When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

RoundsRx

Dashboard

Overview

Recent

Rotations

Quick Reference

Antibiotic Guide Analgesia Guide Sedation Guide Bowel Regimen Electrolyte Replacement Pain Management & Conversions Drug Interactions Anticoag Reversal IV Fluid Guide Inotropes Guide Vasopressors Insulin Guide Code Blue & Rapid Response Procedures Guide ECG Interpretation Lab Interpretation Radiology Quick Ref GCS Pocket Card Admission Orders & I-PASS Landmark Trials

Tools

💎 Clinical Pearls 🧠 Pimp Me Quiz 🧮 Clinical Calculators 📰 What's New 🎓 Intern Survival Guide ✅ Rounding Checklists 🩺 Procedure Guides ⚡ Electrolyte Replacement 💧 IV Fluids Guide 🩸 Transfusion Guide 💓 ECG Pattern Guide 🧪 Lab Interpretation Guide 📱 QR Poster 🔗 Resources 🎙️ Channels & Podcasts 🎮 Medical Games 🏛️ Famous Cases 🎬 Media Library

ℹ️ About

Available offline

EMERGENTICU / FloorGI / Hepatology

Hepatic Encephalopathy & Acute Liver Failure

Neuropsychiatric dysfunction from liver failure. In cirrhosis it's often episodic and reversible -find and treat the precipitant. Acute liver failure (ALF) is a different, more dangerous beast requiring ICU and transplant evaluation.

🔍 Overview

HE vs ALF -Two Different Conditions

Hepatic Encephalopathy (HE): Neuropsychiatric complications in a patient with pre-existing liver disease (cirrhosis). Usually reversible. Graded West Haven criteria 1–4.

Acute Liver Failure (ALF): Rapid hepatic necrosis in a previously healthy liver: coagulopathy (INR > 1.5) + encephalopathy without prior liver disease. Medical emergency requiring ICU + transplant evaluation.

Precipitants of HE -TIPS Mnemonic

T -Toxins/drugs (opioids, benzos, sedatives), Transjugular shunts
I -Infection (SBP is most common! -always tap ascites), Increased protein load (GI bleed)
P -Portal shunting, Portosystemic shunts
S -Sodium low (hyponatremia), Surgical stress, Starvation
Also: Constipation, Dehydration, Electrolyte disturbance (hypokalemia → alkalosis → ↑NH3)

Always perform diagnostic paracentesis in cirrhotic patient with new/worsening HE. SBP is the most commonly missed precipitant. PMN > 250/mm³ → SBP → treat even without symptoms.

Causes of Acute Liver Failure

Acetaminophen toxicity (most common in US -50%)
Viral hepatitis (HAV, HBV, HEV)
Drug-induced (isoniazid, amoxicillin-clavulanate, NSAIDs)
Autoimmune hepatitis
Ischemic hepatitis ("shock liver")
Wilson's disease, Budd-Chiari, pregnancy-related (AFLP, HELLP)

🧪 Workup & Diagnosis

Workup

For Hepatic Encephalopathy

LFTs, INR/PT -severity of liver dysfunction (most critical for staging)
Ammonia -confirms HE but does NOT correlate well with grade. Trend more useful than single value.
BMP -Na (hyponatremia worsens HE), K, BUN/Cr (renal function -HRS?)
CBC -infection? thrombocytopenia (cirrhosis)?
Diagnostic paracentesis -PMN count > 250 = SBP (most commonly missed precipitant); do this early
Blood cultures + UA + urine culture -rule out infection triggering HE
CXR -pulmonary infection
Head CT -if focal neuro deficits or unclear diagnosis (rule out structural cause); not routine

For ALF -Additional

Acetaminophen level -most common cause of ALF in US (50%); check even without clear history
Toxicology screen -rule out other drug/toxin causes
Viral hepatitis panel (HAV IgM, HBsAg, HBV DNA, HCV RNA) -2nd most common etiology group
Autoimmune hepatitis (ANA, ASMA, IgG) -treatable, do not miss
Pregnancy test -AFLP and HELLP are obstetric emergencies
Wilson's disease (ceruloplasmin, Kayser-Fleischer rings, urine copper) -rare but treatable in young patients
Contact transplant hepatology early in ALF -before deterioration

🚨 Management

Management: Hepatic Encephalopathy

Find and Treat the Precipitant

This is the most important step. Treat infection (SBP, pneumonia, UTI). Stop offending medications. Correct electrolytes. Treat GI bleed. Relieve constipation. Correct dehydration.

