Harrison’s Manual of Medicine



Upper Gi Bleeding
Lower Gi Bleeding

1.   Hematemesis: Vomiting of blood or altered blood (“coffee grounds”) indicates bleeding proximal to ligament of Treitz.
2.   Melena: Altered (black) blood per rectum (>100 mL blood required for one melenic stool) usually indicates bleeding proximal to ligament of Treitz but may be as distal as ascending colon; pseudomelena may be caused by ingestion of iron, bismuth, licorice, beets, blueberries, charcoal.
3.   Hematochezia: Bright red or maroon rectal bleeding usually implies bleeding beyond ligament of Treitz but may be due to rapid upper GI bleeding (>1000 mL).
4.   Positive fecal occult blood test with or without iron deficiency.
5.   Symptoms of blood loss: e.g., light-headedness or shortness of breath.
HEMODYNAMIC CHANGES   Orthostatic drop in bp >10 mmHg usually indicates >20% reduction in blood volume (± syncope, light-headedness, nausea, sweating, thirst).
SHOCK   bp <100 mmHg systolic usually indicates <30% reduction in blood volume (± pallor, cool skin).
LABORATORY CHANGES   Hematocrit may not reflect extent of blood loss because of delayed equilibration with extravascular fluid. Mild leukocytosis and thrombocytosis. Elevated BUN is common in upper GI bleeding.
ADVERSE PROGNOSTIC SIGNS   Age >60, associated illnesses, coagulopathy, immunosuppression, presentation with shock, rebleeding, onset of bleeding in hospital, variceal bleeding, endoscopic stigmata of recent bleeding, [e.g., “visible vessel” in ulcer base (see below)].
CAUSES   Common   Peptic ulcer, gastropathy (alcohol, aspirin, NSAIDs, stress), esophagitis, Mallory-Weiss tear (mucosal tear at gastroesophageal junction due to retching), gastroesophageal varices.
Less Common   Swallowed blood (nosebleed); esophageal, gastric, or intestinal neoplasm; anticoagulant and fibrinolytic therapy; hypertrophic gastropathy (Ménétrier’s disease); aortic aneurysm; aortoenteric fistula (from aortic graft); AV malformation; telangiectases (Osler-Rendu-Weber syndrome); Dieulafoy lesion (ectatic submucosal vessel); vasculitis; connective tissue disease (pseudoxanthoma elasticum, Ehlers-Danlos syndrome); blood dyscrasias; neurofibroma; amyloidosis; hemobilia (biliary origin).
EVALUATION   After hemodynamic resuscitation (see below and Fig. 22-1).

FIGURE 22-1. Suggested algorithm for patients with acute UGIB. Recommendations on level of care and time of discharge assume patient is stabilized without further bleeding or other concomitant medical problems. Upper GI endoscopy is the major diagnostic and therapeutic tool. *Some authors suggest endoscopic therapy for adherent clots.

History and physical examination: Drugs (increased risk of upper and lower GI tract bleeding with aspirin and NSAIDs), prior ulcer, bleeding history, family history, features of cirrhosis or vasculitis, etc. Hyperactive bowel sounds favor upper GI source.

Nasogastric aspirate for gross blood, if source (upper versus lower) not clear from history; may be falsely negative in up to 16% of pts if bleeding has ceased or duodenum is the source. Testing aspirate for occult blood is meaningless.

Upper endoscopy: Accuracy >90%; allows visualization of bleeding site and possibility of therapeutic intervention; mandatory for suspected varices, aortoenteric fistulas; permits identification of “visible vessel” (protruding artery in ulcer crater), which connotes high (~50%) risk of rebleeding.

Upper GI barium radiography: Accuracy ~80% in identifying a lesion, though does not confirm source of bleeding; acceptable alternative to endoscopy in resolved or chronic low-grade bleeding.

Selective mesenteric arteriography: When brisk bleeding precludes identification of source at endoscopy.

