Australian Clinical Toxicology Investigators Collaboration randomized trial of different loading infusion rates of N-acetylcysteine.
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Acetaminophen↗
Biomedical subjects
Paul I Dargan
Publications and source records attributed to Paul I Dargan.
The management of tricyclic antidepressant poisoning : the role of gut decontamination, extracorporeal procedures and fab antibody fragments.
Although there have been descriptive, uncontrolled clinical reports of removal of tablet debris by gastric lavage, there have been no clinical studies that have demonstrated that this has any impact on outcome in patients with tricyclic antidepressant (TCA) poisoning. There is also the possibility that lavage may increase drug absorption by pushing tablets into the small intestine. Furthermore, gastric lavage in patients with TCA poisoning may induce hypoxia and a tachycardia potentially increasing the risk of severe complications such as arrhythmias and convulsions. In view of the paucity of evidence that gastric lavage removes a significant amount of drug and the risk of complications associated with the procedure, the routine use of gastric lavage in the management of patients with TCA poisoning is not appropriate. Volunteer studies have shown generally that activated charcoal is more likely to reduce drug absorption if it is administered within 1 hour of drug ingestion. In the one volunteer study that looked at later administration of activated charcoal, there was a 37% decrease in plasma concentration associated with administration of activated charcoal at 2 hours post-ingestion. There have been no clinical studies that enable an estimate of the effect of activated charcoal administration on outcome in the management of patients with TCA poisoning. Volunteer studies have shown that multiple-dose activated charcoal increases the elimination of therapeutic doses of amitriptyline and nortriptyline, but not of doxepin or imipramine; however, these studies cannot be directly extrapolated to the management of patients with TCA poisoning. There have been no well designed controlled studies that have assessed the impact of multiple-dose activated charcoal in the management of patients with TCA poisoning. Because of the large volume of distribution of TCAs, it would not be expected that their elimination would be significantly increased by multiple-dose activated charcoal.Haemoperfusion, haemodialysis and the combination of these procedures do not result in significant removal of TCAs and are not recommended in the management of patients with TCA poisoning.
Animals↗
Duodenal perforation after ibuprofen overdose.
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Adolescent↗
Case report: severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration.
INTRODUCTION: Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, life-threatening features and acute renal failure. Previous reports on the use of extracorporeal procedures such as haemodialysis and haemoperfusion have shown no significant removal of mercury. We report here the successful use of the chelating agent 2,3-dimercaptopropane-1-sulphonate (DMPS), together with continuous veno-venous haemodiafiltration (CVVHDF), in a patient with severe inorganic mercury poisoning. CASE REPORT: A 40-year-old man presented with haematemesis after ingestion of 1 g mercuric sulphate and rapidly deteriorated in the emergency department, requiring intubation and ventilation. His initial blood mercury was 15 580 microg/l. At 4.5 hours after ingestion he was started on DMPS. He rapidly developed acute renal failure and so he was started on CVVHDF for renal support and in an attempt to improve mercury clearance; CVVHDF was continued for 14 days. METHODS: Regular ultradialysate and pre- and post-filtrate blood samples were taken and in addition all ultradialysate generated was collected to determine its mercury content. RESULTS: The total amount of mercury in the ultrafiltrate was 127 mg (12.7% of the ingested dose). The sieving coefficient ranged from 0.13 at 30-hours to 0.02 at 210-hours after ingestion. He developed no neurological features and was discharged from hospital on day 50. Five months after discharge from hospital he remained asymptomatic, with normal creatinine clearance. DISCUSSION: We describe a patient with severe inorganic mercury poisoning in whom full recovery occurred with the early use of the chelating agent DMPS and CVVHDF. There was removal of a significant amount of mercury by CVVHDF. CONCLUSION: We feel that CVVHDF should be considered in patients with inorganic mercury poisoning, particularly those who develop acute renal failure, together with meticulous supportive care and adequate doses of chelation therapy with DMPS.
