Gastroenterology — Acute GI Hemorrhage

101. GI Bleeding

UGIB vs LGIB · resuscitate first · risk-stratify (Glasgow-Blatchford) · PPI + octreotide if cirrhotic · scope timing · Super Compact

Sx: UGIB → hematemesis/coffee-ground emesis + melena · LGIB → hematochezia/BRBPR · lightheadedness/syncope + fatigue · exam: orthostatic VS, pallor, rectal exam (brisk UGIB can present as hematochezia if massive)

Neg: denies tearing back pain + arm BP differential (AoD) · denies wt loss + change in stool caliber + anemia hx (colorectal malignancy) · denies NSAID/anticoag use w/ epigastric pain (PUD) · denies retching before hematemesis (Mallory-Weiss) · denies stigmata of cirrhosis/ascites (variceal)

SHx: ETOH (varices, gastritis, Mallory-Weiss) · tobacco (PUD risk) · NSAID/ASA/anticoagulant use · prior GI bleed/ulcer/H. pylori

Etiology: UGIB: PUD (#1, ~40%) · gastritis/erosions · esophagitis · varices · Mallory-Weiss · malignancy · LGIB: diverticular bleed (#1) · angiodysplasia/AVM · hemorrhoids/anorectal · colitis (ischemic/IBD/infectious) · post-polypectomy · malignancy

RF: NSAID/ASA/anticoagulant/DOAC · H. pylori · cirrhosis/portal HTN · prior GI bleed · age >65 · CKD (angiodysplasia)

Data: CBC (Hgb — may be normal early before hemodilution; trend q4–6h) · type & crossmatch (have 2+ units ready if unstable) · BMP (↑BUN:Cr >20–30 suggests UGIB from absorbed blood) · LFTs + INR/PT + albumin (coagulopathy, cirrhosis) · lactate (hypoperfusion) · coags/fibrinogen (reversal planning) · Glasgow-Blatchford score (0–1 may be outpatient) · ECG/troponin (demand ischemia in CAD/elderly) · type & screen, NG lavage rarely needed · upright/decubitus films if perforation suspected

DDx: hemoptysis (coughed not vomited, frothy/alkaline) · epistaxis/swallowed blood (ENT source) · brisk UGIB presenting as hematochezia (unstable + ↑BUN:Cr → scope upper first) · ischemic colitis (pain + bloody diarrhea, watershed areas)

Home Meds: hold/reverse anticoagulants — warfarin (Coumadin)→vit K + 4F-PCC, dabigatran (Pradaxa)→idarucizumab (Praxbind), factor Xa inhibitors→andexanet alfa (Andexxa) or 4F-PCC · hold NSAIDs/ASA (resume ASA early if secondary CV prevention once hemostasis) · hold antihypertensives if hypotensive

Plan

CONSULT: GI (urgent endoscopy) · IR if refractory/massive (embolization) · Surgery if uncontrolled · Hepatology if variceal/cirrhotic

– Resuscitate first (ABCs): 2 large-bore IVs (≥18g); crystalloid bolus; restrictive transfusion — transfuse PRBC for Hgb <7 (target 7–9), threshold <8 if active CAD/unstable (Villanueva NEJM 2013: restrictive improved survival)
– Protect airway if massive hematemesis/altered mental status → intubate before EGD
– Acid suppression (UGIB): pantoprazole (Protonix) 80 mg IV bolus then 8 mg/hr infusion, or 40 mg IV q12h
– If cirrhosis/variceal suspected: octreotide (Sandostatin) 50 mcg IV bolus then 50 mcg/hr ×3–5d + ceftriaxone (Rocephin) 1 g IV q24h ×7d (SBP/infection prophylaxis, ↓rebleed + mortality)
– Reverse coagulopathy: hold/reverse anticoagulants (see Home Meds); platelets if <50k + active bleed; consider FFP/PCC if INR elevated; tranexamic acid NOT recommended (HALT-IT showed no benefit, ↑VTE)
– Endoscopy timing: EGD within 24h (within 12h if unstable/variceal after resuscitation); colonoscopy after prep for LGIB; CT angiography if brisk/localizing for IR
– Hemostasis: UGIB — clips, thermal, injection, hemospray; variceal — band ligation (esophageal) or cyanoacrylate (gastric); LGIB — clip/cautery, embolization
– H. pylori: test all PUD; treat if positive (clarithromycin triple or bismuth quadruple therapy)
– Brisk hematochezia + hemodynamic instability + ↑BUN:Cr → do EGD first; ~10–15% of "lower" bleeds are massive upper bleeds.
– PT/OT: mobilize once stable; fall-risk assessment given anemia/orthostasis
– Trend daily: Hgb q4–6h while active then daily, VS/orthostatics, urine output, BUN:Cr, recurrent melena/hematochezia, transfusion requirement
– Escalation triggers: SBP <90 or HR >120 despite fluids → massive transfusion protocol + ICU; Hgb drop >2 despite transfusion → repeat scope/IR/surgery; ongoing bleed after 2 endoscopic attempts → IR embolization or surgery
– Discharge checklist: PPI — omeprazole (Prilosec) 40 mg PO daily (continue per ulcer type/duration); H. pylori eradication regimen if positive + confirm cure; stop offending NSAID or add gastroprotection; document anticoagulation resumption plan with timing; iron repletion — ferrous sulfate (Feosol) 325 mg PO daily or IV if intolerant; GI follow-up + repeat scope if malignancy/large ulcer; return precautions (recurrent bleeding, dizziness, black stools)

101. GI Bleeding — Upper & Lower

complete reference · UGIB (PUD/gastritis/esophagitis) + LGIB (diverticular/hemorrhoids/AVM) · scores + full regimens · Full Card

Symptoms / Associated Sx

• UGIB: hematemesis or coffee-ground emesis, melena (black tarry stool), epigastric pain; LGIB: hematochezia / BRBPR, often painless

• Hemodynamic: lightheadedness, syncope, fatigue, dyspnea on exertion (anemia); tachycardia and orthostasis precede hypotension

• Exam: orthostatic vital signs, pallor, conjunctival rim pallor, digital rectal exam (melena vs BRBPR), stigmata of chronic liver disease if variceal

Neg

• Pt denies NSAID/anticoagulant use + epigastric pain relieved by food/antacids — would argue against PUD (still test H. pylori; ulcers can be silent in elderly/NSAID users)

• Pt denies stigmata of cirrhosis (jaundice, ascites, spider angiomata, splenomegaly) — argues against variceal source (but compensated cirrhosis can be occult — check LFTs/platelets; if suspected, add octreotide + ceftriaxone empirically)

• Pt denies weight loss + change in stool caliber + iron-deficiency anemia — argues against colorectal malignancy (colonoscopy still indicated for LGIB workup)

Social History (SHx)

• Alcohol: heavy use → varices, portal hypertensive gastropathy, gastritis, Mallory-Weiss tears (retching)

• Tobacco: increases PUD risk and impairs ulcer healing

• Medications: NSAIDs/ASA, anticoagulants (warfarin, DOACs), antiplatelets, SSRIs (bleeding risk)

• Prior history: known ulcer/H. pylori, prior GI bleed, diverticulosis, AVMs, recent polypectomy

Main Etiology

• Upper (UGIB): peptic ulcer disease most common (~40%; H. pylori + NSAIDs); erosive gastritis/esophagitis; gastroesophageal varices; Mallory-Weiss tear; Dieulafoy lesion; malignancy; aortoenteric fistula (rare, prior graft)

• Lower (LGIB): diverticular bleed most common (painless, often self-limited); angiodysplasia/AVM (elderly, CKD, aortic stenosis); hemorrhoids/anorectal; ischemic colitis; IBD; infectious colitis; post-polypectomy bleeding; colorectal malignancy

• ~10–15% of presumed LGIB (hematochezia) are actually brisk UGIB

RF

• Modifiable: NSAID/ASA use, anticoagulation, H. pylori, alcohol, smoking

• Non-modifiable: age >65, prior GI bleed, cirrhosis/portal hypertension, diverticulosis, CKD (angiodysplasia), coagulopathy

Data

• CBC (Hgb/Hct — may be normal early before equilibration; trend q4–6h during active bleed; MCV low in chronic blood loss)

• Type & crossmatch (2+ units available if hemodynamically unstable or active bleeding)

• BMP (elevated BUN:Cr ratio >20–30 supports UGIB from digested blood protein load)

• LFTs, albumin, INR/PT/PTT (coagulopathy, undiagnosed cirrhosis, baseline before reversal)

• Fibrinogen (guides cryoprecipitate in massive transfusion / cirrhosis)

• Lactate (hypoperfusion, severity)

• Glasgow-Blatchford Score (BUN, Hgb, SBP, HR, melena, syncope, hepatic/cardiac disease; score 0–1 = low risk, candidate for outpatient management)

• Rockall score (post-endoscopy rebleeding/mortality risk)

• ECG + troponin (demand ischemia in CAD/elderly with significant anemia)

• CT angiography (localizes brisk active bleeding ≥0.3–0.5 mL/min; roadmap for IR)

• Tagged RBC scan (detects slower bleeds 0.1–0.5 mL/min when CTA negative and ongoing)

DDx

Hemoptysis (coughed, frothy, alkaline pH vs vomited acidic blood) · epistaxis/oropharyngeal source with swallowed blood (ENT exam) · brisk UGIB masquerading as hematochezia (unstable + ↑BUN:Cr → EGD first) · ischemic colitis (crampy pain + bloody diarrhea, watershed splenic flexure/rectosigmoid)

Home Meds

• Reverse: warfarin (Coumadin) → vitamin K (phytonadione) 10 mg IV + 4-factor PCC (Kcentra); dabigatran (Pradaxa) → idarucizumab (Praxbind) 5 g IV; apixaban (Eliquis)/rivaroxaban (Xarelto) → andexanet alfa (Andexxa) or 4F-PCC 50 units/kg

• Hold: NSAIDs and ASA during active bleed; antiplatelets pending GI/cardiology risk-benefit (resume ASA early if needed for secondary prevention once hemostasis achieved)

• Hold: antihypertensives and diuretics if hypotensive/volume depleted

Plan

CONSULT: GI (urgent/emergent endoscopy) · Interventional Radiology (embolization for refractory/massive bleed) · Surgery (uncontrolled hemorrhage) · Hepatology (variceal bleeding / cirrhosis)

• Resuscitation first: two large-bore IVs (≥18-gauge), crystalloid resuscitation, continuous monitoring; restrictive transfusion strategy — PRBC for Hgb <7 g/dL (target 7–9), use <8 threshold with active CAD or hemodynamic instability (Villanueva NEJM 2013 showed restrictive strategy improved survival and reduced rebleeding)

• Airway: intubate for airway protection before endoscopy if massive hematemesis or altered mental status

• UGIB acid suppression: pantoprazole (Protonix) 80 mg IV bolus then 8 mg/hr continuous infusion (or 40 mg IV q12h) — reduces high-risk stigmata and rebleeding

• If variceal/cirrhosis suspected: octreotide (Sandostatin) 50 mcg IV bolus then 50 mcg/hr infusion ×3–5 days + ceftriaxone (Rocephin) 1 g IV q24h ×7 days (antibiotic prophylaxis reduces infection, rebleeding, and mortality in cirrhotic GI bleed)

• Coagulopathy: reverse anticoagulants per agent (above); platelet transfusion if <50k with active bleeding; PCC/FFP for elevated INR; tranexamic acid NOT recommended (HALT-IT 2020: no mortality benefit, increased VTE/seizure)

• Endoscopy: EGD within 24h of presentation (within 12h after resuscitation if hemodynamically unstable or variceal); colonoscopy after adequate prep for LGIB; therapeutic options — clips, thermal coagulation, injection, hemostatic powder, band ligation (esophageal varices), cyanoacrylate (gastric varices)

• Localization for ongoing LGIB: CT angiography first if brisk; tagged RBC scan for slower bleeds; angiographic embolization by IR if source identified and endoscopy fails

• H. pylori: biopsy/test all peptic ulcers; eradicate if positive (bismuth quadruple or clarithromycin triple therapy) and confirm eradication

• PT/OT: early mobilization once hemodynamically stable; fall-risk precautions given anemia and orthostasis

• Trend daily: Hgb every 4–6h during active bleeding then daily, vital signs and orthostatics, urine output, BUN:Cr trend, recurrence of melena/hematochezia, cumulative transfusion requirement

• Escalation triggers: SBP <90 or HR >120 persisting despite fluid resuscitation → activate massive transfusion protocol + ICU; Hgb drop >2 g/dL despite transfusion or recurrent hematemesis → repeat endoscopy / IR / surgery; failure of two endoscopic hemostasis attempts → IR embolization or operative intervention

• Discharge checklist: PPI — omeprazole (Prilosec) 40 mg PO daily (duration per ulcer size/etiology; high-dose 8 weeks for large/complicated ulcers); complete and confirm H. pylori eradication if positive; discontinue offending NSAID or add gastroprotection; explicit anticoagulation/antiplatelet resumption plan with timing and prescriber communication; iron repletion — ferrous sulfate (Feosol) 325 mg PO daily or IV iron if intolerant/severe; GI follow-up with repeat endoscopy for gastric ulcers (exclude malignancy) or incomplete evaluation; return precautions for recurrent bleeding, melena, lightheadedness

Red Flags

• Hemodynamic instability: SBP <90, HR >120, lactate elevated, altered mental status → massive transfusion protocol + ICU

• Massive hematemesis with airway compromise → intubate before endoscopy

• Variceal bleeding → high mortality; octreotide + antibiotics + urgent banding; consider balloon tamponade (Blakemore) or TIPS if refractory

• Aortoenteric fistula (prior aortic graft + GI bleed) → emergent CT/surgery, often "herald" minor bleed precedes catastrophic hemorrhage

• Ongoing bleeding despite two endoscopic attempts → IR embolization or surgery; do not delay

Senior IM Resident Pearls

• Restrictive transfusion saves lives: target Hgb 7–9 (Villanueva 2013). Over-transfusing raises portal pressure and worsens variceal rebleeding — resist the urge to "top off" a stable patient.

• BUN:Cr ratio is a free localizer: ratio >20–30 in the absence of renal failure points to an upper source (digested blood = nitrogen load). Useful when hematochezia is ambiguous.

• Glasgow-Blatchford 0–1 identifies very-low-risk UGIB who can often be managed as outpatients — know the inputs (BUN, Hgb, SBP, HR, melena, syncope, liver/cardiac disease).

• Cirrhotic with any GI bleed gets antibiotics (ceftriaxone) regardless of confirmed variceal source — prophylaxis independently reduces mortality.

• Common mistake: giving tranexamic acid for GI bleeding — HALT-IT showed no benefit and more thrombotic events; it is not standard of care.

• Resume ASA early for secondary cardiovascular prevention once hemostasis is achieved — stopping it for high-risk patients increases cardiovascular death more than rebleeding.