Lactulose (First-Line)

Lactulose 25–30 g PO/NG q1–2h until bowel movement, then titrate to 2–3 soft stools/day. Mechanism: acidifies colon → traps NH4⁺ → reduces ammonia absorption. If no PO/NG: lactulose enemas 300 mL in 700 mL water retention enema q6h.

🔄 Updated Practice: Old teaching: lactulose enemas are first-line for hepatic encephalopathy. Current practice: oral or NG lactulose is first-line (titrate to 3-4 soft stools per day). Rectal lactulose enemas (300 mL in 700 mL water) are reserved for patients who cannot take oral medications (e.g., grade III-IV HE with aspiration risk). Rifaximin (Xifaxan) 550 mg BID is added for secondary prevention of recurrence.

Rifaximin (Second-Line / Maintenance)

Rifaximin 550 mg PO BID -non-absorbable antibiotic that reduces gut ammonia-producing bacteria. Added to lactulose for recurrent or refractory HE. Significantly reduces HE recurrence Bass, 2010.

Airway Protection

Grade 3–4 HE (stupor/coma) → high risk of aspiration. Consider intubation early for airway protection, especially before procedures (paracentesis, endoscopy, LP).

Swipe for more examples

📋 Case 1, Hepatic Encephalopathy Management

Patient: 62M with alcoholic cirrhosis (Child-Pugh C), brought in confused and somnolent. Asterixis present. NH3 68.
Grade: West Haven Grade 3 (somnolent but arousable, confused, asterixis).
Identify precipitant: Infection (SBP? UTI? Pneumonia?), GI bleed, constipation, medications (benzos, opioids), electrolyte derangement (hypokalemia, hyponatremia), non-compliance with lactulose. Check: CBC, BMP, UA, CXR, blood cultures, diagnostic paracentesis (ALWAYS if ascites -rule out SBP).
Treatment:
- Lactulose (Kristalose) 30mL PO/NG q1-2h until first bowel movement → then titrate to 3-4 soft stools/day. Can give as enema (300mL in 700mL water) if unable to take PO.
- Rifaximin (Xifaxan) 550mg PO BID -add for prevention of recurrence (not just acute treatment). Reduces recurrence by 58%.
- Protein restriction is OUTDATED -maintain 1.2-1.5 g/kg/day protein. Malnutrition worsens encephalopathy.
- Zinc 220mg PO daily -zinc deficiency impairs urea cycle, worsening ammonia metabolism.
- 🔄 Updated Practice: Old teaching: restrict protein intake in hepatic encephalopathy to reduce ammonia production. Current practice: protein restriction is HARMFUL, it worsens malnutrition (which is already severe in cirrhosis) and does NOT improve encephalopathy. Maintain protein intake at 1.2-1.5 g/kg/day. Branched-chain amino acid supplements may help in protein-intolerant patients.
Key: NH3 level does NOT correlate with severity and should NOT be trended. Treat the patient, not the number. Lactulose titrated to stool output is the cornerstone.

📋 Case 2, Refractory Hepatic Encephalopathy

Patient: 61M with cirrhosis (Child-Pugh C), on lactulose and rifaximin, still Grade 3 HE (somnolent, confused). Ammonia 142.
Key concept: FIND THE PRECIPITANT, not just increase lactulose.
Precipitant checklist:
- GI bleed, do rectal exam. Melena?
- Infection / SBP, diagnostic paracentesis if ascites
- Constipation, when was last BM?
- Electrolyte abnormalities, hypokalemia and alkalosis worsen HE. Alkalosis converts NH4+ to NH3 which crosses BBB.
- Medications, benzos, opioids, PPIs. Stop all sedatives.
- Dehydration / renal failure
- Dietary protein excess, rare. Do NOT restrict protein; they need it.
- TIPS, if recent, may need revision.
Treatment:
- Lactulose titrated to 3-4 BMs/day (NOT diarrhea, diarrhea causes dehydration → worsens HE).
- Rifaximin 550 mg BID -non-absorbable antibiotic that reduces ammonia-producing gut bacteria. Add-on to lactulose for recurrent HE; reduces breakthrough episodes by ~50% and HE-related hospitalizations by ~50% per Bass NEJM 2010.
- Treat the precipitant -GI bleed, infection (especially SBP), AKI/dehydration, electrolyte derangement (esp. hypokalemia → ↑ ammonia), constipation, sedatives, dietary protein load, TIPS-related, HCC. Without precipitant control, HE recurs regardless of lactulose dose.
- Consider zinc supplementation (cofactor in the urea cycle; cirrhotics are commonly deficient and modest data support reduced HE recurrence with repletion).
Key Lesson: Refractory HE = hunt for the precipitant. The answer is almost never "more lactulose." Check for GI bleed, SBP, constipation, hypokalemia, and sedating medications.

