Eduovisual
Gastrointestinal
Variceal hemorrhage: acute management and prophylaxis
— Varices present in ~50% of cirrhotics at diagnosis; ~30% of compensated and ~60% of decompensated patients.
— Annual bleeding risk 5–15%; 6-week mortality 15–25% even with modern care.
— Accounts for ~70% of upper GI bleeding in cirrhotics; remaining 30% are peptic ulcer, portal hypertensive gastropathy, Mallory-Weiss.
— Known cirrhotic with hematemesis, coffee-ground emesis, melena, or hematochezia (brisk bleed).
— Hemodynamic instability + stigmata of chronic liver disease (spider angiomata, palmar erythema, caput medusae, ascites, splenomegaly).
— Alcohol use disorder, HCV/HBV, NAFLD/MASH, hemochromatosis, autoimmune hepatitis with sudden GI bleed.
— Non-cirrhotic portal hypertension: portal vein thrombosis, schistosomiasis, splenic vein thrombosis (isolated gastric varices), congenital hepatic fibrosis.
— Esophageal varices (most common bleed source).
— Gastric varices (Sarin classification): GOV1 (lesser curve extension, treated like esophageal), GOV2 and IGV1 (fundic—think splenic vein thrombosis if isolated), IGV2.
— Ectopic varices: duodenal, rectal, stomal—rare but high mortality.
Board pearl: In any cirrhotic with new hematemesis, assume variceal bleed and start octreotide + ceftriaxone empirically before endoscopy confirms the source—do not wait for EGD to begin therapy.
— Large-volume painless hematemesis (bright red or coffee-ground), often with melena or hematochezia if brisk.
— Syncope, lightheadedness, dyspnea on standing → suggests ≥15% blood volume loss.
— May present as hepatic encephalopathy triggered by absorbed nitrogenous blood load—asterixis, confusion in a cirrhotic = look for occult GI bleed.
— Liver disease etiology: alcohol quantity/duration, IVDU, transfusions pre-1992, obesity/diabetes (MASH), family history (hemochromatosis, Wilson, α1-antitrypsin).
— Prior variceal bleed: rebleed risk ~60% within 1–2 years without secondary prophylaxis.
— Prior endoscopy: Were varices documented? Size? Red wale marks? On band ligation program?
— Medications: NSAIDs (worsen renal function, ulcer risk), nonselective beta-blockers (NSBBs—were they on prophylaxis?), anticoagulants, SSRIs.
— Recent procedures: TIPS, paracentesis, recent banding (post-banding ulcer bleed 5–15 days later).
— Symptoms of decompensation: ascites, jaundice, confusion, weight loss.
— Known cirrhosis or stigmata.
— Large-volume bleed without prior dyspepsia.
— Hemodynamic instability disproportionate to apparent blood loss (splanchnic pooling).
— Straining, vomiting, alcohol binge, infection (SBP), portal vein thrombosis, hepatocellular carcinoma development, NSAIDs, antiplatelets.
Step 3 management: On initial encounter in a cirrhotic with suspected upper GI bleed, simultaneously (1) place 2 large-bore IVs, (2) type and cross 2 units PRBCs, (3) draw CBC/CMP/coags/lactate/blood cultures, (4) start octreotide 50 mcg bolus then 50 mcg/hr drip, (5) give IV ceftriaxone 1 g, (6) call GI for EGD within 12 hours. Do not delay antibiotics for endoscopy—SBP/bacteremia prophylaxis reduces mortality, a high-yield CCS order.
— Class I loss (<15%, <750 mL): normal HR/BP, mild anxiety.
— Class II (15–30%): HR >100, narrowed pulse pressure, orthostasis, anxiety.
— Class III (30–40%): HR >120, SBP <90, tachypnea, confusion → massive transfusion protocol territory.
— Class IV (>40%): moribund, no urine output.
— Orthostatic vitals: ↓SBP ≥20 or ↑HR ≥30 on standing = significant volume loss.
— Scleral icterus, spider angiomata (SVC distribution), palmar erythema, Dupuytren contracture, parotid enlargement, gynecomastia, testicular atrophy, terry nails, clubbing.
— Caput medusae (recanalized umbilical vein) vs inferior vena cava obstruction (flow direction: caput flows away from umbilicus; IVC obstruction flows cephalad).
— Ascites with flank dullness, shifting dullness, fluid wave (sensitivity rises with volume).
— Splenomegaly (portal hypertension), hepatomegaly or shrunken nodular liver.
— Asterixis (flapping tremor on wrist extension), fetor hepaticus, somnolence, disorientation—West Haven grading I–IV.
— New encephalopathy in a stable cirrhotic = hunt for precipitant: GI bleed, infection, electrolytes, constipation, sedatives, TIPS.