Hepatology — Decompensated Cirrhosis

102. Decompensated Cirrhosis

4 decompensations: ascites · HE · variceal bleed · HRS · find the precipitant (infection/bleed/med) · MELD-Na for transplant · Super Compact

Sx: ascites/abdominal distension + LE edema · confusion/asterixis (HE) · hematemesis/melena (varices) · ↓UOP + rising Cr (HRS) · jaundice, fatigue (decompensation = ascites, HE, variceal bleed, or jaundice)

Neg: denies fever + abd pain + ascites tenderness (SBP — still tap to exclude) · denies focal neuro deficit + headache (intracranial cause of AMS) · denies nephrotoxin/volume loss preceding AKI (ATN/prerenal vs HRS) · denies new mass/portal vein thrombus on imaging (HCC)

SHx: ETOH (amount, duration, last drink — withdrawal risk) · IVDU/transfusion/tattoos (HCV/HBV) · metabolic risk (obesity, DM → MASH) · acetaminophen/herbal/OTC use

Etiology: alcohol-associated · MASH (NAFLD) · chronic HCV/HBV · autoimmune/PBC/PSC · hemochromatosis/Wilson/A1AT · decompensation triggers: infection (SBP), GI bleed, dietary indiscretion/constipation (HE), nonadherence to diuretics/lactulose, HCC, portal vein thrombosis, nephrotoxins/NSAIDs

RF: ongoing alcohol use · uncontrolled viral hepatitis · obesity/DM (MASH) · NSAID use (precipitates HRS/AKI) · medication nonadherence

Data: CBC (thrombocytopenia from portal HTN/hypersplenism, anemia) · CMP (Na — hyponatremia for MELD-Na/prognosis; Cr for HRS; K) · LFTs + bili + albumin (synthetic function) · INR/PT (synthetic function, MELD) · ammonia (supports HE but do not trend/use to titrate — clinical diagnosis) · MELD-Na (bili, INR, Cr, Na — transplant priority + mortality) · Child-Pugh (bili, albumin, INR, ascites, HE) · diagnostic paracentesis (cell count w/ PMN ≥250 = SBP; albumin for SAAG ≥1.1 = portal HTN; culture, total protein) · blood/urine cultures · lactate · RUQ US w/ Dopplers (ascites, PVT, HCC screen) · AFP · viral hepatitis serologies

DDx: SBP (ascitic PMN ≥250 — treat even without symptoms) · HRS vs prerenal vs ATN (no response to albumin challenge + no other cause = HRS-AKI) · HCC (LI-RADS lesion, ↑AFP) · acute alcoholic hepatitis (Maddrey ≥32, recent heavy drinking, AST:ALT >2)

Home Meds: continue/titrate nonselective β-blocker — nadolol (Corgard) or carvedilol (Coreg) for varices (hold if SBP <90 or HRS/SBP) · continue lactulose (Enulose) + rifaximin (Xifaxan) for HE · continue/adjust diuretics — spironolactone (Aldactone) + furosemide (Lasix) (hold if AKI/HRS or hyponatremia) · avoid NSAIDs, nephrotoxins, sedatives

Plan

CONSULT: Hepatology (all; transplant eval) · GI (variceal banding) · IR (TIPS, refractory ascites/HRS) · Nephrology (HRS/RRT) · Nutrition

— Always: identify and treat the precipitant (infection, GI bleed, constipation, nonadherence, nephrotoxin, HCC).

ASCITES: sodium restriction <2 g/day; diuretics — spironolactone (Aldactone) 100 mg + furosemide (Lasix) 40 mg PO daily (100:40 ratio, titrate up to 400:160); large-volume paracentesis (LVP) for tense ascites with albumin 6–8 g/L removed if >5 L; refractory → TIPS or serial LVP.
SBP: ascitic PMN ≥250 → cefotaxime (Claforan) 2 g IV q8h (or ceftriaxone 2 g IV q24h) ×5d + albumin 1.5 g/kg day 1 and 1 g/kg day 3 (prevents HRS, ↓mortality); secondary prophylaxis — ciprofloxacin (Cipro) 500 mg PO daily or TMP-SMX.
HEPATIC ENCEPHALOPATHY: lactulose (Enulose) 30 mL PO/NG q1–2h until BM then titrate to 2–3 soft BMs/day (PR retention enema if obtunded) + rifaximin (Xifaxan) 550 mg PO BID; treat precipitant; avoid sedatives; protein restriction NOT recommended (worsens catabolism).
VARICEAL BLEED: resuscitate (restrictive Hgb 7–9) → octreotide (Sandostatin) 50 mcg IV bolus then 50 mcg/hr ×3–5d + ceftriaxone (Rocephin) 1 g IV q24h ×7d + urgent EGD band ligation; refractory → balloon tamponade (Blakemore) bridge → TIPS; nonselective β-blocker for secondary prophylaxis once stable.
HEPATORENAL SYNDROME (HRS-AKI): stop diuretics + nephrotoxins; volume challenge albumin 1 g/kg/day ×2d; if no response → vasoconstrictor: terlipressin (Terlivaz) 0.85–2 mg IV q6h (or norepinephrine in ICU, or midodrine + octreotide + albumin) + albumin 20–40 g/day; definitive = liver transplant; RRT as bridge.
– A cirrhotic with AMS, fever, or AKI gets a diagnostic paracentesis — SBP is frequently asymptomatic and missing it is lethal.
– PT/OT: mobilize, fall precautions (HE/deconditioning); nutrition consult — adequate protein 1.2–1.5 g/kg, late-evening snack to reduce catabolism
– Trend daily: mental status/asterixis, weight + abdominal girth, Na/K/Cr, BMs per day (lactulose titration), MELD-Na, signs of bleeding/infection
– Escalation triggers: grade 3–4 HE or airway risk → ICU + airway protection; rising Cr despite albumin → vasoconstrictor + nephrology; variceal bleed uncontrolled → TIPS; refractory ascites/HRS → transplant evaluation expedited
– Discharge checklist: lactulose titrated to 2–3 BMs/day + rifaximin (Xifaxan) 550 mg PO BID; diuretics with sodium restriction reinforced; nonselective β-blocker dosing; SBP prophylaxis if indicated; alcohol cessation referral; hepatology + transplant follow-up; HCC surveillance US + AFP q6mo; vaccinate (HAV, HBV, pneumococcal, influenza); return precautions (confusion, fever, bleeding, decreased urine, worsening swelling)

102. Decompensated Cirrhosis

complete reference · ascites + HE + variceal bleed + HRS · MELD-Na / Child-Pugh · full regimens + transplant pathway · Full Card

Symptoms / Associated Sx

• Ascites: progressive abdominal distension, early satiety, weight gain, lower extremity edema, umbilical hernia

• Hepatic encephalopathy: confusion, day-night reversal, asterixis, lethargy progressing to coma; precipitated by infection/bleed/constipation/nonadherence

• Variceal bleeding: hematemesis, melena, hemodynamic instability

• HRS: oliguria with rising creatinine; stigmata — jaundice, palmar erythema, spider angiomata, caput medusae, gynecomastia, splenomegaly

Neg

• Pt denies focal neurologic deficit + headache + papilledema — argues against intracranial cause of altered mental status (but low threshold for CT head if HE atypical, trauma, or anticoagulated)

• Pt denies recent nephrotoxin/NSAID, volume loss, or shock preceding AKI — supports HRS over prerenal azotemia or ATN (urine sodium low <10 in HRS; muddy brown casts suggest ATN)

• Pt denies new hepatic mass, rising AFP, or portal vein thrombus on imaging — argues against HCC as decompensation driver (continue surveillance imaging)

Social History (SHx)

• Alcohol: quantify amount, duration, time of last drink (withdrawal risk requires CIWA monitoring and prophylaxis)

• Viral risk: IV drug use, transfusions before 1992, tattoos, sexual history (HCV/HBV)

• Metabolic: obesity, type 2 diabetes, hyperlipidemia (MASH/MASLD)

• Hepatotoxins: acetaminophen total daily dose, herbal/OTC supplements

Main Etiology

• Chronic causes: alcohol-associated liver disease, MASH (metabolic dysfunction-associated steatohepatitis), chronic hepatitis C and B, autoimmune hepatitis, PBC/PSC, hereditary hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency

• Decompensation precipitants (always hunt for these): infection (SBP, UTI, pneumonia), GI/variceal bleeding, constipation or dietary protein/sodium load (HE), diuretic/lactulose nonadherence, nephrotoxins/NSAIDs, hepatocellular carcinoma, portal vein thrombosis, dehydration, TIPS dysfunction

RF

• Modifiable: ongoing alcohol use, uncontrolled viral hepatitis, obesity/diabetes, NSAID use, medication nonadherence, dietary indiscretion

• Non-modifiable: established cirrhosis with portal hypertension, prior decompensation, high MELD-Na

Data

• CBC (thrombocytopenia from hypersplenism/portal HTN is a clue to cirrhosis; anemia from bleeding/marrow suppression)

• CMP (hyponatremia = poor prognosis and MELD-Na component; creatinine for HRS/AKI; potassium with diuretics)

• LFTs, total/direct bilirubin, albumin (synthetic function; AST:ALT >2 suggests alcohol; low albumin = chronicity)

• INR/PT (synthetic function and MELD component; not a reliable bleeding predictor in cirrhosis — rebalanced hemostasis)

• Ammonia (may support HE but is a clinical diagnosis — do NOT trend ammonia to titrate therapy)

• MELD-Na score (bilirubin, INR, creatinine, sodium → transplant priority and 90-day mortality)

• Child-Pugh class (bilirubin, albumin, INR, ascites, encephalopathy → A/B/C prognosis)

• Diagnostic paracentesis (cell count + differential: PMN ≥250/mm³ = SBP; ascitic albumin for SAAG ≥1.1 g/dL = portal hypertension; total protein; culture in blood culture bottles at bedside)

• Blood and urine cultures, lactate (occult infection as precipitant)

• RUQ ultrasound with Doppler (ascites, hepatic/portal vein patency, splenomegaly, nodularity; portal vein thrombosis)

• AFP + cross-sectional imaging (HCC surveillance/diagnosis; multiphase CT or MRI for LI-RADS)

• Viral hepatitis serologies, iron studies, autoimmune panel (establish/confirm etiology if not known)

DDx

Spontaneous bacterial peritonitis (ascitic PMN ≥250 — treat even if asymptomatic) · HRS vs prerenal azotemia vs ATN (no response to 2-day albumin challenge + no nephrotoxin/shock + bland sediment = HRS-AKI) · hepatocellular carcinoma (LI-RADS 5 lesion, elevated AFP, can precipitate decompensation/PVT) · acute alcoholic hepatitis (Maddrey discriminant function ≥32, recent heavy intake, fever, leukocytosis, AST:ALT >2)

Home Meds

• Continue/titrate: nonselective beta-blocker — nadolol (Corgard) 40 mg PO daily or carvedilol (Coreg) 6.25 mg PO BID for variceal prophylaxis (hold if SBP <90, active SBP, or HRS — can worsen outcomes)

• Continue: lactulose (Enulose) titrated to 2–3 BMs/day + rifaximin (Xifaxan) 550 mg PO BID for HE

• Continue/adjust: diuretics — spironolactone (Aldactone) + furosemide (Lasix) (hold if AKI/HRS, hyponatremia <125, or hypovolemia)

• Avoid: NSAIDs, aminoglycosides, IV contrast when avoidable, benzodiazepines/sedatives (precipitate HE)

Plan

CONSULT: Hepatology (all cases; liver transplant evaluation) · GI (variceal band ligation) · Interventional Radiology (TIPS for refractory ascites/variceal bleed) · Nephrology (HRS, renal replacement) · Nutrition (protein/calorie optimization)

• Universal first step — identify and treat the precipitant: pan-culture, diagnostic paracentesis, review medications/adherence, assess for GI bleed and constipation, imaging for HCC/PVT

• Ascites: dietary sodium <2 g/day; spironolactone (Aldactone) 100 mg + furosemide (Lasix) 40 mg PO daily, maintain 100:40 ratio, titrate to max 400:160; therapeutic large-volume paracentesis for tense/symptomatic ascites with albumin 6–8 g per liter removed when >5 L drained (prevents post-paracentesis circulatory dysfunction); refractory ascites → TIPS (if no significant HE, preserved cardiac/renal function) or serial LVP

• SBP: ascitic PMN ≥250/mm³ → cefotaxime (Claforan) 2 g IV q8h or ceftriaxone (Rocephin) 2 g IV q24h ×5 days + IV albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 (reduces HRS and mortality); secondary prophylaxis — ciprofloxacin (Cipro) 500 mg PO daily or TMP-SMX DS daily

• Hepatic encephalopathy: lactulose (Enulose) 30 mL PO/NG every 1–2h until bowel movement, then titrate to 2–3 soft stools/day (retention enema 300 mL in 700 mL water if obtunded/unable to take PO) + rifaximin (Xifaxan) 550 mg PO BID; correct precipitant; avoid sedatives; do NOT protein-restrict (worsens sarcopenia) — target 1.2–1.5 g/kg protein

• Variceal bleeding: resuscitate with restrictive transfusion (Hgb 7–9); octreotide (Sandostatin) 50 mcg IV bolus then 50 mcg/hr ×3–5 days + ceftriaxone (Rocephin) 1 g IV q24h ×7 days + urgent EGD with endoscopic band ligation within 12h; balloon tamponade (Sengstaken-Blakemore) as temporizing bridge; salvage TIPS for uncontrolled or early rebleeding; nonselective beta-blocker + repeat banding for secondary prophylaxis once stable

• Hepatorenal syndrome (HRS-AKI): discontinue diuretics and nephrotoxins; volume expansion with albumin 1 g/kg/day ×2 days (max 100 g/day) to exclude prerenal; if creatinine fails to improve → vasoconstrictor therapy: terlipressin (Terlivaz) 0.85–2 mg IV q6h (preferred where available), or norepinephrine infusion in ICU, or midodrine + octreotide combination, each + IV albumin 20–40 g/day; renal replacement therapy as a bridge; definitive treatment is liver transplantation

• PT/OT: early mobilization with fall precautions (encephalopathy, deconditioning, sarcopenia); nutrition consult for adequate protein and a late-evening snack to limit overnight catabolism

• Trend daily: mental status and asterixis grade, daily weight and abdominal girth, sodium/potassium/creatinine, number of bowel movements (lactulose titration target), MELD-Na, signs of new bleeding or infection

• Escalation triggers: grade 3–4 HE or aspiration/airway risk → ICU and airway protection; creatinine rising despite albumin → vasoconstrictor + nephrology; uncontrolled variceal bleeding → balloon tamponade then TIPS; refractory ascites or HRS not responding → expedite transplant evaluation

• Discharge checklist: lactulose titrated to 2–3 BMs/day + rifaximin (Xifaxan) 550 mg PO BID; spironolactone/furosemide doses with sodium restriction education; nonselective beta-blocker if indicated; SBP prophylaxis if prior SBP or low ascitic protein; alcohol cessation referral and CIWA-guided withdrawal management during stay; hepatology and transplant clinic follow-up; HCC surveillance ultrasound + AFP every 6 months; vaccinate for hepatitis A, hepatitis B, pneumococcus, and influenza; return precautions for confusion, fever, GI bleeding, decreased urine output, worsening abdominal swelling

Red Flags

• Grade 3–4 hepatic encephalopathy with airway compromise → ICU, intubation for airway protection

• SBP — high short-term mortality; treat empirically at PMN ≥250 before culture results; missed SBP precipitates HRS and death

• Active variceal hemorrhage → octreotide + antibiotics + urgent banding; balloon tamponade and TIPS for refractory bleeding

• HRS with rapidly rising creatinine → urgent vasoconstrictor + albumin + transplant evaluation; poor prognosis without transplant

• Acute-on-chronic liver failure (multi-organ failure on cirrhosis) → ICU, transplant urgency; assess with CLIF-C ACLF

• New rapid decompensation → exclude HCC, portal vein thrombosis, and occult infection

Senior IM Resident Pearls

• Tap the belly. Every cirrhotic admitted with ascites, AMS, fever, or AKI gets a diagnostic paracentesis. SBP is often silent and a PMN ≥250 mandates treatment regardless of symptoms.