📋 Case 3, HE Mimicker: Wernicke's Encephalopathy in Cirrhosis

Patient: 55M with alcoholic cirrhosis, admitted with confusion, ataxia, and nystagmus. Team starts lactulose for presumed HE. Ammonia is only 45 (mildly elevated, does not correlate with HE severity).
Clinical course: After 48h of lactulose, no improvement. Re-examine: classic triad of confusion + ataxia + ophthalmoplegia = Wernicke's encephalopathy from thiamine deficiency, NOT hepatic encephalopathy.
Treatment:
- IV thiamine 500mg TID × 3 days → 250mg daily × 5 days (high-dose Caine criteria dosing).
- Must give thiamine BEFORE glucose (glucose without thiamine precipitates Wernicke's).
- Improvement expected within hours to days.
Key Lesson: Not all confusion in cirrhotics is HE. Wernicke's and HE overlap significantly in alcoholic liver disease. Always give IV thiamine empirically. Ammonia levels do NOT reliably diagnose or exclude HE.

Management: Acute Liver Failure (ALF)

ICU admission -all ALF patients
N-acetylcysteine (NAC) -for acetaminophen ALF (and emerging evidence for non-acetaminophen ALF). 150 mg/kg IV over 1h, then 12.5 mg/kg/hr × 4h, then 6.25 mg/kg/hr × 16h. Start immediately if APAP toxicity possible.
Liver transplant evaluation immediately -contact transplant center
Manage ICP (cerebral edema risk in ALF) -head of bed 30°, avoid hypotonic fluids, consider ICP monitoring
Correct coagulopathy only if actively bleeding (do NOT give FFP prophylactically -INR is prognostic)
Avoid

💊 Medications

Medications -Hepatic Encephalopathy

Drug	Dose	Route	Notes
Lactulose (Kristalose) 1ST LINE	30 mL PO q1–2h until first BM → titrate to 3–4 soft stools/day	PO/NG/PR	Cornerstone of HE treatment. Acidifies colon → traps NH4+ → reduces ammonia absorption. Enema (300 mL in 700 mL water) if unable to take PO. Titrate to stool output, NOT ammonia level.
Rifaximin (Xifaxan)	550 mg PO BID	PO	Non-absorbable antibiotic. Added to lactulose for recurrence prevention -reduces HE recurrence by 58% RFHE, 2010. Not just for acute treatment. Well tolerated, minimal systemic absorption.
Zinc sulfate	220 mg PO daily	PO	Zinc deficiency impairs the urea cycle, worsening ammonia metabolism. Adjunctive therapy. Common deficiency in cirrhosis.
LOLA (L-ornithine L-aspartate)	Per protocol	PO/IV	Adjunct therapy. Provides substrates for ammonia metabolism (urea cycle and glutamine synthesis). Evidence modest -use as add-on when lactulose + rifaximin insufficient.
Metronidazole (Flagyl)	250 mg PO TID	PO	Only if rifaximin unavailable. Reduces ammonia-producing gut bacteria. Limit duration -neurotoxicity with prolonged use (peripheral neuropathy, cerebellar dysfunction). Not first-line.

Protein restriction is OUTDATED. Maintain 1.2–1.5 g/kg/day protein. Malnutrition worsens encephalopathy and increases mortality. Branched-chain amino acids (BCAA) may be beneficial if intolerant of standard protein.

📋 On Rounds

On Rounds

Pimp Questions

How does lactulose work in hepatic encephalopathy?

Lactulose is metabolized by colonic bacteria to lactic acid and acetic acid, lowering colonic pH. This acidic environment converts NH3 (which freely crosses intestinal epithelium) to NH4⁺ (which is charged and cannot be absorbed). It also acts as an osmotic cathartic, reducing intestinal transit time and ammonia absorption.

Why should you NOT give FFP prophylactically in ALF?

