Hepatic Staging and CLD Complications

MELD-Na and Child-Pugh, then the complications: HRS, HPS and the Maddrey function · v1.2

  • Enter the standard liver biochemistry, then grade the two bedside findings, ascites and encephalopathy, as you actually find them.
  • You get the Child-Pugh class, which is what operative risk and most drug dosing advice were written against, alongside the classic MELD-Na, which estimates 90-day mortality.
  • The two scores answer different questions and will not always point the same way.
  • The second tab scores the decompensating events, alcoholic hepatitis, hepatorenal syndrome and hepatopulmonary syndrome, when the presentation calls for it.

  • Transplant priority. The score here measures severity, and OPTN allocation in the United States moved to MELD 3.0 on 13 July 2023, which this tool does not compute.
  • Children and adolescents under 18. Child-Pugh and MELD-Na were derived and validated in adults.
  • Acute liver failure in a previously normal liver, which is assessed against transplant criteria written for it rather than against these scores.
  • The day-to-day management of ascites, encephalopathy and variceal bleeding, which the scores here grade rather than treat.
If the liver disease is alcohol-related, two other tools apply during this admission. Quantify the intake and screen for a use disorder with the Alcohol Unit Calculator and AUD Assessment. More urgently, a patient admitted with alcoholic hepatitis or decompensated cirrhosis who has stopped drinking will withdraw, usually on day 2 or 3: the Alcohol Withdrawal: CIWA-Ar and Thiamine Protocol covers that, and it selects lorazepam rather than chlordiazepoxide once cirrhosis is decompensated. Note that confusion in this patient is hepatic encephalopathy until proved otherwise, and the benzodiazepines that treat withdrawal will worsen it.

1. Laboratory Values

2. Bedside Findings

Scope of this tool. Both scores were built for chronic liver disease. Acute liver failure in a previously healthy liver is a different assessment against different criteria, and this tool does not cover it. Neither score names the cause of the cirrhosis, and neither replaces a referral: transplant listing follows a centre's own assessment and never a number produced here. Child-Pugh also rests on two graded findings, ascites and encephalopathy. Two clinicians can read the same patient a class apart, so record what you graded and on what. The MELD-Na here is the classic formula, with creatinine held between 1.0 and 4.0 mg/dL and set to 4.0 mg/dL on dialysis, which means it stops discriminating once the renal failure is worse than that. It is not the score the OPTN uses for allocation in the United States: that has been MELD 3.0 since 13 July 2023, which adds the patient's sex and the serum albumin and caps creatinine at 3.0 mg/dL. In India, allocation sits with the state appropriate authority under NOTTO and follows that state's rules, so treat the number here as a severity index and not as a place in a queue. It is not validated in children.

  • Three decompensating events are worked up here: the severity of alcoholic hepatitis by Maddrey's discriminant function, hepatorenal syndrome against the International Club of Ascites criteria, and hepatopulmonary syndrome.
  • Fill in only the section your patient's presentation calls for.
  • Each is scored on its own, and a section left blank is simply not reported.

A. Maddrey's Discriminant Function (Alcoholic Hepatitis)

B. Hepatorenal Syndrome (HRS-AKI) Criteria

C. Hepatopulmonary Syndrome (HPS) Criteria

Evidence & Clinical Pearls

1. Pathophysiology: Why Sodium Is in MELD-Na

The original MELD score used Bilirubin, INR and Creatinine alone. Sodium was added because a low sodium in cirrhosis is not really a sodium problem. In advanced cirrhosis, portal hypertension drives the release of systemic vasodilators, nitric oxide chief among them. The splanchnic bed dilates, the effective arterial blood volume falls, the baroreceptors read that as underfilling, and non-osmotic Anti-Diuretic Hormone (ADH) is released whatever the plasma osmolality is doing. The ADH holds on to free water, and the sodium falls by dilution. So a serum sodium < 135 mEq/L is a reading of how far the portal hypertension has gone, and it predicts survival on its own, over and above the other three terms. That is what earned it a place in the allocation formula.

2. Practice Advisory: Corticosteroids Before Infection Has Been Excluded

The Sepsis Caution in India: A Maddrey's Discriminant Function (mDF) ≥ 32 defines severe alcoholic hepatitis with a high 1-month mortality, and that is the threshold at which corticosteroids, Prednisolone 40mg/day, are classically given. The arithmetic cannot tell whether the patient is also infected. Before those steroids are started, exclude the occult infections that present quietly in a cirrhotic, meaning UTI, SBP and pneumonia, and think about latent Tuberculosis, which in this population is a live question and not a formality. A cirrhotic patient with untreated sepsis has little defence left, and steroids take away what remains.

3. Illness Scripts: AKI in Cirrhosis

Condition Pathophysiology Volume Challenge Response
Pre-Renal Azotaemia True volume depletion (over-diuresis, GI bleed, severe vomiting/diarrhoea). Rapidly improves with IV Albumin/Fluids.
Hepatorenal Syndrome (HRS-AKI) Extreme splanchnic vasodilation leading to compensatory, intense renal vasoconstriction. The kidneys are histologically normal but functionally starved of blood. Refractory to volume expansion. Requires vasoconstrictors (Terlipressin) + Albumin to reverse splanchnic pooling.
Acute Tubular Necrosis (ATN) Direct structural damage to renal tubules (ischaemic shock, nephrotoxic drugs, contrast). Refractory to volume expansion. Urine will show muddy brown casts.