• Don't trend ammonia. HE is a clinical diagnosis; a normal ammonia doesn't exclude it and a high one doesn't grade it. Titrate lactulose to bowel movements, not to ammonia.

• Albumin with SBP is not optional — 1.5 g/kg day 1 and 1 g/kg day 3 reduces HRS and mortality (Sort NEJM 1999).

• Don't protein-restrict in HE. Old teaching; it worsens sarcopenia and outcomes. Feed these patients (1.2–1.5 g/kg) with a late-evening snack.

• SAAG ≥1.1 = portal hypertension (cirrhosis, heart failure, Budd-Chiari); <1.1 = non-portal (malignancy, TB, pancreatic). It localizes the cause of ascites instantly.

• Hold the beta-blocker in SBP, hypotension, or HRS — in advanced disease nonselective beta-blockers can reduce cardiac output and worsen renal perfusion ("window hypothesis").

• Common mistake: reflexively transfusing FFP/platelets for an elevated INR before a procedure. Cirrhosis is a rebalanced hemostatic state; INR does not predict bleeding and prophylactic transfusion is usually unnecessary.

Gastroenterology — Acute Pancreatitis

103. Acute Pancreatitis

2 of 3 dx criteria · find the cause (gallstones/ETOH/triglycerides) · aggressive early fluids · no routine antibiotics · Super Compact

Sx: severe epigastric pain radiating to back + constant · nausea/vomiting · epigastric tenderness/guarding · fever/tachycardia (Cullen/Grey-Turner sign = late hemorrhagic, rare)

Neg: denies tearing chest/back pain + arm BP differential (AoD) · denies exertional/pleuritic CP + ECG changes (ACS/inferior MI) · denies rebound/rigidity + free air (perforated viscus) · denies RUQ pain + Murphy sign + fever (acute cholecystitis/cholangitis)

SHx: ETOH (amount, chronicity, last drink — #2 cause + withdrawal) · gallstone risk (female, obesity, rapid wt loss) · hypertriglyceridemia/DM/diet · recent ERCP or new meds

Etiology: gallstones (#1, ~40%) · alcohol (#2, ~30%) · hypertriglyceridemia (TG >1000, #3) · post-ERCP · drugs (azathioprine, valproate, GLP-1, thiazides, didanosine) · hypercalcemia · trauma · autoimmune · idiopathic

RF: gallstones/biliary disease · alcohol use · hypertriglyceridemia >500–1000 · obesity · hypercalcemia · certain medications

Data: lipase (≥3× ULN — more specific than amylase; degree does not equal severity) · CMP (glucose, Ca — hypocalcemia = severe; renal fxn for fluids) · LFTs (ALT >3× ULN suggests gallstone etiology) · triglycerides (>1000 = HTG cause) · CBC (Hct — hemoconcentration = third-spacing/severity; WBC) · CRP (>150 at 48h = severe) · BUN (rising BUN at 24h = strong mortality predictor) · lactate · RUQ ultrasound (gallstones/CBD dilation — first-line for etiology) · CT w/ contrast (only if dx unclear or no improvement at 48–72h — necrosis/complications, not for diagnosis early) · BISAP/APACHE II for severity

DDx: perforated peptic ulcer (free air, peritonitis, sudden onset) · acute cholecystitis/cholangitis (RUQ, Murphy, Charcot triad, ↑bili) · mesenteric ischemia (pain out of proportion, lactate, AF/vascular dz) · inferior MI (ECG, troponin — can mimic epigastric pain)

Home Meds: hold culprit drugs (azathioprine, valproate, thiazides, GLP-1 agonists, estrogen) · hold nephrotoxins during AKI risk · continue/adjust insulin (needed for HTG pancreatitis) · hold PO intake initially then advance

Plan

CONSULT: GI (ERCP if cholangitis/biliary obstruction) · Surgery (cholecystectomy same admission for gallstone; necrosectomy if infected necrosis) · IR/Endo (drainage of infected collections) · Endocrine (HTG management)

– Diagnosis (2 of 3): characteristic epigastric pain · lipase/amylase ≥3× ULN · imaging consistent with pancreatitis
– Fluids (cornerstone): goal-directed moderate resuscitation — lactated Ringer's preferred over NS (less acidosis, possibly less inflammation), e.g. bolus then 1.5–3 mL/kg/hr, titrate to urine output ≥0.5 mL/kg/hr, HR, BUN/Hct trend (WATERFALL 2022: aggressive overhydration caused more fluid overload — avoid over-resuscitation)
– Analgesia: opioids — hydromorphone (Dilaudid) 0.5–1 mg IV q2–4h PRN or fentanyl; scheduled antiemetics — ondansetron (Zofran) 4 mg IV q8h
– Nutrition: early enteral feeding — start low-fat oral diet within 24–48h as tolerated (mild); NJ/NG tube feeding if cannot tolerate PO; NPO/TPN no longer routine (early enteral ↓infection vs parenteral)
– NO prophylactic antibiotics for sterile necrosis/predicted severe disease; antibiotics only for confirmed/suspected infected necrosis or cholangitis — carbapenem (meropenem) penetrates necrosis
– Gallstone pancreatitis: urgent ERCP within 24–48h ONLY if concurrent cholangitis or persistent biliary obstruction; cholecystectomy same admission for mild gallstone pancreatitis (↓recurrence)
– Alcohol pancreatitis: CIWA-guided withdrawal management, thiamine before glucose, alcohol cessation counseling
– Hypertriglyceridemia (TG >1000): insulin infusion (activates lipoprotein lipase) ± apheresis if severe/organ failure; fibrate — fenofibrate (Tricor) once eating; control DM; avoid causative meds
– Degree of lipase elevation does NOT correlate with severity — assess severity with BISAP, BUN/Hct trend, CRP, and organ failure, not the lipase number.
– PT/OT: early mobilization once pain controlled; VTE prophylaxis
– Trend daily: pain, ability to tolerate diet, BUN + Hct (hemoconcentration/resuscitation adequacy), Ca, glucose, creatinine, fluid balance/UOP, signs of organ failure or infection
– Escalation triggers: persistent SIRS/organ failure >48h → ICU (severe pancreatitis); fever + clinical decline at >7–10d → CT for infected necrosis → drainage/abx; rising BUN or Hct despite fluids → reassess resuscitation; abdominal compartment syndrome → decompression
– Discharge checklist: etiology addressed (cholecystectomy scheduled/done, alcohol cessation, TG control with fenofibrate (Tricor) + statin + diet); tolerating diet with controlled pain on PO regimen; diabetes management if applicable; avoid culprit medications documented; GI/surgery follow-up; return precautions (worsening pain, fever, vomiting, inability to eat, jaundice)

103. Acute Pancreatitis

complete reference · gallstone + alcohol + hypertriglyceridemia subtypes · severity scores · full management · Full Card

Symptoms / Associated Sx

• Acute, severe, constant epigastric pain classically radiating to the back, often relieved by leaning forward; nausea and vomiting

• Exam: epigastric tenderness, guarding, decreased bowel sounds (ileus), fever, tachycardia; signs of dehydration/SIRS

• Rare late hemorrhagic signs: periumbilical (Cullen) or flank (Grey-Turner) ecchymosis indicating retroperitoneal hemorrhage

Neg

• Pt denies tearing chest/back pain + inter-arm BP differential — argues against aortic dissection (CT angiography if any suspicion; dissection can mimic and is catastrophic)

• Pt denies sudden diffuse abdominal rigidity + free air on imaging — argues against perforated viscus (upright film/CT for free air)

• Pt denies RUQ pain + positive Murphy + Charcot triad (fever, jaundice, RUQ pain) — argues against acute cholangitis (but gallstone pancreatitis can coexist — check LFTs and biliary imaging)

Social History (SHx)

• Alcohol: quantify amount and chronicity, time of last drink (second most common cause; withdrawal risk → CIWA, thiamine)

• Gallstone risk factors: female sex, obesity, rapid weight loss, pregnancy, family history

• Metabolic: hypertriglyceridemia, poorly controlled diabetes, high-fat diet

• Recent ERCP, new medications, abdominal trauma

Main Etiology

• Gallstones — most common (~40%); obstruction at ampulla; ALT >3× ULN is predictive

• Alcohol — second most common (~30%); usually chronic heavy use

• Hypertriglyceridemia — third; typically triglycerides >1000 mg/dL

• Other: post-ERCP, medications (azathioprine, valproate, GLP-1 agonists, thiazides, didanosine, estrogens), hypercalcemia, trauma, autoimmune (IgG4), pancreatic tumor obstruction, infections, scorpion sting (classic exam trivia); idiopathic ~10–15%

RF

• Modifiable: alcohol use, hypertriglyceridemia, obesity, causative medications, smoking

• Non-modifiable: cholelithiasis/biliary anatomy, hypercalcemia/hyperparathyroidism, genetic (PRSS1, SPINK1), prior pancreatitis

Data

• Lipase (≥3× ULN diagnostic; more sensitive/specific and longer-lasting than amylase; magnitude does NOT correlate with severity)

• CMP (glucose, calcium — hypocalcemia indicates fat saponification/severity; creatinine and electrolytes for fluid management)

• LFTs (ALT >150 / >3× ULN strongly suggests gallstone etiology; bilirubin/alk phos for biliary obstruction)

• Triglycerides (>1000 mg/dL implicates hypertriglyceridemia as cause)

• CBC with Hct (hemoconcentration from third-spacing reflects severity; rising Hct = inadequate resuscitation; WBC for SIRS)

• BUN (rising BUN at 24h is one of the strongest predictors of mortality)

• CRP (>150 mg/L at 48h predicts severe disease)

• Lactate, ABG (hypoperfusion, organ dysfunction in severe disease)

• RUQ ultrasound (first-line for etiology — gallstones, CBD dilation; limited by bowel gas)

• Contrast-enhanced CT abdomen (NOT for early diagnosis; reserve for diagnostic uncertainty or to assess necrosis/complications at 48–72h or with clinical deterioration)

• MRCP/EUS (occult biliary etiology, microlithiasis, ductal anatomy)

• Severity scores (BISAP: BUN >25, impaired mental status, SIRS, age >60, pleural effusion; APACHE II; Ranson's — historical)

DDx

Perforated peptic ulcer (free air, sudden peritonitis) · acute cholecystitis / ascending cholangitis (RUQ pain, Murphy sign, Charcot triad, marked ↑bilirubin) · mesenteric ischemia (pain out of proportion to exam, lactate, AF/vasculopathy) · inferior MI (epigastric presentation — get ECG and troponin)

Home Meds

• Hold: potential culprit drugs — azathioprine, valproate, thiazides, GLP-1 receptor agonists, estrogens, didanosine

• Hold: nephrotoxins (NSAIDs, ACEi) during AKI risk and active resuscitation

• Continue/adjust: insulin — required as therapy in hypertriglyceridemia-induced pancreatitis; manage hyperglycemia

• Diet: hold oral intake initially, then advance to early low-fat diet as tolerated

Plan

CONSULT: GI (ERCP for cholangitis/persistent obstruction; management of collections) · Surgery (same-admission cholecystectomy for gallstone pancreatitis; necrosectomy for infected necrosis) · Interventional Radiology/advanced endoscopy (step-up drainage of infected necrosis) · Endocrinology (severe hypertriglyceridemia)

• Diagnosis (2 of 3): characteristic epigastric pain; lipase or amylase ≥3× upper limit of normal; cross-sectional imaging consistent with pancreatitis

• Fluid resuscitation (cornerstone): lactated Ringer's preferred (less metabolic acidosis, possible anti-inflammatory benefit vs normal saline); goal-directed moderate rate (e.g. initial bolus then ~1.5–3 mL/kg/hr) titrated to urine output ≥0.5 mL/kg/hr, heart rate, MAP, and downtrending BUN/Hct — the WATERFALL trial (2022) showed aggressive over-resuscitation increased fluid overload without benefit, so avoid overhydration

• Analgesia and antiemetics: opioids — hydromorphone (Dilaudid) 0.5–1 mg IV q2–4h PRN or fentanyl; ondansetron (Zofran) 4 mg IV q8h scheduled/PRN

• Nutrition: early enteral nutrition — advance to a low-fat oral diet within 24–48h in mild disease as tolerated; nasojejunal or nasogastric feeding if oral intake not tolerated; routine NPO and TPN are outdated — early enteral feeding lowers infectious complications versus parenteral

• Antibiotics: NO prophylactic antibiotics for sterile necrosis or predicted severe pancreatitis; reserve antibiotics for confirmed or strongly suspected infected necrosis or concurrent cholangitis — a carbapenem (meropenem (Merrem) 1 g IV q8h) penetrates pancreatic necrosis well

• Gallstone pancreatitis: urgent ERCP within 24–48h only if concurrent cholangitis or persistent common bile duct obstruction (not for all gallstone pancreatitis); perform cholecystectomy during the same admission for mild gallstone pancreatitis to prevent recurrence

• Alcohol-related: CIWA-protocol monitoring and benzodiazepine prophylaxis for withdrawal, thiamine 100–500 mg IV before glucose, folate, alcohol cessation counseling and referral

• Hypertriglyceridemia-induced (TG >1000): IV insulin infusion (activates lipoprotein lipase to lower triglycerides) with glucose monitoring ± dextrose; plasmapheresis/apheresis if severe disease or organ failure; once eating, start fibrate — fenofibrate (Tricor) 145 mg PO daily; optimize diabetes; eliminate dietary fat and offending agents

• PT/OT: early mobilization once pain is controlled; pharmacologic VTE prophylaxis

• Trend daily: pain control and diet tolerance, BUN and Hct (resuscitation adequacy and severity), calcium, glucose, creatinine, fluid balance and urine output, SIRS criteria and evolving organ failure

• Escalation triggers: persistent SIRS or organ failure beyond 48h → ICU (severe acute pancreatitis); new fever/clinical decline beyond 7–10 days → contrast CT for infected walled-off necrosis → step-up drainage and targeted antibiotics; rising BUN/Hct despite fluids → reassess resuscitation strategy; tense distended abdomen with rising airway/bladder pressures → evaluate for abdominal compartment syndrome

• Discharge checklist: etiology definitively addressed — cholecystectomy performed or scheduled for gallstone disease, alcohol cessation resources, triglyceride control with fenofibrate (Tricor) ± statin and dietary fat restriction, diabetes optimization; tolerating oral diet with adequate pain control on an oral regimen; list of medications to avoid documented; GI and/or surgery follow-up; return precautions for worsening or recurrent pain, fever, persistent vomiting, inability to maintain hydration, or jaundice

Red Flags

• Persistent organ failure >48h (respiratory, cardiovascular, renal) → severe acute pancreatitis, ICU care, high mortality

• Infected pancreatic necrosis (gas in collection, clinical deterioration at 1–4 weeks) → step-up drainage + carbapenem; avoid early open necrosectomy

• Ascending cholangitis with gallstone pancreatitis (Charcot triad, hypotension/confusion = Reynolds pentad) → emergent ERCP

• Hypocalcemia, rising BUN, hemoconcentration, and elevated CRP → markers of severe disease

• Abdominal compartment syndrome from aggressive fluids/third-spacing → bladder pressure monitoring, decompression

• Hemorrhagic signs (Cullen/Grey-Turner) or pseudoaneurysm bleeding (splenic artery) → emergent imaging/IR

Senior IM Resident Pearls

• Lipase magnitude ≠ severity. A lipase of 3,000 is not "worse" than 900. Stratify severity with BISAP, rising BUN, hemoconcentration, CRP, and organ failure — not the enzyme level.