Radioisotope scanning (e.g., 99Tc tagged to red blood cells or albumin); used primarily as screening test to confirm bleeding is rapid enough for arteriography to be of value or when bleeding is intermittent and of unclear origin.
CAUSES   Anal lesions (hemorrhoids, fissures), rectal trauma, proctitis, colitis (ulcerative colitis, Crohn’s disease, infectious colitis, ischemic colitis, radiation), colonic polyps, colonic carcinoma, angiodysplasia (vascular ectasia), diverticulosis, intussusception, solitary ulcer, blood dyscrasias, vasculitis, connective tissue disease, neurofibroma, amyloidosis, anticoagulation.
EVALUATION   See below and Fig. 22-2.

FIGURE 22-2. Suggested algorithm for patients with acute LGIB. *If massive bleeding does not allow time for colonic lavage, proceed to angiography.

History and physical examination.

In the presence of hemodynamic changes, perform upper endoscopy followed by colonoscopy. In the absence of hemodynamic changes, perform anoscopy and either flexible sigmoidoscopy or colonoscopy: Exclude hemorrhoids, fissure, ulcer, proctitis, neoplasm.

Colonoscopy: Often test of choice, but may be impossible if bleeding is massive.

Barium enema: No role in active bleeding.

Arteriography: When bleeding is severe (requires bleeding rate >0.5 mL/ min; may require prestudy radioisotope bleeding scan as above); defines site of bleeding or abnormal vasculature.
Surgical exploration (last resort).
BLEEDING OF OBSCURE ORIGIN   Often small-bowel source. Consider small-bowel enteroclysis x-ray (careful barium radiography via peroral intubation of small bowel), Meckel’s scan, enteroscopy (small-bowel endoscopy), or exploratory laparotomy with intraoperative enteroscopy.

Upper and Lower GI Bleeding

Venous access with large bore IV (14–18 gauge); central venous line for major bleed and pts with cardiac disease; monitor vital signs, urine output, Hct (fall may lag). Gastric lavage of unproven benefit but clears stomach before endoscopy. Iced saline may lyse clots; room-temperature tap water may be preferable. Intubation may be required to protect airway.

Type and cross match blood (6 units for major bleed).

Surgical standby when bleeding is massive.

Support blood pressure with isotonic fluids (normal saline); albumin and fresh frozen plasma in cirrhotics. Packed red blood cells when available (whole blood if massive bleeding); maintain Hct >25–30. Fresh frozen plasma and vitamin K (10 mg SC or IV) in cirrhotics with coagulopathy.

IV calcium (e.g., up to 10–20 mL 10% calcium gluconate IV over 10– 15 min) if serum calcium falls (due to transfusion of citrated blood). Empirical drug therapy (antacids, H2 receptor blockers, omeprazole) of unproven benefit.

Specific measures: Varices: IV vasopressin (0.4–0.9 U/min) with nitroglycerin IV, SL, or transdermally to maintain systolic bp >90 mmHg, Blakemore-Sengstaken tube tamponade, endoscopic sclerosis, or band ligation; propranolol or nadolol in doses sufficient to cause beta blockade reduces risk of recurrent or initial variceal bleeding (do not use in acute bleed) (Chap. 156); ulcer with visible vessel or active bleeding: endoscopic bipolar, heater-probe, or laser coagulation or injection of epinephrine; gastritis: embolization or vasopressin infusion of left gastric artery; GI telangiectases: ethinylestradiol/norethisterone (0.05/1.0 mg PO qd) may prevent recurrent bleeding, particularly in pts with chronic renal failure; diverticulosis: mesenteric arteriography with intraarterial vasopressin; angiodysplasia: colonoscopic bipolar or laser coagulation, may regress with replacement of stenotic aortic valve.

Indications for emergency surgery: Uncontrolled or prolonged bleeding, severe rebleeding, aortoenteric fistula. For intractable variceal bleeding, consider transjugular intrahepatic portosystemic shunt (TIPS).


For a more detailed discussion, see Laine L: Gastrointestinal Bleeding, Chap. 44, p. 252, in HPIM-15.


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