Ascendency of the Black Bottle (Activated Charcoal)

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PEDIATRICS

Vol. 80 No. 6 December

1987

949

COMMENTARIES

Opinions expressed in these commentaries are those of the authors and not necessarily those of the American Academy of Pediatrics or its Committees.

Ascendency

of the Black

Bottle

(Activated

Charcoal)

Previous well-established guidelines for the man-agement of poisonous ingestions in children are undergoing significant change. The time-honored practice of syrup of ipecac-induced vomiting as the primary means of gastrointestinal decontamination now frequently yields to the administration of ac-tivated charcoal. Practitioners and emergency room physicians who are increasingly relying on advice from and participation in treatment by regional poison control centers need to understand the ra-tionale behind what many consider contradictions to accepted teaching.

A case in point was a recent letter to the Amen-can Academy of Pediatrics from a pediatrician questioning the treatment of an ingestion of poison in a toddler. The regional poison control center contacted for advice recommended activated char-coal as the preferred treatment rather than induc-tion of emesis with syrup of ipecac or gastric lavage. Since 1966, when legislation allowed over-the-counter sale of syrup of ipecac, it became firmly established as the preferred first aid treatment in a suspected poisoning. Frequent education cam-paigns have encouraged the acquisition of a 30-mL bottle for every home with young children. Al-though the safety and efficacy of syrup of ipecac in inducing vomiting in children is well established, there have been rare fatalities associated with its

use.’3 Recent studies have questioned the efficacy of ipecac in removing significant amounts of

in-gested products. An editorial in the British Medical Journal questioned its usefulness and suggested that its use be reconsidered in favor of activated

charcoal.4

The use of charcoal in medicine goes back to the time of Hippocrates, and an example of its

effi-ciency in offering protection against an arsenic tnioxide ingestion was demonstrated by Bertrand in i918. Holt and Holz5 brought activated charcoal into modern usage with their classical review “The Black Bottle.”

Activated charcoal is the residue from the de-structive distillation of various organic materials, treated to increase its adsorptive power. Further enhancement of the charcoal’s adsorptive capacity is accomplished by treatment with steam, air, car-bon dioxide, oxygen, zinc chloride, sulfuric acid, phosphoric acid, or a combination of some of these substances at temperatures ranging from 500#{176}Cto 900#{176}C.This treatment is referred to as activation, the activating agent presumably removing

sub-stances previously adsorbed on the charcoal and

breaking down the granules of carbon into smaller ones having a greater total surface area.6 The effec-tiveness of activated charcoal lies in its small par-tide size and large surface area, allowing the ad-sorption of a variety of chemical agents by offering alternative binding sites and thereby reducing their absorption from the gastrointestinal tract. The power to adsorb persists for several hours after administration and has been referred to as “the catch-up phenomena.”7

Recently, “superactive” charcoals have been de-veloped similar to those used in treating water supplies. These charcoal antidotes have a binding area of up to 3,000 m2/g.8’9

Where indicated (Figs. 1 and 2) activated char-coal has the capability of inactivating a larger

quan-tity of an ingested substance than the approxi-mately 30% that could be removed by syrup of ipecac-induced vomiting.” A recent study indicated that activated charcoal may be the more appropni-ate initial emergency department treatment for in-gested chemical and drug overdoses. This study questioned whether gastric emptying as initial treatment of all emergency department drug over-dose patients should be the accepted standard of care.’2 Gastric lavage in obtunded patients may be of little value more than one hour postingestion, and the use of syrup of ipecac does not benefit

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Acetaminophen Aconitine Amphetamines Antimony Antipynine Arsenic Atropine Barbiturates Camphor Cantharides Carbamazepine Chlordane Chloroquine Chlorpromazine Chiorpheniramine Cocaine Colchicine Dapsone 2,4-Dichlorophenoxyacetic acid Digitalis Digitoxin Diphenyhydantoin Ergotamine Ethchlorvynol Glutethimide Hexachiorophene Imipramine Iodine Ipecac Isoniazid Kerosene Malathion Mefenamic acid Meprobamate Mercuric chloride Methotrexate Methyl salicylate Methylene blue Morphine Muscanine Narcotics Nicotine Nortriptyline Opium Oxalates Paracetamol Parathion Penicillin Phenobarbital Phenolphthalein Phenothiazines Phenylbutazone Phenylpropanolamine Phenytoin Phosphorus Potassium Pnimaquine Probenecid Propantheline Propoxyphene Quinacrine Quinidine Quinine Salicylamide Salicylates Selenium Silver Stramonium Strychnine Sulfonamides Theophylline Tolbutamide Tnicyclic antidepressants

Alkali Ferrous sulfate Boric acid Isopropanol Chlorpropamide* Methanol Cyanide Mineral acids DDT5 N-Methyl carbamate8

Ethanol Sodium and potassium hydroxide

Sodium metasilicate

950

PEDIATRICS

Vol. 80 No. 6 December

1987

Fig 1. Compounds adsorbed by activated charcoal. Ef-ficacy to adsorb some of these compounds has not been

Fig 2. Compounds with little or no adsorption by acti-vated charcoal. 8Authors of Poisindex consider these to be effectively adsorbed by activated charcoal. Modified from Mofenson et al.’#{176}

patients who seek medical attention hours after an overdose.’2

A limiting

factor

to wide acceptance

of activated

charcoal as a home first aid measure for appropriate ingestions of poisons is its poor acceptance by chil-dren and the difficulty parents can have adminis-tering an appropriate dose of 1 to 2 g/kg. This resistance can be overcome in the emergency de-partment by administration via gastric intubation if necessary.

It is in this setting

that greater

reliance

on activated charcoal as the preferred gastrointes-tinal decontaminent may find its place because compliance can be assured.

It should

no longer

come

as a surprise

to the

practitioner when informed that activated charcoal

subjected to careful scientific study. Modified from Mo-fenson et a!.’#{176}

is advised in preferance to syrup of ipecac or gastric lavage. Even the assumption that activated char-coal should not be administered when the oral antidote N-acetylcysteine is given for acetamino-phen intoxication has been challenged.’3”4 Further studies will determine agents in which activated charcoal is effective.

A discussion

of merits

of the

various

available

charcoal preparations, the additives used to en-hance palatability, and the concomitant use of ca-thartics is beyond the scope of this commentary.

REFERENCES

JOSEPH GREENSHER,

MD

HOWARD C. MOFENSON, MD THOMAS

R.

CARACCIO, PHARMD Department of Pediatrics

Winthrop-University Hospital Mineola, NY, and

The Long Island Regional Poison Control Center East Meadow, NY

1. Robertson WO: Syrup of ipecac associated fatality: A case report. Vet Hum Toxicol 1979;21:87

2. Smith PR, Smith DM: Acute ipecac poisoning-Report of a case and review ofthe literature. NEnglJMed 1961;265:523

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COMMENTARIES

951

3. Manno BR, Manno JE: Toxicology of ipecac: A review. Clin Toxicol 1977;1O:221

4. Vale JA, Meredith TJ, Proudfoot AT: Syrup of ipeca-cuanha-It is really useful? Br Med J 1986;293:1321

5. Holt LE, Holz PH: The black bottle. J Pediatr 1963;63:306

6. Swinyard EA: Gastrointestinal drugs, in Osol A, Chase GD, Gennaro AR, et al (cdi): Remington’s Pharmaceutical Sci-ences, ed 16. Easton, PA, Mack Publishing Co, 1980, chapter 40,p 752

7. Park GD, Spector R, Goldberg MJ, et al: Expanded role of charcoal therapy in the poisoned and overdosed patient.

Arch Intern Med 1986;146:969

8. Cooney DO: A “superactive” charcoal for antidotal use in poisonings. Clin Toxicol 1977;11:387

9. Cooney DO, Kane RP: Superactive charcoal adsorbs drugs as fast as standard antidotal charcoal. Jr Clin Toxicol

1980;16:123

10. Mofenson HC, Caraccio TR, Greensher J, et al: Gastroin-testinal dialysis with activated charcoal and cathartic in the treatment of adolescent intoxications. Clin Pediatr