• No prophylactic antibiotics. One of the most common errors. Antibiotics are for infected necrosis or cholangitis, not for sterile necrosis or "looks sick."

• Don't CT too early. CT in the first 48–72h underestimates necrosis and rarely changes management; reserve it for diagnostic uncertainty or deterioration.

• Moderate, not maximal, fluids. WATERFALL (2022) overturned the aggressive-hydration dogma — goal-directed LR titrated to urine output and BUN beats high fixed rates that cause fluid overload.

• Feed early. Early enteral nutrition reduces infectious complications and mortality versus TPN — start a low-fat diet within 24–48h when tolerated.

• Same-admission cholecystectomy for mild gallstone pancreatitis prevents recurrence — don't discharge with the gallbladder still in and a plan to "schedule later."

• Common mistake: treating hypertriglyceridemia pancreatitis with a fibrate alone acutely — the acute therapy is an insulin infusion (± apheresis); fibrates are for maintenance once the patient is eating.

Gastroenterology / Surgery — Mechanical Bowel Obstruction

104. Small Bowel Obstruction (SBO)

adhesions vs hernia vs malignancy · partial vs complete · find strangulation early · NPO + NG decompression + fluids · surgery if ischemia/complete/fails · Super Compact

Sx: crampy intermittent abdominal pain + distension · nausea/bilious vomiting (feculent if distal) · obstipation (no flatus/stool = complete) · exam: distension, high-pitched/tinkling then absent bowel sounds, surgical scars, hernia at orifices (constant severe pain + peritonism → strangulation)

Neg: denies fever + peritoneal signs + lactate (strangulation/ischemia) · denies absent stool/flatus w/ diffuse dilation incl colon (ileus vs mechanical) · denies pain out of proportion + AF/vascular hx (mesenteric ischemia) · denies prior cancer + weight loss + new mass (malignant obstruction)

SHx: prior abdominal/pelvic surgery (adhesions #1) · malignancy hx + prior radiation · hernia history · IBD/Crohn's (strictures)

Etiology: adhesions (#1 in developed world, ~60–75%; prior surgery) · hernia (#2; incarcerated inguinal/femoral/ventral/internal) · malignancy (#3; primary or metastatic, esp colon/ovarian/peritoneal) · Crohn's strictures · intussusception · gallstone ileus · volvulus · radiation enteritis

RF: prior abdominopelvic surgery · known hernia · intra-abdominal malignancy · prior radiation · Crohn's disease

Data: CBC (leukocytosis/left shift → strangulation/ischemia) · BMP (hypokalemia, metabolic alkalosis from vomiting; volume status; renal fxn) · lactate (↑ suggests ischemia/strangulation — late/insensitive) · type & screen (pre-op) · VBG · CT abdomen/pelvis w/ IV contrast (study of choice — transition point, complete vs partial, closed-loop, ischemia signs: bowel wall thickening, pneumatosis, portal venous gas, reduced enhancement, free fluid) · upright/supine films (dilated loops >3 cm, air-fluid levels, paucity of colonic gas — screening only) · water-soluble contrast (Gastrografin) challenge (prognostic + therapeutic for adhesive partial SBO)

DDx: paralytic ileus (post-op/metabolic, diffuse dilation incl colon, no transition point) · large bowel obstruction (colonic dilation, distal point — colon CA/volvulus) · mesenteric ischemia (pain out of proportion, lactate, AF) · Ogilvie/colonic pseudo-obstruction (massive colonic dilation, no mechanical cause)

Home Meds: hold all PO meds (NPO) · hold opioids/anticholinergics that worsen ileus where possible · convert essential meds to IV · hold oral hypoglycemics, adjust insulin while NPO

Plan

CONSULT: Surgery (early — for any strangulation, complete obstruction, closed-loop, hernia, or failure of conservative management) · GI (if malignant obstruction or stent candidate) · Oncology (malignant etiology)

– Initial: NPO; NG tube to low intermittent suction for decompression (relieves distension/vomiting); IV crystalloid resuscitation (LR); strict I&Os, Foley; correct electrolytes (replete K, correct hypochloremic metabolic alkalosis)
– Analgesia + antiemetics: opioids judiciously — hydromorphone (Dilaudid) 0.5 mg IV q3–4h PRN; ondansetron (Zofran) 4 mg IV q8h
– VTE prophylaxis: enoxaparin (Lovenox) 40 mg SC daily (or heparin if renal/peri-op)
– Adhesive partial SBO (no ischemia): trial of conservative management 24–48h; water-soluble contrast challenge — Gastrografin 100 mL via NG; contrast reaching colon on film within 24h predicts resolution and may itself promote it; failure to progress → surgery
– Operative indications (don't delay): signs of strangulation/ischemia, complete obstruction, closed-loop, incarcerated/strangulated hernia, perforation, or failure of conservative trial → exploratory laparotomy/laparoscopy, lysis of adhesions, hernia repair, or resection of nonviable bowel
– Hernia: incarcerated/strangulated → urgent surgical reduction/repair; do not reduce if signs of ischemia (reduces dead bowel)
– Malignant obstruction: CT staging, GI/oncology/surgery for stent vs surgical bypass vs decompressive measures; dexamethasone + octreotide for inoperable malignant bowel obstruction symptom control
– Antibiotics: broad-spectrum (e.g. piperacillin-tazobactam (Zosyn) 3.375 g IV q6h) for suspected strangulation/ischemia/perforation or peri-operatively — not routine for simple obstruction
– Closed-loop obstruction and early strangulation can have a deceptively benign exam and normal labs — the CT signs (and clinical trajectory) drive the decision, not a single normal WBC/lactate.
– PT/OT: early mobilization to promote motility once stable/post-op
– Trend daily: abdominal exam (distension, tenderness, peritonism), NG output, passage of flatus/stool, WBC, lactate, electrolytes, fluid balance
– Escalation triggers: rising lactate/WBC, worsening/constant pain, peritoneal signs, fever, tachycardia, or CT ischemia signs → emergent surgery; no resolution by 48–72h of conservative management → surgery
– Discharge checklist: resolution confirmed (passing flatus/stool, tolerating diet, NG removed); etiology addressed (hernia repaired, malignancy plan, adhesion counseling); diet advanced as tolerated; surgery/GI/oncology follow-up; return precautions (recurrent pain, distension, vomiting, no stool/flatus)

104. Small Bowel Obstruction (SBO)

complete reference · adhesions + hernia + malignancy · CT-driven decisions · conservative trial vs operative · Full Card

Symptoms / Associated Sx

• Crampy, intermittent, colicky abdominal pain with progressive distension; nausea and vomiting (bilious proximally, feculent with distal/long-standing obstruction)

• Obstipation — inability to pass flatus or stool suggests complete obstruction; partial obstruction may still pass some gas/stool

• Exam: abdominal distension, early high-pitched/tinkling bowel sounds progressing to absent, prior surgical scars, careful exam of all hernia orifices (inguinal, femoral, umbilical, incisional)

• Constant (rather than colicky) pain, fever, tachycardia, and peritoneal signs raise concern for strangulation/ischemia

Neg

• Pt denies fever + focal peritoneal signs + rising lactate — argues against strangulation/bowel ischemia (but early strangulation can be subtle; CT findings and trajectory override reassuring labs)

• Pt denies diffuse gas including a dilated colon without a transition point — argues against paralytic ileus (ileus = no mechanical block, often post-op/metabolic/opioid)

• Pt denies pain out of proportion to exam + atrial fibrillation/vascular disease — argues against acute mesenteric ischemia (CT angiography if suspected — a can't-miss mimic)

Social History (SHx)

• Prior abdominal or pelvic surgery — the dominant risk factor (adhesions cause most SBOs in developed countries)

• Malignancy history and prior abdominopelvic radiation (radiation enteritis, peritoneal disease)

• Known or prior hernias

• Inflammatory bowel disease, particularly Crohn's (fibrostenotic strictures)

Main Etiology

• Adhesions — most common cause (~60–75%); from prior surgery; can occur years later

• Hernia — second most common; incarcerated/strangulated inguinal, femoral, ventral, incisional, or internal hernias; leading cause in patients without prior surgery

• Malignancy — primary small bowel tumors, or more often extrinsic compression/peritoneal carcinomatosis (colorectal, ovarian, gastric)

• Other: Crohn's strictures, intussusception (often with a lead point in adults), gallstone ileus (pneumobilia + ectopic gallstone + SBO = Rigler triad), volvulus, radiation enteritis, foreign body/bezoar

RF

• Modifiable: hernia repair when elective reduces incarceration risk; minimizing repeat surgery limits adhesions

• Non-modifiable: prior abdominopelvic surgery, intra-abdominal malignancy, prior radiation, Crohn's disease, congenital adhesive bands

Data

• CBC with differential (leukocytosis with left shift raises concern for strangulation/ischemia, though normal counts do not exclude it)

• BMP (hypokalemia and hypochloremic metabolic alkalosis from vomiting; volume depletion; renal function)

• Lactate (elevation supports ischemia/strangulation but is a late and insensitive marker)

• VBG, magnesium, phosphate (acid-base and repletion before any operation)

• Type and screen (pre-operative preparation)

• CT abdomen/pelvis with IV contrast (imaging of choice — identifies transition point, distinguishes partial vs complete, detects closed-loop obstruction, and shows ischemia signs: bowel wall thickening, mural pneumatosis, portal venous gas, decreased/absent wall enhancement, mesenteric edema, free fluid)

• Plain abdominal radiographs (upright + supine) (dilated small bowel loops >3 cm, air-fluid levels in a step-ladder pattern, paucity of colonic gas; useful for screening but far less sensitive than CT)

• Water-soluble contrast (Gastrografin) challenge (in adhesive partial SBO — contrast reaching the colon within 24h predicts successful nonoperative resolution and is therapeutic)

DDx

Paralytic ileus (no mechanical transition point, diffuse dilation including colon; post-op, opioids, electrolyte derangement) · large bowel obstruction (colonic dilation to a distal point — colorectal cancer, sigmoid/cecal volvulus) · acute mesenteric ischemia (pain out of proportion, lactate, embolic source) · Ogilvie syndrome / acute colonic pseudo-obstruction (massive colonic dilation without mechanical cause; risk of cecal perforation)

Home Meds

• Hold: all oral medications (patient is NPO); convert essential medications to IV

• Hold/minimize: opioids and anticholinergics that impair motility where clinically feasible

• Adjust: hold oral hypoglycemics and adjust insulin regimen while NPO; hold diuretics if volume depleted

Plan

CONSULT: Surgery (early involvement for any strangulation, complete or closed-loop obstruction, hernia, or failure of conservative management) · GI (malignant obstruction, stent candidacy) · Oncology (malignant etiology) · Palliative care (inoperable malignant bowel obstruction)

• Supportive core: NPO; nasogastric tube to low intermittent suction for proximal decompression; aggressive IV crystalloid (lactated Ringer's) resuscitation; Foley catheter with strict intake/output; correct electrolytes — replete potassium and correct hypochloremic, hypokalemic metabolic alkalosis

• Analgesia and antiemetics: opioids used judiciously — hydromorphone (Dilaudid) 0.5 mg IV q3–4h PRN; ondansetron (Zofran) 4 mg IV q8h

• VTE prophylaxis: enoxaparin (Lovenox) 40 mg SC daily (or unfractionated heparin 5000 units SC q8h if renal impairment or imminent surgery)

• Adhesive partial SBO without ischemia: trial of nonoperative management for 24–48h with serial exams; water-soluble contrast challenge — Gastrografin 100 mL via NG tube with follow-up radiograph; contrast in the colon within 24h predicts (and helps achieve) resolution, while failure to progress mandates surgery

• Operative management (do not delay) for: signs of strangulation or ischemia, complete obstruction, closed-loop obstruction, incarcerated/strangulated hernia, perforation, or failure of an appropriate conservative trial — exploratory laparoscopy or laparotomy with adhesiolysis, hernia reduction and repair, and resection of nonviable bowel

• Hernia: incarcerated or strangulated hernia requires urgent surgical management; avoid forceful reduction if ischemia is suspected (risk of reducing nonviable bowel into the abdomen)

• Malignant obstruction: CT staging and multidisciplinary input (surgery, GI, oncology) for endoscopic stenting, surgical bypass/resection, or decompression; for inoperable malignant bowel obstruction, symptom control with dexamethasone, octreotide (antisecretory), antiemetics, and a venting gastrostomy as needed

• Antibiotics: broad-spectrum coverage (e.g. piperacillin-tazobactam (Zosyn) 3.375 g IV q6h) when strangulation, ischemia, or perforation is suspected and perioperatively — not routine for uncomplicated mechanical obstruction

• PT/OT: early mobilization to promote return of motility once stable or post-operatively

• Trend daily: serial abdominal exams (distension, tenderness, peritoneal signs), nasogastric output, return of flatus/stool, white count, lactate, electrolytes, and fluid balance

• Escalation triggers: rising lactate or white count, worsening or constant pain, new peritoneal signs, fever, tachycardia, or CT signs of ischemia → emergent operative exploration; failure to resolve within 48–72h of conservative management → surgery

• Discharge checklist: documented resolution (passing flatus and stool, tolerating diet, NG tube removed); underlying cause addressed (hernia repaired, malignancy treatment plan, counseling on adhesion recurrence risk); diet advanced as tolerated; surgery/GI/oncology follow-up arranged; return precautions for recurrent crampy pain, distension, vomiting, or obstipation

Red Flags

• Strangulation/ischemia: constant severe pain, fever, tachycardia, peritoneal signs, rising lactate/WBC → emergent surgery

• Closed-loop obstruction on CT → high risk of rapid ischemia even with a benign exam → urgent surgery

• Incarcerated/strangulated hernia → urgent operative repair; tender irreducible hernia is a surgical emergency

• Complete obstruction (no flatus/stool, no colonic gas) → lower likelihood of spontaneous resolution, lower threshold for surgery

• Pneumatosis intestinalis or portal venous gas → transmural ischemia until proven otherwise

• Feculent vomiting + profound distension → distal/long-standing obstruction with aspiration risk → secure airway/decompress

Senior IM Resident Pearls

• Examine every hernia orifice and the old scars. A missed incarcerated femoral hernia (more common in women, high strangulation risk) is a classic trap.

