Acute liver failure: Case

This girl presents severe acetaminophen-induced acute liver failure at 48 hours after a large intentional overdose. The international normalised ratio of 6.1, the markedly elevated transaminases, the grade two encephalopathy, the renal dysfunction, and the arterial pH of 7.26 confirm advanced hepatic failure with multiorgan involvement. The acetaminophen level being below the treatment line reflects the 48-hour interval but does not alter the management, because N-acetylcysteine is given regardless of the level once hepatotoxicity is established. [1]

Clinical findings

The pattern is unequivocally that of severe acetaminophen-induced acute liver failure at the peak of the hepatotoxic phase, which typically occurs around 72 hours after ingestion. The international normalised ratio of 6.1 reflects profound loss of hepatic synthetic function, the transaminases in the thousands indicate massive hepatocyte necrosis, and the falling arterial pH of 7.26 signals accumulating lactate and failing clearance, a grave prognostic sign. The grade two encephalopathy confirms that the failing liver is no longer clearing ammonia, and the renal dysfunction signals emerging multiorgan failure. [1]

The differential at presentation included other causes of acute liver failure, but the history of a large intentional acetaminophen overdose 48 hours earlier makes the diagnosis clear. The psychosocial context is essential: an intentional overdose in an adolescent requires parallel psychiatric assessment alongside the medical management, because the underlying self-harm behaviour determines the long-term outcome as much as the hepatic recovery. [1]

Investigations and diagnosis

The diagnosis is severe acetaminophen-induced acute liver failure. The international normalised ratio of 6.1 with grade two encephalopathy far exceeds the paediatric threshold, and the arterial pH of 7.26 places her in a high-risk category. A full workup excludes co-existing causes: autoimmune markers, a viral screen, and a metabolic screen are sent, and the acetaminophen level confirms the exposure even though it is below the treatment line at 48 hours. Serial international normalised ratios, arterial blood gases, ammonia, renal function, and electrolytes are monitored every few hours to track the trajectory, because the trend determines the transplant decision. [1]

The team calculates that she meets adult King's College Criteria for paracetamol-induced failure on the basis of the arterial pH below 7.3 with the international normalised ratio, creatinine, and encephalopathy grade, but recognises that these adult criteria are not validated in children and are used only as one data point alongside the dynamic trend, not as the sole determinant of the transplant decision. [1]

Management and outcome

Management begins immediately with intravenous N-acetylcysteine at a loading dose of 150 milligrams per kilogram over 60 minutes, then 50 milligrams per kilogram over 4 hours, then 100 milligrams per kilogram over 16 hours, continued beyond the standard 21-hour protocol until the international normalised ratio falls below 1.5. The airway is monitored given the grade two encephalopathy and the risk of progression. Hypoglycaemia is prevented with a continuous dextrose infusion, the coagulopathy is managed with restraint with products reserved for bleeding, and neuroprotective intensive care is begun with the head elevated and hypercapnia avoided. Broad-spectrum antibiotics are started because the failing liver and invasive monitoring predispose to sepsis. [2]

The paediatric hepatology and transplant teams are involved from admission, and she is listed for urgent transplantation given the severity and the falling arterial pH. Over the next 24 hours, with continuing N-acetylcysteine and supportive care, her international normalised ratio peaks and then begins to fall, her arterial pH improves, and her encephalopathy lightens. As the trend reverses, the transplant is deferred and she continues supportive care, and over the following week her liver function recovers. The multidisciplinary plan then addresses the psychosocial needs: a comprehensive mental health assessment, risk evaluation, and the engagement of adolescent mental health services, because the first year after acute liver failure carries a measurable burden of impaired quality of life and neurocognitive function that benefits from structured follow-up. [3]