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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.
NAPQI, also known as NAPBQI or N-acetyl-p-benzoquinone imine, is a toxic byproduct produced during the xenobiotic metabolism of the analgesic paracetamol (acetaminophen). [1] It is normally produced only in small amounts, and then almost immediately detoxified in the liver.
This type of adverse effect that results from pharmaceutical drug exposure is commonly due to interactions of the drug with its intended target. In this case, both the therapeutic and toxic targets are the same. To avoid toxicity during treatment, many times the drug needs to be changed to target a different aspect of the illness or symptoms.
As of 2016, benzodiazepines were most likely to cause fatal overdose in Australia, [20] with diazepam (Valium) being the drug most responsible. [12] While fatal overdoses are highly associated with drugs such as opiates, cocaine and alcohol, [ 2 ] deaths from other drugs such as caffeine are extremely rare.
Paracetamol, [a] or acetaminophen, [b] is a non-opioid analgesic and antipyretic agent used to treat fever and mild to moderate pain. [13] [14] [15] It is a widely available over-the-counter drug sold under various brand names, including Tylenol and Panadol. Paracetamol relieves pain in both acute mild migraine and episodic tension headache.
The Rumack–Matthew nomogram, also known as the acetaminophen nomogram, is an acetaminophen toxicity nomogram. It plots serum concentration of acetaminophen against the time since ingestion, in order to predict possible liver toxicity and allow a clinician to decide whether to proceed with N-Acetylcysteine (NAC) treatment.
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For paracetamol overdose, it works by increasing the level of glutathione, an antioxidant that can neutralize the toxic breakdown products of paracetamol. [9] When inhaled, it acts as a mucolytic by decreasing the thickness of mucus. [14] Acetylcysteine was initially patented in 1960 and came into medical use in 1968.