Step 2 CK · Internal Medicine · Gastroenterology

GI Bleeding

Name: GI Bleeding
Creator: Veli Bakalov, MD

Localize it, resuscitate it, score it, scope it

Gastroenterology·GI Bleeding·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Upper GI bleed = proximal to the ligament of Treitz (hematemesis, coffee-ground emesis, melena, BUN:Cr over 30); lower GI bleed = distal (hematochezia), though a brisk upper bleed can also cause hematochezia.
Melena needs only ~50 mL of blood and ~14 h of transit; the initial hemoglobin may be normal before hemodilution, so recheck serially.
Resuscitate with two large-bore IVs, crystalloid, type and cross, airway protection for massive hematemesis, and reversal of anticoagulation.
Transfuse restrictively at Hb under 7 g/dL (under 8 with cardiovascular disease); restrictive transfusion improved survival in acute upper GI bleeding.
Glasgow-Blatchford is used before endoscopy (0–1 = safe for outpatient care); Rockall predicts rebleeding and mortality after endoscopy.
Peptic ulcer bleed: IV PPI and endoscopy within 24 h; treat spurting (Forrest Ia) or a visible vessel (IIa) with epinephrine plus thermal/clip, leave a clean base (III) alone.
Variceal bleed: octreotide + prophylactic IV ceftriaxone (lowers mortality) + endoscopic band ligation; balloon tamponade or TIPS for refractory bleeding.
Diverticulosis is the most common lower GI bleed (painless, stops spontaneously in ~75–80%); angiodysplasia (cecum/ascending colon) is linked to aortic stenosis (Heyde), ESRD, and HHT.
Brisk lower bleed → CT angiography (~0.3–0.5 mL/min) then catheter embolization; iron-deficiency anemia in an older adult → colonoscopy plus EGD, then capsule endoscopy if both are negative.

Localizing the bleed

The ligament of Treitz is the dividing line. An upper GI bleed (UGIB) arises proximal to it and presents with hematemesis, coffee-ground emesis, or melena. A lower GI bleed (LGIB) arises distal to it and presents with hematochezia, bright red or maroon. A brisk upper bleed can also cause hematochezia when transit is fast, so hematochezia with hemodynamic instability should prompt a search for an upper source.

Upper vs lower GI bleeding

Feature	Upper GI bleed	Lower GI bleed
Presentation	Hematemesis, coffee-ground emesis, melena	Hematochezia
BUN:creatinine	Often >30: digested blood is a protein load, and volume loss adds prerenal azotemia	Usually normal: no protein load
Leading causes	Peptic ulcer disease (most common), varices	Diverticulosis (most common), angiodysplasia
First procedure	Upper endoscopy (EGD)	Colonoscopy after bowel prep

Only about 50 mL of upper-tract blood can produce melena, but it takes roughly 14 hours of gut transit to turn stool black.

Hemoglobin lags. The first hemoglobin can be normal because hemodilution has not yet occurred. Recheck it serially and judge severity by vital signs.

Resuscitation and risk stratification

ABCs and two large-bore IVs16–18 gauge; crystalloid; type and crossmatch. Protect the airway for massive hematemesis or altered mental status.
Correct coagulopathyReverse anticoagulation and hold offending agents (anticoagulants, antiplatelets, NSAIDs).
Transfuse restrictivelyAt Hb <7 g/dL.
Risk-stratifyGlasgow-Blatchford score.
Start drugsIV PPI, or octreotide plus ceftriaxone for suspected varices.
Endoscopy within 24 hoursTo diagnose and treat.

<7 g/dLtransfusion threshold (target 7–9)

<8 g/dLreasonable threshold with active cardiovascular disease

Restrictive transfusion saves lives. In acute UGIB, restrictive transfusion improved survival compared with a liberal strategy (Villanueva, NEJM 2013). A stable patient without cardiac disease and an Hb just above 7 is observed and rechecked, not transfused. Over-transfusion also raises portal pressure and can provoke variceal rebleeding.

