Paracetamol poisoning | |
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Other names | Acetaminophen toxicity, paracetamol toxicity, acetaminophen poisoning, paracetamol overdose, acetaminophen overdose, Tylenol toxicity |
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Paracetamol | |
Specialty | Toxicology |
Symptoms | Early: Non specific, feeling tired, abdominal pain, nausea Later: Yellowish skin, blood clotting problems, confusion |
Complications | Liver failure, kidney failure, pancreatitis, low blood sugar, lactic acidosis. |
Usual onset | After 24 hours (toxicity)[1] |
Causes | Paracetamol (acetaminophen) usually > 7 g[2][1] |
Risk factors | Alcoholism, malnutrition, certain other hepatotoxic medications[1] |
Diagnostic method | Blood levels at specific times following use[1] |
Differential diagnosis | Alcoholism, viral hepatitis, gastroenteritis[1] |
Treatment | Activated charcoal, acetylcysteine, liver transplant[1] |
Prognosis | Death occurs in ~0.1%[1] |
Frequency | >100,000 per year (US)[1] |
Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen).[2] Most people have few or non-specific symptoms in the first 24 hours following overdose. These symptoms include feeling tired, abdominal pain, or nausea. This is typically followed by absence of symptoms for a couple of days, after which yellowish skin, blood clotting problems, and confusion occurs as a result of liver failure. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks.[3][4] Without treatment, death from toxicity occurs 4 to 18 days later.[5]
Paracetamol poisoning can occur accidentally or as an attempt to die by suicide. Risk factors for toxicity include alcoholism, malnutrition, and the taking of certain other hepatotoxic medications.[1] Liver damage results not from paracetamol itself, but from one of its metabolites, N-acetyl-p-benzoquinone imine (NAPQI).[6] NAPQI decreases the liver's glutathione and directly damages cells in the liver.[7] Diagnosis is based on the blood level of paracetamol at specific times after the medication was taken.[1] These values are often plotted on the Rumack-Matthew nomogram to determine level of concern.[1]
Treatment may include activated charcoal if the person seeks medical help soon after the overdose.[1] Attempting to force the person to vomit is not recommended.[6] If there is a potential for toxicity, the antidote acetylcysteine is recommended.[1] The medication is generally given for at least 24 hours.[6] Psychiatric care may be required following recovery.[1] A liver transplant may be required if damage to the liver becomes severe. The need for transplant is often based on low blood pH, high blood lactate, poor blood clotting, or significant hepatic encephalopathy. With early treatment liver failure is rare.[6] Death occurs in about 0.1% of cases.[1]
Paracetamol poisoning was first described in the 1960s.[6] Rates of poisoning vary significantly between regions of the world.[8] In the United States more than 100,000 cases occur a year.[1] In the United Kingdom it is the medication responsible for the greatest number of overdoses.[7] Young children are most commonly affected.[1] In the United States and the United Kingdom, paracetamol is the most common cause of acute liver failure.[9][1]