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CASE STUDY/ASSIGNMENT-2
rapidly absorbed from the gastrointestinal tract, and peak serum concentrations
are usually achieved within 2 hours. Delayed absorption can occur especially
release preparations.
N-acetyl-p-benzoquioneimine (NAPQI).
Observed hepatocyte damage typically progresses with cell lysis on the second
four stages. During the first 24 hours after exposure (stage 1), patients may be
(including right upper quadrant pain and tenderness) may occur and serum
after 1 to 3 months.
synthase) in other organs. In rare cases, isolated renal injury, cardiac toxicity,
either liver failure or hypotension. Likely mechanisms for this finding include
hours, and unknown time or >24 hours before presentation. The risk of
hepatotoxicity increases with the lag time between ingestion and initiation of
acetylcysteine therapy.
for acetylcysteine therapy has been determined until the completion of the
For patients who present to the ED within 4 hours and are likely to have a
paracetamol concentration.
If the clinical laboratory can report the paracetamol concentration within the
therapy is necessary.
determined, the need for acetylcysteine therapy can be determined with the use
of the nomogram.
For patients who present >4 hours but <24 hours following paracetamol
presentation.
after ingestion, await the paracetamol concentration and plot the result on the
or >66 micromole/L) suggests that the patient may be at risk for developing
and the serum transaminases are not elevated, the acetylcysteine can be
discontinued.
downtrending transaminases (at least two values) and there are no signs of
reported to the regional poison control center for both data collection purposes