NOTES:

Decompensated Cirrhosis

• Definition
  Decompensated cirrhosis (HE, variceal bleed, ascites): ~1–2 year survival

• Pathophysiology
  Cascade: Fibrotic liver obstructs portal flow → portal hypertension → splanchnic vasodilation pools blood away from central circulation → low effective arterial volume → RAAS/sympathetic activation causes Na/H₂O retention and renal vasoconstriction, worsening ascites/edema and risking HRS. Liver synthetic failure drops albumin (low oncotic pressure → edema) and clotting factors (coagulopathy); poor toxin clearance drives HE via ammonia.

• Compensated cirrhosis: ~10–15 year survival

• Late decompensation in cirrhosis
  Recurrent variceal bleeding, refractory ascites, hepatorenal syndrome, recurrent encephalopathy, and severe jaundice — these signal very high mortality and mandate urgent transplant evaluation.

• Creatinine (Cr)
  Detects AKI and hepatorenal syndrome, part of the MELD score; even small rises in cirrhosis are significant because muscle mass is low and Cr underestimates renal dysfunction.

• BUN
  Helps assess renal perfusion and volume status; in a GI bleed, BUN often rises from absorbed blood protein, and high BUN with rising Cr signals prerenal state or HRS in decompensated cirrhosis.

• Sodium (Na)
  Hyponatremia reflects severe vasodilation and RAAS/ADH activation (“hepatorenal physiology”) and is a poor prognostic sign; included in MELD-Na for transplant priority.

• Albumin
  Made by the liver; low levels indicate impaired synthetic function and more advanced, decompensated disease and are used in Child–Pugh. Low albumin also contributes to ascites and edema.

• Total bilirubin
  Elevates with impaired hepatic excretion or cholestasis and is another key marker of severity; included in both MELD and Child–Pugh scores.

• INR
  Reflects reduced hepatic synthesis of clotting factors; elongated INR shows synthetic failure and correlates with prognosis and bleeding risk; part of MELD and informs procedural/transfusion decisions.
  Normal INR: 0.8–1.2 (lab-specific); >1.5 in cirrhosis reflects synthetic failure.
  In cirrhosis, the liver produces clotting factors (except VIII) and anticoagulants (protein C/S, antithrombin), creating a rebalanced hemostasis—elevated INR reflects synthetic failure, not true bleeding risk, so correcting it with FFP rarely helps and risks overload (use only for procedures needing INR <2; vitamin K ineffective unless deficient). Patients risk both bleeding (varices, gastropathy) and clotting (PVT, DVT)—provide DVT prophylaxis unless actively bleeding or platelets critically low.

• Hemoglobin/Hematocrit
  Look for anemia from variceal or other GI bleeding, chronic disease, or nutritional deficiencies.

• WBC
  Leukocytosis may signal infection (SBP, pneumonia, UTI), a major trigger of decompensation; leukopenia can reflect hypersplenism.

• Platelets
  Thrombocytopenia reflects portal hypertension and splenomegaly and is one of the earliest lab clues to cirrhosis; also feeds into noninvasive scores (APRI, FIB-4).

• RUQ US with Doppler
  Assess for portal vein thrombosis and evaluate ascites volume. If thrombosis suspected → CT with contrast to confirm.
  Every 6 months ultrasound to detect early hepatocellular carcinoma.

Home Meds / Substances to Check

• Diuretics (e.g., spironolactone, furosemide)
  Assess for overdiuresis causing hepatorenal syndrome or hyponatremia; hold if Cr ↑ >50% or Na <130.

• Beta-blockers (e.g., propranolol, carvedilol)
  Safe/essential for varices but hold in refractory ascites, SBP, or systolic BP <90 (risk HRS).

• NSAIDs
  Stop immediately (risk AKI, GI bleed); switch to acetaminophen ≤2 g/day.

• Lactulose/rifaximin
  Confirm adherence/dosing for HE control; overtitration causes dehydration.

• Antibiotics
  Review for MDRO emergence in SBP/variceal bleed contexts.

• Hold statins (myopathy risk), metformin (if Cr up), benzodiazepines (worsen HE).

• Alcohol use
  Recent intake triggers decompensation; quantify for transplant exclusion (6 months abstinence).

• Recent infections/paracentesis
  SBP clues; prior quinolones raise MDRO suspicion.

• GI bleed symptoms
  Melena, BUN rise; variceal history mandates endoscopy.

• HE episodes
  Triggers (constipation, GI bleed, TIPS); rifaximin candidacy.

• Volume status/weight
  Ascites progression, diuretic response.

• MELD-Na (6–50+)
  Predicts 90-day mortality for transplant waitlist priority; ≥15 prompts referral, ≥20 ICU/transplant urgency in SBP/HRS/variceal bleed.

• Child-Pugh (5–15, A–C)
  Quick synthetic/severity assessment; Class B/C (>7) confirms decompensation and flags high mortality—guides beta-blockers, diuretics, HCC screening.

• CLIF-ACLF (ICU only)
  For acute-on-chronic liver failure with organ failures (e.g., shock, respiratory failure); superior to MELD for short-term ICU mortality but requires additional data.

• HOLD BB with refractory ascites, SBP, systolic BP <90 mmHg, shock, or acute kidney injury (e.g., hepatorenal syndrome), as they can worsen renal perfusion.

• Transplant Indications
  Consider liver transplantation for decompensated cirrhosis, non-metastatic hepatocellular carcinoma, type 1 HRS, or fulminant failure; MELD score predicts mortality and prioritizes allocation. Contraindications: active substance abuse, untreated extrahepatic cancer, severe extrahepatic organ failure, noncompliance/poor support. Early hepatology referral is essential.

