A fictional 31-year-old presents after staggered paracetamol ingestion with worsening confusion, hypoglycaemia, acidosis and rising INR.
Listen for the assumption.
The paracetamol concentration is low, so the antidote can probably stop.
In staggered exposure with evolving liver failure, what matters more than one concentration?
The clinical trajectory: encephalopathy, glucose, acid-base status, renal function and coagulation. I will involve critical care and a specialist liver unit now.
Choose an answer below and reveal the reasoning to see consultant feedback at every checkpoint. The full consultant-led synthesis follows after all three decisions.
Go to the first decision ↓The picture develops.
- New confusion and recurrent hypoglycaemia
- Metabolic acidosis and acute kidney injury
- INR rising after staggered paracetamol exposure
Commit before you reveal.
After you select an option, reveal the model reasoning and the consultant’s feedback.
Hear the senior team refine the plan.
The registrar tests the plan, the consultant synthesises the key principle, and the SHO confirms the safer next steps.
Obtain a precise exposure history, but do not let uncertainty delay antidote and specialist advice under the appropriate pathway.
Early referral protects the chance of safe transfer. The liver unit guides prognostication, transplant assessment and ongoing therapy.
I will record glucose and neurological trends, organ support and the agreed receiving-centre plan.
What must remain explicit.
- Use current local toxicology and acute-liver-failure guidance.
- Involve critical care and a specialist liver unit early.
- This case does not replace TOXBASE or specialist advice.
Where reasoning fails.
- Relying on one drug concentration
- Delaying specialist discussion
- Treating INR alone
Acute liver failure after [exposure pattern], neurology [trend], glucose/acid-base/renal/coagulation [trend], antidote [status] and liver-unit discussion [time/plan].
What feature would trigger referral even before overt encephalopathy?