The INR in ALF reflects global coagulation factor deficiency and is used as a prognostic marker (part of King's College criteria for transplant listing). Correcting the INR with FFP obscures this prognostic marker without proven clinical benefit. Reserve FFP for active bleeding or before invasive procedures only.

What are the precipitants of hepatic encephalopathy and what's the mnemonic?

HEPATICS: H emorrhage (GI bleed → protein load → ammonia) · E lectrolytes (hypokalemia → increased renal ammonia production; hyponatremia) · P roteins (excessive dietary protein -rare cause, over-taught) · A nything that causes dehydration (diuretics, vomiting, diarrhea) · T IPS (shunting portal blood past the liver) · I nfection/SBP (most commonly missed precipitant -always do paracentesis) · C onstipation (decreased ammonia elimination) · S edatives (benzodiazepines, opioids -enhanced GABA sensitivity in cirrhosis). Most important: SBP and infection -check paracentesis fluid in every cirrhotic with altered mental status, even without abdominal pain or fever.

Why do you not chase the ammonia number?

Ammonia levels do not correlate well with the severity of hepatic encephalopathy and should not guide treatment. Reasons: (1) Ammonia is only one of many neurotoxins in HE -manganese, mercaptans, short-chain fatty acids, and inflammatory cytokines all contribute. (2) Venous ammonia levels don't reflect brain ammonia (arterial is slightly more reliable but still imperfect)

Clinical Examples

📋 Case 1, Overt HE Precipitated by GI Bleed

Patient: 61M with alcohol-related cirrhosis (Child-Pugh B), presents with confusion and asterixis. Found to have melena. Family reports increasing somnolence over 24 hours.

Key findings: Temp 37.4°C, HR 104, BP 102/58. Disoriented to time and place, asterixis present, no focal neurological deficits. West Haven Grade III. Hgb 7.8 (baseline 10.2), ammonia 142, Cr 1.6. CT head: no acute abnormality.

Management:

Lactulose 30 mL PO/NG q1-2h until first bowel movement, then titrate to 2-3 soft stools/day
Add rifaximin 550 mg BID (especially if recurrent episodes) Bass, 2010
Treat precipitant: GI bleed workup, transfuse to Hgb 7, start octreotide and ceftriaxone
Check for other precipitants: infection (SBP screen with paracentesis), electrolytes (hypokalemia, hyponatremia), constipation, medications (benzodiazepines, opioids)

Teaching point: Always identify and treat the precipitant. GI bleed is a common trigger because blood in the gut is a massive protein/nitrogen load that gut bacteria convert to ammonia. The ammonia level does NOT guide treatment -- treat the clinical grade.

📋 Case 2, Lactulose-Refractory HE

Patient: 58F with NASH cirrhosis, admitted 3 days ago with Grade III HE. On lactulose 30 mL q6h with 3-4 stools/day but remains persistently confused and intermittently combative.

Key findings: Still disoriented, asterixis present, no improvement in West Haven grade despite adequate lactulose. All precipitants addressed: no infection, electrolytes corrected, no offending medications. Ammonia trending down but mental status unchanged.

Management:

Ensure lactulose is actually producing stools (not just charted). Consider lactulose enemas (300 mL in 700 mL water PR) if oral route inadequate
Add rifaximin 550 mg BID if not already on it
Consider zinc supplementation 220 mg BID (cofactor for urea cycle; often deficient in cirrhotics)
Rule out alternative diagnoses: Wernicke encephalopathy (give thiamine), subdural hematoma, metabolic encephalopathy, occult seizures (consider EEG)

Teaching point: When HE does not respond to lactulose, broaden the differential. Cirrhotic patients can have multiple simultaneous causes of altered mental status. Do not anchor on HE alone.

📋 Case 3, Covert HE Affecting Quality of Life

Patient: 64M with compensated HCV cirrhosis (Child-Pugh A), referred by hepatologist for cognitive complaints. Wife reports he has become forgetful, has difficulty managing finances, and had a minor car accident last month. No overt confusion or asterixis.

Key findings: Alert, oriented x3, no asterixis. However, psychometric testing (Stroop test, number connection test) is abnormal. Ammonia 68. MRI brain: no structural abnormality. Diagnosis: Covert (minimal) hepatic encephalopathy.