Spontaneous Bacterial Peritonitis

Ascites

Presents with abdominal distension and increased abdominal girth, fever, abdominal pain, AMS. Patient reports weight gain, dyspnea; exam positive for fluid wave.

Hx of (alcoholic, hepatitis C, metabolic) cirrhosis diagnosed at ** with previous decompensation and complication of **.
Home medications (diuretics, midodrine, prophylactic BB…).

• Diagnostic paracentesis fluid sent in all patients

  • (Cell count/diff (neutrophil count ≥250/mm³ confirms SBP and start treatment), Gram stain, aerobic/anaerobic cultures, albumin, total protein — if indicated add glucose/LDH (peritonitis), cytology (malignancy), amylase (pancreatic), AFB/ADA (TB).)

• Serum albumin (for SAAG calculation).

• Calculate SAAG (Serum albumin − Ascites albumin)

  • ≥1.1 g/dL → Portal hypertension (cirrhosis, HF, portal/hepatic vein thrombosis).

  • <1.1 g/dL → No portal hypertension (malignancy, TB, pancreatitis, nephrotic syndrome).

• Ascitic fluid total protein helps differentiate cirrhosis from other high-SAAG (≥1.1 g/dL) causes:

  • Low protein (<1.5–2.5 g/dL) classic for cirrhosis.

  • High protein (>2.5 g/dL) with high SAAG suggests HF, Budd-Chiari, pulmonary hypertension → obtain echocardiogram.

• Dietary sodium restriction (<2 g/day).

• Tense ascites → large-volume paracentesis first if indicated, then start/adjust diuretics.

• Albumin (25% hyperoncotic solution) 6–8 g per liter removed after large-volume paracentesis (>5 L).

• Spironolactone primary + furosemide (100:40 ratio) to maintain potassium balance.

• Muscle cramps → baclofen 10 mg/day, titrated weekly up to 30 mg/day.

• Consider TIPS if requiring multiple paracenteses despite optimized diuretics.

Paracentesis fluid sent for cell count/diff (PMN), Gram stain and cultures (inoculated bedside), albumin and total protein (for SAAG), plus glucose/LDH if secondary peritonitis suspected, cytology if malignancy suspected, amylase if pancreatic source suspected, AFB/ADA if TB suspected.

SBP

• Ceftriaxone 1 g IV daily for 5–7 days.

• If no improvement within 48 hours or PMNs fail to decrease by ≥25%, consider resistant organisms → broaden to meropenem.

• Albumin: 1.5 g/kg day 1 and 1 g/kg day 3 to reduce HRS risk.

• Prophylaxis after ≥1 SBP episode: ciprofloxacin 500 mg daily or TMP-SMX DS daily.

Decompensated Cirrhosis / Esophageal Variceal Bleeding

• Presentation: Hematemesis ± melena, Signs of hypovolemia (pallor, tachycardia, hypotension, oliguria), may trigger HRS/HE; Cirrhosis stigmata (jaundice, ascites, spider angiomata).

• Hold home diuretics if Cr ↑ >50% or Na <130; hold BB/BP meds in refractory ascites, SBP, systolic BP <90, shock, AKI/HRS.

• PPIs not primary treatment for variceal bleed (octreotide/terlipressin + endoscopy are); give empirically until EGD confirms non-variceal source; helpful post-banding.

• 2 large-bore IVs for rapid volume/blood; avoid central lines initially.

• Octreotide immediately when suspected; reduces portal pressure; continue 2–5 days; monitor glucose.

• Ceftriaxone 1 g daily for up to 7 days.

• Secondary prevention:

  • Carvedilol 3.125 mg BID → titrate to 6.25 mg BID.

  • Propranolol 20–40 mg BID → titrate; max 320 mg/day (160 mg/day if ascites).

  • Target HR 50–60 bpm; avoid if SBP ≤90 mmHg; consider TIPS if intolerant.

• TIPS
  Decompresses portal hypertension; indicated in refractory ascites or high-risk variceal bleed. Early placement (within 72h, ideally 24h) reduces rebleeding/mortality. Risks: hepatic decompensation, pulmonary HTN, 30–40% encephalopathy.

• GI consult; EGD within 12 hours preferred.

Decompensated Cirrhosis / Hepatic Encephalopathy

Clinical diagnosis: altered mental status, asterixis, somnolence. Ammonia levels not required.

• Protect airway (intubate if needed).

• Lactulose 20–30 g every 1–2 hours until BM, then titrate to 2–3 soft stools/day. Enema option.

• Rifaximin 550 mg BID (or TID).

• Zinc adjunct.

• Polyethylene glycol may be effective.

• NG tube if needed.

Decompensated Cirrhosis / Hepatorenal Syndrome

• HRS
  Splanchnic vasodilation → low effective arterial volume → RAAS/vasopressin activation → renal vasoconstriction → AKI. Hyponatremia = poor prognosis. Liver transplant definitive.

Plan

• RUQ US with Doppler; if thrombus suspected → CTA.

• Hold diuretics, BB, NSAIDs, opioids/benzos, metformin/statins.

• Albumin 1 g/kg (max 100 g/day), then 20–40 g/day.

• Midodrine 5–15 mg q8h + octreotide 100–200 mcg q8h (or 50 mcg/hr IV).

• Shock → ICU, norepinephrine.

• RRT individualized for transplant candidates.

• Refer to hepatology.

• Follow every 6 months with ultrasound for HCC screening.

• Discuss lifestyle modification and alcohol cessation.