The Child-Pugh score relies heavily on subjective clinical parameters (ascites and encephalopathy) and is primarily used to adjust pharmacological dosing and assess perioperative mortality risk. The MELD-Na score relies strictly on objective laboratory values and is the international gold standard used by the Organ Procurement and Transplantation Network (OPTN/UNOS) for predicting 90-day mortality and prioritising liver transplantation allocation.
2. Alcoholic Hepatitis & Corticosteroids (mDF)
Maddrey’s Discriminant Function (mDF) identifies patients with severe alcoholic hepatitis who are at high risk for short-term mortality. An mDF ≥ 32 indicates a potential survival benefit from corticosteroid therapy (e.g., Prednisolone), provided there are no contraindications.
Clinical Caveat: Historically, Pentoxifylline was considered the alternative if steroids were contraindicated. However, the landmark STOPAH trial (2015) definitively demonstrated that Pentoxifylline offers no survival benefit in severe alcoholic hepatitis. Its routine use is no longer supported by robust evidence.
HRS is essentially a diagnosis of exclusion. The defining pathophysiological mechanism is extreme splanchnic vasodilation causing severe renal vasoconstriction. Because the kidneys themselves are structurally intact, the criteria strictly require ruling out intrinsic renal disease (via urinalysis and US) and proving that the AKI does not reverse with simple volume expansion (albumin loading). Confirmed HRS-AKI often requires treatment with splanchnic vasoconstrictors (Terlipressin or Noradrenaline) combined with IV albumin.
4. Hepatopulmonary Syndrome (HPS)Characterised by the triad of liver disease, impaired oxygenation, and intrapulmonary vascular dilatations (IPVDs). Diagnosis relies on demonstrating a widened A-a gradient or hypoxaemia, combined with a positive contrast-enhanced echocardiogram (showing bubbles in the left atrium 3-6 cardiac cycles after right atrial opacification). Liver transplantation is the only definitive therapy.
An elevated INR in a cirrhotic patient represents decreased synthesis of procoagulant factors, but the liver also stops synthesising anticoagulant factors (like Protein C and S). Therefore, a high INR does not mean the patient is “auto-anticoagulated.” Cirrhotic patients remain at high risk for VTE and portal vein thrombosis despite an elevated INR. Do not withhold DVT prophylaxis solely based on a high INR.
Algorithm References & Evidence Base
- Pugh RN, et al. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg. 1973.
- Organ Procurement and Transplantation Network (OPTN). Policies: MELD Score. US Department of Health and Human Services.
- Maddrey WC, et al. Corticosteroid therapy of alcoholic hepatitis. Gastroenterology. 1978.
- Angeli P, et al. Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites. J Hepatol. 2015.
- Thursz MR, et al. (STOPAH Trial). Prednisolone or pentoxifylline for alcoholic hepatitis. N Engl J Med. 2015.
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