Acute Liver Failure in India: Causes, Warning Signs and Emergency Treatment

Acute liver failure is the sudden loss of liver function — jaundice, a clotting abnormality and confusion — in someone with no previous liver disease. In India the commonest cause today is hepatitis A, followed by rat-killer poisoning. In a 2025 multicentre Indian study, only 57% survived three weeks without a transplant. Any jaundiced patient who becomes drowsy or confused needs a liver ICU the same day.
— Dr Chetan Kalal, DM Hepatology, Gleneagles Hospital Mumbai

A 22-year-old engineering student from Thane, otherwise fit, develops fever and vomiting, then yellow eyes. The family is told it is “jaundice” and to rest at home with a light diet. On day nine he sleeps through the afternoon, and by evening he does not recognise his mother. That change — from jaundiced but lucid to jaundiced and confused — is the moment ordinary hepatitis becomes acute liver failure, and it is the single most important thing any family in India can learn to recognise. (This is an illustrative scenario, not a specific patient.)

Acute liver failure is rare, but it kills young people, and it kills them quickly. Most patients are in their twenties. Many reach a liver unit later than they should, because the early phase looks like the self-limiting hepatitis that millions of Indians recover from every year. I have spent much of my career on this disease, beginning in the liver ICU at ILBS New Delhi, where I led the MAHAL randomised trial on treating brain swelling in ALF, and now at Gleneagles Hospital Mumbai, where our team recently published on monitoring the brain in these patients in the Journal of Hepatology. This guide explains what ALF is, what causes it in India today, which warning signs mean “go now”, and how modern ICU care and transplantation change the odds.

What acute liver failure is — and what it is not

The European Association for the Study of the Liver (EASL) defines ALF as an acute abnormality of liver tests in a person without underlying chronic liver disease, accompanied by a coagulopathy of liver origin and a clinically apparent change in consciousness from hepatic encephalopathy. All three elements matter. Jaundice alone, even deep jaundice, is not liver failure. Jaundice with a rising INR is severe acute liver injury, a warning. Jaundice, coagulopathy and encephalopathy together are acute liver failure.

The absence of prior liver disease is what separates ALF from acute-on-chronic liver failure (ACLF), in which a patient with existing cirrhosis or chronic liver disease decompensates suddenly. The distinction is not academic. Their causes differ, their prognostic scores differ, and the liver’s capacity to recover differs — a previously healthy liver can regenerate completely if the patient is kept alive long enough, which is why so much of ALF care is about buying time.

Specialists also classify ALF by how quickly encephalopathy follows jaundice. In the King’s College classification, hyperacute liver failure — encephalopathy within seven days of jaundice — carries a high risk of brain swelling yet includes many patients who survive with medical treatment alone. When the interval is eight to 28 days, prognosis without transplantation is much poorer; subacute cases, developing over five to twelve weeks, look less dramatic but also do badly. In the MAHAL cohort at ILBS, the median interval from jaundice to encephalopathy was eight days.

For a broader overview of how we assess these patients at Gleneagles, see our acute liver failure service page.

What causes acute liver failure in India today

Ask most Indian doctors what causes ALF here and they will say hepatitis E. That was the classical teaching, and in the MAHAL trial cohort from ILBS, hepatitis E was indeed the single commonest cause, at 33.3%. The picture is shifting. A 2025 multicentre study by Roy and colleagues from four tertiary centres — Kolkata, Jaipur, Chandigarh and Hyderabad — analysed 183 ALF patients admitted between 2021 and 2023. Hepatitis A was now the commonest cause, at 44.2%. Rodenticide poisoning came second, at 10.3%.

Both findings deserve attention. Hepatitis A in childhood is usually trivial; as sanitation improves, fewer Indians are infected as children, more meet the virus as adults, and adults are the ones who develop liver failure. The authors’ own conclusion was a call for universal hepatitis A vaccination. Rat-killer paste containing yellow phosphorus is cheap, freely available and taken deliberately in self-harm, especially by young people. In a series of 96 patients from Puducherry who had swallowed a 3% yellow phosphorus paste, symptoms typically appeared about 48 hours after ingestion, 36.5% died, and most deaths came within a week — so anyone who has swallowed it must be admitted even if they look well.

Other important causes are drugs — anti-tuberculosis therapy above all in India, along with paracetamol overdose and herbal or dietary supplements, which we discuss in our guide to drug-induced liver injury — hepatitis B (new infection or a flare), hepatitis E in pregnant women — who, particularly in the Indian subcontinent, are at higher risk of severe disease and liver failure, with dangers to both mother and baby — autoimmune hepatitis, Wilson disease in teenagers and young adults, tropical infections, and, in a minority, no identifiable cause.

Warning signs: when jaundice becomes an emergency

Most people with jaundice recover. The skill lies in recognising the few who will not, while there is still time to move them. These are the signs that should send a jaundiced patient to a hospital with a liver unit the same day, not after the next routine blood test.