• CT is the decision-maker. It distinguishes partial vs complete, finds the transition point and closed loops, and shows ischemia signs that a normal WBC/lactate will miss — don't be reassured by benign labs.

• Gastrografin challenge is both prognostic and therapeutic in adhesive partial SBO — contrast reaching the colon within 24h predicts nonoperative resolution.

• "The sun should not set on a complete SBO" is dated dogma, but closed-loop and strangulating obstructions genuinely don't wait — escalate early.

• SBO without prior surgery? Think hernia or malignancy first — the absence of adhesions shifts your differential.

• Common mistake: reducing a strangulated hernia at the bedside — you can push dead bowel back inside and lose the diagnosis. Get surgery.

• Distinguish ileus from mechanical SBO before blaming opioids — a transition point on CT means mechanical obstruction that decompression alone may not fix.

Hepatobiliary — Biliary Infection

105. Acute Cholangitis

infection of obstructed bile duct · Charcot triad / Reynolds pentad · Tokyo Guidelines grading · antibiotics + urgent biliary drainage (ERCP) · Super Compact

Sx: fever/rigors + RUQ pain + jaundice (Charcot triad) · + hypotension + AMS = Reynolds pentad (suppurative, emergency) · nausea, pruritus, dark urine/pale stool

Neg: denies isolated RUQ pain + Murphy w/o jaundice/ductal dilation (acute cholecystitis) · denies painless jaundice + weight loss + Courvoisier (malignant obstruction) · denies hepatitic transaminitis pattern w/o obstruction (viral/alcoholic hepatitis) · denies RLQ migration (appendicitis)

SHx: gallstone risk (female, obesity, age) · prior biliary surgery/ERCP/stent · alcohol use · known choledocholithiasis/PSC/stricture

Etiology: choledocholithiasis (#1 — stone obstructs CBD + ascending infection) · benign stricture · malignant obstruction (cholangiocarcinoma, pancreatic head, ampullary) · stent occlusion/blockage · post-ERCP · parasitic (Clonorchis, Ascaris — endemic areas); organisms: E. coli, Klebsiella, Enterococcus, Enterobacter

RF: choledocholithiasis/gallstones · prior biliary instrumentation or indwelling stent · biliary stricture/PSC · malignancy · age

Data: CBC (leukocytosis/left shift; leukopenia=severe) · CMP/LFTs (cholestatic pattern: ↑↑ALP + ↑GGT + ↑direct bili out of proportion to transaminases) · lactate (sepsis severity) · blood cultures ×2 (before abx — frequently positive, guides therapy) · coags (pre-procedure; ↑INR from cholestasis/sepsis) · lipase (concurrent gallstone pancreatitis) · CRP/procalcitonin · RUQ ultrasound (first-line: CBD dilation >6 mm, stones, intrahepatic ductal dilation) · MRCP/EUS (define obstruction if US equivocal, pre-ERCP) · CT (if dx unclear, complications, malignancy) · Tokyo Guidelines 2018 grading (I mild / II moderate / III severe w/ organ dysfunction)

DDx: acute cholecystitis (Murphy+, no ductal dilation, no/mild jaundice) · gallstone pancreatitis (↑lipase, epigastric→back) · liver abscess (fever + focal lesion on imaging) · malignant biliary obstruction (painless jaundice, mass, may become infected)

Home Meds: hold anticoagulants/antiplatelets (pre-ERCP — reverse if needed) · hold oral meds if NPO for procedure · continue essential meds IV · hold nephrotoxins during sepsis/AKI

Plan

CONSULT: GI/Advanced endoscopy (URGENT ERCP for biliary drainage) · IR (PTC drainage if ERCP fails/unavailable) · Surgery (if ERCP/PTC not feasible) · ICU (Grade III / Reynolds pentad)

– Diagnosis (Tokyo Guidelines 2018): (A) systemic inflammation — fever/rigors or labs; (B) cholestasis — jaundice or abnormal LFTs; (C) imaging — biliary dilation or evidence of cause. Suspected = A + (B or C); Definite = A + B + C
– Resuscitate: IV fluids, sepsis bundle, lactate-guided resuscitation, pressors + ICU if shock (Grade III)
– Empiric antibiotics (early, after cultures): piperacillin-tazobactam (Zosyn) 4.5 g IV q6h; alternatives — ceftriaxone (Rocephin) 2 g IV q24h + metronidazole (Flagyl) 500 mg IV q8h, or carbapenem (meropenem 1 g IV q8h) for severe/healthcare-associated/prior resistance; cover Enterococcus in severe or post-instrumentation cases; de-escalate to cultures
– Biliary drainage (definitive): ERCP with sphincterotomy + stone extraction ± stent — urgent/emergent (within 24h, sooner if Grade III/septic shock); if ERCP fails or unavailable → percutaneous transhepatic cholangiography (PTC) drainage by IR, or surgical decompression as last resort
– Source control timing: Grade I (mild) — abx + drainage as needed, often elective; Grade II (moderate) — early drainage; Grade III (severe) — organ support + emergent drainage
– Duration: antibiotics 4–7 days after adequate source control (longer with bacteremia/Enterococcus/incomplete drainage)
– Definitive prevention: cholecystectomy after recovery for gallstone-related cholangitis to prevent recurrence
– Cholangitis is a "drain or die" diagnosis — antibiotics alone do not treat an obstructed, infected duct; the obstruction must be relieved, urgently if septic.
– PT/OT: mobilize post-procedure once stable
– Trend daily: temp/fever curve, WBC, LFTs/bilirubin (should fall after drainage), lactate, hemodynamics, blood culture results, drain output
– Escalation triggers: hypotension/AMS (Reynolds pentad) → ICU + emergent drainage; no clinical improvement after drainage → reassess for inadequate drainage, abscess, or resistant organism; rising lactate/organ failure → sepsis escalation
– Discharge checklist: complete antibiotic course; biliary obstruction relieved/stent documented with removal/exchange plan; interval cholecystectomy scheduled if gallstone etiology; LFTs trending to normal; GI/surgery follow-up; return precautions (fever, RUQ pain, jaundice, confusion)

105. Acute Cholangitis

complete reference · Tokyo Guidelines 2018 diagnosis + grading · empiric antibiotics + urgent ERCP · Full Card

Symptoms / Associated Sx

• Charcot triad: fever/rigors, right upper quadrant pain, and jaundice (present in a minority — sensitivity ~50–70%, so absence does not exclude)

• Reynolds pentad: Charcot triad plus hypotension and altered mental status — indicates suppurative cholangitis and septic shock, a true emergency

• Associated: nausea/vomiting, pruritus, dark urine, pale/acholic stools, malaise

Neg

• Pt denies isolated RUQ pain with a positive Murphy sign but without jaundice or ductal dilation — argues for acute cholecystitis rather than cholangitis (cholecystitis lacks the cholestatic jaundice and duct dilation of an obstructed CBD)

• Pt denies painless progressive jaundice + weight loss + palpable nontender gallbladder (Courvoisier) — argues against malignant biliary obstruction (though malignancy can obstruct and then become infected)

• Pt denies a hepatocellular transaminitis pattern (AST/ALT in the thousands) without obstruction — argues against acute viral or alcoholic hepatitis (cholangitis shows a cholestatic pattern with duct dilation)

Social History (SHx)

• Gallstone risk factors: female sex, obesity, increasing age, rapid weight loss

• Prior biliary surgery, ERCP, sphincterotomy, or indwelling biliary stent (stent occlusion is a common cause)

• Alcohol use; known primary sclerosing cholangitis, biliary strictures, or prior choledocholithiasis

Main Etiology

• Choledocholithiasis — most common; a CBD stone obstructs bile flow, bile becomes infected, and pressure drives bacterial translocation into the bloodstream

• Benign biliary strictures (post-surgical, PSC, chronic pancreatitis)

• Malignant obstruction — cholangiocarcinoma, pancreatic head cancer, ampullary or duodenal tumors

• Stent occlusion or blockage; post-ERCP cholangitis

• Parasitic infection in endemic regions (Clonorchis sinensis, Ascaris lumbricoides)

• Common organisms: E. coli, Klebsiella, Enterobacter, Enterococcus, and anaerobes (especially after instrumentation)

RF

• Modifiable: timely management of choledocholithiasis; stent exchange before occlusion; cholecystectomy after gallstone disease

• Non-modifiable: prior biliary instrumentation, PSC/strictures, malignancy, older age, prior cholangitis

Data

• CBC with differential (leukocytosis with left shift; leukopenia <4k is a severity/Tokyo marker)

• Comprehensive metabolic panel / LFTs (cholestatic pattern: markedly elevated alkaline phosphatase and GGT with elevated direct bilirubin disproportionate to transaminases)

• Lactate (sepsis severity and resuscitation target)

• Blood cultures ×2 (obtain before antibiotics — frequently positive and guide targeted therapy)

• Coagulation studies (pre-procedure planning; INR may rise from cholestasis-related vitamin K malabsorption or sepsis)

• Lipase (concurrent gallstone pancreatitis)

• CRP / procalcitonin (inflammatory burden, severity grading)

• RUQ ultrasound (first-line — common bile duct dilation >6 mm, choledocholithiasis, intrahepatic ductal dilation; readily available)

• MRCP or endoscopic ultrasound (define the level and cause of obstruction when ultrasound is equivocal and to plan ERCP)

• CT abdomen (when diagnosis is unclear, to assess complications, or evaluate for malignancy)

• Tokyo Guidelines 2018 severity grade (Grade I mild; Grade II moderate; Grade III severe — associated with organ dysfunction: cardiovascular, neurologic, respiratory, renal, hepatic, or hematologic)

DDx

Acute cholecystitis (positive Murphy, no/mild jaundice, no ductal dilation) · gallstone pancreatitis (elevated lipase, epigastric pain to the back) · pyogenic liver abscess (fever + focal hepatic lesion on imaging) · malignant biliary obstruction (painless jaundice, mass, may secondarily infect)

Home Meds

• Hold/reverse: anticoagulants and antiplatelets in anticipation of ERCP with sphincterotomy (reverse if active bleeding risk)

• Hold: oral medications if NPO for procedure; convert essentials to IV

• Hold: nephrotoxins (NSAIDs, ACEi) during sepsis/AKI

Plan

CONSULT: GI / advanced endoscopy (urgent ERCP for biliary drainage) · Interventional Radiology (percutaneous transhepatic drainage if ERCP fails or is unavailable) · Surgery (open decompression if both fail) · ICU (Grade III / Reynolds pentad / septic shock)

• Diagnosis (Tokyo Guidelines 2018): (A) systemic inflammation — fever/rigors or inflammatory labs; (B) cholestasis — jaundice or abnormal LFTs; (C) imaging — biliary dilation or evidence of an etiology. Suspected = A + (B or C); Definite = A + B + C

• Resuscitation: IV fluids, sepsis bundle, lactate-guided resuscitation; vasopressors and ICU admission for septic shock (Grade III)

• Empiric antibiotics (start early, after blood cultures): piperacillin-tazobactam (Zosyn) 4.5 g IV q6h; alternatives — ceftriaxone (Rocephin) 2 g IV q24h plus metronidazole (Flagyl) 500 mg IV q8h, or a carbapenem (meropenem (Merrem) 1 g IV q8h) for severe, healthcare-associated, or resistance-risk cases; add enterococcal coverage in severe disease or after biliary instrumentation; de-escalate based on culture and sensitivity

• Biliary drainage (the definitive therapy): ERCP with sphincterotomy and stone extraction, with stent placement as needed — urgent within 24h, and emergent in Grade III/septic shock; if ERCP fails or is unavailable, percutaneous transhepatic biliary drainage by IR; surgical decompression only if endoscopic and percutaneous approaches are not feasible

• Drainage timing by severity: Grade I (mild) — antibiotics with drainage if no response, often elective; Grade II (moderate) — early biliary drainage; Grade III (severe) — organ support plus emergent drainage once stabilized enough to undergo the procedure

• Antibiotic duration: 4–7 days after adequate source control; longer with persistent bacteremia, Enterococcus/resistant organisms, or incomplete drainage

• Definitive prevention: interval cholecystectomy after recovery for gallstone-related cholangitis to prevent recurrence

• PT/OT: mobilize after the procedure once hemodynamically stable

• Trend daily: fever curve, white count, LFTs and bilirubin (expected to fall after successful drainage), lactate, hemodynamics, blood culture results, and biliary drain output if placed

• Escalation triggers: hypotension or altered mental status (Reynolds pentad) → ICU and emergent drainage; failure to improve after drainage → reassess for inadequate drainage, undrained segment, abscess, or resistant organism; rising lactate or new organ dysfunction → escalate sepsis management

• Discharge checklist: complete the antibiotic course; document relief of obstruction and any stent with a plan for removal/exchange; schedule interval cholecystectomy if gallstone etiology; confirm LFTs are trending toward normal; arrange GI and surgery follow-up; return precautions for recurrent fever, RUQ pain, jaundice, or confusion

Red Flags

• Reynolds pentad (Charcot triad + hypotension + altered mental status) → suppurative cholangitis/septic shock → ICU + emergent biliary drainage

• Grade III cholangitis with any organ dysfunction → emergent decompression, do not wait for "optimization"

• Failure to improve after antibiotics alone → the duct must be drained; antibiotics cannot sterilize an obstructed system

• Persistent bacteremia or new hepatic abscess after drainage → inadequate source control, reimage

• Coagulopathy from cholestasis/sepsis → correct (vitamin K, reversal) before sphincterotomy to reduce post-ERCP bleeding

Senior IM Resident Pearls

• Drain or die. Cholangitis is an obstructed, infected, high-pressure space — antibiotics buy time but the cure is mechanical decompression (ERCP). Septic patients need it emergently, not "in the morning."

• Charcot triad is insensitive. Only about half of patients have all three; fever + cholestatic LFTs + duct dilation is enough to act on. Don't wait for jaundice.

• Cholestatic vs hepatocellular pattern tells you where the problem is: ALP/GGT/direct bilirubin out of proportion = obstruction; AST/ALT in the thousands = hepatocyte injury.

• Cover Enterococcus in severe disease and after biliary instrumentation — it is commonly missed by standard regimens.

