Hyperacute liver failure and various other toxicities: case reportA 30-year-old woman developed hyperacute liver failure, hepatic encephalopathy, acidaemia, hyperlactataemia, hypotension, hypoglycaemia, reduced physical capacity, confusion, nausea, abdominal pain and agitation following paracetamol overdose.The woman presented to the emergency department with confusion, nausea and abdominal pain. Her history revealed that she was seen 3 days before the presentation for suspected ingesting of paracetamol in an overdose up to 30g at some point between her initial presentation and current presentation. An examination showed right upper quadrant pain, prolonged capillary refill time of >5 seconds, dry mucous membranes and cool peripheries. She appeared disorientated and confused, with a Glasgow coma score of 13 (E3V4M6). Her vital signs were as follows: pulse rate: 110 bpm, BP: 85/40mm Hg, oxygen saturations: 99% on room air and RR: 24 breaths/minute. Arterial blood gas showed hyperlactataemia and acidaemia. The CT scan showed a homogenous liver with patent portal vein, hepatic veins and hepatic artery without evidence of infective abdominal pathology. Her head CT scan was normal. Hence, she was admitted to the critical care unit. Based on her laboratory findings and symptoms, a diagnosis of significant acute coagulopathy, encephalopathy and jaundice in the context of hyperacute liver failure due to paracetamol overdose was made.Therefore, the woman was treated with acetylcysteine [N-acetyl-l-cysteine], fluid resuscitation and 0.9% of sodium chloride. Due to hypotension, she underwent insertion of arterial and central venous lines for pressure monitoring, alongside norepinephrine [noradrenaline] administration. She also received glucose infusion for hypoglycaemia. In view of progressive hepatic encephalopathy with agitation and confusion, she was intubated in critical care. Following discussion with the regional transplant centre, she was treated with unspecified antifungals and broad-spectrum antibiotics. She underwent dialysis catheter insertion for initiation of haemofiltration. She also received renal replacement therapy with continuous venovenous haemodiafiltration (CVVHDF). Treatment with sodium chloride [hypertonic saline] was given to increase her sodium level. No increase in intracranial pressure was noted. She was kept sedated and ventilated until her serum ammonia levels stablised. Her condition improved, and after 8 days, she was weaned from mechanical ventilation. After 3 weeks of hospitalisation, she was discharged. She had required intensive rehabilitation input. Despite discharge from the hospital, her physical capacity was significantly reduced.