— Rectal exam mandatory: melena confirms upper GI source; hematochezia + instability suggests massive upper bleed.
— NG lavage no longer routine (low sensitivity, doesn't change management).
— Petechiae/ecchymoses from thrombocytopenia.
— Track marks (HCV risk).
Board pearl: Cirrhotics may have baseline low SBP (90s) from hyperdynamic circulation—a "normal" pressure of 110 may actually represent significant volume depletion. Trend HR, mental status, and lactate, not absolute BP. Target MAP ~65, Hgb 7–8 g/dL (restrictive transfusion improves survival vs liberal in variceal bleeds—Villanueva NEJM 2013).
— CBC: baseline Hgb may underestimate loss before equilibration (~24 hr); platelets often <100k (hypersplenism).
— CMP: ↑BUN out of proportion to Cr (digested blood protein load), look for AKI (hepatorenal trigger), hyponatremia, hyperkalemia.
— LFTs: AST/ALT (usually <300 in cirrhosis; >1000 suggests ischemic/alcoholic flare), bilirubin, albumin, alk phos.
— Coags: INR reflects synthetic function—do NOT use INR to estimate bleeding risk in cirrhosis (rebalanced hemostasis); fibrinogen more useful, target >150.
— Lactate (hypoperfusion marker), ammonia (only if encephalopathy clinically unclear—not for grading), type and cross 2–4 units.
— Blood cultures × 2 (bacteremia in 20% of cirrhotic GI bleeds).
— Pregnancy test in reproductive-age women before imaging/meds.
— Child-Pugh (bilirubin, albumin, INR, ascites, encephalopathy): A 5–6, B 7–9, C 10–15—correlates with mortality.
— MELD-Na: prognosis + transplant priority; MELD >18 predicts higher 6-week mortality.
— AIMS65, Glasgow-Blatchford, Rockall for general UGIB risk stratification.
— CXR: rule out aspiration, perforation; upright if perforation suspected.
— RUQ ultrasound with Doppler: portal vein patency (PVT contraindicates TIPS), splenic vein thrombosis (isolated fundic varices), ascites, HCC screening if not recent.
— CT abdomen with contrast if perforation, mesenteric ischemia, or HCC suspected once stable.
Key distinction: BUN/Cr ratio >30 in upper GI bleed reflects absorbed nitrogen + prerenal state—useful but less reliable in cirrhotics with low muscle mass (falsely low Cr). Always interpret Cr alongside cystatin C if available, and watch for hepatorenal syndrome (Cr rising despite volume).
— Timing: within 12 hours of presentation after hemodynamic resuscitation (AASLD/Baveno VII).
— Earlier (<6 hr) does NOT improve outcomes and may worsen them if patient under-resuscitated.
— Pre-EGD prep: airway assessment (intubate if active hematemesis, encephalopathy, aspiration risk), erythromycin 250 mg IV 30–90 min pre-procedure (prokinetic, improves visualization).
— Diagnostic + therapeutic: identify source, grade varices (small <5 mm vs large ≥5 mm), red wale marks (high-risk stigmata), and perform endoscopic band ligation (EVL) for esophageal varices or cyanoacrylate injection for gastric varices.
— Balloon tamponade (Sengstaken-Blakemore, Minnesota, Linton tubes): temporizing measure for uncontrolled bleeding; max 24 hours; complications include esophageal necrosis, perforation, asphyxiation if displaced. Must intubate first.
— Self-expanding covered esophageal stents (Danis stent): newer alternative to balloon, fewer complications, up to 7 days.
— TIPS (transjugular intrahepatic portosystemic shunt): salvage or early/preemptive TIPS (see chunk 8).
— Capsule endoscopy, push enteroscopy, deep enteroscopy: for suspected ectopic small bowel varices.
— CT angiography: active extravasation, ectopic varices, surgical planning.
— Mesenteric angiography: rare for varices; more for embolization of arterial bleeds.
— Gold standard for portal pressure (transjugular hepatic vein catheterization).
— HVPG ≥20 mmHg measured within 24 hr of bleed predicts treatment failure and rebleeding—indication for early TIPS.
— Mostly research/tertiary centers in the US.
CCS pearl: On Step 3 CCS, the correct order set after stabilization is: NPO, IV access ×2, NS or LR bolus, type and cross, octreotide drip, ceftriaxone, PPI drip (held after EGD if varices confirmed), GI consult for EGD within 12 hours, ICU bed. Forgetting antibiotics or airway protection loses points.
— Airway: Low threshold to intubate before EGD if active hematemesis, GCS <8, severe encephalopathy, or aspiration risk. Cirrhotics tolerate aspiration poorly.
— Breathing: Supplemental O2, monitor SpO2.
