8.1 GI Bleeding & Acute Hepatic Failure

Gastrointestinal Bleeding

Gastrointestinal (GI) bleeding is a high-frequency CCRN emergency that tests your ability to recognize the source, resuscitate, and sequence definitive care. The anatomic dividing line is the ligament of Treitz (the duodenojejunal junction). Bleeding proximal to it is upper GI bleeding (UGIB); bleeding distal to it is lower GI bleeding (LGIB).

Upper vs. Lower: Reading the Presentation

• Hematemesis — vomiting bright red blood or coffee-ground material (blood altered by gastric acid) always indicates an upper source.
• Melena — black, tarry, foul stool from digested blood, usually upper (or slow right-colon) bleeding.
• Hematochezia — bright red or maroon blood per rectum, typically lower. A caveat tested often: a brisk upper GI bleed can move so fast it presents as hematochezia, so hemodynamic instability with hematochezia should not exclude an upper source.

Varices vs. Peptic Ulcer

The two most exam-relevant UGIB causes behave differently:

Peptic ulcer disease remains the single most common UGIB cause overall; variceal bleeding carries the highest mortality. Diverticulosis and angiodysplasia dominate LGIB.

Resuscitation Priorities

Apply A-B-C. Protect the airway in massive hematemesis or altered mental status (aspiration and airway soiling kill quickly). Establish two large-bore IVs (16-18 gauge) or central access, and send type and crossmatch, CBC, coagulation panel, and lactate.

Resuscitate with balanced crystalloid and blood products. A key evidence point: use a restrictive transfusion strategy, transfusing packed red cells to keep hemoglobin above roughly 7 g/dL in stable patients. Trials show restrictive transfusion improves survival and lowers rebleeding, particularly in variceal patients—over-transfusion raises portal venous pressure and provokes further hemorrhage. Activate the massive transfusion protocol (balanced RBC:plasma:platelets) for ongoing hemorrhage, and correct coagulopathy and thrombocytopenia. Glasgow-Blatchford and Rockall scores risk-stratify and guide disposition.

Endoscopy and Pharmacology

Esophagogastroduodenoscopy (EGD) is both diagnostic and therapeutic and is generally performed within 24 hours of UGIB—urgently (within 12 hours) for suspected variceal bleeding once the patient is resuscitated. Start drugs before scope results:

• Octreotide (a somatostatin analog): 50 mcg IV bolus then 50 mcg/hr infusion. It causes splanchnic vasoconstriction, reducing portal blood flow and portal pressure—the mechanism that controls variceal bleeding. PPIs do not lower portal pressure.
• Proton pump inhibitor (PPI): high-dose IV (e.g., pantoprazole 80 mg bolus then 8 mg/hr or intermittent dosing) raises gastric pH and stabilizes the clot over an ulcer.
• Prophylactic antibiotics (ceftriaxone) in cirrhotic GI bleeders reduce spontaneous bacterial peritonitis, rebleeding, and mortality.

When endoscopy fails or is delayed in exsanguinating variceal bleeding, balloon tamponade (Sengstaken-Blakemore/Minnesota tube) is a temporizing rescue bridge—airway must be secured first. Transjugular intrahepatic portosystemic shunt (TIPS) treats refractory variceal bleeding but can precipitate encephalopathy.

Acute Hepatic Failure

Acute liver failure (ALF) is rapid hepatocellular dysfunction with coagulopathy (INR >=1.5) and encephalopathy in a patient without prior cirrhosis. Acetaminophen toxicity is the leading U.S. cause; N-acetylcysteine is the antidote and benefits even non-acetaminophen ALF.

Hepatic Encephalopathy and Ammonia

Hepatic encephalopathy (HE) reflects accumulation of gut-derived neurotoxins, chiefly ammonia, that the failing liver cannot clear. Asterixis (flapping tremor) is the classic sign. The West Haven scale grades severity:

Ammonia loosely correlates with severity; a level above ~150-200 mcmol/L in ALF signals risk of cerebral edema and intracranial hypertension. Treat with lactulose, a nonabsorbable disaccharide titrated to 2-3 soft stools per day—it acidifies the colon, trapping ammonia as ammonium for excretion. Rifaximin is an adjunct. Critically, identify precipitants: GI bleeding, infection, hypokalemia, constipation, dehydration, and sedatives (which must be avoided).

Coagulopathy, Hepatorenal Syndrome, Portal Hypertension

The liver synthesizes clotting factors, so ALF causes a rising INR/PT—used as a prognostic marker, not a prophylactic correction target. Give vitamin K and plasma only for active bleeding or procedures. Hepatorenal syndrome (HRS) is functional renal failure from splanchnic vasodilation triggering renal vasoconstriction; treat with albumin plus vasoconstrictors (terlipressin, or norepinephrine/midodrine-octreotide), with liver transplant definitive. Portal hypertension (hepatic venous pressure gradient >5 mmHg; varices bleed above ~12 mmHg) drives varices, ascites, and splenomegaly. Cerebral edema is a leading ALF cause of death: elevate the head, maintain normonatremia, and use hypertonic saline or mannitol for surges.

Ascites, SBP, and Lower GI Bleeding

Ascites from portal hypertension is managed with sodium restriction and diuretics; large-volume paracentesis requires albumin replacement to prevent post-paracentesis circulatory dysfunction. Spontaneous bacterial peritonitis (SBP) is diagnosed when ascitic fluid polymorphonuclear count is >=250 cells/mm3; treat empirically with a third-generation cephalosporin (cefotaxime/ceftriaxone) plus albumin, which reduces renal impairment and mortality. Suspect SBP in any cirrhotic with fever, abdominal pain, or new encephalopathy.

For lower GI bleeding, resuscitate identically, then localize with colonoscopy; CT angiography or tagged red-cell scintigraphy finds brisk bleeds, and angiographic embolization or surgery treats refractory cases. Diverticular bleeding is often self-limited, whereas angiodysplasia and ischemic colitis recur.

Common Exam Traps

• Hematochezia with shock may be a fast upper bleed—do not rule out UGIB.
• Do not over-transfuse varices; a higher hemoglobin raises portal pressure and rebleeding.
• Sedatives worsen hepatic encephalopathy—avoid them and hunt for precipitants.
• A high INR in ALF is a prognostic marker, so do not correct it prophylactically.