Intravenous N-acetylcysteine: still the treatment of choice for paracetamol poisoning.

Prescott, L. F.; Illingworth, R N; Critchley, J. A. J. H.; Proudfoot, A. T.

doi:10.1136/bmj.280.6206.46-b

Cited by 245 publications

(91 citation statements)

References 18 publications

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“…6 NAC is thought to have a therapeutic effect in acetaminophen toxicity by regeneration of reduced glutathione. 3 Complete recovery following treatment with NAC in this case also highlights the fact that newborns and young children are more resilient to hepatic necrosis and failure than older children and adults. This may be related to reduced rates of metabolism by the CYP450 system in the neonatal liver and the newborn's increased ability to synthesize glutathione.…”

Section: Discussionmentioning

confidence: 56%

“…6 Hepatotoxicity from an acetaminophen overdose is mediated by the reactive metabolic intermediate N-acetyl-p-benzoquinoneimine (NAPQI), which is normally detoxified by reduced glutathione. 3 The reserves of glutathione needed for detoxification of NAPQI may be depleted after supratherapeutic or repeated therapeutic doses of acetaminophen. 6 NAC is thought to have a therapeutic effect in acetaminophen toxicity by regeneration of reduced glutathione.…”

Section: Discussionmentioning

confidence: 99%

“…7 Currently, there are two published intravenous NAC treatment protocols that are used in acetaminophen overdose in children and adults. 3 Anaphylactoid reactions (which can occur in up to 10% of patients) tend to be more significant with intravenous NAC compared to oral NAC. There are few toxicokinetic data of neonatal acetaminophen overdose available, 8 and the protocol used to treat acetaminophen toxicity in this case was based on adult studies.…”

Section: Discussionmentioning

confidence: 99%

“…A complete blood count revealed a WBC count of 13 600/mm, 2 hematocrit 66.4% and platelets of 154 000/mm. 3 Cerebral spinal fluid analysis was normal. The baby received intravenous volume expansion, dextrose and ampicillin and cefotaxime.…”

Section: Introductionmentioning

confidence: 97%

“…Treatment with a 20 h intravenous NAC infusion protocol 3 was initiated with a 150 mg/kg bolus of NAC given over 15 min, followed by a 50 mg/kg dose over 4 h and then 100 mg/kg over 16 h. A concentration of 40 mg/ml in 5% dextrose was used to avoid volume overload and hyponatremia. 3 Subsequent doses of NAC were given in 100 mg/kg aliquots over 16 h until the acetaminophen concentration was undetectable. Other supportive measures included transfusions of fresh frozen plasma and cryoprecipitate to correct coagulopathy; fluid boluses and furosemide to induce diuresis; high dextrose and restricted protein; ranitidine for blood-tinged gastric aspirates; and enteral lactulose therapy to cause increased stooling.…”

Section: Introductionmentioning

confidence: 99%

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Acetaminophen-induced hepatic failure with encephalopathy in a newborn

