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Activated Charcoal: Activated charcoal is produced by pyrolysis of organic material, such as wood, and an activation process which cleanses and fragments the charcoal by exposure to an oxidizing gas compound of steam, oxygen, and acids at high temperatures resulting in increased surface area through the creation of numerous external and internal pores. These pores serve as reservoirs to adsorb substances admixed with activated charcoal, making it a useful adsorbent for specified toxins.
Activated charcoal is pharmacologically inert and is not absorbed in the gastrointestinal tract.Activated charcoal will adsorb a variety of organic and inorganic substances, but is especially effective in adsorbing compounds within a molecular weight range of l00 to 1,000 Daltons (AMU's).1Several other physiologic and physicochemical factors influence the adsorptive capacity of activated charcoal including: pH, charcoal:drug ratio, gastric contents, and adsorption kinetics.2
Much of the published scientific literature which studied the adsorptive capacity of activated charcoal was conducted using In vitro models. A considerable amount of the research may be invalid since the effects of physiologic pH were not taken into consideration or held constant. Using research models which simulate the gastric environment, some toxins were not adsorbed by activated charcoal. This data was inappropriately extended to imply that activated charcoal did not adsorb a toxin and therefore had no efficacy in the management of that type of poisoning incident. However, the research failed to consider that the increased pH of the small intestine provides a receptive environment for the adsorption of the toxin by activated charcoal. Activated charcoal will effectively adsorb acidic, alkaline and neutral substances (not to suggest use of activated charcoal in poisonings caused by corrosive agents2). The extent of adsorption will be dependent upon the relative solubility of the drug at a specified pH.
The optimal dosage ratio of activated charcoal to toxin is described as 10:1.3,4,17,18 Numerous factors contribute to and interfere with adsorptive capacity, therefore, the 10:1 ratio may not be valid in the clinical setting. Furthermore, a primary application of activated charcoal is in adult patients who have intentionally ingested a toxin for drug abuse or suicidal purposes. These patients may not freely provide information about the substance or amount ingested, or have a decreased level of consciousness. Under these conditions it is difficult to determine the ingestion history, making it impractical to use the 10:1 ratio. The 10:1 ratio is also impractical when large amounts of toxin have been ingested (i.e., an overdose of 50 gm of aspirin would then require 500 gm [1.1 lbs.] of activated charcoal).
Gastric contents may also compete with ingested toxins and compromise the adsorption of the toxins by activated charcoal.2 If activated charcoal is to be administered to a patient known to have ingested a large meal in close proximity to the time of treatment, a larger dose of activated charcoal may be appropriate.
Under appropriate physiologic conditions activated charcoal adsorbs toxins instantaneously. This adsorptive process is reversible and an equilibrium between free and bound toxin will exist. According to the law of mass action the amount of free drug decreases as the dose of activated charcoal increases. Therefore, large doses of activated charcoal can favor the equilibrium toward greater toxin adsorption and efficacy. There is limited evidence that desorption of a toxin from activated charcoal may occur.19Therefore, there is a potential for toxin readsorption and enhanced toxicity. The current standard of care is to administer a cathartic with single doses of activated charcoal to hasten the elimination of the toxin/activated charcoal complex from the gastrointestinal tract.5 Cathartics should be used with extreme care during multiple dose activated charcoal therapy and it is not recommended to use a cathartic with each dose of activated charcoal.5
Sorbitol: Sorbitol is a hexahydric sugar alcohol which primarily serves as an osmotic cathartic in Actidose with Sorbitol.6 A secondary advantage of using sorbitol is as a palatability enhancer to decrease the innate gritty texture of activated charcoal and to provide a sweet vehicle to increase patient compliance. Sorbitol is poorly absorbed during its transit through the gastrointestinal tract.Absorbed sorbitol is metabolized by the liver and slowly converted to fructose. Insulin is not necessary for intracel-lular transport of sorbitol, therefore customary cathartic doses can be safely used by patients with diabetes mellitus.
As a hyperosmotic cathartic sorbitol produces a hygroscopic action resulting in increased water in the large intestine and increased intraluminal pressure which stimulates catharsis. Studies have been conducted in healthy adult human volunteers using therapeutic amounts of activated charcoal and sorbitol.8,9 Catharsis of activated charcoal occurred in an average of 1.0 - 1.5 hours and persisted for 8 - 12 hours. Fourteen poisoned patients are reported in one series representing a wide range of toxins and dosages of sorbitol resulting in the onset of catharsis in an average of 7.7 hours.10 The onset of action may be expected to be longer in patients who have ingested toxins which decrease bowel motility, such as pharmacological agents and plants with anticholinergic properties, and drugs like narcotics.20
Sorbitol does not compromise the adsorptive capacity of activated charcoal.11,12
1. Activated Charcoal, Antidotal and Other Medicinal Uses, Marcel Dekker, New York, 1980.
2. Clinical Pharmacokinetics. 1982; 7: 465-489
3. Handbook of Common Poisonings in Children, American Academy of Pediatrics, Evanston, 1983
4. Am J Emerg Med. 1985; 3: 280-283
5. Poisindex Information System, Micromedix, Denver, 1991
6. J Pediatrics. 1981; 98: 157-158
7. Diabetes Care. 1978; 1: 223-230
8. Clinical Toxicology. 1985; 22: 529-536
9. Ann. Emerg. Med. 1985; 14: 1152-1155
10. Clinical Toxicology. 1985; 23: 579-587
11. J. Pharmacol. Exp. Ther. 1982; 221: 656-663
12. Am. J. Hosp. Pharm. 1978, 35:1355-1359
17. Medical Toxicology. New York, Elsevier, 1988
18. Clinical Management of Poisoning and Drug Overdose. Philadelphia, W.B. Saunders Co., 1990
19. Arch Intern Med. 1987; 147: 1390-1392
20. Clin Toxicol. 1989; 27: 91-99
Last reviewed on RxList: 11/6/2008
This monograph has been modified to include the generic and brand name in many instances.
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