Guide — Gastrointestinal
Cirrhosis & Portal Hypertension
Cirrhosis is end-stage liver disease characterized by irreversible hepatic fibrosis. Portal hypertension — elevated pressure in the portal venous system — drives its most dangerous complications: varices, ascites, and hepatic encephalopathy.
13 min read · Gastrointestinal
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Pathophysiology
Chronic liver injury from any cause leads to hepatic inflammation, stellate cell activation, collagen deposition, and fibrosis. Over time, normal hepatocytes are replaced by fibrotic tissue, disrupting architecture and blood flow.
| Common Cause | Mechanism |
|---|---|
| Alcohol-related liver disease | Ethanol directly toxic to hepatocytes; acetaldehyde activates stellate cells; leads to steatohepatitis then fibrosis |
| Nonalcoholic fatty liver disease (NAFLD/NASH) | Metabolic syndrome, obesity, T2DM — fat accumulation leads to hepatic inflammation and fibrosis |
| Chronic hepatitis B or C | Viral-induced inflammation and immune-mediated hepatocyte destruction over decades |
| Autoimmune hepatitis | Immune-mediated attack on hepatocytes — responds to immunosuppression but can progress if untreated |
| Primary biliary cholangitis (PBC) | Autoimmune destruction of intrahepatic bile ducts — chronic cholestasis leads to fibrosis |
| Hemochromatosis / Wilson's disease | Iron/copper deposition causes oxidative injury and fibrosis |
Portal hypertension develops when portal vein pressure exceeds 10 mmHg (normal: 5–10 mmHg). Complications develop when it exceeds 12 mmHg: varices form at pressure >10–12 mmHg, and variceal bleeding risk increases substantially above 12 mmHg.
Ascites
Ascites is the accumulation of fluid in the peritoneal cavity. It is the most common complication of cirrhosis, occurring in 50–60% of patients within 10 years of diagnosis.
Pathophysiology
- ✦Portal hypertension → increased hydrostatic pressure
- ✦Hypoalbuminemia → decreased oncotic pressure
- ✦Sodium and water retention (RAAS activation)
- ✦Splanchnic vasodilation → compensatory renal vasoconstriction
Assessment Findings
- ✦Abdominal distension, tense and tender abdomen
- ✦Shifting dullness on percussion
- ✦Positive fluid wave (>1.5 L fluid present)
- ✦Flank dullness, bulging flanks
- ✦Umbilical hernia, scrotal/labial edema
Diagnosis
- ✦Abdominal ultrasound (most sensitive)
- ✦Paracentesis: SAAG ≥1.1 g/dL = portal hypertension-related ascites
- ✦Serum-ascites albumin gradient (SAAG) differentiates causes
Treatment
- ✦Sodium restriction: <2 g/day
- ✦Diuretics: spironolactone (aldosterone antagonist) ± furosemide
- ✦Large-volume paracentesis (LVP) for refractory ascites
- ✦TIPS for refractory cases
- ✦Liver transplant — definitive treatment
Spontaneous bacterial peritonitis (SBP) is a life-threatening infection of ascitic fluid. Signs: fever, abdominal pain, altered mental status. Diagnosed by ascitic fluid PMN >250 cells/mm³. Treat with IV cefotaxime.
Esophageal & Gastric Varices
Varices are dilated, thin-walled collateral vessels that develop when portal hypertension diverts blood to the systemic venous system via the portosystemic shunts.
| Aspect | Details |
|---|---|
| Location | Esophageal varices (most common), gastric varices, anorectal varices, caput medusae (umbilical) |
| Bleeding risk | Present in 50% of cirrhotics. Annual bleed risk 10–30%. Mortality per episode 15–20%. |
| Presentation | Massive hematemesis (bright red), melena, hemodynamic instability, tachycardia, hypotension |
| Primary prevention | Non-selective beta-blockers (propranolol, nadolol, carvedilol) — reduce portal pressure. EGD surveillance every 1–3 years. |
| Acute treatment | IV octreotide (5 days) + endoscopic band ligation. IV antibiotics (norfloxacin or ceftriaxone). Terlipressin where available. |
| Secondary prevention | Band ligation every 2–4 weeks until obliteration. Non-selective beta-blocker. TIPS for recurrent/refractory bleeding. |
| Balloon tamponade | Sengstaken-Blakemore tube: temporizing measure for refractory variceal bleed. Bridge to TIPS or surgery. |
Hepatic Encephalopathy
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome from the accumulation of nitrogenous waste (primarily ammonia) that the diseased liver cannot metabolize.