— Circulation: 2 large-bore (16–18 g) peripheral IVs > central line for rapid resuscitation. Crystalloid bolus 500–1000 mL initially; avoid over-resuscitation (worsens portal pressure and rebleeding).
— Restrictive Hgb threshold 7 g/dL, target 7–8 g/dL (Villanueva trial: lower mortality, fewer rebleeds vs liberal).
— Exception: active ACS, massive ongoing bleed, symptomatic anemia → liberalize.
— Platelets: transfuse if <50k in active bleed.
— FFP: controversial—do not correct INR routinely (volume overload worsens portal pressure); reserve for fibrinogen replacement or massive transfusion.
— Fibrinogen concentrate/cryoprecipitate if fibrinogen <100–150.
— Avoid recombinant factor VIIa (no benefit, thrombotic risk).
— Vasoactive: octreotide 50 mcg IV bolus → 50 mcg/hr × 2–5 days (splanchnic vasoconstriction ↓ portal flow).
— Antibiotic: ceftriaxone 1 g IV daily × 5–7 days (or fluoroquinolone if low local resistance) → reduces SBP, rebleeding, and mortality.
— PPI drip (pantoprazole 80 mg bolus → 8 mg/hr) until source identified; discontinue or oral if varices confirmed and no ulcer.
— Warfarin: vitamin K + 4F-PCC; DOACs: andexanet/idarucizumab if life-threatening.
— Child-Pugh C, MELD >19, HVPG ≥20, active bleeding at EGD → high risk for failure → consider early TIPS within 72 hr.
Step 3 management: The mortality-reducing triad in acute variceal bleed is vasoactive drug + endoscopic therapy + prophylactic antibiotics. Forgetting antibiotics is the single most common error on board questions.
— Octreotide (US standard): somatostatin analog; 50 mcg IV bolus → 50 mcg/hr continuous infusion × 2–5 days. Mechanism: inhibits glucagon → splanchnic vasoconstriction → ↓ portal pressure. Side effects: hyperglycemia, bradycardia, mild QT prolongation.
— Somatostatin (250 mcg bolus → 250 mcg/hr): used outside US.
— Terlipressin (vasopressin analog, 2 mg IV q4h then 1 mg q4h): FDA-approved 2022 for hepatorenal syndrome, also effective for variceal bleed. Risks: ischemia (digital, mesenteric, cardiac), hyponatremia—avoid in CAD/PVD.
— Vasopressin (with nitroglycerin to offset ischemia): largely replaced by above.
— Ceftriaxone 1 g IV q24h × 5–7 days—preferred, especially in Child-Pugh B/C, ascites, prior fluoroquinolone use, or hospital with fluoroquinolone resistance.
— Ciprofloxacin 400 mg IV q12h if low resistance and ceftriaxone contraindicated.
— Continue 5–7 days or until bleeding controlled and patient stable.
— Empiric pantoprazole 80 mg IV bolus → 8 mg/hr until EGD identifies source.
— If varices only → discontinue PPI (no proven benefit, may ↑ SBP, C. diff, hepatic encephalopathy in cirrhosis).
— If concomitant ulcer or post-banding → continue oral PPI.
— Prophylactic lactulose titrated to 2–3 soft stools/day in any cirrhotic with GI bleed to prevent precipitated hepatic encephalopathy.
— Add rifaximin 550 mg BID if overt encephalopathy develops.
— Beta-blockers acutely (impair hemodynamic response, worsen renal perfusion)—hold NSBB during acute bleed, resume after bleeding controlled.
— NSAIDs, aminoglycosides, sedating opioids/benzos (precipitate encephalopathy).
Board pearl: Hold NSBBs during the acute bleed to allow compensatory tachycardia and adequate MAP; restart after hemostasis as part of secondary prophylaxis. This is a classic Step 3 distractor question.
— Rubber bands placed at varices; superior to sclerotherapy (fewer strictures, ulcers).
— Hemostasis ~90%; rebleed rate ~20% within 6 weeks without secondary prophylaxis.
— Complications: post-banding ulcer bleed (5–15 days post), chest pain, dysphagia, esophageal stricture.
— Repeat EVL every 2–4 weeks until variceal eradication, then surveillance EGD at 3–6 months, then annually.
— GOV1 (lesser curve, esophageal extension): treat with EVL.
— GOV2 and IGV1 (fundic): cyanoacrylate (glue) injection or endoscopic ultrasound-guided coil ± glue; consider BRTO (balloon-occluded retrograde transvenous obliteration) if gastrorenal shunt present.
— Creates shunt between portal and hepatic veins via stent → ↓ portal pressure.
— Salvage TIPS: for failure of endoscopic + pharmacologic therapy (~10–20% of cases).
— Early/preemptive TIPS (within 72 hours): in high-risk patients—Child-Pugh C (<14 points) or Child-Pugh B with active bleeding at EGD, or HVPG ≥20 mmHg—reduces rebleeding and mortality (García-Pagán NEJM 2010).
— Target post-TIPS HVPG <12 mmHg.
— Contraindications: Child-Pugh C >13, MELD >18–20 (relative), heart failure (right-sided), severe pulmonary hypertension, polycystic liver, uncontrolled sepsis, hepatic encephalopathy (relative).
— Complications: new/worsened hepatic encephalopathy (~25–35%), stent stenosis, hemolysis, hepatic infarction.
— Bridge to definitive therapy only; max 24 hours; intubate first.
— Apply gastric balloon traction (~500 mL) ± esophageal balloon (30–45 mmHg, deflate q4–6 hr).
— Distal splenorenal shunt (Warren) or portocaval shunt—rare since TIPS era; consider in non-cirrhotic portal hypertension or TIPS failure.
— Splenectomy curative for isolated gastric varices from splenic vein thrombosis ("sinistral/left-sided portal hypertension"—classic pancreatitis/pancreatic cancer association).
CCS pearl: If after EVL + octreotide the patient continues to bleed, the next step is balloon tamponade as a bridge, then TIPS—not repeat EGD endlessly. Order interventional radiology consult early.
— Higher baseline cardiovascular disease → liberalize transfusion threshold to Hgb 8 if active CAD/ACS.
— Polypharmacy: review anticoagulants, antiplatelets, NSAIDs, SSRIs (all increase bleeding).
— Higher procedural risk for TIPS (cardiac dysfunction, encephalopathy).
— Delirium risk with hospitalization, sedation, benzo use—avoid benzos for alcohol withdrawal where possible, use phenobarbital or careful CIWA-protocol.
— Goals-of-care conversation early: variceal bleed in Child-Pugh C elderly without transplant candidacy carries 50%+ mortality.
— Cr is falsely low in cirrhotics (sarcopenia); use cystatin C-based eGFR if available.
— Hepatorenal syndrome (HRS-AKI): Cr ↑ ≥0.3 mg/dL within 48 hr or ≥1.5× baseline within 7 days, no improvement after 2 days of albumin 1 g/kg/day and diuretic withdrawal, no shock, no nephrotoxin, no structural disease.
— Treat: terlipressin + albumin (FDA-approved 2022) or midodrine + octreotide + albumin if terlipressin unavailable.
— Avoid: NSAIDs, IV contrast when possible, aminoglycosides, ACEi/ARB acutely.
— Adjust drug doses: ceftriaxone (no adjustment), ciprofloxacin (↓ if CrCl <30), PPIs (no adjustment but limit duration), lactulose (no adjustment).
— Avoid acetaminophen >2 g/day; acetaminophen preferred over NSAIDs for pain.
— Sedation: short-acting agents (fentanyl > morphine; avoid benzos; use small-dose midazolam reversibly if needed).
— Beta-blockers: avoid in refractory ascites with SBP <90, Na <130, or AKI—associated with ↑ mortality (paracentesis-induced circulatory dysfunction). Use carvedilol cautiously.
— "Rebalanced hemostasis"—INR does NOT predict bleeding; do not transfuse FFP to "correct" INR for procedures.
— Use viscoelastic testing (TEG/ROTEM) when available for transfusion guidance.
Key distinction: A cirrhotic with INR 2.5 and platelets 60 is not auto-coagulopathic—endogenous anticoagulants (protein C, antithrombin) are also reduced. Transfuse based on active bleeding and fibrinogen <150, not INR alone.
— Variceal bleeding peaks in 2nd trimester and labor (peak plasma volume + IVC compression ↑ portal pressure).
— Causes: pre-existing cirrhosis, non-cirrhotic portal hypertension (idiopathic, schistosomiasis, congenital hepatic fibrosis), Budd-Chiari, portal vein thrombosis.
— Pre-pregnancy: screen with EGD; band high-risk varices before conception.
— Beta-blockers (propranolol, nadolol) are reasonable in pregnancy (category C) but monitor fetal growth, bradycardia, hypoglycemia at birth.
— EVL safe in pregnancy; preferred over sclerotherapy.
— TIPS: technically feasible but exposes fetus to fluoroscopy—reserve for life-threatening.
— Delivery: elective C-section or assisted vaginal delivery with short 2nd stage (avoid prolonged Valsalva) for known large varices.
— Causes: biliary atresia, extrahepatic portal vein obstruction, congenital hepatic fibrosis, cystic fibrosis liver disease, autoimmune hepatitis.
— Extrahepatic portal vein obstruction (EHPVO) is the most common cause of pediatric variceal bleeding worldwide.