• Use the Tokyo Guidelines to both diagnose and grade — the grade drives how urgently the duct is drained.

• Common mistake: treating "cholangitis" with antibiotics and admitting for observation without arranging drainage — the obstruction is the disease.

• Don't forget the gallbladder. Schedule interval cholecystectomy after gallstone cholangitis or the patient comes back.

Hepatobiliary — Gallbladder Inflammation

106. Acute Cholecystitis

cystic duct obstruction → GB inflammation/infection · Murphy sign · US first-line · abx + early lap chole · Tokyo grading · Super Compact

Sx: constant RUQ/epigastric pain >6h (vs self-limited biliary colic) · radiates to right shoulder/scapula · nausea/vomiting · fever · Murphy sign (inspiratory arrest on RUQ palpation) · post-fatty-meal onset

Neg: denies jaundice + ductal dilation + cholestatic LFTs (cholangitis/CBD stone) · denies epigastric→back pain + ↑lipase (pancreatitis) · denies exertional/substernal CP + ECG changes (ACS/inferior MI) · denies RLQ migration + anorexia (appendicitis)

SHx: gallstone risk — "4 Fs" (female, forty, fertile, fat) · rapid weight loss/bariatric · ETOH · TPN/critical illness/fasting (acalculous)

Etiology: calculous (~90% — stone impacted in cystic duct → obstruction, inflammation, secondary infection) · acalculous (~10% — critically ill, TPN, fasting, ischemia/stasis; higher morbidity) · organisms: E. coli, Klebsiella, Enterococcus

RF: cholelithiasis · female sex/age/obesity · rapid weight loss · pregnancy · critical illness/TPN (acalculous) · diabetes

Data: CBC (leukocytosis/left shift) · CMP/LFTs (mild ↑ALP/bili common; markedly ↑bili/ALP → suspect CBD stone/cholangitis) · lipase (exclude concurrent pancreatitis) · CRP (severity, Tokyo grading) · blood cultures (if febrile/toxic) · RUQ ultrasound (first-line: gallstones, GB wall >3 mm, pericholecystic fluid, sonographic Murphy, distension) · HIDA scan (most sensitive — nonvisualization of GB confirms cystic duct obstruction; use if US equivocal) · CT (complications: gangrene, perforation, emphysematous, or alternative dx) · Tokyo Guidelines 2018 grading (I/II/III)

DDx: biliary colic (transient pain <6h, no fever/inflammation) · acute cholangitis (jaundice + ductal dilation + Charcot) · gallstone pancreatitis (↑lipase) · PUD/perforation (epigastric, free air) · inferior MI/hepatitis (ECG/troponin; transaminitis)

Home Meds: hold oral meds if NPO pre-op · hold/reverse anticoagulants pre-op · continue essential meds IV · hold nephrotoxins if AKI; resume after

Plan

CONSULT: Surgery (early lap cholecystectomy — definitive) · IR (percutaneous cholecystostomy tube if high surgical risk / Grade III) · GI (if concurrent choledocholithiasis needing ERCP)

– Diagnosis (Tokyo Guidelines 2018): (A) local signs — Murphy, RUQ pain/mass; (B) systemic — fever, ↑CRP/WBC; (C) imaging consistent. Suspected = A + B; Definite = A + B + C
– Supportive: NPO, IV fluids (LR), correct electrolytes; analgesia — ketorolac (Toradol) 15–30 mg IV (NSAID effective for biliary pain) or opioid; antiemetics — ondansetron (Zofran) 4 mg IV q8h
– Antibiotics: Grade I (mild) — often abx not strictly required if early chole, but commonly cefazolin (Ancef) or ceftriaxone (Rocephin) 1–2 g IV q24h; Grade II/III or toxic — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h or ceftriaxone + metronidazole (Flagyl) 500 mg IV q8h; add Enterococcus coverage in severe/healthcare-associated
– Definitive — early laparoscopic cholecystectomy: ideally within 24–72h of symptom onset (early beats delayed/interval surgery — fewer complications, shorter stay); intraop cholangiogram if CBD stone suspected
– High surgical risk / Grade III / unfit: percutaneous cholecystostomy tube (IR) for drainage as a bridge or temporizing measure, with interval cholecystectomy when stabilized
– If concurrent choledocholithiasis/cholangitis: ERCP before or after cholecystectomy to clear the duct
– Duration of antibiotics: stop within 24h after uncomplicated cholecystectomy; continue 4–7 days if perforation/abscess/gangrene or no source control
– Acalculous cholecystitis in the ICU patient is easily missed and progresses to gangrene/perforation quickly — low threshold for HIDA/CT and cholecystostomy in the critically ill with unexplained sepsis.
– PT/OT: early mobilization post-op; VTE prophylaxis — enoxaparin (Lovenox) 40 mg SC daily
– Trend daily: RUQ exam, fever curve, WBC, LFTs (rising bili → consider retained CBD stone), drain output if cholecystostomy
– Escalation triggers: worsening pain/peritonism, rising WBC/lactate, hemodynamic instability → suspect gangrene/perforation/emphysematous cholecystitis → urgent surgery; failure to improve on abx within 24–48h → image for complications
– Discharge checklist: cholecystectomy done or interval surgery scheduled; cholecystostomy care/follow-up if placed; antibiotics completed/stopped appropriately; LFTs normalizing; diet advanced; surgery follow-up; return precautions (recurrent RUQ pain, fever, jaundice)

106. Acute Cholecystitis

complete reference · calculous + acalculous · Tokyo Guidelines · early laparoscopic cholecystectomy · Full Card

Symptoms / Associated Sx

• Constant right upper quadrant or epigastric pain lasting >4–6h (distinguishing it from self-limited biliary colic), often after a fatty meal, radiating to the right shoulder or scapula

• Nausea, vomiting, anorexia, low-grade fever

• Exam: Murphy sign (inspiratory arrest during deep RUQ palpation), RUQ tenderness/guarding, occasionally a palpable tender gallbladder

Neg

• Pt denies jaundice + common bile duct dilation + markedly cholestatic LFTs — argues against choledocholithiasis/cholangitis (mild LFT elevation is common in cholecystitis, but marked elevation suggests a ductal stone)

• Pt denies epigastric pain radiating to the back + elevated lipase — argues against gallstone pancreatitis (check lipase; the two can coexist)

• Pt denies substernal/exertional chest pain + ECG changes + troponin rise — argues against acute coronary syndrome (inferior MI can present as RUQ/epigastric pain — get an ECG in the right patient)

Social History (SHx)

• Classic gallstone risk: female, forties, fertile, overweight ("4 Fs"); also family history, rapid weight loss, bariatric surgery

• Alcohol use; pregnancy

• Critical illness, prolonged fasting, total parenteral nutrition, major surgery/trauma (acalculous cholecystitis)

Main Etiology

• Calculous cholecystitis (~90%): a gallstone impacts in the cystic duct, causing obstruction, gallbladder distension, inflammation, and secondary bacterial infection

• Acalculous cholecystitis (~10%): gallbladder stasis and ischemia in critically ill, fasting, TPN-dependent, or post-operative patients; higher rates of gangrene and perforation, often diagnosed late

• Common organisms when infected: E. coli, Klebsiella, Enterococcus, Enterobacter

RF

• Modifiable: obesity, rapid weight loss, TPN duration, gallstone disease management

• Non-modifiable: female sex, increasing age, pregnancy, prior gallstones, critical illness (acalculous), diabetes

Data

• CBC with differential (leukocytosis with left shift)

• CMP / LFTs (mild elevations in alkaline phosphatase and bilirubin are common; markedly elevated bilirubin/ALP should prompt evaluation for a CBD stone or cholangitis)

• Lipase (exclude concurrent gallstone pancreatitis)

• CRP (inflammatory severity and Tokyo grading)

• Blood cultures (febrile or toxic-appearing patients)

• RUQ ultrasound (first-line) (gallstones, gallbladder wall thickening >3 mm, pericholecystic fluid, sonographic Murphy sign, gallbladder distension)

• HIDA (cholescintigraphy) (most sensitive/specific — nonvisualization of the gallbladder indicates cystic duct obstruction; use when ultrasound is equivocal)

• CT abdomen (detect complications — gangrenous, emphysematous, or perforated cholecystitis — and evaluate alternative diagnoses)

• Tokyo Guidelines 2018 severity grade (Grade I mild, Grade II moderate with marked local inflammation, Grade III severe with organ dysfunction)

DDx

Biliary colic (transient pain <4–6h, no fever or inflammatory signs) · acute cholangitis (jaundice + ductal dilation + Charcot triad) · gallstone pancreatitis (elevated lipase, epigastric-to-back pain) · perforated peptic ulcer (free air, sudden peritonitis) · inferior MI or acute hepatitis (ECG/troponin; transaminitis pattern)

Home Meds

• Hold: oral medications if NPO for surgery; convert essential medications to IV

• Hold/reverse: anticoagulants and antiplatelets pre-operatively

• Hold: nephrotoxins during AKI; resume post-operatively

Plan

CONSULT: Surgery (early laparoscopic cholecystectomy — definitive treatment) · Interventional Radiology (percutaneous cholecystostomy tube for high surgical risk or Grade III) · GI (concurrent choledocholithiasis requiring ERCP)

• Diagnosis (Tokyo Guidelines 2018): (A) local signs of inflammation — Murphy sign, RUQ pain/mass; (B) systemic signs — fever, elevated CRP/WBC; (C) characteristic imaging findings. Suspected = A + B; Definite = A + B + C

• Supportive care: NPO, IV fluids (lactated Ringer's), electrolyte correction; analgesia with ketorolac (Toradol) 15–30 mg IV (NSAIDs are effective for biliary pain) or an opioid; antiemetic — ondansetron (Zofran) 4 mg IV q8h

• Antibiotics: Grade I (mild) — cefazolin (Ancef) or ceftriaxone (Rocephin) 1–2 g IV q24h (and sometimes deferred if very early cholecystectomy planned); Grade II/III or toxic — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h, or ceftriaxone plus metronidazole (Flagyl) 500 mg IV q8h; add enterococcal coverage in severe or healthcare-associated disease

• Definitive treatment — early laparoscopic cholecystectomy: ideally within 24–72h of symptom onset; early surgery is superior to delayed/interval cholecystectomy (fewer complications, shorter total stay); intraoperative cholangiogram if a CBD stone is suspected

• High surgical risk / Grade III / unfit for surgery: percutaneous cholecystostomy tube placed by IR to drain and decompress as a temporizing or bridging measure, with interval cholecystectomy once the patient is stabilized

• Concurrent choledocholithiasis or cholangitis: ERCP to clear the duct, sequenced before or after cholecystectomy depending on presentation

• Antibiotic duration: discontinue within 24h after uncomplicated cholecystectomy; continue 4–7 days for perforation, abscess, gangrenous cholecystitis, or inadequate source control

• PT/OT: early mobilization post-operatively; VTE prophylaxis — enoxaparin (Lovenox) 40 mg SC daily

• Trend daily: RUQ exam, fever curve, white count, LFTs (rising bilirubin suggests a retained CBD stone), and cholecystostomy drain output if placed

• Escalation triggers: worsening pain or peritoneal signs, rising WBC/lactate, or hemodynamic instability → suspect gangrene, perforation, or emphysematous cholecystitis → urgent surgery; failure to improve on antibiotics within 24–48h → cross-sectional imaging for complications

• Discharge checklist: cholecystectomy completed or interval surgery scheduled; cholecystostomy tube care and follow-up if placed; antibiotics completed or appropriately stopped; LFTs normalizing; diet advanced as tolerated; surgical follow-up; return precautions for recurrent RUQ pain, fever, or jaundice

Red Flags

• Gangrenous cholecystitis (severe pain, high fever, marked leukocytosis) → urgent cholecystectomy

• Emphysematous cholecystitis (gas in the gallbladder wall, often diabetic/male, Clostridium) → high mortality, emergent surgery + broad antibiotics

• Perforation with bile peritonitis or pericholecystic abscess → emergent surgery

• Acalculous cholecystitis in a critically ill patient → rapid progression to gangrene; low threshold for imaging and drainage

• Marked jaundice/cholestasis → evaluate for concurrent CBD stone or cholangitis (different urgency, needs ERCP)

Senior IM Resident Pearls

• Early cholecystectomy wins. Operating within 24–72h beats waiting weeks for an "interval" procedure — fewer complications, shorter overall stay. Don't reflexively cool people off first.

• Mild LFT bumps are fine; big ones are not. Markedly elevated bilirubin/ALP in "cholecystitis" should make you look for a CBD stone or cholangitis before the OR.

• Think acalculous in the ICU. Unexplained sepsis in a fasting, TPN-dependent, or post-op critically ill patient — image the gallbladder; it progresses fast and is easy to miss.

• HIDA is the tiebreaker. When the ultrasound is equivocal, nonvisualization of the gallbladder on HIDA confirms cystic duct obstruction.

• NSAIDs work for biliary pain and may even reduce progression of biliary colic to cholecystitis — ketorolac is a reasonable first-line analgesic.

• Cholecystostomy is a bridge, not a cure. The high-risk patient still usually needs interval cholecystectomy once stabilized.

• Common mistake: stopping at "gallstones on ultrasound." Stones are common and incidental — you need wall thickening, pericholecystic fluid, or a sonographic Murphy to call cholecystitis.