4. Contraindications in Cirrhosis

Avoid NSAIDs and ACE Inhibitors: In cirrhosis the kidney is already vasoconstricted, and what holds the afferent arteriole open is locally made prostaglandin. That is a single point of failure. An NSAID blocks the prostaglandin and the afferent arteriole closes down; an ACE inhibitor removes the efferent tone that was propping up the filtration pressure. Either one can tip a compensated patient into acute renal failure, and it happens quickly.
Abbreviations A-a (Alveolar-Arterial) · ACE (Angiotensin-Converting Enzyme) · ADH (Antidiuretic Hormone) · AKI (Acute Kidney Injury) · ATN (Acute Tubular Necrosis) · AUD (Alcohol Use Disorder) · CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol, revised) · CLD (Chronic Liver Disease) · GFR (Glomerular Filtration Rate) · GI (Gastrointestinal) · HPS (Hepatopulmonary Syndrome) · HRS (Hepatorenal Syndrome) · HRS-AKI (Hepatorenal Syndrome - Acute Kidney Injury) · INR (International Normalised Ratio) · mDF (Maddrey's Discriminant Function) · MELD (Model for End-Stage Liver Disease) · MELD-Na (Model for End-Stage Liver Disease - Sodium) · Na⁺ (Sodium) · NSAID (Non-Steroidal Anti-Inflammatory Drug) · OPTN (Organ Procurement and Transplantation Network) · PaO₂ (Partial Pressure of Arterial Oxygen) · PT (Prothrombin Time) · SBP (Spontaneous Bacterial Peritonitis) · sCr (Serum Creatinine) · TB (Tuberculosis) · UTI (Urinary Tract Infection)
References
  1. Pugh RN, et al. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg. 1973;60(8):646-649.
  2. Organ Procurement and Transplantation Network. OPTN Policies, Policy 9: Allocation of Livers and Liver-Intestines. Rockville, MD: US Department of Health and Human Services, Health Resources and Services Administration; 2023.
  3. Maddrey WC, et al. Corticosteroid therapy of alcoholic hepatitis. Gastroenterology. 1978;75(2):193-199.
  4. 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;62(4):968-974.
  5. Kamath PS, Wiesner RH, Malinchoc M, et al. A model to predict survival in patients with end-stage liver disease. Hepatology. 2001;33(2):464-470.
  6. Kim WR, Biggins SW, Kremers WK, et al. Hyponatremia and mortality among patients on the liver-transplant waiting list. N Engl J Med. 2008;359(10):1018-1026.
  7. Kim WR, Mannalithara A, Heimbach JK, et al. MELD 3.0: The Model for End-Stage Liver Disease updated for the modern era. Gastroenterology. 2021;161(6):1887-1895.e4.
  8. Organ Procurement and Transplantation Network. Updates to medical urgency scoring of liver transplant candidates in effect. Effective 13 July 2023. Rockville, MD: HRSA; 2023.
  9. Thursz MR, Richardson P, Allison M, et al. Prednisolone or pentoxifylline for alcoholic hepatitis (STOPAH). N Engl J Med. 2015;372(17):1619-1628.
  10. Louvet A, Naveau S, Abdelnour M, et al. The Lille model: a new tool for therapeutic strategy in patients with severe alcoholic hepatitis treated with steroids. Hepatology. 2007;45(6):1348-1354.
  11. Sarin SK, Choudhury A, Sharma MK, et al. Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL): an update. Hepatol Int. 2019;13(4):353-390.
  12. European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406-460.
How to Cite This Tool

DOIhttps://doi.org/10.5281/zenodo.22401586

AMA Style:Umakanth S. Hepatic Staging and CLD Complications. Version 1.2. MEDiscuss Clinical Decision Support System. Published 2026. Accessed . https://mediscuss.org/cdss/hepatic-assessment. doi:10.5281/zenodo.22401586

Vancouver Style:Umakanth S. Hepatic Staging and CLD Complications [Internet]. Version 1.2. MEDiscuss.org; 2026 [cited ]. Available from: https://mediscuss.org/cdss/hepatic-assessment. doi:10.5281/zenodo.22401586

Disclaimer and scope
Disclaimer: This decision-support system is written for healthcare professionals. It does not substitute clinical judgment, and the treating physician retains absolute responsibility for every diagnostic, dosing and therapeutic decision. The algorithms are built on the evidence as it stands, and the evidence moves. Verify the output against your current institutional protocol, and against the patient in front of you.
© 2026 MEDiscuss.org. All rights reserved. Provided free of charge for clinical use. Unauthorised reproduction or redistribution is strictly prohibited.
Category Risk Scores & Diagnostic PathwaysPathway
Specialties Gastroenterology & Hepatology

Written and maintained by

Dr Shashikiran Umakanth

Last revised 24 August 2026

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