Gastroenterology & Nutrition

Liver Cirrhosis

Irreversible replacement of normal liver architecture by fibrous septa and regenerative nodules causes both failing synthetic function and obstructed blood flow, so every complication is one of these two mechanisms playing out.

In a nutshell

Cirrhosis replaces normal liver architecture with fibrous septa and regenerative nodules, causing failing synthetic function (coagulopathy, hypoalbuminaemia, jaundice) and portal hypertension (varices, ascites, splenomegaly) as its two core mechanisms. Decompensation is usually triggered by an identifiable precipitant.

Classic presentation

A patient with known chronic liver disease presenting with jaundice, ascites, confusion (encephalopathy) or a variceal bleed, often precipitated by infection, GI bleeding or constipation.

Key points

Every complication of cirrhosis follows from either failing synthetic function or portal hypertension: map new findings onto one of these two mechanisms.
Coagulopathy, hypoalbuminaemia and jaundice reflect loss of functioning hepatocyte mass, not a bleeding or renal problem in isolation.
Portal hypertension opens portosystemic collaterals at the gastro-oesophageal junction (varices), umbilicus and rectum, and drives ascites via splanchnic hydrostatic pressure and renal sodium retention.
Hepatic encephalopathy results from ammonia bypassing the liver via portosystemic shunts and failing hepatic clearance, treated with lactulose first-line and rifaximin for secondary prevention of recurrent episodes.
Decompensation is usually precipitated by an identifiable trigger (infection, GI bleed, constipation, electrolyte disturbance) that must be actively sought and treated.
Severity and transplant candidacy are quantified with Child-Pugh and MELD (six-monthly in compensated disease), and in the UK with UKELD, where a score of 49 or more is the national minimal listing criterion for transplant.

First-line investigation

LFTs, albumin and INR alongside liver ultrasound with elastography, with endoscopy to screen for varices and Child-Pugh/MELD scoring for severity.

Management

Stage and treat the cause

Confirm the aetiology, separate compensated from decompensated disease, address alcohol or viral/metabolic drivers, and involve hepatology when cirrhosis or high complication risk is identified.^1,2

Surveil for cancer and varices

Arrange six-monthly HCC surveillance and endoscopic variceal screening unless the person is starting a NICE-supported non-selective beta-blocker pathway for primary prevention of decompensation.^1,8,2

Prevent variceal bleeding and decompensation

Use cautious specialist prescribing of carvedilol first choice or propranolol if contraindicated for clinically significant portal hypertension, and offer band ligation when beta-blockers are unsuitable or cannot be taken reliably.^1,11,10

Treat ascites, SBP and bleeding urgently

Tap new or deteriorating ascites, use specialist diuretic or paracentesis pathways, avoid routine SBP prophylaxis, and treat suspected variceal bleeding as an emergency with antibiotics, vasoactive treatment and urgent endoscopy.^1,4,6,10

Treat encephalopathy and its trigger

Search actively for infection, bleeding, constipation, renal or electrolyte disturbance and sedatives; treat overt encephalopathy with lactulose and add rifaximin for recurrence despite lactulose under the NICE pathway.^1,5,3,10

Escalate for transplant assessment

Refer early after decompensation, refractory complications, persistent synthetic dysfunction or a concerning UKELD trajectory; UKELD 49 or more is the national minimal listing criterion, but clinical deterioration should prompt discussion sooner.^7,3

Include nutrition and palliative care

Address nutrition, vaccination, alcohol support and symptom burden; involve palliative care alongside hepatology when transplant is unsuitable or advanced liver disease is causing substantial symptoms.^2,3,12

Exam traps

A raised INR in cirrhosis reflects reduced clotting factor synthesis, not vitamin K deficiency alone, and does not reliably predict bleeding risk the way it does on warfarin.
Every decompensation episode should trigger a search for a precipitant (infection, bleeding, constipation, sedatives) rather than being treated as spontaneous.
Spontaneous bacterial peritonitis should be actively excluded (low threshold for ascitic tap) in any cirrhotic patient with ascites and new deterioration, even without classic peritonism.
Carvedilol is first-choice over propranolol for primary prevention of decompensation and variceal bleeding but should be avoided in severe hepatic impairment (for example large-volume or refractory ascites).
Routine antibiotic SBP prophylaxis is not given to all cirrhotic patients with ascites; it is reserved for those at high risk (low ascitic protein with a high Child-Pugh or MELD score) or where infection would jeopardise transplant/TIPS candidacy.

Illustrations

Normal liver architecture versus cirrhosisDiagram contrasting normal hepatic lobular architecture with fibrous septa surrounding regenerative nodules, and the resulting obstruction to sinusoidal blood flow.PassFinals · original

Portosystemic collateral pathways in portal hypertensionDiagram showing collateral flow opening at the gastro-oesophageal junction (varices), umbilicus (caput medusae) and rectum (haemorrhoids) as portal pressure rises.PassFinals · original

Cirrhotic liver (gross pathology)Explanted liver showing the diffuse nodularity of cirrhosis.Centers for Disease Control and Prevention/ Dr. Edwin P. Ewing, Jr, Wikimedia Commons · CC0

Key sources

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.