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Paracetamol overdose

Introduction

Paracetamol (aka acetaminophen) is a widely used over the counter analgesic medication. In its recommended dose it is safe and effective. However, it also has the potential to cause severe liver damage (and potentially death) when taken in overdose. Liver damage is often delayed by several days – and this gives a window of opportunity to prevent this damage from occurring with the use of acetylcysteine.

Paracetamol overdose is the single most common cause of acute liver injury in the western world. 

Paracetamol overdose can be either intentional (i.e. in a suicide or self-harm attempt) or unintentional. Overdose may often be “staggered” – i.e. taken over several days, weeks or months in doses higher than the recommended dose. These cases are harder to diagnose and manage as the paracetamol concentration doe not follow the normal “nomogram” pattern (see below). Examples of toxic doses in staggered overdose include:

Most cases are straightforward and can be managed according to local protocols – an example of which is given in the treatment section below. The difficulty is in recognising and treating more complex cases. Guidelines can often vary widely between jurisdictions.

Patients who present early should be given activated charcoal to prevent absorption. Patients who are at risk of liver damage should be given an intravenous infusion of N-acetylcysteine (NAC). You can use the nomogram to assess who is at risk. Special cases include large/ massive overdoses, accidental liquid ingestion in children and staggered overdose.

Only a very small percentage of patients will develop hepatotoxicity – often defined as ALT > 1000U/L. Only a very small percentage of these patients will develop liver failure. Typically ALT will rise for 3-4 days before recovering.

Mechanism

It is also worth noting here the role of the cytochrome P450 system. Problems with this system do NOT increase the risk of paracetamol toxicity – because the toxicity is related to NAPQI. If there is a reduction in cytochrome P450 efficacy – then LESS NAPQI is produced and in fact – toxicity may even be reduced.

Signs and Symptoms

Signs and symptoms typically do not develop until 24 hours after ingestion.

Investigations

Paracetamol level and ALT are the most important tests

Patients at high risk of hepatotoxicty should also have:

The Nomogram

Paracetamol Nomogram. Taken from LITFL – Paracetamol Toxicology

The is a graph used to estimate the need for treatment. It is also an excellent predictor or risk of liver damage for those “above the line”. To compare the patient to the nomogram the time of ingestion needs to be known, as well as the serum paracetamol level.

The nomogram should only be use if all the following are met:

Patients with levels more than double the nomogram line are at increased risk and should be given modified acetylcysteine regimens.

Always check the units on the nomogram! They are available in both mg/L and umol/L – and you will need to be using the same units as the serum paracetamol level result.
The nomogram is only validated for use between 4 hours and 16b hours after ingestion – but can be extrapolated (with caution) up to 24 hours.

Management

Management if <8 hours after ingestion

Activated Charcoal

Not suitable in many instances. Give 50mg activated charcoal orally if:

Acetylcysteine

An example protocol would include:

Repeat ALT and paracetamol levels 2 hours before completion of NAC (see above in investigations section).

R

Management if >8 hours after ingestion

Give acetylcystiene if >12g or >150mg/Kg has been ingested, regardless of current plasma level (don’t wait for blood result)

Liver transplant

Should be considered if:

References

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