Liver Cirrhosis Nursing Guide

Definition & Causes

Cirrhosis is the end-stage of chronic liver disease characterised by irreversible hepatic fibrosis and nodular regeneration, leading to portal hypertension and hepatocellular failure.

Common Causes

Global/GCC Common

NAFLD/NASH — fastest growing cause globally; extremely prevalent in GCC (obesity, T2DM epidemic)
Hepatitis B — common in East/Southeast Asian expat populations in GCC
Hepatitis C — common in Egyptian and some South Asian expats
Autoimmune hepatitis
Wilson's disease, haemochromatosis (genetic)

Western-Dominant (Less Common in GCC)

Alcohol-related liver disease (ARLD) — less common in GCC Muslim population; but seen in non-Muslim expats
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)

Child-Pugh Score (Severity of Cirrhosis)

Parameter	1 point	2 points	3 points
Bilirubin (µmol/L)	<34	34–50	>50
Albumin (g/L)	>35	28–35	<28
PT prolongation (seconds)	<4	4–6	>6
Ascites	None	Mild	Moderate/severe
Encephalopathy grade	None	Grade 1–2	Grade 3–4

Class	Total Score	1-Year Survival
A — Compensated	5–6	~100%
B — Mild decompensation	7–9	~80%
C — Severe decompensation	10–15	~45%

MELD score (Model for End-stage Liver Disease) uses bilirubin, INR, and creatinine to predict 90-day mortality and is used internationally for liver transplant listing priority. Higher MELD = more urgent transplant need.

Complications of Cirrhosis

Portal hypertension (portal pressure >12 mmHg) causes most serious complications:

Complication	Mechanism	Key Management
Ascites	Portal hypertension + hypoalbuminaemia + sodium retention	Salt restriction (2g/day), spironolactone + furosemide, paracentesis if tense
Spontaneous Bacterial Peritonitis (SBP)	Bacterial translocation infecting ascitic fluid	Cefotaxime IV; ciprofloxacin prophylaxis long-term
Hepatic Encephalopathy (HE)	Ammonia + other toxins bypass liver → brain	Lactulose; rifaximin; treat precipitants
Variceal bleeding	Portal HTN → oesophageal/gastric varices → rupture	Terlipressin, ceftriaxone, band ligation, TIPS
Hepatorenal syndrome (HRS)	Renal vasoconstriction in setting of advanced cirrhosis	Terlipressin + albumin; transplant
Hepatocellular carcinoma (HCC)	Nodular regeneration → malignant transformation	Ultrasound + AFP surveillance every 6 months
Coagulopathy	Reduced synthesis of clotting factors II, V, VII, IX, X	Vitamin K; FFP/PCC for bleeding; avoid routine correction unless bleeding

Ascites Management

Diagnosis — SAAG (Serum-Ascites Albumin Gradient)

SAAG = Serum albumin − Ascites albumin

SAAG ≥ 11 g/L = portal hypertension (cirrhosis, heart failure, BCS)
SAAG < 11 g/L = non-portal hypertension (malignancy, TB, pancreatitis, nephrotic syndrome)

Ascites Management Steps

Sodium restriction — <2 g/day (88 mmol/day) dietary sodium
Diuretics — Spironolactone 100mg/day (aldosterone antagonist, potassium-sparing) + furosemide 40mg/day; ratio 100:40 maintained to prevent electrolyte imbalance; weigh daily — target 0.5 kg/day weight loss (1 kg if peripheral oedema also present)
Paracentesis — for tense/refractory ascites; drain up to 5 L; give IV albumin 8g per litre drained >5 L (prevents post-paracentesis circulatory dysfunction = PPCD)

Spontaneous Bacterial Peritonitis (SBP)

SBP = medical emergency. Diagnostic criteria: ascitic fluid PMN (neutrophil) count ≥ 250/mm³ (even without positive culture).

Symptoms: fever, abdominal pain, confusion (encephalopathy), deteriorating liver function — but may be clinically silent
ALWAYS perform diagnostic ascitic tap in any cirrhotic patient admitted to hospital
Treatment: IV cefotaxime 2g TDS × 5 days (or IV ceftriaxone 1g OD)
IV albumin 1.5g/kg on day 1 + 1g/kg on day 3 — reduces hepatorenal syndrome risk (SORT trial)
Secondary prophylaxis: norfloxacin 400mg OD (or ciprofloxacin) long-term after first episode
Primary prophylaxis: norfloxacin for variceal bleed patients and low-protein ascites (<15g/L)

Hepatic Encephalopathy (HE)

HE is a neuropsychiatric syndrome caused by accumulation of ammonia and other toxins in patients with liver failure, leading to cerebral dysfunction.