1985;24:678

11. Corby DG, Decker WJ, Moran MJ, et al: Clinical compari-son of pharmacologic emetics in children. Pediatrics

1968;42:361

12. Kulig K, Bar-Or D, Cantrill SV, et al: Management of acutely poisoned patients without gastric emptying. Ann

Emerg Med 1985;14:562-567

13. Renzi FP, Donvan JW, Morgan L, et al: Concomitant use of activated charcoal and N-acetylcysteine. Ann Emerg Med

1984;14:400

14. Spyker DA: Activated charcoal reborn: Progress in poison

management. Arch Intern Med 1985;145:43

Heart

Block

Secondary

to

Erythromycin-lnduced

Carbamazepine

Toxicity

Toxic elevations of serum levels of carbamaze-pine have been reported recently in children treated concurrently with erythromycin.’3 Similar toxic interaction has been recognized longer in adults.4 The toxic effects described are confusion, somno-lence, ataxia, vertigo, and nystagmus, sometimes associated with vomiting and hyponatremia. We report the case of a 10-year-old boy with sinus arrest and atrioventricular (A-V) block. The poten-tial for carbamazepine to depress A-V conduction and ventricular automaticity is recognized in adults,5’#{176} particularly those with preexisting A-V conduction defects.6”#{176} However, this is the first reported case of serious conduction disturbances occurring with carbamazepine toxicity in a child.

CASE REPORT

A 10-year-old boy with severe spastic quadraplegia required maintenance therapy with carbamazepine (100

mg, three times per day), clobazam (5 mg, twice per day), and valproic acid (125 mg, four times per day) to control his chronic seizure disorder. (A respiratory arrest second-ary to pneumonia had caused severe hypoxic-ischemic injury when he was 5 weeks of age.) The plasma level of carbamazepine was 9.0 mg/mL at an outpatient checkup

3 weeks prior to hospital admission. Five days prior to the toxic event, weeping hemorrhagic lesions in the left

axilla required treatment for possible secondary infection.

His family practitioner prescribed erythromycin (125 mg, four times per day). During the next four days, the child became progressively more drowsy. The erythromycin was discontinued on telephone advice from the seizure clinic. The following evening, he required hospitalization because he remained drowsy, was cold to the touch, and unable to feed.

On admission, his axillary temperature was 35#{176}C,heart

rate was 20 beats per minute, and BP was unrecordable. Heart rate failed to respond to atropine (0.5 mg IV) but increased to 100 beats per minute with an isuprel infusion (0.2 g/kg/min). BP could then be measured at 110/50 mm Hg. Initial blood gas results were pH 7.33, Pco, 40

mm Hg, Po2 63 mm Hg, bicarbonate 21 mEqjL, base

deficit -4.4 (capillary). Bicarbonate therapy was not used. The child’s respiratory rate was 16 breaths per minute initially and respiratory effort adequate; however, eight hours after admission, his breathing became labored and he required intubation and assisted ventilation.

Laboratory investigation showed a plasma

carbama-zepine concentration of 39 g/mL (therapeutic range 8

to 12 zg/mL) and vaiproic acid of 81 zg/mL (range 50 to 100 g/mL). Serum sodium was 126 mEqJL, decreasing to 121 mEcijL during the next nine hours.

Management following restoration of heart rate and BP included rewarming, nasogastric administration of

charcoal, and a half-strength Fleet enema every six hours. Thirty-six hours after admission, his carbamazepine level

had decreased to 15 zg/mL. Serum sodium value was

normal. He was weaned from the isuprel infusion and

tolerated extubation the following day. Subsequently,

carbamazepine was recommended at the same mainte-nance dosage as prior to admission and monitored levels

remained stable within the therapeutic range.

The ECG recording at the time of admission showed sinus arrest and junctional bradycardia with a heart rate of 30 beats per minute (Figure, A). Second-degree A-V block, Mobitz type II, developed and then first-degree

A-V block during his recovery (Figure, B). Chest

roentgen-ography at that time showed no cardiomegaly, and there

was no murmur heard. The ECG became normal when

carbamazepine levels returned to levels within the normal therapeutic range (Figure, C). No underlying conduction defect or evidence of subclinical cardiac disease were detected.

DISCUSSION

Carbamazepine has been available since the early

1960s. This is the first case described with heart

block of a child resulting from toxic levels of car-bamazepine. Goulden et a!1 recently reported the

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1987;80;949

Pediatrics

JOSEPH GREENSHER, HOWARD C. MOFENSON and THOMAS R. CARACCIO