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Using Activated Charcoal in Medical Toxicology

By Richard J. Geller, MD, MPH


Activated charcoal is the single most widely used method of gastrointestinal (GI) decontamination for the treatment of the poisoned patient. Generically, decontamination refers to efforts to inhibit absorption of drugs and poisons after exposure. Annual American Association of Poison Control Centers data documents use patterns for each of the 4 general methods of GI decontamination in cases reported to America’s 62 poison control centers. Data for 2004 reveal that, of 2,438,644 human exposures, 130,938 patients were given single dose activated charcoal (5.4% of patients), gastric lavage was performed in 16,179 patients (0.66%), 4,701 received syrup of ipecac (0.19%) and 2,961 (0.12%) underwent whole bowel irrigation. (1)


Activated charcoal is prepared by pyrolysis of wood or other carbonaceous material, and then oxidation of the pyrolyzed product with steam or carbon dioxide. The fine particles which result have a surface area of 1,000 – 2,000 m2 per gram. (2) The surface of activated charcoal contains several moieties that adsorb drugs and poisons to varying degrees. (3)


Activated charcoal is available in many preparations for many uses. It is used in California to purify drinking water contaminated with substances such as 1,2-dibromo-3-chloropropane (DBCP). Charcoal prepared for medicinal use must meet USP standards for adsorptive capacity, purity, and microbial contamination. While pharmaceutical activated charcoal is available as a suspension in either water or sorbitol, the plain aqueous preparation is usually preferred. If sorbitol is used, only one dose is given, as repeated use of the cathartic has caused serious fluid and electrolyte disturbances, and often provokes abdominal cramping. Activated charcoal in either water or sorbitol is usually sold as 50 grams charcoal in 240 ml total volume.


Activated charcoal is often recommended in a dose by weight that is ten times the weight of the estimated drug or poison ingested, to a maximum single dose of 100 grams in adults. The precise appropriate dose of charcoal in any given ingestion is, however, unknown. The 10:1 charcoal to drug ratio is based on multiple studies looking at the ability of activated charcoal to retard absorption when given at varying charcoal to toxin ratios. In one such study, Chin(4) used a rat model to investigate the effectiveness of charcoal:drug ratios of 1:1, 2:1, 4:1 and 8:1 for exposures to phenobarbital, chloroquine and isoniazid. Reduction of absorption at 1:1 ratios for the 3 drugs was 7%, 20% and 1.2%, and for 8:1 ratios was 89%, 96% and 80%.

It is far easier to achieve a 10:1 ratio of charcoal to drug for overdoses of medicines usually prescribed in microgram quantities, i.e., digoxin and levothyroxin, than for drugs normally used in much higher doses, such as aspirin. It would be hard to find a digoxin overdose for which the administration of 50 grams of charcoal would not achieve at least a 10:1 ratio, as 5 grams of digoxin equals a dose of 20,000 tablets of 0.25 mg each. On the other hand, 100 grams of charcoal would be optimal for aspirin ingestions of just 10 grams or less, yet ASA overdoses often involve a much higher dose. For this reason, repeat dosing of activated charcoal may be needed to approach the desired ratio. Additional doses of charcoal can be given at intervals of 2-4 hours.

Multiple dose activated charcoal

In some cases, the rate of elimination of a drug that has already been absorbed can be accelerated by giving Multiple Dose of Activated Charcoal (MDAC). Drugs that are removed by this method either undergo extensive entero-hepatic reabsorption or are drugs that have an unusual affinity for charcoal, and can be attracted across the capillary-gut interface for adsorption. This is referred to as “gastrointestinal dialysis.” Examples of such agents where MDAC may be of benefit are theophylline and carbamazepine, and ingestions of cardiac glycoside containing plants.

Efficacy of activated charcoal in the poisoned patient

Activated charcoal is effective at adsorbing experimentally a wide variety of pharmaceutical and toxic agents. Generally, most medications undergo some adsorption by charcoal. Alcohols, metals including iron and lithium, and strong acids and bases are poorly adsorbed.

Clinical use has been predicated on the belief that adsorption to charcoal prevents systemic absorption of the drug or poison, and can thus positively affect outcome, doing so in a manner which is safe. What do we really know about the clinical benefit and risk of activated charcoal? Unfortunately, we have insufficient scientific studies addressing the use of gastrointestinal decontamination.

In 1985, 15.0% of calls to poison centers resulted in the administration of syrup of ipecac and 4.6 % resulted in administration of activated charcoal. In 1995, only 2.3% got ipecac and 7.7% got charcoal. By 2004, ipecac use was down to 0.2% and charcoal use had declined to 5.6%.

It is not a simple matter to study the effectiveness of any modality of gastrointestinal decontamination, nor to apply the body of collected science to a given patient. The decision to employ a GI decontamination procedure involves a large number of variables germane to the specific case, and this has made relevant, generalizable, study difficult if not impossible. At a minimum, the effectiveness of decontamination involves: 1) the drug or poison ingested, 2) the dose, 3) patient weight, 4) time since ingestion, 5) the medical status of the patient at the time decontamination is contemplated, 6) the binding affinity of the drug or poison to charcoal, 7) operator skill and 8) patient cooperation. When confronted with the need to treat an altered patient who ingested 1,500 mg diphenhydramine 2 hours ago, it is highly unlikely that you will be able to find a study describing the benefit of charcoal in your particular patient.