Grading (West Haven Criteria)

Grade	Consciousness	Cognition/Behaviour
Covert / Minimal	Normal	Only detectable on psychometric testing
Grade I	Mild drowsiness	Shortened attention span, mild confusion
Grade II	Moderate drowsiness	Disorientation, inappropriate behaviour, asterixis (flapping tremor)
Grade III	Marked somnolence	Gross disorientation, bizarre behaviour, unable to perform mental tasks
Grade IV	Coma	Unresponsive to stimuli

Precipitants (ABCDE mnemonic)

Alcohol binge (in non-Muslim patients)
Bleeding (GI variceal/peptic — ammonia load from blood protein)
Constipation (increased ammonia absorption)
Drugs (sedatives, opioids, diuretics causing electrolyte disturbance)
Electrolyte imbalance (hyponatraemia, hypokalaemia) / Infection (SBP, UTI, pneumonia)

Treatment

Lactulose 30–50 mL 2–4× daily (target 2–3 soft stools/day) — reduces intestinal ammonia production and absorption; titrate to avoid diarrhoea
Rifaximin 550mg BD — non-absorbable antibiotic reducing ammonia-producing gut bacteria; primary and secondary prevention
Treat precipitants (antibiotics for infection, lactulose for constipation, stop sedatives)
Protein restriction: AVOID in HE — protein restriction is OUTDATED and harmful (causes malnutrition). Give adequate protein (1.2–1.5 g/kg/day) including branched-chain amino acids
Grade III–IV HE: airway protection, ICU, consider liver transplantation evaluation

Asterixis (flapping tremor): Ask patient to hold arms extended with wrists dorsiflexed. Non-rhythmic, asynchronous flapping = grade II HE. Also seen in uraemia and CO₂ retention.

GCC-Specific Liver Disease Context

NAFLD/NASH Epidemic in GCC ▼

Non-alcoholic fatty liver disease (NAFLD) and its progressive form NASH (non-alcoholic steatohepatitis) are the most common causes of liver disease in GCC countries. The GCC has among the highest rates of obesity, metabolic syndrome, and type 2 diabetes in the world. Saudi Arabia has NAFLD prevalence estimates of 15–30% of the adult population. NAFLD can progress to cirrhosis and HCC without ever developing overt symptoms. Regular ultrasound surveillance is recommended for high-risk patients.

Viral Hepatitis in GCC Expat Populations ▼

Hepatitis B is highly prevalent among East Asian and some South Asian expat workers in GCC. Hepatitis C (HCV) is particularly prevalent among Egyptian expatriates who received contaminated schistosomiasis treatment before 1990. Both can progress silently to cirrhosis and HCC. GCC hospitals should screen all high-risk patients with HBsAg, anti-HCV. Effective treatments now exist for both (tenofovir/entecavir for HBV; direct-acting antivirals — sofosbuvir-based regimens — for HCV with >95% cure rate).

Liver Transplantation in GCC ▼

Liver transplantation is offered at major GCC centres (King Faisal Specialist Hospital Riyadh, Cleveland Clinic Abu Dhabi, Hamad Medical Corporation Qatar). Waiting lists are shorter than in Western countries for some indications. Living donor liver transplant (LDLT) is increasingly used, with Islamic religious scholars generally permitting living donation. Nurses in transplant centres require advanced competency in post-transplant immunosuppression management (tacrolimus, mycophenolate, prednisolone) and rejection monitoring.

MCQ Practice — Liver Cirrhosis

Q1. A cirrhotic patient with ascites undergoes diagnostic paracentesis. Ascitic fluid PMN count is 380/mm³. Culture is pending. What is the diagnosis and immediate treatment?

A) Normal finding — repeat tap in 48 hours

B) Culture-negative ascites — watch and wait

C) Spontaneous bacterial peritonitis — start IV cefotaxime immediately

D) Malignant ascites — arrange CT abdomen

✅ C — SBP is diagnosed by ascitic PMN ≥250/mm³, regardless of culture result (many are culture-negative). Start IV cefotaxime (or ceftriaxone) immediately. DO NOT wait for culture results. Also give IV albumin 1.5g/kg day 1 and 1g/kg day 3 to prevent hepatorenal syndrome.

Q2. A cirrhotic patient develops grade III hepatic encephalopathy. The nurse should AVOID administering which of the following?

A) Lactulose via NGT

B) IV vitamin K

C) IV morphine for pain — opioids are hepatically metabolised and accumulate

D) Oral rifaximin

✅ C — Opioids and sedatives (benzodiazepines) are precipitants of HE and should be avoided. They accumulate in liver failure and worsen encephalopathy. Use paracetamol (cautiously, max 2g/day in cirrhosis) for pain. Lactulose and rifaximin are treatments for HE.

Q3. When performing large volume paracentesis (>5 litres) in a cirrhotic patient with refractory ascites, what must be co-administered to prevent post-paracentesis circulatory dysfunction?

A) IV 0.9% saline 1L per litre drained

B) IV albumin 8g per litre drained beyond 5 litres

C) IV furosemide 40mg to prevent oedema reaccumulation

D) Oral spironolactone doubled after the procedure

✅ B — IV albumin 8g per litre drained (for paracentesis >5L) is the evidence-based intervention to prevent post-paracentesis circulatory dysfunction (PPCD), which causes haemodynamic instability and worsens renal function. Saline is not adequate replacement for albumin in this context.

Q4. What is the current dietary protein recommendation for a patient with grade II hepatic encephalopathy?

A) Strict protein restriction to <40g/day to reduce ammonia production

B) Nil by mouth until encephalopathy resolves

C) Adequate protein intake 1.2–1.5g/kg/day — protein restriction is harmful and outdated

D) Protein-free IV dextrose only until mental state improves

✅ C — Protein restriction in HE is an outdated practice that causes sarcopenia and worsens outcomes. Current guidelines recommend 1.2–1.5g/kg/day protein including branched-chain amino acids (leucine, isoleucine, valine). Treat HE with lactulose and rifaximin, not starvation.

Liver Cirrhosis — Nursing Guide