2007

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We report a case of oral acetaminophen toxicity in a term newborn infant successfully treated with a 20 h intravenous N-acetylcysteine infusion protocol without any adverse effects. This case report supports the use of N-acetylcysteine to treat neonatal acetaminophen toxicity and highlights the need for better education of parents regarding the appropriate use and dosage of acetaminophen in newborns. Journal of Perinatology (2007Perinatology ( ) 27, 133-135. doi:10.1038 Keywords: Neonatal acetaminophen toxicity; hepatic failure; N-acetylcysteine IntroductionAcetaminophen is an efficacious and safe analgesic used often in newborns. 1 Although it is relatively safe, acetaminophen toxicity is well documented and can lead to liver failure and even death. The risk of developing toxicity is, in general, thought to be lower in children than in adults. N-acetylcysteine (NAC) is the treatment of choice for acetaminophen overdose in older children and adults. To date, there are no documented neonatal cases of oral acetaminophen toxicity with hepatic encephalopathy. We report a case of oral acetaminophen toxicity presenting with hepatic encephalopathy and oliguric renal failure in a term newborn infant successfully treated with intravenous NAC without observable adverse effects.Case report A four day-old term male infant was brought to the emergency department after episodic emesis and decreased level of arousal. He was born to a 24 year-old mother following an uncomplicated pregnancy by normal spontaneous vaginal delivery at 41 weeks gestational age. Apgar scores were 9 at 1 min and 9 at 5 min. He was discharged on the second postnatal day after circumcision.One day later he became sleepy, fed poorly and vomited approximately 10 times in 24 h. The baby was evaluated by a visiting nurse, who sent him to the emergency department. On examination he was moderately dehydrated, lethargic and poorly responsive to stimulation. Gastric lavage produced blood-tinged aspirates. Significant laboratory findings included glucose 27 mg/dl (normal: 45 to 120 mg/dl), Na 149 mEq/l (normal: 135 to 148 mEq/l), K 5.9 mEq/l, Cl 110 mEq/l (normal: 91 to 111 mEq/l), CO 2 18 mEq/l, BUN 40 mg/dl, creatinine 3.2 mg/dl (normal: 0.3 to 1 mg/dl), total serum bilirubin 9 mg/dl with a conjugated fraction of 1.4 mg/dl, serum ammonia 114 mmol/l (normal: 56 to 92 mmol/l), AST 718 IU/l (normal: 20 to 65 IU/l), ALT 978 IU/l (normal: <54 IU/L), PT 51.9 s (normal; 10.1 to 15.9 s), PTT 45.7 s (normal: 31.3 to 54.3 s), INR 5.4 (normal: 0.96 to 1.04), D-dimer 5.9 mg/l, factor V assay 57% and fibrinogen 61 mg/dl (normal: 1.67 to 3.09 g/l). A complete blood count revealed a WBC count of 13 600/mm, 2 hematocrit 66.4% and platelets of 154 000/mm. 3 Cerebral spinal fluid analysis was normal. The baby received intravenous volume expansion, dextrose and ampicillin and cefotaxime. He was admitted to the neonatal intensive care unit with a presumptive diagnosis of sepsis with renal failure, liver failure and coagulopathy. An arterial blood gas analysis after fluid boluses ...

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Acetaminophen-induced hepatic failure with encephalopathy in a newborn

2007

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Treatment of severe acetaminophen poisoning with intravenous acetylcysteine

Prescott¹

1981

Archives of Internal Medicine

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Intravenous (IV) acetylcysteine, cysteamine, and methionine treatments were compared in patients with severe acetaminophen poisoning; a control group consisted of patients receiving supportive therapy only. Acetylcysteine proved the safest and most effective mode of treatment. Acetylcysteine was effective in preventing liver damage, hepatic failure, renal damage, and death when given eight to ten hours after poisoning. When treatment was delayed for ten to 24 hours, results were the same as in the supportive-therapy group. The alanine aminotransferase (ALT) activity remained normal in 76% of the patients treated within ten hours, as compared with 40% in both cysteamine- and methionine-treated groups and with 16% in the supportive-therapy group. The ingestion-treatment interval for complete protection with all three drugs was eight hours; beyond that time, the incidence of damage increased steadily. After 15 hours, all treatments were pointless. Based on my experience, IV administration is preferable, since nausea and vomiting may limit the effectiveness of oral therapy.

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Treatment of acetaminophen poisoning. The use of oral methionine

Vale¹

1981

Archives of Internal Medicine

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One hundred thirty-two cases of severe acetaminophen (paracetamol) poisoning were treated with oral methionine. Seven of 96 patients who received the antidote within ten hours of ingestion of the overdose had severe liver damage (aspartate transaminase level, greater than 1,000 IU/L), but none of these patients died. Thirty-six patients received methionine between ten and 24 hours of ingestion; severe liver damage occurred in 47%, and two patients died. The treatment protocol for oral methionine is simple, and therapy is complete within 12 hours as compared with three days for oral acetylcysteine and 20 hours for intravenous acetylcysteine. Side effects from methionine were unimportant. Oral methionine is as effective as acetylcysteine in preventing severe liver damage and death after acetaminophen overdose. However, as with acetylcysteine, it must be given within ten hours of ingestion to be effective.

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Intravenous N-acetylcysteine: still the treatment of choice for paracetamol poisoning.

Cited by 245 publications

References 18 publications

Acetaminophen-induced hepatic failure with encephalopathy in a newborn

Acetaminophen-induced hepatic failure with encephalopathy in a newborn

Treatment of severe acetaminophen poisoning with intravenous acetylcysteine

Treatment of acetaminophen poisoning. The use of oral methionine

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