Hepatobiliary — Biliary Obstruction

107. Biliary Obstruction / Choledocholithiasis

CBD stone or stricture/mass · cholestatic LFTs + ductal dilation · risk-stratify → ERCP vs MRCP/EUS · clear duct + treat cause · Super Compact

Sx: RUQ/epigastric pain + jaundice · dark urine + pale/acholic stools + pruritus · nausea · may be asymptomatic with only abnormal LFTs (painless jaundice + wt loss → suspect malignancy)

Neg: denies fever/rigors + hypotension/AMS (cholangitis/Reynolds — if present escalate) · denies hepatitic AST/ALT in thousands w/o dilation (hepatocellular injury) · denies hemolysis labs (↑indirect bili, ↑LDH, ↓hapto → prehepatic jaundice) · denies Murphy + GB wall changes (cholecystitis)

SHx: gallstone risk (female, obesity, age) · prior cholecystectomy (retained/recurrent CBD stone) · alcohol · weight loss/malignancy risk · prior biliary surgery/PSC

Etiology: choledocholithiasis (#1 — CBD stone, primary or migrated from GB) · benign stricture (post-op, chronic pancreatitis, PSC) · malignant obstruction (pancreatic head, cholangiocarcinoma, ampullary, nodal) · parasitic · Mirizzi syndrome (stone in cystic duct compressing CHD)

RF: cholelithiasis · prior cholecystectomy · increasing age · chronic pancreatitis/PSC · malignancy risk factors

Data: CMP/LFTs (cholestatic pattern: ↑↑direct bili + ↑↑ALP + ↑GGT >> transaminases) · CBC (WBC — leukocytosis suggests superimposed cholangitis) · lipase (gallstone pancreatitis) · coags/INR (↑ from fat-soluble vit K malabsorption; pre-procedure) · GGT (confirms biliary source of ↑ALP) · CA 19-9 (if malignancy suspected — not for acute dx) · RUQ ultrasound (first: CBD >6 mm, ductal dilation, stones) · MRCP (noninvasive, defines stones/strictures/anatomy) · EUS (most sensitive for small distal CBD stones; tissue if mass) · ERCP (diagnostic + therapeutic — reserve for high-probability/therapeutic intent) · ASGE risk stratification (high/intermediate/low likelihood of CBD stone)

DDx: acute cholangitis (obstruction + infection: fever, Charcot) · malignant obstruction (painless jaundice, mass, Courvoisier, ↑CA19-9) · hepatocellular jaundice (hepatitis — AST/ALT pattern) · hemolysis/Gilbert (indirect hyperbilirubinemia, normal ALP)

Home Meds: hold/reverse anticoagulants/antiplatelets pre-ERCP · hold oral meds if NPO for procedure · continue essentials IV · supplement vitamin K if coagulopathic from cholestasis

Plan

CONSULT: GI (ERCP for stone extraction / stent) · Surgery (cholecystectomy ± CBD exploration; if ERCP fails) · Oncology + IR/EUS (if malignant obstruction — tissue + stent) · Hepatology (PSC/complex)

– Risk-stratify (ASGE) for CBD stone: high probability (CBD stone on US, total bili >4 + dilated CBD, ascending cholangitis) → proceed directly to ERCP; intermediate → MRCP or EUS first to confirm before ERCP; low → cholecystectomy with intraoperative cholangiogram, no upfront ERCP
– If cholangitis present (fever + cholestasis + obstruction): this is a "drain or die" emergency — blood cultures ×2, empiric antibiotics now — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h (or ceftriaxone (Rocephin) 2 g IV q24h + metronidazole (Flagyl) 500 mg IV q8h; carbapenem if severe/healthcare-associated) — sepsis resuscitation, then urgent ERCP biliary drainage within 24h (emergent if septic shock/Reynolds pentad); PTC drainage if ERCP fails
– Supportive: IV fluids, analgesia, antiemetics; correct coagulopathy — vitamin K (phytonadione) 10 mg IV/SC if INR elevated from cholestasis
– Definitive — clear the duct: ERCP with sphincterotomy + stone extraction (balloon/basket) ± temporary stent; large/impacted stones → mechanical lithotripsy, cholangioscopy with laser/EHL; failed ERCP → percutaneous (PTC) or surgical CBD exploration
– Gallbladder still in place + gallstone source: laparoscopic cholecystectomy (same admission preferred) after duct cleared to prevent recurrence
– Malignant obstruction: EUS/ERCP for tissue diagnosis + biliary stent (metal vs plastic per resectability); staging CT/MRI; multidisciplinary oncology/surgery planning; relieve obstruction before chemotherapy
– Stricture: brushings/biopsy to exclude malignancy; dilation ± stenting
– A dilated CBD with cholestatic LFTs and no fever is obstruction; add fever/leukocytosis and it becomes cholangitis — the same anatomy, but the second one needs urgent drainage.
– PT/OT: mobilize post-procedure
– Trend daily: LFTs/bilirubin (should fall after duct cleared), WBC/fever (watch for post-ERCP cholangitis/pancreatitis), lipase (post-ERCP pancreatitis), coags
– Escalation triggers: fever + rising WBC + worsening LFTs → cholangitis → urgent drainage; post-ERCP severe abdominal pain + ↑lipase → post-ERCP pancreatitis management; failure of bilirubin to fall after drainage → retained stone/incomplete clearance → reimage/repeat
– Discharge checklist: duct clearance documented; cholecystectomy done/scheduled if gallstone source; stent in place noted with removal/exchange plan; malignancy pathway arranged if applicable; LFTs trending down; GI/surgery/oncology follow-up; return precautions (fever, jaundice, RUQ pain, pale stools)

107. Biliary Obstruction / Choledocholithiasis

complete reference · CBD stones + strictures + malignant obstruction · ASGE risk stratification · ERCP vs MRCP/EUS · Full Card

Symptoms / Associated Sx

• Right upper quadrant or epigastric pain with jaundice; dark urine, pale/acholic stools, and pruritus from cholestasis

• Nausea, anorexia; may be entirely asymptomatic with only incidentally abnormal LFTs

• Painless, progressive jaundice with weight loss and a palpable nontender gallbladder (Courvoisier sign) shifts suspicion toward malignant obstruction

Neg

• Pt denies fever/rigors + hypotension + altered mental status — argues against acute cholangitis superimposed on the obstruction (if present, escalate to urgent drainage)

• Pt denies a hepatocellular pattern (AST/ALT in the thousands) without ductal dilation — argues against acute hepatitis as the cause of jaundice

• Pt denies indirect hyperbilirubinemia with normal ALP, elevated LDH, and low haptoglobin — argues against hemolysis or Gilbert syndrome (prehepatic/unconjugated causes)

Social History (SHx)

• Gallstone risk factors: female sex, obesity, increasing age, rapid weight loss

• Prior cholecystectomy (retained or recurrent CBD stones)

• Alcohol use; weight loss and constitutional symptoms (malignancy risk)

• Prior biliary surgery, chronic pancreatitis, primary sclerosing cholangitis (stricture risk)

Main Etiology

• Choledocholithiasis — most common; either secondary stones that migrate from the gallbladder into the CBD or primary stones formed within the duct

• Benign strictures — post-surgical, chronic pancreatitis, PSC

• Malignant obstruction — pancreatic head adenocarcinoma, cholangiocarcinoma, ampullary carcinoma, or malignant porta hepatis nodes

• Mirizzi syndrome — a stone impacted in the cystic duct or gallbladder neck extrinsically compresses the common hepatic duct

• Parasitic obstruction in endemic regions

RF

• Modifiable: gallstone disease management, timely cholecystectomy

• Non-modifiable: prior cholecystectomy, age, chronic pancreatitis/PSC, malignancy risk factors

Data

• CMP / LFTs (cholestatic pattern — elevated direct bilirubin, alkaline phosphatase, and GGT out of proportion to transaminases; degree of bilirubin elevation aids ASGE risk stratification)

• CBC (leukocytosis suggests superimposed cholangitis)

• Lipase (concurrent gallstone pancreatitis)

• Coagulation studies / INR (may be elevated from impaired vitamin K absorption in chronic cholestasis; needed before ERCP/sphincterotomy)

• GGT (confirms a biliary/hepatic source of an elevated alkaline phosphatase)

• CA 19-9 (when malignancy is suspected — supportive, not diagnostic, and falsely elevated by cholestasis itself)

• RUQ ultrasound (first-line) (common bile duct dilation >6 mm, intrahepatic ductal dilation, choledocholithiasis; limited sensitivity for distal CBD stones)

• MRCP (noninvasive, excellent for defining stones, strictures, and biliary/pancreatic ductal anatomy)

• Endoscopic ultrasound (EUS) (most sensitive for small distal CBD stones and microlithiasis; allows tissue sampling of masses)

• ERCP (both diagnostic and therapeutic — reserve for high probability of a stone or when intervention is intended, given pancreatitis/bleeding/perforation risks)

• ASGE risk stratification (combines bilirubin, CBD diameter, and clinical features into high/intermediate/low likelihood of choledocholithiasis to guide which test comes next)

DDx

Acute cholangitis (obstruction plus infection — fever, Charcot triad) · malignant biliary obstruction (painless jaundice, weight loss, Courvoisier sign, mass on imaging) · hepatocellular jaundice (viral/alcoholic hepatitis — transaminase-predominant) · hemolysis or Gilbert syndrome (unconjugated hyperbilirubinemia, normal alkaline phosphatase)

Home Meds

• Hold/reverse: anticoagulants and antiplatelets before ERCP with anticipated sphincterotomy

• Hold: oral medications if NPO for procedure; convert essentials to IV

• Supplement: vitamin K (phytonadione) for coagulopathy from chronic cholestasis

Plan

CONSULT: GI (ERCP for stone extraction and/or stenting) · Surgery (cholecystectomy with or without CBD exploration; salvage if ERCP fails) · Oncology + EUS/IR (malignant obstruction — tissue diagnosis and stenting) · Hepatology (PSC or complex strictures)

• Risk-stratify for a CBD stone (ASGE): high probability (CBD stone visualized on ultrasound, total bilirubin >4 mg/dL with a dilated CBD, or clinical ascending cholangitis) → proceed directly to ERCP; intermediate probability → confirm first with MRCP or EUS before committing to ERCP; low probability → laparoscopic cholecystectomy with intraoperative cholangiogram rather than upfront ERCP

• If cholangitis is present (fever + cholestasis on a background of obstruction): treat as a biliary emergency — obtain blood cultures, start empiric antibiotics immediately (piperacillin-tazobactam (Zosyn) 4.5 g IV q6h, or ceftriaxone (Rocephin) 2 g IV q24h plus metronidazole (Flagyl) 500 mg IV q8h; a carbapenem such as meropenem 1 g IV q8h for severe or healthcare-associated disease, with enterococcal coverage in severe cases), resuscitate per sepsis protocol, and proceed to urgent ERCP biliary drainage within 24h (emergent in septic shock or Reynolds pentad — Charcot triad plus hypotension and altered mental status); percutaneous transhepatic drainage if ERCP fails or is unavailable; antibiotics continue 4–7 days after adequate drainage

• Supportive: IV fluids, analgesia, antiemetics; correct coagulopathy with vitamin K (phytonadione) 10 mg IV/SC if the INR is elevated from cholestasis

• Definitive — clear the duct: ERCP with sphincterotomy and stone extraction by balloon or basket, with a temporary stent as needed; large or impacted stones may require mechanical lithotripsy or cholangioscopy-guided laser/electrohydraulic lithotripsy; if ERCP fails, percutaneous transhepatic approach or surgical CBD exploration

• Gallbladder in situ with a gallstone source: laparoscopic cholecystectomy (preferably same admission) after the duct is cleared, to prevent recurrent stones and biliary events

• Malignant obstruction: EUS/ERCP for tissue diagnosis and biliary stenting (self-expanding metal stent if unresectable, plastic if resection planned or short-term); staging cross-sectional imaging; multidisciplinary oncology and surgical planning; relieve obstruction and normalize bilirubin before systemic chemotherapy

• Stricture: brushings and biopsy to exclude malignancy; balloon dilation with or without stenting

• PT/OT: mobilization after the procedure

• Trend daily: LFTs and bilirubin (should fall after the duct is cleared), white count and fever curve (post-ERCP cholangitis), lipase (post-ERCP pancreatitis), and coagulation studies

• Escalation triggers: fever with rising WBC and worsening LFTs → cholangitis requiring urgent drainage; severe post-ERCP abdominal pain with elevated lipase → manage post-ERCP pancreatitis; failure of bilirubin to decline after drainage → retained stone or incomplete clearance, reimage and repeat intervention

• Discharge checklist: documented duct clearance; cholecystectomy performed or scheduled for a gallstone source; any stent recorded with a removal/exchange plan; malignancy diagnostic and treatment pathway arranged when applicable; LFTs trending down; GI/surgery/oncology follow-up; return precautions for fever, jaundice, RUQ pain, or pale stools

Red Flags

• Fever + leukocytosis on a background of obstruction → ascending cholangitis → urgent biliary drainage

• Painless jaundice + weight loss + Courvoisier sign → malignant obstruction until proven otherwise → tissue + staging

• Rising bilirubin with worsening coagulopathy → significant cholestasis; correct vitamin K before intervention

• Post-ERCP severe pain with elevated lipase → post-ERCP pancreatitis (most common serious complication)

• Gallstone pancreatitis with persistent obstruction → may need urgent ERCP

Senior IM Resident Pearls

• Risk-stratify before you scope. ERCP carries real risk (pancreatitis, bleeding, perforation) — use ASGE criteria so high-probability stones go straight to ERCP while intermediate ones get a confirmatory MRCP/EUS first.

• Pattern recognition on the LFTs: cholestatic (ALP/GGT/direct bilirubin dominant) points to obstruction; hepatocellular (AST/ALT dominant) points to liver parenchyma. This single read directs the entire workup.

• Obstruction vs cholangitis is one fever apart. A dilated duct with cholestasis but no fever is plumbing; add fever/leukocytosis and it's an infected, high-pressure system needing urgent drainage.

• EUS finds what ultrasound misses — small distal CBD stones and microlithiasis hide near the ampulla where transabdominal ultrasound is blind.

• Don't forget the gallbladder. After clearing a CBD stone in a patient with an intact gallbladder, same-admission cholecystectomy prevents recurrence.

• CA 19-9 is a soft sign. It rises with benign cholestasis too — never diagnose malignancy on CA 19-9 alone; get tissue.

• Common mistake: sending every jaundiced gallstone patient straight to ERCP — low-probability patients are better served by cholecystectomy with intraoperative cholangiogram, sparing them procedural risk.