Management:

Start rifaximin 550 mg BID (shown to improve cognitive function and driving performance in covert HE)
Lactulose 15-30 mL titrated to 2-3 soft stools/day
Counsel on driving safety: covert HE significantly impairs reaction time and is a recognized cause of motor vehicle accidents
Optimize nutrition: adequate protein intake (1.2-1.5 g/kg/day -- protein restriction is HARMFUL and outdated). Consider branched-chain amino acid supplementation

Teaching point: Covert HE affects up to 80% of cirrhotic patients and significantly impairs quality of life. Protein restriction is a harmful myth -- adequate protein intake is essential. Always screen for driving safety concerns.

📋 Sample Presentation

"Mr. Alvarez is a 54-year-old with decompensated cirrhosis from alcohol who presented with confusion and asterixis. This represents Grade 2 hepatic encephalopathy. We performed diagnostic paracentesis on admission which showed PMN count of 312 -consistent with SBP. He was started on cefotaxime and albumin per SBP protocol. Ammonia on admission was 118. He was started on lactulose -currently having 2–3 soft stools per day. He is more alert today, following commands, with ammonia down to 74. We are adding rifaximin for recurrence prevention. Rifaximin was not on his outpatient regimen. Repeat paracentesis is planned on day 5 to confirm SBP resolution."

Monitoring -Hepatic Encephalopathy

Parameter	Frequency	Target / Action
West Haven grade	q4–8h (more frequent if worsening)	Track mental status: orientation, asterixis, somnolence. Grade 3–4 → consider ICU for airway protection.
Asterixis	Each assessment	Negative myoclonus ("liver flap"). Presence confirms HE. Disappearance suggests improvement.
Orientation	Each assessment	Person, place, time, situation. Serial number connection test if able to participate.
Lactulose stool output	Strict I&O tracking	Target 3–4 stools/day. Too few → increase lactulose. Excessive diarrhea → dehydration → worsens HE.
Ammonia level	On admission only	Do NOT trend ammonia -it does NOT correlate with severity. An initial elevated ammonia supports the diagnosis but serial levels do not guide treatment. Treat clinically.
BMP (K+, Na+, Cr, BUN)	Daily	Hypokalemia → metabolic alkalosis → increased renal ammonia production → worsens HE. Hyponatremia worsens cerebral edema. Cr for HRS surveillance.
Infection workup	On admission + any worsening	CBC, blood cultures, UA/UCx, CXR, diagnostic paracentesis (rule out SBP -most commonly missed precipitant). Repeat paracentesis with any AMS change.

Treat the patient, not the ammonia number. Lactulose titrated to stool output + finding/treating the precipitant are the cornerstones. If mental status is improving, the treatment is working regardless of what the ammonia says.

⚡ Summary

Summary

HE First Move

Find the precipitant. Tap ascites (rule out SBP). Treat infection. Lactulose to 2–3 stools/day.

Medications

Lactulose (first-line). Rifaximin 550 mg BID added for recurrent/refractory HE RFHE, 2010.

Airway

Grade 3–4 HE → intubate for airway protection especially before procedures.

ALF

ICU + NAC (especially for APAP) + transplant evaluation immediately. Do not delay listing.

SBP Rule

Always tap ascites in new/worsening HE. PMN > 250 = SBP. Treat with cefotaxime + albumin.

Common Pitfall

Giving FFP in ALF (obscures prognosis). Not tapping ascites. Giving lactulose without finding precipitant.

📄 One Pager

GI · Hepatology · One Pager

Hepatic Encephalopathy / ALF

Find the precipitant first -especially SBP. Tap ascites. Lactulose to 2–3 stools/day. Add rifaximin for recurrence. ALF → ICU + NAC + transplant evaluation.

⚡ Precipitants -TIPS

T -Toxins/drugs, TIPS shunts
I -Infection (SBP!), increased protein
P -Portal shunting
S -Sodium (hyponatremia), starvation
Also: constipation, dehydration, hypokalemia

🧪 Always Tap Ascites

PMN > 250/mm³ = SBP
Treat: cefotaxime 2g IV q8h + albumin 1.5 g/kg day 1, 1 g/kg day 3
Most commonly missed precipitant

💊 HE Treatment

Lactulose25–30g q1–2h → 2–3 stools/day

Rifaximin550 mg PO BID Bass, 2010

Treat precipitantMost important step

🆘 ALF Management

ICU admission
NAC (especially APAP)
Transplant evaluation NOW
Do NOT correct INR prophylactically

⚠️ Pitfalls

Not tapping ascites
FFP prophylactically (obscures prognosis)
Grade 3–4 → intubate early
Lactulose without finding cause