— Management mirrors adult: octreotide (weight-based), ceftriaxone, EVL feasible >10 kg.
— Meso-Rex bypass (mesenteric-to-left portal vein shunt) is curative for EHPVO—uniquely pediatric option.
— NSBBs less well-studied; use cautiously.
— Preserved synthetic function → better tolerated bleeding, lower mortality, but recurrence common.
— Splenic vein thrombosis → isolated gastric varices → splenectomy curative (think pancreatitis or pancreatic cancer history).
— Portal vein thrombosis: anticoagulation often appropriate even with varices (after primary prophylaxis with EVL or NSBB).
— Variceal bleed → reassess MELD, expedite transplant evaluation if not done.
— Avoid TIPS-related encephalopathy compromising candidacy.
— Concurrent alcoholic hepatitis (Maddrey's >32) → consider steroids if no contraindication; address withdrawal, thiamine before glucose, folate, MV.
Board pearl: A young patient with isolated gastric fundic varices and no cirrhosis → suspect splenic vein thrombosis from chronic pancreatitis or pancreatic mass; CT pancreas + splenectomy is curative.
— Early rebleeding (within 5 days): 10–20%—associated with active bleeding at EGD, HVPG ≥20, Child-Pugh C, large varices.
— Late rebleeding (5 days to 6 weeks): ~60% without secondary prophylaxis; drops to ~20% with NSBB + EVL.
— 6-week mortality: 15–25% overall; up to 60% in Child-Pugh C.
— Hypovolemic shock, MI (demand ischemia), stroke.
— Acute kidney injury / HRS-AKI (precipitated by hypoperfusion, contrast, NSAIDs).
— Ischemic hepatitis ("shock liver"): AST/ALT >1000, rapid normalization.
— Spontaneous bacterial peritonitis (SBP): ascites PMN ≥250/mm³; classic post-bleed complication—ceftriaxone prophylaxis reduces incidence.
— Bacteremia, aspiration pneumonia, UTI, catheter-related infections.
— Hepatic encephalopathy—nitrogen load from gut blood + hypoperfusion + infection.
— Worsening ascites, jaundice, coagulopathy.
— Acute-on-chronic liver failure (ACLF): ≥1 extrahepatic organ failure on background cirrhosis—high short-term mortality, may need transplant urgently.
— EVL: post-banding ulcer bleed (5–15 days), strictures, chest pain, perforation.
— TIPS: new/worsened hepatic encephalopathy (~30%), shunt stenosis/thrombosis, right heart failure, hemolysis, hepatic ischemia.
— Balloon tamponade: esophageal necrosis, perforation, asphyxiation (tube migration), aspiration.
— Sclerotherapy (rarely used now): strictures, mediastinitis, ulceration.
— TRALI, TACO (especially in cirrhotics with reduced cardiac reserve), citrate toxicity (hypocalcemia) → check ionized Ca during massive transfusion, replete.
— Recurrent varices, portal vein thrombosis (post-banding inflammation), chronic anemia, deconditioning, depression.
Step 3 management: Any cirrhotic post-bleed with new fever, abdominal pain, or encephalopathy → diagnostic paracentesis for SBP, blood cultures, urinalysis. PMN ≥250 = empiric ceftriaxone + IV albumin (1.5 g/kg day 1, 1 g/kg day 3) to prevent HRS.
— Active hematemesis with hemodynamic instability (SBP <90, HR >120, lactate >4).
— Need for intubation (airway protection, severe encephalopathy, ongoing massive bleed).
— Requirement for vasopressors or massive transfusion protocol.
— Child-Pugh C or MELD >18 with active bleeding.
— Status post-TIPS or salvage procedure in first 24 hr.
— Concomitant organ failures (AKI, ACLF, respiratory failure).
— Hemodynamically stable post-EGD with successful banding, no rebleeding signs, Child-Pugh A/B early.
— Continued octreotide drip × 2–5 days.
— GI/Hepatology — emergent for EGD, longitudinal management, transplant referral.
— Interventional Radiology — TIPS evaluation, especially Child-Pugh B with active bleed or Child-Pugh C <14.
— Anesthesia/Critical Care — airway, intubation pre-EGD if unstable.
— Transplant Hepatology — MELD ≥15 or recurrent decompensation.
— Surgery — backup if shunt surgery / splenectomy considered; rarely first-line.
— Addiction Medicine/Social Work — alcohol use disorder pathway, post-discharge supports.
— Palliative Care — Child-Pugh C non-transplant candidate, recurrent bleeds, dementia.
— MELD ≥15, recurrent variceal bleed despite secondary prophylaxis, refractory ascites, HRS, hepatopulmonary syndrome, HCC within Milan criteria.
— EMTALA-compliant transfer once stabilized; accepting facility documented.
