≥12 (
), BUN <18,  melena, syncope, heart failure, liver disease (
Lancet
2009;373;42)