Hepatology — Alcohol-Associated Liver Disease

108. Severe Alcoholic Hepatitis

recent heavy use + rapid jaundice · AST:ALT >2, both <~400 · Maddrey ≥32 / MELD = severe · steroids by Lille · abstinence + nutrition · Super Compact

Sx: rapid-onset jaundice + RUQ pain/tender hepatomegaly · fever · anorexia/weight loss · in recent heavy drinker · ± ascites, HE, signs of decompensation (presents over weeks, often after a binge or just after stopping)

Neg: denies AST/ALT in thousands + viral/toxin exposure (acute viral/ischemic/acetaminophen hepatitis — different pattern) · denies biliary dilation + cholestatic-only LFTs (obstruction/cholangitis) · denies new mass + ↑AFP (HCC) · denies infection/GI bleed as sole driver (decompensation precipitant — still screen)

SHx: alcohol — quantify amount + duration + time of last drink (withdrawal risk) · prior alcohol-associated liver disease/cirrhosis · viral hepatitis risk · acetaminophen/other hepatotoxins

Etiology: chronic heavy alcohol use → hepatocyte injury, steatohepatitis, neutrophilic inflammation; often superimposed on underlying alcohol-associated fibrosis/cirrhosis; recent heavy intake the proximate trigger

RF: heavy/prolonged alcohol use · female sex (greater susceptibility) · obesity/metabolic syndrome · underlying cirrhosis · concurrent viral hepatitis · malnutrition

Data: LFTs (AST:ALT >2, classically both <~300–400; AST rarely >500 — if higher, reconsider dx) · bilirubin (↑↑ direct/total — severity + Maddrey/MELD/Lille) · INR/PT (synthetic function, Maddrey) · CBC (leukocytosis/neutrophilia even without infection; macrocytosis; thrombocytopenia) · CMP (Cr — AKI/HRS worsens prognosis; Na; glucose) · GGT (↑, supports alcohol) · Maddrey discriminant function (4.6×(PT−control) + total bili; ≥32 = severe) · MELD (>20 severe; prognosis) · viral hepatitis serologies + acetaminophen level + autoimmune/iron/ceruloplasmin (exclude other causes) · cultures/CXR/UA/ascitic tap (infection screen — common + alters steroid decision) · RUQ US w/ Doppler (exclude obstruction, HCC, PVT)

DDx: acute viral/ischemic/acetaminophen hepatitis (AST/ALT in thousands, exposure) · decompensated cirrhosis from other cause (no recent heavy use, alt etiology) · ascending cholangitis/obstruction (cholestatic, ductal dilation, Charcot) · NASH/drug-induced liver injury (history, milder, no heavy alcohol)

Home Meds: stop all alcohol; hold hepatotoxins (avoid acetaminophen >2 g/day; stop methotrexate etc.) · continue thiamine + folate + multivitamin · hold nephrotoxins (NSAIDs) · adjust sedatives — use CIWA-guided withdrawal management cautiously (lorazepam preferred in liver disease)

Plan

CONSULT: Hepatology (severity, steroids, transplant candidacy) · Nutrition (aggressive feeding) · Social work/Addiction medicine (alcohol use disorder treatment) · Transplant center (early referral in steroid-nonresponders at experienced centers)

– Diagnose & stage: clinical AH (recent heavy use, rapid jaundice, AST:ALT >2 with both typically <400) + calculate Maddrey DF and MELD; biopsy (transjugular) only if diagnosis uncertain
– Universal supportive care (benefits all): complete alcohol cessation; thiamine 100–500 mg IV before any glucose, then daily; folate, multivitamin; aggressive nutrition — 1.2–1.5 g/kg protein and 35 kcal/kg/day, enteral/NG feeding if intake poor (malnutrition is universal and drives mortality — do NOT protein-restrict)
– Withdrawal: CIWA-guided benzodiazepines — lorazepam (Ativan) preferred (no hepatic oxidation); monitor for HE
– Screen & treat infection before and during steroids (cultures, CXR, UA, diagnostic paracentesis) — active uncontrolled infection is a contraindication to steroids
– Corticosteroids (severe only, Maddrey ≥32 or MELD >20): prednisolone (not prednisone — no hepatic conversion needed) 40 mg PO daily ×28 days then taper; contraindicated with active infection, GI bleeding, HRS, uncontrolled — stabilize first
– Assess response — Lille score at day 7: Lille <0.45 = responder → complete 28-day course; Lille ≥0.45 = nonresponder → stop steroids (no benefit, ongoing infection risk) and pursue transplant evaluation
– Manage decompensation inline: ascites — sodium restriction (<2 g/day) + diuretics (spironolactone (Aldactone) 100 mg + furosemide (Lasix) 40 mg PO daily, 100:40 ratio) + large-volume paracentesis with albumin 6–8 g/L removed if tense; HE — lactulose 30 mL PO/NG titrated to 2–3 soft stools/day + rifaximin (Xifaxan) 550 mg PO BID, identify precipitants (infection, GI bleed, electrolytes); variceal bleed — octreotide (Sandostatin) 50 mcg IV bolus then 50 mcg/h, ceftriaxone (Rocephin) 1 g IV daily prophylaxis, urgent EGD with band ligation, restrictive transfusion (Hgb 7); HRS-AKI — albumin 1 g/kg/day + vasoconstrictor (norepinephrine, or midodrine + octreotide) + nephrology — portends very poor prognosis
– Transplant: early liver transplant for carefully selected steroid-nonresponders at experienced centers improves survival (challenges traditional abstinence-period requirements)
– STOPAH (2015): prednisolone gave a modest short-term (28-day) mortality benefit with no benefit at 90 days/1 year, and pentoxifylline showed no benefit — set expectations and prioritize abstinence + nutrition + infection control.
– PT/OT: mobilization, nutrition reinforcement, fall precautions if HE
– Trend daily: bilirubin/INR (Lille trajectory), mental status (HE), Cr (HRS), infection signs/cultures, glucose, electrolytes, nutritional intake
– Escalation triggers: grade 3–4 HE/airway → ICU; rising Cr/HRS → vasoconstrictor + albumin + transplant eval; new/uncontrolled infection → stop steroids, treat; multi-organ failure (ACLF) → ICU + transplant urgency
– Discharge checklist: structured alcohol use disorder treatment (counseling, pharmacotherapy — naltrexone/acamprosate as liver function allows), thiamine/folate/multivitamin, nutrition plan, hepatology + transplant follow-up, HCC/varices surveillance per cirrhosis, vaccinate (HAV/HBV/pneumococcal/influenza), return precautions (confusion, bleeding, fever, jaundice worsening, decreased urine)

108. Severe Alcoholic Hepatitis

complete reference · Maddrey / MELD severity · prednisolone by Lille response · abstinence + nutrition + transplant · Full Card

Symptoms / Associated Sx

• Rapid-onset jaundice (over weeks) in a patient with recent heavy alcohol use, often presenting during or shortly after a period of increased drinking

• RUQ/epigastric pain, tender hepatomegaly, fever, anorexia, nausea, weight loss, malaise

• Signs of hepatic decompensation: ascites, hepatic encephalopathy, peripheral edema; features of chronic liver disease if underlying cirrhosis

Neg

• Pt denies AST/ALT elevations in the thousands + viral prodrome/toxin or acetaminophen exposure — argues against acute viral, ischemic, or acetaminophen-induced hepatitis (alcoholic hepatitis classically has AST:ALT >2 with both usually <300–400)

• Pt denies biliary ductal dilation + an isolated cholestatic LFT pattern + Charcot triad — argues against biliary obstruction or cholangitis

• Pt denies a new hepatic mass + rising AFP — argues against hepatocellular carcinoma as the driver (still screen given underlying liver disease)

Social History (SHx)

• Alcohol: quantify daily amount, duration of heavy use, and time of last drink (withdrawal risk and timing of CIWA monitoring)

• Prior alcohol-associated liver disease or established cirrhosis, prior episodes of alcoholic hepatitis

• Viral hepatitis risk factors; use of acetaminophen and other hepatotoxins

• Nutritional status and social supports (central to prognosis and recovery)

Main Etiology

• Chronic heavy alcohol use drives hepatocyte injury, steatosis progressing to steatohepatitis, neutrophilic inflammation, and ballooning degeneration (Mallory-Denk bodies on histology)

• Frequently superimposed on underlying alcohol-related fibrosis or cirrhosis

• A recent increase in alcohol intake is typically the proximate trigger for the acute episode

RF

• Modifiable: amount and duration of alcohol use, obesity/metabolic syndrome, malnutrition, concurrent viral hepatitis

• Non-modifiable: female sex (greater susceptibility per gram of alcohol), genetic predisposition, established cirrhosis

Data

• LFTs (AST:ALT ratio >2 is characteristic; both transaminases usually <300–400 and AST rarely exceeds 500 — higher values should prompt reconsideration of the diagnosis)

• Total/direct bilirubin (marked elevation reflects severity and feeds the Maddrey, MELD, and Lille scores)

• INR/PT (synthetic dysfunction; component of Maddrey discriminant function and MELD)

• CBC (leukocytosis with neutrophilia can occur without infection; macrocytosis from alcohol/folate deficiency; thrombocytopenia from portal hypertension/marrow suppression)

• CMP (creatinine — AKI/hepatorenal syndrome markedly worsens prognosis; sodium; glucose)

• GGT (elevated, supports an alcohol-related process)

• Maddrey discriminant function (4.6 × [patient PT − control PT] + total bilirubin; a value ≥32 defines severe disease and historically guided steroid use)

• MELD score (>20 indicates severe disease; prognostic and used for transplant assessment)

• Viral hepatitis serologies, acetaminophen level, autoimmune markers, iron studies, ceruloplasmin (systematically exclude other causes of acute liver injury)

• Infection workup — blood and urine cultures, chest radiograph, diagnostic paracentesis if ascites (infection is common, worsens outcomes, and is a contraindication to steroids until controlled)

• RUQ ultrasound with Doppler (exclude biliary obstruction, assess for HCC and portal vein thrombosis)

• Transjugular liver biopsy (reserved for diagnostic uncertainty; confirms alcoholic steatohepatitis when the clinical picture is atypical)

DDx

Acute viral, ischemic, or acetaminophen hepatitis (transaminases in the thousands, identifiable exposure) · decompensated cirrhosis from another etiology (no recent heavy drinking, alternative cause) · ascending cholangitis/biliary obstruction (cholestatic pattern, ductal dilation, Charcot triad) · NASH or drug-induced liver injury (history, generally milder, absent heavy alcohol use)

Home Meds

• Stop: all alcohol; treat withdrawal with CIWA-guided benzodiazepines (lorazepam (Ativan) preferred — not hepatically oxidized)

• Hold/limit: hepatotoxins — limit acetaminophen to ≤2 g/day, stop methotrexate and other hepatotoxic agents; avoid NSAIDs (renal/HRS risk)

• Continue: thiamine, folate, and a multivitamin; treat magnesium/phosphate deficiencies

Plan

CONSULT: Hepatology (severity assessment, steroid decision, transplant candidacy) · Nutrition (aggressive enteral support) · Addiction medicine / Social work (alcohol use disorder treatment) · Transplant center (early referral for selected steroid-nonresponders at experienced programs)

• Diagnose and stage: clinical diagnosis of alcoholic hepatitis (recent heavy use, rapid jaundice, AST:ALT >2 with transaminases typically <400) after excluding other causes; calculate Maddrey discriminant function and MELD; transjugular biopsy only when the diagnosis is uncertain

• Universal supportive care (benefits every patient): complete and immediate alcohol cessation; thiamine 100–500 mg IV before any glucose-containing fluids, then daily; folate and multivitamin; aggressive nutrition targeting 1.2–1.5 g/kg/day protein and ~35 kcal/kg/day with enteral or nasogastric feeding if oral intake is inadequate — malnutrition is nearly universal and independently predicts mortality, so do not protein-restrict even with encephalopathy

• Alcohol withdrawal: CIWA-Ar–guided benzodiazepines, using lorazepam (Ativan) given its lack of hepatic oxidative metabolism; monitor closely for precipitating hepatic encephalopathy

• Screen for and treat infection before and during corticosteroid therapy — blood/urine cultures, chest radiograph, and diagnostic paracentesis; active uncontrolled infection contraindicates steroids and must be treated first

• Corticosteroids for severe disease (Maddrey ≥32 or MELD >20): prednisolone 40 mg PO daily for 28 days followed by a taper (prednisolone is used rather than prednisone because it does not require hepatic conversion); contraindicated with active infection, GI bleeding, or hepatorenal syndrome until these are controlled

• Assess steroid response with the Lille score at day 7: a score <0.45 identifies responders who should complete the 28-day course; a score ≥0.45 identifies nonresponders in whom steroids should be stopped (no survival benefit and continued infection risk) and transplant evaluation pursued

• Manage hepatic decompensation inline:

• • Ascites: sodium restriction (<2 g/day) with diuretics — spironolactone (Aldactone) 100 mg plus furosemide (Lasix) 40 mg PO daily, titrated in a 100:40 ratio; large-volume paracentesis for tense or refractory ascites with IV albumin 6–8 g per liter of fluid removed

• • Hepatic encephalopathy: lactulose 30 mL PO/NG titrated to 2–3 soft stools daily, plus rifaximin (Xifaxan) 550 mg PO BID; identify and treat precipitants (infection, GI bleeding, electrolyte derangement, constipation) — and do not protein-restrict

• • Variceal bleeding: octreotide (Sandostatin) 50 mcg IV bolus then 50 mcg/h infusion, prophylactic ceftriaxone (Rocephin) 1 g IV daily, urgent EGD with endoscopic band ligation, restrictive transfusion to a hemoglobin target of 7 g/dL, and consideration of TIPS for refractory bleeding

• • Hepatorenal syndrome (HRS-AKI): IV albumin 1 g/kg/day with a vasoconstrictor (norepinephrine in the ICU, or midodrine plus octreotide on the floor; terlipressin where available) and nephrology involvement; HRS-AKI in this setting carries a particularly poor prognosis

• Early liver transplantation for carefully selected corticosteroid-nonresponders at experienced centers improves survival and increasingly challenges rigid pre-transplant abstinence requirements

• PT/OT: mobilization, ongoing nutritional reinforcement, and fall precautions if encephalopathic

• Trend daily: bilirubin and INR (Lille trajectory), mental status (encephalopathy), creatinine (hepatorenal syndrome), signs of infection and culture results, glucose and electrolytes, and nutritional intake

• Escalation triggers: grade 3–4 encephalopathy or airway compromise → ICU and airway protection; rising creatinine/HRS → vasoconstrictor plus albumin and transplant evaluation; new or uncontrolled infection → discontinue steroids and treat; multi-organ failure (acute-on-chronic liver failure) → ICU and urgent transplant consideration

• Discharge checklist: structured alcohol use disorder treatment (counseling and pharmacotherapy such as naltrexone or acamprosate as hepatic function permits); thiamine, folate, and multivitamin; a nutrition plan; hepatology and transplant follow-up; HCC surveillance with ultrasound (± AFP) every 6 months and endoscopic varices surveillance; vaccination for hepatitis A, hepatitis B, pneumococcus, and influenza; return precautions for confusion, bleeding, fever, worsening jaundice, or decreased urine output

Red Flags

• Hepatorenal syndrome / rising creatinine → markedly worse prognosis → vasoconstrictor + albumin + expedited transplant evaluation

• Grade 3–4 hepatic encephalopathy with airway risk → ICU, airway protection

• Active uncontrolled infection or sepsis → contraindicates steroids; treat first, as it is a leading cause of death

• GI/variceal bleeding → octreotide (Sandostatin) infusion, prophylactic ceftriaxone, urgent EGD with band ligation, restrictive transfusion (Hgb 7); contraindicates steroids until controlled

• Lille ≥0.45 at day 7 (steroid nonresponse) → very high short-term mortality → stop steroids, pursue transplant

• Acute-on-chronic liver failure with multi-organ failure → ICU, transplant urgency

Senior IM Resident Pearls

• AST:ALT >2 with modest absolute values is the fingerprint — if transaminases are in the thousands, it is not alcoholic hepatitis; look for viral, ischemic, or acetaminophen injury.

• Prednisolone, not prednisone. The diseased liver can't reliably convert prednisone to its active form — use prednisolone, and only in severe disease (Maddrey ≥32 / MELD >20) after excluding infection and bleeding.

• STOPAH reset expectations (2015): prednisolone offers at most a modest 28-day mortality benefit and none at 90 days or 1 year; pentoxifylline showed no benefit. Abstinence, nutrition, and infection control drive long-term outcomes.

• Check the Lille score at day 7. Nonresponders (≥0.45) get no further benefit from steroids and should stop — continuing only adds infection risk.

• Feed them. Malnutrition is universal and lethal; never protein-restrict, even with encephalopathy — use a late-evening snack and enteral feeding if needed.

• Lorazepam for withdrawal in liver disease — it bypasses hepatic oxidation, unlike diazepam/chlordiazepoxide whose active metabolites accumulate.

• Common mistake: giving steroids to a patient with occult infection — always pan-culture and tap the ascites first; an untreated infection turns a steroid course lethal.