Precipitating Factors
- ✦GI bleed (blood = protein load)
- ✦Infection (SBP, UTI, pneumonia)
- ✦Constipation (increased ammonia absorption)
- ✦Medication: benzodiazepines, opioids, diuretics
- ✦Electrolyte imbalance: hypokalemia, alkalosis
Clinical Signs
- ✦Asterixis (flapping tremor of outstretched hands)
- ✦Confusion, disorientation, personality change
- ✦Slurred speech, sleep disturbance
- ✦Fetor hepaticus (musty breath)
- ✦Coma (severe cases — West Haven Grade 4)
Diagnosis
- ✦Clinical assessment using West Haven Criteria
- ✦Serum ammonia (elevated, but not required)
- ✦EEG: triphasic waves in moderate/severe HE
- ✦Rule out other causes: CT head, metabolic panel
Treatment
- ✦Lactulose (first-line): traps ammonia in gut as NH4+, promotes elimination via diarrhea
- ✦Rifaximin (adjunctive): non-absorbable antibiotic reduces ammonia-producing gut bacteria
- ✦Treat precipitating cause
- ✦Dietary protein: moderate restriction (0.5–0.8 g/kg) — avoid complete protein restriction
Laboratory Findings
| Lab | Finding | Significance |
|---|---|---|
| AST / ALT | Elevated (may normalize in end-stage) | Hepatocyte damage; AST:ALT ratio >2:1 = alcoholic hepatitis |
| ALP / GGT | Elevated | Cholestasis, biliary obstruction; GGT elevated with alcohol |
| Total bilirubin | Elevated (jaundice if >2.5 mg/dL) | Impaired conjugation and excretion by failing liver |
| Albumin | Decreased (<3.5 g/dL) | Reduced synthetic function — marker of liver function |
| INR / PT | Elevated (coagulopathy) | Decreased clotting factor synthesis (factors II, VII, IX, X) |
| Ammonia | Elevated | Hepatic encephalopathy — impaired urea cycle |
| Platelets | Decreased (thrombocytopenia) | Splenomegaly from portal HTN → platelet sequestration; decreased TPO |
| Sodium | Decreased (hyponatremia) | Dilutional — free water retention from ADH and RAAS activation |
Nursing Priorities
Monitor for variceal bleeding signs
Hematemesis, melena, or hematochezia in cirrhosis = potential variceal bleed. Vital signs q4h minimum. Have IV octreotide and large-bore IV access ready. Know facility protocol for massive GI hemorrhage.
Assess and manage ascites
Daily weights (>1 kg/day gain = fluid accumulation). Measure abdominal girth. Sodium-restricted diet (<2 g/day). Administer spironolactone and furosemide as ordered. Monitor for SBP: fever + abdominal pain + altered mental status.
Monitor neurological status for hepatic encephalopathy
Assess orientation, asterixis (flapping tremor), sleep-wake cycle changes. Administer lactulose as ordered — titrate to 2–4 soft stools per day. Check ammonia level as ordered. Avoid benzodiazepines and opioids.
Coagulopathy and bleeding precautions
INR is elevated — minimize invasive procedures. Use smallest needle gauge for venipuncture. Apply pressure after any puncture site. Monitor for spontaneous bruising, gum bleeding, epistaxis. Do NOT give IM injections.
Nutritional support
Avoid protein restriction unless severe refractory encephalopathy. Small frequent meals. Supplement B vitamins (especially thiamine in alcohol-related cirrhosis). Zinc supplementation may reduce HE risk. Monitor albumin and prealbumin.
Skin integrity and infection prevention
Assess for jaundice, skin breakdown from edema, pressure injuries. Pruritus management (cholestyramine, antihistamines). Strict hand hygiene — cirrhotic patients are immunocompromised. Monitor for SBP, UTI, and pneumonia.
NCLEX Pearls
- ✦Cirrhosis is IRREVERSIBLE — distinguish from other liver diseases that may be treated and reversed. Only liver transplant addresses end-stage disease.
- ✦Lactulose for hepatic encephalopathy: mechanism = acidifies the colon (traps NH3 as NH4+) and acts as a cathartic. Goal = 2–4 soft stools per day.
- ✦Asterixis (flapping tremor) = hallmark sign of hepatic encephalopathy. Test by having patient extend arms and dorsiflex wrists.
- ✦SAAG ≥1.1 = portal hypertension-related ascites. SAAG <1.1 = non-portal hypertension cause (malignancy, TB, pancreatitis).
- ✦Spironolactone + furosemide for ascites: ratio 100 mg:40 mg. Spironolactone is primary (counteracts hyperaldosteronism), furosemide potentiates diuresis.
- ✦Coagulopathy in cirrhosis: elevated INR from decreased factor synthesis. Platelets low from splenomegaly. Avoid IM injections and minimize invasive procedures.
- ✦Spontaneous bacterial peritonitis (SBP): fever + abdominal pain + altered mental status in cirrhotic patient = get diagnostic paracentesis. PMN >250 = positive.
- ✦Varices: prophylaxis with non-selective beta-blockers (propranolol, nadolol). Acute treatment: IV octreotide + band ligation. These are two separate approaches.
- ✦Child-Pugh and MELD scores are used to assess cirrhosis severity and transplant candidacy — MELD uses bilirubin, INR, and creatinine.
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with American College of Gastroenterology (ACG) / AGA · ASPEN (nutrition support). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →