Acetaminophen Toxicity Clinical Presentation
- Author: Susan E Farrell, MD; Chief Editor: Asim Tarabar, MD more...
History and Physical Examination
The clinical course of acetaminophen (APAP) toxicity generally is divided into 4 phases. Physical examination findings may vary, depending on the phase of toxicity.
Clinical evidence of end-organ toxicity is often delayed 24-48 hours after an acute ingestion.
Because antidotal therapy is most effective when initiated within 8 hours after an ingestion, it is important to obtain an accurate history of the time(s) of ingestion, the quantity, and the formulation of APAP ingested. In addition, the history should include any co-ingestants, which may delay APAP absorption (eg, anticholinergic drugs or opioids).
The serum APAP concentration is the basis for diagnosis and treatment, even in the absence of symptoms. After a single ingestion, N -acetylcysteine (NAC) therapy is guided by the serum APAP concentration.
Phase 1 (0-24 h)
Patients may be asymptomatic or report anorexia, nausea or vomiting, and malaise. Physical examination may reveal pallor and diaphoresis. A subclinical rise in serum transaminase levels begins approximately 12 hours after an acute ingestion.
Phase 2 (18-72 h)
Patients generally develop right upper quadrant abdominal pain, anorexia, nausea, and vomiting. Right upper quadrant tenderness, tachycardia, and hypotension may be present. There is a continued rise in serum transaminase levels.
Phase 3 (72-96 h)
Patients may have continued nausea and vomiting, abdominal pain, and a tender hepatic edge. Hepatic necrosis and dysfunction are associated with jaundice, coagulopathy, hypoglycemia, and hepatic encephalopathy. Acute renal failure develops in some critically ill patients. Death from multiorgan failure may occur.
Phase 4 (4 d to 3 wk)
Patients who survive critically illness in Phase 3 have complete resolution of symptoms and complete resolution of organ failure.
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