— Average length of stay for uncomplicated variceal bleed: 4–7 days.
— Discharge criteria: hemodynamic stability, 48 hr without rebleeding, tolerating oral intake/meds, NSBB initiated, follow-up scheduled.
CCS pearl: On CCS, transfer to ICU is itself a billable order that triggers the appropriate monitoring frequency. Don't forget to change location to ICU when ordering pressors, intubation, or massive transfusion—the simulator scores location-appropriate care.
— Most common UGIB cause overall; in cirrhotics, co-exists in 30%.
— Risk factors: H. pylori, NSAIDs, stress (ICU), steroids, smoking.
— EGD: ulcer with Forrest classification (Ia spurting → III clean base).
— High-risk stigmata (Forrest Ia/Ib/IIa/IIb) → endoscopic therapy + PPI drip 72 hr.
— Test/treat H. pylori; stop NSAIDs.
— Diffuse mosaic/snakeskin mucosa in cirrhotics, often without discrete ulcer.
— Causes chronic blood loss > acute bleed; treat with NSBBs, iron, occasional argon plasma coagulation.
— Linear red stripes in antrum; associated with cirrhosis, scleroderma, CKD.
— APC or radiofrequency ablation preferred; does NOT respond to TIPS (key distinction from PHG).
— Longitudinal mucosal tear at GE junction after retching/vomiting (e.g., alcohol binge, hyperemesis).
— Usually self-limited; endoscopic clips or epinephrine injection if active.
— Aberrant submucosal artery, often proximal stomach; massive recurrent bleed without obvious ulcer.
— Endoscopic clips, banding, or thermal therapy.
— Prior aortic graft + "herald" bleed → catastrophic exsanguination.
— CT angiography or EGD to 4th portion of duodenum; emergent surgery.
— Gastric/esophageal cancer—weight loss, dysphagia, occult bleeding; biopsy at EGD.
— Pill esophagitis (doxycycline, bisphosphonates, NSAIDs, KCl), infectious (CMV/HSV/Candida in immunocompromised).
— Post-ERCP, liver biopsy, trauma; classic triad RUQ pain, jaundice, GI bleed (Quincke triad).
Key distinction: A cirrhotic with UGIB has non-variceal source in ~30% of cases—do not assume variceal until EGD confirms. However, empiric octreotide + ceftriaxone is still indicated while awaiting EGD because of high pretest probability and mortality benefit.
— Massive brisk upper bleed can present as hematochezia (10–15% of UGIB).
— Diverticular bleed (most common LGIB), angiodysplasia, ischemic colitis, IBD flare, colorectal cancer, post-polypectomy.
— Workup: rule out upper source with NG lavage or EGD first if unstable; then colonoscopy.
— Angiodysplasia, NSAID enteropathy, Meckel diverticulum (young patients), small bowel tumor (GIST, lymphoma), aortoenteric fistula.
— Workup: capsule endoscopy, deep enteroscopy, CT/MR enterography, tagged RBC scan, angiography.
— Hemoptysis: bright red, frothy, alkaline pH, cough, mixed with sputum.
— Hematemesis: dark/coffee-ground, acidic pH, nausea, food particles.
— Massive hemoptysis = bronchiectasis, TB, lung cancer, AV malformation, anticoagulation.
— Posterior nosebleed swallowed → "hematemesis"; check nasopharynx, dental sources.
— Spontaneous bacterial peritonitis → distributive shock without overt bleed.
— Sepsis from any source (UTI, cellulitis, pneumonia).
— Adrenal insufficiency of cirrhosis ("hepatoadrenal syndrome").
— Cardiac: cirrhotic cardiomyopathy, demand ischemia.
— Hepatorenal syndrome with volume contraction.
— DIC, severe thrombocytopenia, drug-induced (heparin, warfarin, DOACs, antiplatelets), uremic platelet dysfunction.
— Rare but reported—swallowed blood, self-induced; consider only after thorough workup.
— Spontaneous esophageal rupture after forceful vomiting → chest pain, subcutaneous emphysema, mediastinitis (Hamman crunch); CT with oral contrast.
Board pearl: A cirrhotic with hypotension but no overt bleeding still needs a diagnostic paracentesis (rule out SBP), blood cultures, urinalysis, and CXR—occult infection causes 20–30% of decompensations.
— Nonselective beta-blockers (NSBBs):
— Carvedilol 6.25 mg BID, titrate to 12.5 mg BID (preferred—dual α/β blockade, greater HVPG reduction).
— Propranolol 20 mg BID, titrate to max tolerated (up to 320 mg/day) or nadolol 20–40 mg daily.
— Target: resting HR 55–60, SBP >90, no symptomatic hypotension.