Risk scores.

Glasgow-Blatchford: used before endoscopy. It uses only clinical and lab data: BUN, hemoglobin, systolic BP, pulse, melena, syncope, and hepatic or cardiac disease. A score of 0–1 identifies very-low-risk patients who can be managed as outpatients.
Rockall: used after endoscopy to predict rebleeding and mortality.
AIMS65: a quick mortality predictor.

Nonvariceal upper GI bleeding

Peptic ulcer disease is the most common cause of UGIB. Start IV pantoprazole (a PPI) and perform endoscopy within 24 hours. IV erythromycin before endoscopy speeds gastric emptying and improves the view. Afterward, test and treat H. pylori and stop NSAIDs.

Endoscopic hemostasis. Use two modalities together: epinephrine injection plus a thermal probe or clip. Epinephrine alone is not enough. After successful therapy of a high-risk lesion, continue high-dose PPI for about 72 hours.

Forrest classification of ulcer stigmata

Stigma	Class	Rebleeding risk	Endoscopic therapy?
Active arterial spurting	Ia	Highest	Yes
Active oozing	Ib	High	Yes
Nonbleeding visible vessel	IIa	High	Yes
Adherent clot	IIb	Intermediate	Consider
Flat pigmented spot	IIc	Low	No
Clean base	III	Lowest	No

Variceal bleeding

Suspect varices in any patient with cirrhosis or portal hypertension who has hematemesis, and start treatment before endoscopy:

Octreotide: a somatostatin analog that reduces splanchnic blood flow and portal pressure.
Prophylactic IV ceftriaxone: reduces infection and mortality in any patient with cirrhosis and GI bleeding.
Endoscopic band ligation: the definitive treatment, performed urgently (ideally within 12 hours).
Rescue for refractory bleeding: balloon tamponade as a bridge, then TIPS.

Prophylactic ceftriaxone is a proven mortality intervention in cirrhotic GI bleeding. Fresh frozen plasma given to "normalize" the INR, and liberal transfusion, are not.

After the bleed. Prevent recurrence with a nonselective β-blocker plus serial band ligation until the varices are eradicated.

Lower GI bleeding

Diverticulosis is the most common cause of acute LGIB. It causes painless, often large-volume hematochezia that stops spontaneously in about 75–80% of cases. Once the patient is stable, colonoscopy after a prep is both diagnostic and therapeutic.

Angiodysplasia is the next major cause. These tortuous, dilated submucosal vessels lie in the cecum and ascending colon of older adults and cause painless overt or occult bleeding. Associations:

Aortic stenosis: Heyde syndrome, in which turbulent flow destroys large von Willebrand multimers and causes acquired von Willebrand deficiency
End-stage renal disease
Hereditary hemorrhagic telangiectasia

When the bleed is too brisk to scope

Test	Detectable bleeding rate	Role
CT angiography	~0.3–0.5 mL/min	Fast; localizes active brisk bleeding in an unstable patient
Tagged red-cell scan	~0.1–0.4 mL/min	Detects slower or intermittent bleeding; localization is less precise
Catheter angiography	Needs brisker bleeding	Therapeutic: embolizes the culprit vessel after localization

Occult and obscure bleeding

Occult bleeding shows up as a positive fecal immunochemical test (FIT) or iron-deficiency anemia with no visible blood.

In an older adult, iron-deficiency anemia requires colonoscopy to exclude colorectal cancer.
Add upper endoscopy (evaluate both ends).
If both are negative, capsule endoscopy evaluates the small bowel.

Obscure bleeding is bleeding with no source found on EGD and colonoscopy. It usually comes from the small bowel, from angiodysplasia or tumors.

New iron-deficiency anemia in a man or a postmenopausal woman is GI cancer until proven otherwise. Never attribute it to diet and simply give iron.