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The Journal of Emergency Medicine, Vol. 39, No. 5, pp. 655–661, 2010Copyright © 2010 Elsevier Inc.

Printed in the USA. All rights reserved0736-4679/$–see front matter

Letters

to the Editor

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A CASE OF CARBAMAZEPINENTOXICATION IN A YOUNG BOY

To the Editor:

arbamazepine, a commonly used anticonvulsant, is gen-rally a safe drug. However, it has at times been associatedith cases of severe toxicity and death. Its pharmacologicalroperties include sedation, anticholinergic, antidysrhyth-ic, muscle relaxant, antidiuretic, and antidepressant ef-

ects (1). Carbamazepine is available in enteral solid anduspension formulations (2). In contrast to the solid formu-ation that is known to have slow and unpredictable absorp-ion, therapeutic loading doses of carbamazepine suspen-ion provide quick and predictable absorption in bothhildren and adults (2). Pharmacokinetic studies have dem-nstrated rapid absorption of the suspension resulting ineak and therapeutic concentrations within 2 h of ingestion2). In this letter, we discuss the case of a young boy whoas followed for epilepsy for 2 years and who had a

arbamazepine tablet intake equal to 100 mg/kg.A 7-year-old boy presented to our Emergency Depart-

ent due to loss of consciousness. He had a history ofpilepsy diagnosed 2 years prior at another center and wasreated with carbamazepine pills at a dose of 200 mg twice

day. It was determined that 6 h before presentation, heook 10 carbamazepine pills, which was equal to 100 mg/g, and 1 h afterward he became unconscious. He did notevelop seizures, but vomited three times at home. Hisamily history was unremarkable. On physical examination,e appeared ill in general. On neurological examination, head decreased level of consciousness and stupor; Glasgowoma Scale score was 6. The remainder of the physicalxamination was normal. On laboratory examination, com-lete blood count, liver, renal function tests, serum electro-ytes, arterial blood gas analysis, prothrombin time, andctive partial thromboplastin time were all in the normalange, and urinalysis and electrocardiogram were similarlyormal. The patient was hospitalized with a diagnosis ofcute carbamazepine intoxication and was followed in thentensive care unit. Gastric lavage was performed and sixaily doses of activated charcoal, 1 gm/kg/dose, were given.he patient did not develop cardiac dysrhythmias. Twelveours after the hospitalization he began seizing, which was

reated with diazepam. Supportive care was also given to v

655

he patient. The serum carbamazepine level was 25 ug/mLn the third day of hospitalization. When he was dischargedn the fourth day of hospitalization, complete blood count,iver and kidney function tests, prothrombin time, activeartial thromboplastin time, and brain magnetic resonancemaging were all within normal limits. The patient wasreated with phenytoin, two doses for a total of 5 mg/kg/ay, and was followed-up for 2 months by our pediatricolyclinics. He did not have any seizures during this periodnd remained with normal neurological function.

In acute carbamazepine intoxication, the neurologicalystem is primarily affected. The signs range from nystag-us, ataxia, dysarthria, lethargy, and seizures to coma and

espiratory depression, many of which our patient had (3).n adults, serum concentrations � 40 �g/mL are usuallyredictive of serious toxicity, and this blood level is asso-iated with coma, respiratory depression, seizures, and dys-hythmias (4). However, children are known to developevere manifestations at lower serum concentrations (5–7).t is reported that, in children, this peak level varies between7 and 35 �g/mL (5–7). The reason for this lower thresholds unknown (3). It should be noted that, of the neurologicalanifestations of severe toxicity, coma without hypoxia or

ypotension is generally not associated with residual neu-ological sequelae; however, status epilepticus is a rare butminous complication (1,3). In our patient, the plasma levelf carbamazepine was 25 �g/mL, but we measured thisalue on the third day of hospitalization. Peak plasma levelsf carbamazepine would have been higher had it beeneasured on the first day of admission. Although seizuresere controlled with diazepam, stupor was observed in ouratient with no dysrhythmia, hypotension, cardiac toxicity,r hypoxia.

The concern for cardiac toxicity must always be con-idered when dealing with carbamazepine ingestion.ne-third of patients will characteristically develop a

inus tachycardia that is secondary to the anticholinergicffects (3). Hypotension, conduction delays, and QTccorrected QT time in electrocardiography) prolongation� 420 ms) have been reported (3). In our patient, thetems mentioned above were not found.

The management of carbamazepine overdoses is sup-ortive. Activated charcoal, which binds carbamazepineffectively, should be given early (3). Multiple-dose acti-

ated charcoal prevents enterohepatic recirculation and

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656 Letters to the Editor

hould be used if no contraindication exists (e.g., anticho-inergic ileus) (8). Cardiac monitoring should take place,nd seizures should be treated with benzodiazepines (3).arly treatment is very important in these situations. Incute carbamazepine intoxication, due to the wide distribu-ion capacity and high binding to plasma proteins, conven-ional hemodialysis is not useful. However, there are fewtudies that report that albumin-enhanced continuous veno-enous hemodialysis may be an optimal and cost-effectiveption for the treatment of toxic-level ingestions of protein-ound drugs like carbamazepine that are not amenable tolearance by conventional dialysis protocols (9). