170 Tox icolog y
SPECIFIC POISONS
Paracetamol
DIAGNOSIS
1 Paracetamol overdose is common and potentially lethal.
2 Hepatocellular necrosis is the major complication of paracetamol toxicity.
Factors that enhance the potential for hepatotoxicity, and therefore morbid-
ity and mortality, include:
(i) Late presentation with delayed antidote administration,
especially if over 24 h.
(ii) Staggered overdose: multiple supra-therapeutic ingestions over a
number of days.
(iii) Glutathione deficiency in starvation and debilitating illness such
as AIDS.
(iv) Enzyme-inducing drugs such as carbamazepine, phenobarbitone
(phenobarbital), rifampicin or isoniazid.
(v) Regular alcohol use.
3 Determine the time since ingestion, total paracetamol consumed and the
patient’s weight:
(i) Patients who have taken >10 g (20 tablets) or >200 mg/kg over a
period of <8 h are considered at risk from severe liver damage.
(ii) The greatest risk of hepatotoxicity is related to the extent of delay
beyond 8 h until antidote treatment with N-acetylcysteine (NAC)
is commenced.
(iii) Hepatotoxicity may also occur in patients who take repeated or
staggered doses, or sustained-release preparations.
4 The patient is usually asymptomatic, but can present in fulminant hepatic
failure with abdominal pain, vomiting, hypoglycaemia, tender hepato-
megaly, jaundice and encephalopathy.
5 Gain i.v. access and send bloods for full blood count (FBC), urea and
electrolytes (U&Es), liver function tests (LFTs), prothrombin index (PTI)
(international normalized ratio [INR]) and a blood sugar level.
(i) These bloods become more important if the patient presents over
8 h after ingestion, and are essential if presentation is delayed
beyond 24 h or more.
(ii) Send a paracetamol level once 4 h or more have elapsed since
overdose.
MANAGEMENT
1 Resuscitation is rarely required unless the patient is in fulminant hepatic
failure.
(i) Administer 50% dextrose 50 mL i.v. if the patient is
hypoglycaemic.