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Paracetamol Poisoning

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A poison is any substance which, when taken into the body in sufficient quantity, may either endanger life or seriously impair body functions (IHCD 1999).


Poisons come in many forms and can enter the body in many ways: Inhalation – fumes, gases; Ingestion – liquids or solids by mouth; Injection – needles, animal and insect bites; Absorption – pesticides or herbicides through the skin and eyes.
In the field of accident and emergency we see cases of poisoning that are both accidental and intentional. A massive 85% of these cases involve just three types of drug: Paracetamol 45% Benzodiazepines 20% Antidepressants 20% (Daly; Harrison, 2001).

As the majority of our cases come from these non-corrosive types of poisons the author will concentrate only on overdoses of drugs, with the second section solely devoted to the most common of these; Paracetamol.

Clinical Signs of Poisoning

The majority of drugs effect the nervous system and produce some common signs: ▪ Slow, shallow respiration’s ▪ Lethargy and reduction in activity ▪ Vomiting and diarrhoea ▪ Loss of consciousness
Some drugs though, such as Paracetamol are asymptomatic during the early stages of poisoning.

Although in the majority of cases our treatment in the field for poisoning will be the same irrespective of the drug involved, certain signs can point to the type of drug taken. Below are some examples of these.

➢ Eyes: Pinpoint – opioids. Dilated – tricylics, cocaine. ➢ CNS Drowsiness – alcohol, sedatives, opioids, hypnotics. ➢ Confusion/Ataxia/Excitability – alcohol, tricyclics, antihistimines, salbutamol, solvents. ➢ Dystonia – metaclopramide, phenothiazenes ➢ Cardiac arrythmias – tricyclics, amphetamines, digoxin, blockers. ➢ Hypertension with tachycardia – amphetamines. ➢ Hypertension – sedatives, narcotics, hypnotics, tricyclics, alcohol. ➢ Sweating – salicylates (e.g. aspirin). ➢ Hyperventilation – salicylates, opioids, sedatives, hypnotics. ➢ Hypothermia – amphetamines, salicylates, ecstacy, alcohol. (BAEM, 1997)


✓ Ensure open airway ✓ Administer 100% oxygen ✓ Assist ventilation if necessary ✓ Carry out CPR if required ✓ Do not induce vomiting, if pt does vomit keep sample for hospital analysis ✓ Provide milk or water to dilute and delay absorption if the poison is unknown. This must not delay transport to hospital. ✓ Place in recovery position if unconscious. ✓ Keep pt still and quiet to reduce pulse rate ✓ Not allowing pt to walk (IHCD, 1997)
It would also be sensible to attach the pt to an ECG. If paramedic available the pt could be cannulated for IV access. If opiate overdose is evident, the paramedic should administer naloxone titrated against response up to 1600mcg.
Remember to treat other associated conditions, such as hypothermia and hypotension following WAST guidelines.

As part of good management it is important to gain an accurate history. This should include what was taken, the time it was taken and the amount. The pt statement as to these should be accepted with caution. They may give false information (intentionally or otherwise), therefore any circumstantial evidence should be looked for: i.e. empty bottles/wrappers, loose tablets. All should be retained and taken to hospital with the pt. It is also sometimes difficult to get history from children. In paediatric cases suspect diagnosis of overdose from abnormal behaviour, convulsions, ataxia and GI disturbance (BAEM, 1997).



Paracetamol is the most widely used pharmaceutical analgesic and antipyretic drug in the world, and the most common pharmaceutical associated with both accidental and intentional poisoning (Farrell, 2002). The drug is also known as Acetimophen and
N-acetyl-p-aminophenol (APAP).

Harrison/Daly; state that there are 70,000 cases of APAP poisoning cases in the UK every year. Out of these 70,000 approximately 200 patients die due to liver damage.


The maximum daily dose of APAP is 4g in adults and 90mg/kg in children. The dose at which paracetamol becomes toxic seems to be a matter of debate. Farrell suggests that a toxic dose in adults is 7g, while Harrison/Daly state that a dose of 10-15g is needed to produce severe liver damage. They do agree though that in adults ingestion of 150mg/kg in one dose is a toxic amount.

Taken in normal amounts, APAP is rapidly absorbed from the stomach and small intestine. In the liver it is metabolised to non-toxic agents, these are then eliminated in the urine. In acute or accumulated overdose the normal metabolic method is saturated, therefore the APAP is metabolised by the liver in to a toxic agent; N-acetyl-p-benzoquinine-imine (NAPQI). In small amounts this toxin binds with other agents in the body to be rapidly removed from the system. In excess NAPQI cannot be removed so readily, and so it is free to bind to vital proteins and the lipid bilayer of hepatocytes, resulting in necrosis in the liver.

With supportive care and antidotal therapy the majority of patients survive.
Fewer than 4% of patients who suffer hepatoxicity develop liver failure; fatalities or liver transplant occur in less than half of these patients (Farrell, 2002).

Patients with malnutrition, aids, alcohol abuse or anorexia nervosa are all at increased risk from APAP overdose. While paediatrics under 5 appear to fare better than adults after APAP poisoning.

Signs and Symptoms

These vary depending on the phase of toxicity; they can therefore give an estimate of time since ingestion.

Phase 1 (0-24 hours)

• Asymptomatic • Malaise • Diaphoresis • Nausea • Vomiting (very low incidence, Ferren; 2002)

Phase 2 (18-72 hours)

• Right upper abdo pain • Tachycardia • Hypotension

Phase 3 (72-96 hours)

• Tender hepatic edge • Jaundice • GI bleed • Hepatic encephalopathy • Renal failure • Fatality


Care prior to reaching Accident and Emergency is the same as mentioned in Section 1 under management.

Once in the A&E department there are several methods of treatment.

• Supportive therapy: IV fluids, oxygen therapy, cardiac monitoring.

• Gastric decontamination: If the patient presents with 1-2hours post ingestion oralactivated charcoal is given to absorb the drug. If an inhibiting co-ingestant may have been involved it can be administered later.

Oral activated charcoal should also be administered if the time of ingestion is unknown. There is a minimal benefit if post ingestion is greater than 4 hours.

• Administer N-acetylcysteine (NAC): This is the antidote also known as Parvolex. It works by a number of protective mechanisms. Early after overdose it will prevent the formation and accumulation of the toxin NAPQI. The drug also function as an anti-inflammatory and antioxidant and has positive inotropic and vasodilating effects, improving microcirculation and oxygen delivery to tissues. Vasodilating effects decrease morbidity even when hepatoxicity is well established.

NAC is most effective when administered within 8 hours of ingestion. (Farrell, 2002)


Farrell, SE. 2002. Toxicity, Acetaminophen. EMedicine Journal. (vol 3, No 1)

Harrison R; Daly, L. 2001. Acute Medical Emergencies. A Nursing guide. Churchill/livingstone.

Herren, K. 2002. Vomiting In Paracetamol Overdose. EMJ. (June Ed, p.248)

Oxford. 1998. Concise Medical Dictionary (5th Ed). Oxford University Press.

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