Activated charcoal (AC) and N-acetylcysteine (NAC) are used in the treatment of acetaminophen toxicity. Antiemetics are used to relieve nausea and vomiting, which can result from both acetaminophen toxicity and from AC and oral NAC administration.
Gastrointestinal (GI) decontamination with oral AC is selectively used in the emergency treatment of poisoning caused by some drugs and chemicals. The network of pores present in AC adsorbs 100-1000 mg of drug per gram of charcoal. AC does not dissolve in water.
Consider GI decontamination with AC in any patient who presents within 1 hour after the ingestion. Maximum effect is achieved if AC is used within 1 hour post ingestion. AC may be helpful more than 4 hours post-ingestion, if co-ingestion with an agent that slows gut motility occurred or if a sustained-release preparation was ingested.
AC adsorbs acetaminophen, but its use has been controversial, because AC may absorb oral NAC. Although AC reduces the bioavailability of NAC, the small decrease in the NAC bioavailability is unlikely to reduce the effectiveness of oral NAC as an antidote.
NAC counteracts acetaminophen toxicity both directly and indirectly. NAC is converted to cysteine, which replenishes glutathione stores, thus providing a substrate for conjugation with the toxic metabolite of APAP, N -acetyl-p -benzoquinoneimine (NAPQI). NAC also directly detoxifies NAPQI to nontoxic metabolites.
Administer all doses of NAC as directed under the guidance of a regional poison control center. Shortened courses of NAC administration have been found to be effective in preventing liver toxicity in select patients with APAP overdose. [39, 40]
Activated charcoal (AC) is the drug of choice for gastric decontamination and is used for emergency treatment in poisoning caused by drugs and chemicals. A network of pores absorbs 100-1000 mg of drug per gram of charcoal. AC prevents absorption by adsorbing the drug in the intestine. AC does not dissolve in water and for maximum effect, administer this agent within 1 hour after ingestion of poison.
N-acetylcysteine (NAC) is the drug of choice for the prevention and treatment of APAP-induced hepatotoxicity. This medication is approved by the US Food and Drug Administration (FDA) for both oral and intravenous (IV) administration. For the maximum hepatoprotective effects, administer NAC within 8-10 hours of an acute APAP ingestion.
Three treatment protocols are recognized: 72-hour oral, 21-hour IV, and 48-hour IV. The entire NAC protocol, either oral or IV regimen, should be completed even if serumacetaminophen concentrations decrease.
The oral form of NAC, Mucomyst, is available as a 20% solution (200 mg/mL). This should be diluted to 5% solution (50 mg/mL) with fruit juice or carbonated beverage. Aggressive antiemetic therapy is indicated in patients with nausea or vomiting due to acetaminophen-induced hepatic injury or foul sulfur odor of the solution. If the patient vomits within 60 min of administration, repeat the dose.
If failure to tolerate oral formulation persists, switch to the IV preparation (Acetadote). When administered intravenously, dilute NAC in 5% dextrose solution (D5W) and infuse per the recommended intravenous protocol for acute (within 8-10 h) or late-presenting or chronic acetaminophen ingestion.
Emesis is frequently associated with APAP toxicity and is a common adverse effect of both AC and oral NAC administration. For these reasons, antiemetic therapy is often necessary to facilitate the successful administration of oral NAC. Persistent nausea or vomiting precludes oral NAC administration; in this situation, NAC should be administered intravenously.
Antiemetics that do not decrease gastric motility or significantly alter mental status are the drugs of choice; anticholinergic drugs such as prochlorperazine are not considered beneficial, in part because of their propensity to cause both of these adverse effects. Phenothiazines may also contribute to the potential toxicity associated with other anticholinergic drugs, if they are co-ingested with APAP-containing formulations.
Metoclopramide functions as an antiemetic by blocking dopamine receptors in the chemoreceptor trigger zone of the central nervous system. It also enhances gastrointestinal motility and accelerates gastric emptying time. This agent is of low cost and is generally considered an initial drug of choice for the treatment of nausea.
Ondansetron is a selective 5-hydroxytryptamine (5HT3) receptor antagonist. This drug blocks serotonin by acting on the vagus nerve peripherally and at the chemoreceptor trigger zone of the central nervous system (CNS). Ondansetron is considered more effective than metoclopramide, with fewer adverse effects, but it is more costly than metoclopramide.
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