There are 4 lines of inquiry in the medical literature addressing the potential utility of activated charcoal in the treatment of poisoned patients. In vitro studies document that charcoal can adsorb a large number of substances in the test tube, and this evidence has generated enthusiasm over many years that adsorption could be used to decrease absorption, and thus to improve outcome. Human case reports provide testimony that charcoal has been used successfully here and there, but do little to prove efficacy. Human volunteer studies, in which subjects were given subtoxic dose of a marker drug followed by activated charcoal after a delay of 5, 10 or 60 minutes, show reduced systemic absorption of the drug. However, because the doses given were subtoxic, it is difficult to extrapolate to an overdose. Animal studies have employed toxic doses, yet extrapolating from animals to the human gastrointestinal tract and to human liver/kidney elimination is of unknown scientific soundness. Unfortunately, randomized clinical studies evaluating outcome after drug overdose are very difficult to perform and standardize, and until recently show little clinical evidence of benefit. In fact, a position paper published in 2005 by the American Academy of Clinical Toxicology on the use of single dose charcoal(3) concluded “There is no evidence that the administration of activated charcoal improves clinical outcome.” However, a recent article from Sri Lanka did suggest that MDAC may improve outcome following yellow oleander ingestion.(5)

Potential Harm from Use of Activated Charcoal

Activated charcoal has long been employed in the treatment of poisoned patients under the assumption that it is a safe therapy. Yet this assumption is under challenge.(3,6,7) Complications of single dose activated charcoal administration include emesis, corneal abrasions and, most importantly, pulmonary aspiration.

The precise frequency of these complications is unknown. Certainly the medical literature is not overflowing with case reports documenting adverse reactions occurring with charcoal use. Supporters of charcoal point to this relative paucity documenting harm from charcoal as evidence that charcoal is safe. However, there is no central registry to report such complications. Attempts to publish case reports purporting to show harm from activated charcoal may be subject to editorial bias and thus remain unpublished.

Seger(8) has attempted to summarize the literature reports of adverse events associated with charcoal, including deaths associated with aspiration of charcoal. She concluded, “We must reassess if the harm caused by the administration of SDAC is greater then the harm caused by the poisoning. If this is the case, and benefit cannot be demonstrated, the practice of administering SDAC should be abandoned in the mild to moderately poisoned patient.”

The American Academy of Clinical Toxicology, in its position statement on single dose activated charcoal, was sufficiently alarmed by the potential for aspiration to write: “Activated charcoal is contraindicated if the patient has an unprotected airway, such as in a patient with a depressed state of consciousness without endotracheal intubation.”

Some toxicologists do not believe that charcoal causes pulmonary aspiration. These experts maintain that charcoal is inert and that aspiration is more likely caused by the drug or poison, and may have occurred in the absence of charcoal administration. Other experts maintain that, if 240-480 ml of “black goo” is instilled into stomach, distending its walls, with subsequent emesis and aspiration, activated charcoal is simply not an innocent bystander. They also note a case report in which aspirated charcoal was followed by death from bronchiolitis obliterans in which massive amounts of charcoal were histologically found within the scar tissue of a foreign body reaction.(8)


Activated charcoal can bind many drugs and poisons in vitro, and in vivo can decrease gastrointestinal absorption. While outcome has not been shown to be changed by charcoal in studies to date (with the possible exception of yellow oleander), this may be possible when it is used properly in the correct situation. On the other hand, the hazards of activated charcoal use may not be fully appreciated, and the medical literature may not represent a complete picture of complications caused, past or future.

Physicians should consider using activated charcoal in the treatment of selected poisoned patients with severe or potentially severe intoxications where improved outcome is possible. We recommend health care providers consider using activated charcoal in conjunction with a specialist in poison information or a medical toxicologist.

Primum non nocere.


  1. Watson WA, Litovitz TL, Rodgers GC Jr, Klein-Schwartz W, Reid N, Youniss J, Flanagan A, Wruk KM. 2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2005 Sep; 23(5):589-666.
  2. Gaudreault P. Activated charcoal revisited. Clin Ped Emerg Med 2005; (6):76-80.
  3. Chyka PA, Seger D, Krenzelok EP, Vale JA. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: Single-dose activated charcoal. Clin Toxicol (Phila). 2005; 43(2):61-87. Review.
  4. Chin L, Picchioni AL, Bourn WM, Laird HE. Optimal antidotal dose of activated charcoal. Toxicol Appl Pharmacol. 1973 Sep;26(1):103-8.
  5. de Silva HA, Fonseka MM, Pathmeswaran A, Alahakone DG, Ratnatilake GA, Gunatilake SB, Ranasinha CD, Lalloo DG, Aronson JK, de Silva HJ. Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomised, placebo-controlled trial. Lancet. 2003 Jun 7;361(9373):1935-8.
  6. Geller RJ, Ekins BR. Death complicating gastrointestinal decontamination – time to rethink “routine therapy”? Vet and Human Toxicol; Volume 35, Number 4, (Aug 1993): 335. Abstract, paper presented at the International Congress of Clinical Toxicology, New York, New York, September 11, 1993.
  7. Elliott CG, Colby TV Kelly TM Hicks HG. Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest. 1989 Sep;96(3):672-4.
  8. Seger D. Single-dose activated charcoal-backup and reassess. J Toxicol Clin Toxicol. 2004;42 (1):101-10.