Any change in behaviour or consciousness. Excessive sleepiness, irritability, confusion, inappropriate talk, reversal of the sleep-wake cycle, or a flapping tremor of the outstretched hands. Families notice these first. Grade I encephalopathy can be subtle, and it progresses fast. Bleeding — from the gums, nose, injection sites, or in vomit or stool — signals that the liver is no longer making clotting factors. Persistent vomiting and inability to keep fluids down. Jaundice deepening after the first week rather than settling. Low blood sugar, which can present as sweating, confusion or a seizure. Reduced urine output, a sign the kidneys are failing alongside the liver.

On blood tests, the number that matters most is the INR (prothrombin time). A rising INR in a jaundiced patient is the earliest objective marker of a failing liver, well before confusion appears. Any patient with acute hepatitis and an INR of 1.5 or more should be discussed with a hepatologist.

Pregnancy, poisoning, and paracetamol overdose all lower the threshold for admission further. So does any jaundiced patient taking anti-tuberculosis treatment. Please do not wait for symptoms to “settle” with home remedies or herbal preparations; several of those products are themselves causes of liver injury.

Inside the liver ICU: what treatment actually involves

There is no single drug that reverses acute liver failure. Treatment is intensive organ support while the liver either regenerates or a donor liver is found, combined with specific treatment of the cause wherever one exists.

Treating the cause. Paracetamol poisoning has an antidote, N-acetylcysteine (NAC). NAC also helps some patients whose liver failure has another cause: in a US randomised trial of 173 patients with non-paracetamol ALF, intravenous NAC improved transplant-free survival from 27% to 40% overall, and from 30% to 52% in those with early (grade I–II) encephalopathy. Patients already in deep coma did not benefit, which is one more reason early referral matters. Hepatitis B is treated with antivirals, and drugs suspected of causing injury are stopped at once.

Protecting the brain. The most feared complication is cerebral oedema — swelling of the brain driven partly by ammonia — which can raise intracranial pressure to the point of herniation. Patients with advanced encephalopathy are usually sedated and ventilated to protect the airway. Brain swelling is treated with osmotic agents. In the MAHAL trial, which I led at ILBS with 51 patients, hypertonic saline and mannitol lowered intracranial pressure indices to a similar degree at 12 hours, but rebound rises in pressure occurred in 20% of the mannitol group and none of the saline group, and new kidney injury was more frequent with mannitol. Monitoring the brain non-invasively, without drilling into the skull in patients whose blood does not clot, is the problem our Gleneagles team addressed in our 2026 Journal of Hepatology letter on a multimodal, haemostasis-informed neuromonitoring pathway. Venous ammonia levels help in decision-making too, a point I first argued in Hepatology in 2018.

Preventing and treating infection. This is where many ALF patients are actually lost. In 143 patients at PGIMER Chandigarh, 76.9% developed bacterial or fungal infection, most with multidrug-resistant organisms. Thirty-day survival was 17.3% in infected patients against 75.8% in uninfected ones, and no patient with fungal infection survived. Meticulous line care, surveillance cultures and early, targeted antibiotics are therefore not housekeeping. They are life-saving treatment.

Plasma exchange and kidney support. High-volume plasma exchange removes toxins and inflammatory mediators and replaces clotting factors. In a European randomised trial of 182 patients, it improved overall hospital survival from 47.8% to 58.7%, largely by increasing transplant-free survival. About a third of patients in the 2025 Indian multicentre study received plasma exchange, and a similar proportion received continuous renal replacement therapy, which also helps control ammonia.

Prognosis and when a transplant is needed

The central decision in ALF is whether this liver will recover on its own. Get it right and a young patient walks out with their own liver. Get it wrong one way and a patient receives a transplant they did not need; get it wrong the other way and the window closes.

Specialists use prognostic tools such as the King’s College criteria, combined with the trajectory of INR, lactate, encephalopathy grade, kidney function and the underlying cause. In the Indian multicentre study, 40.4% of patients met King’s College criteria at admission, and meeting them carried roughly a tenfold higher risk of death; lactate, advanced encephalopathy and low haemoglobin were also independent predictors. Seven-, 14- and 21-day transplant-free survival were 65.5%, 60.1% and 57.3%.

The most uncomfortable number in that study is 3.8% — the proportion of patients who actually received a liver transplant. With roughly four in ten patients dying without one, that gap reflects the realities of transplantation in India: deceased donor organs are scarce, and most transplants rely on a living family donor who must be evaluated urgently, often within a day or two. Families facing this decision deserve a frank discussion early, while there is still time to assess a donor, rather than in the final hours. A centre with an active transplant hepatology team, a liver ICU and a living donor programme gives a patient with ALF the full range of options.

Survivors who recover without a transplant usually regain normal liver function, because a previously healthy liver regenerates. They need follow-up to make sure the cause has been dealt with, and vaccination against hepatitis A and B where appropriate.

References

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