— Avoid/discontinue NSBBs if: refractory ascites with SBP <90, Na <130, AKI, SBP episode (controversial—may continue if hemodynamically tolerated; AASLD allows carvedilol in compensated decompensated patients with caution).
— EVL sessions every 2–4 weeks until variceal eradication, then surveillance EGD at 3–6 months, then every 6–12 months.
— Continue ceftriaxone/ciprofloxacin to complete 5–7 days total.
— Long-term SBP prophylaxis (norfloxacin or TMP-SMX) only if prior SBP, ascites protein <1.5 with renal/hepatic dysfunction.
— Continue if any encephalopathy episode—lactulose titrated to 2–3 soft stools/day ± rifaximin 550 mg BID for recurrent encephalopathy.
— Alcohol cessation — naltrexone, acamprosate, baclofen (preferred in cirrhosis); refer to AA, intensive outpatient.
— HCV: direct-acting antivirals (sofosbuvir-velpatasvir) regardless of fibrosis.
— HBV: entecavir or tenofovir (TAF preferred if CKD/bone disease).
— MASH: weight loss, GLP-1 agonists, treat diabetes/dyslipidemia.
Step 3 management: Discharge bundle = NSBB + EVL follow-up + lactulose if any HE + alcohol cessation plan + transplant referral if MELD ≥15 + hep A/B vaccines + 2-week outpatient follow-up. Missing the NSBB or EVL schedule is the most common board-question pitfall.
— Hepatology within 1–2 weeks post-discharge: review bleeding plan, titrate NSBB, schedule next EVL.
— Repeat EGD every 2–4 weeks until variceal eradication (typically 2–4 sessions), then EGD at 3–6 months, then every 6–12 months for surveillance.
— HCC surveillance: ultrasound ± AFP every 6 months for all cirrhotics.
— Routine labs every 3–6 months: CBC, CMP, INR, AFP; MELD recalculation.
— Target resting HR 55–60, SBP ≥90.
— Check HR/BP at clinic visits and self-monitored at home.
— If carvedilol intolerance (hypotension, dizziness) → switch to propranolol or reduce dose.
— Daily weights, low-sodium diet (<2 g/day), fluid restriction if Na <125.
— Spironolactone/furosemide titration; diagnostic paracentesis with each admission (SBP screen).
— Brief intervention at every visit; pharmacotherapy (naltrexone, acamprosate, baclofen—baclofen safest in cirrhosis).
— Refer AA/SMART recovery, intensive outpatient, residential rehab.
— PEth (phosphatidylethanol) or urine EtG for objective monitoring—useful in transplant candidates.
— Late-evening snack to reduce overnight catabolism and sarcopenia.
— Protein 1.2–1.5 g/kg/day—do NOT restrict protein for encephalopathy (worsens sarcopenia).
— Branched-chain amino acid supplementation in select patients.
— Vitamin D, zinc, thiamine, folate replacement.
Board pearl: Do NOT protein-restrict cirrhotics with encephalopathy—this is an outdated practice. Maintain 1.2–1.5 g/kg/day protein to preserve muscle mass; treat HE with lactulose/rifaximin instead.
— EGD/TIPS during active hemorrhage with altered mental status (encephalopathy): if patient lacks capacity, obtain consent from healthcare proxy or next of kin under state hierarchy; document emergency exception if life-threatening and surrogate unreachable.
— Alcohol intoxication ≠ automatic incapacity, but acute confusion + life-threatening bleed triggers emergency doctrine.
— Document capacity assessment: understanding, appreciation, reasoning, choice.
— Child-Pugh C, non-transplant candidate, recurrent variceal bleed → palliative care consult; discuss prognosis (1-year mortality often >50%).
— DNR/DNI orders do NOT preclude EGD or TIPS—clarify each intervention separately.
— Advance directives reviewed and documented.
— Failure to schedule outpatient EGD for variceal eradication is a major safety gap—rebleeding peaks in first 6 weeks post-discharge.
— Medication reconciliation: ensure NSBB initiated, lactulose dose clear, PPI discontinued if appropriate, alcohol cessation pharmacotherapy in place.
— Warm handoff to hepatology, with appointment scheduled before discharge.
— Patient education on warning signs (recurrent hematemesis, melena, confusion, fever, abdominal pain) with clear return-precaution instructions.
— Impaired driving from hepatic encephalopathy: some states (e.g., CA, PA) mandate physician reporting of medical conditions impairing driving; counsel patient not to drive during active HE.
— Suspected elder abuse/neglect if cirrhosis complications result from caregiver issues—mandatory reporter laws apply.
— Most US programs no longer require fixed sobriety periods; multidisciplinary assessment of relapse risk is standard.
— Avoid stigma-based exclusion; document objective criteria.
— Over-transfusion increases rebleeding and mortality—respect the restrictive threshold (Hgb 7).