Acute Kidney Injury↗
Management of paracetamol poisoning.
Paracetamol is the most common substance involved in self-poisoning in the UK. The main advances made over the past five years in the management of early paracetamol poisoning, identification of risk factors for paracetamol poisoning, understanding of the mechanisms and management of late paracetamol poisoning and issues concerning the prevention of paracetamol poisoning are discussed.
Acetaminophen↗
Multiple toxicity from 3,4-methylenedioxymethamphetamine ("ecstasy").
There have been no published case series illustrating "ecstasy" (3,4-methylenedioxymethamphetamine [MDMA]) toxicity in a group of patients who have ingested ecstasy in the same environment. We report a series of 7 patients who ingested ecstasy in a nightclub and presented with varying degrees of MDMA toxicity. Three patients presented with features of severe MDMA toxicity. One died within an hour of hospital admission, another died 4 days later, after developing fulminant hepatic failure, and the third recovered after 12 days in intensive care. MDMA was identified in the serum of all 7 patients. High serum MDMA concentrations correlated with severe clinical and biochemical features including coma, hyperpyrexia, cardiovascular compromise, acidosis, and hyperkalaemia. "Poisoned ecstasy" was widely reported by the media as being responsible for the adverse effects observed. This report highlights a relationship between serum concentrations and toxic effects of MDMA, and the ongoing need to educate the public about the dangers of this substance.
Adolescent↗
Acetaminophen poisoning: an update for the intensivist.
Acetaminophen overdose is common and can result from deliberate/nonstaggered or accidental/staggered ingestion. Patients presenting within 24 h of an acetaminophen overdose can safely be managed on medical wards. Early management of nonstaggered overdose is guided by the plasma acetaminophen concentration, whereas management of accidental/staggered ingestion is guided by ingested dose. Ingested dose and time from ingestion to presentation are important prognostic factors in accidental/staggered ingestion. Acetaminophen-induced acute liver failure (ALF) requires meticulous supportive care in an intensive care unit (ICU), with early identification and transfer of patients who are likely to require liver transplantation to a specialist liver centre. The modified King's College Hospital criteria (incorporating lactate into the traditional criteria) represent the best tool for identifying patients who require transplantation.
Acetaminophen↗
Should a lower treatment line be used when treating paracetamol poisoning in patients with chronic alcoholism?: a case against.
The widespread practice of using a lower plasma paracetamol (acetaminophen) concentration threshold for the treatment of paracetamol poisoning in patients with chronic alcoholism has been introduced on the basis of anecdotal case reports. In animals, acute alcohol loading inhibits toxic metabolic activation of paracetamol whilst chronic alcohol administration results in cytochrome P450 (CYP) 2E1 induction with increased toxic metabolic activation of paracetamol by CYP2E1 and increased hepatotoxicity. However, due to species differences in CYP expression, activity and induction, it is not possible extrapolate the results of these animal studies to clinical situations in humans. Isoenzymes are also responsible for the metabolic activation of paracetamol in humans and human studies to date have not convincingly demonstrated increased toxic metabolic activation of paracetamol in patients with chronic alcoholism. Acute alcohol ingestion at the time of a paracetamol overdose is probably protective and the timing and chronicity of alcohol intake is therefore crucial in the interpretation of the effects of alcohol on paracetamol overdose. One of the problems in the interpretation of the literature to date is that insufficient information is available on the timing of alcohol intake in relation to the ingestion of paracetamol. Whilst it is possible that chronic exposure to excessive amounts of alcohol does predispose patients with paracetamol overdose to hepatotoxicity, a critical review of the literature reveals that the evidence to date does not support this. A prospective, controlled study is required. On the basis of the scientific evidence to date, use of the 100 line for patients with chronic alcoholism, in countries where the 200 line represents the standard treatment line, is unjustified.
Acetaminophen↗