Activated Charcoal for Acute Poisoning: One Toxicologist’s Journey

Abstract

When I began studying clinical toxicology in 1981, the issue of gastrointestinal decontamination after acute ingestion seemed pretty well settled: “universal antidote,” apomorphine and salt–water emesis were no longer used [1, 2]; and I was taught that barring a specific contraindication, the awake patient was given syrup of ipecac to induce emesis, and the drowsy or uncooperative patient was lavaged [3]. After gastric emptying, everyone received activated charcoal (AC). The only controversy seemed to be over whether one should add a cathartic to speed gastrointestinal transit [4]. Within a few years, my comfortable assumptions were upset by several prospective randomized trials that cast doubt on the value of gastric emptying prior to AC [5–8]. Merigian even challenged the ritual of routine oral AC when he assigned a subgroup of asymptomatic overdose patients to observation without charcoal and found no difference in outcome [8]. At about the same time, case reports of adverse outcomes in patients given AC began to appear [9–12]. (Ironically, when reviewing the literature in preparation for the present article, I found skepticism about gastrointestinal decontamination dating back to the 1940s. As summarized by Matthew [13], Harstad and Danish colleagues reported in 1942 that relatively little phenobarbital was recovered by lavage even shortly after overdose [14] and this, along with their finding of particles of charcoal in the lungs of patients who died, led them to call for the abandonment of gastric lavage for poisoning.) In recent years, my colleagues and I have continued to debate the value of various methods of gastric decontamination and the role and risks of activated charcoal, and it is clear to me that the issue remains muddy. Some have taken a firm stand that no treatment should be recommended that is not supported by evidence from a randomized controlled trial (RCT). Position statements published jointly by the American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists have adopted a generally conservative view (i.e., lacking evidence, these procedures should not be used routinely) [15–18]. Others have argued that quality RCTs are few and flawed and that we may never have all the evidence we need to guide management of every case. A number of thorough and thoughtful reviews and editorials have summarized the literature and have attempted to provide guidance for the selected use of gastric emptying or activated charcoal [19–23]. In this brief review, I will attempt to answer the following questions about activated charcoal: what is it and what does it bind to? What do animal studies and human volunteer studies reveal about its efficacy in simulated overdose? What evidence is there from case reports and controlled trials for its benefit in humans? What are the potential risks of administering activated charcoal? And finally, how can we put our knowledge about charcoal to use in managing specific patients? Project not funded by any external sources