— Watch for TACO/TRALI in cirrhotics with low cardiac reserve.
— Door-to-EGD <12 hr, antibiotic prophylaxis administration, vasoactive drug timing, follow-up scheduled.
Step 3 management: Always document a capacity assessment before proceeding under emergency consent in a confused cirrhotic, and secure outpatient EGD before discharge—missed follow-up causes preventable rebleeds and is a sentinel-event-level safety failure.
— ≥5 mmHg = portal hypertension.
— ≥10 mmHg = clinically significant portal hypertension; varices develop.
— ≥12 mmHg = bleeding risk threshold.
— ≥20 mmHg within 24 hr of bleed = high rebleed/mortality → early TIPS.
— Antibiotics (ceftriaxone) — ↓ mortality, infections, rebleed.
— Vasoactive drugs (octreotide/terlipressin) — ↓ bleeding, transfusion.
— EVL — first-line endoscopic therapy.
— Early TIPS in high-risk patients — ↓ rebleeding, mortality.
— Restrictive transfusion (Hgb 7) — ↓ mortality vs liberal.
— Octreotide = somatostatin analog → ↓ splanchnic flow.
— Terlipressin = vasopressin analog → also approved for HRS-AKI.
— Carvedilol > propranolol/nadolol for portal pressure reduction (α blockade).
— Rifaximin = non-absorbable antibiotic for HE (gut microbiome modulation).
— GOV1 = lesser curve esophageal extension (EVL).
— GOV2 = greater curve / fundus (cyanoacrylate/coil).
— IGV1 = isolated fundic (think splenic vein thrombosis if no cirrhosis).
— IGV2 = elsewhere in stomach.
— ~2/3 of cirrhotics develop varices.
— ~1/3 of varices bleed.
— ~1/3 of bleeds are fatal (historically; now lower with modern care).
Board pearl: Antibiotic prophylaxis (ceftriaxone) reduces mortality in variceal bleed independent of bleeding control—it's the single most under-ordered intervention on board CCS cases.
— Stem: 55M known cirrhotic, hematemesis, BP 88/52, HR 124.
— Answer: IV access × 2, crystalloid, type/cross, octreotide + ceftriaxone, EGD within 12 hr. Distractors: PPI alone, FFP for INR, immediate TIPS.
— Stem asks for the intervention that reduces mortality MOST.
— Answer: ceftriaxone (or fluoroquinolone). Distractors: PPI, FFP, octreotide alone.
— Stem: Hgb 7.5, stable variceal bleeder post-EGD, no CAD.
— Answer: observe; transfuse only if Hgb <7. Liberal transfusion = worse outcome.
— Stem: Child-Pugh B with active bleeding at EGD, or Child C <14.
— Answer: early TIPS within 72 hours. Distractor: continue medical therapy only.
— Stem: history of chronic pancreatitis, EGD shows isolated fundic varices.
— Answer: CT pancreas, splenectomy curative. Distractor: EVL or TIPS.
— Stem: Day 1 of bleed, asks about NSBB.
— Answer: hold acutely, restart after hemostasis. Distractor: start immediately.
— Stem: Cirrhotic with SBP 82, Na 126, AKI, on propranolol.
— Answer: discontinue NSBB.
— Stem: confused cirrhotic, no overt bleed.
— Answer: workup for SBP, GI bleed, electrolytes, infection; don't protein-restrict, give lactulose ± rifaximin.
— Answer: NSBB + repeat EGD in 2–4 weeks + outpatient hepatology + alcohol cessation + vaccines.
— Stem: INR 2.0, platelets 70, active variceal bleed.
— Answer: do NOT routinely transfuse FFP; consider platelets if <50 with active bleed, cryo if fibrinogen <150. Distractor: FFP to correct INR.
— Stem: Cr rises after bleed, no shock, no nephrotoxin.
— Answer: albumin challenge, then terlipressin + albumin (or midodrine + octreotide + albumin).
Key distinction: When the question asks "MOST important next step," prioritize ABCs → vasoactive + antibiotic + EGD within 12 hr, in that order; when asking "MOST reduces mortality," the answer is almost always antibiotic prophylaxis.
Variceal hemorrhage is a hemodynamically and hepatically lethal emergency managed by the triad of vasoactive drug (octreotide) + prophylactic antibiotic (ceftriaxone) + early endoscopic band ligation, with restrictive transfusion, early TIPS for high-risk patients, and lifelong secondary prophylaxis using a nonselective beta-blocker plus serial EVL.
Board pearl: The single intervention with the largest independent mortality reduction in acute variceal hemorrhage is prophylactic ceftriaxone—give it before, during, or immediately after EGD, never skip it, and continue for 5–7 days regardless of whether overt infection is identified.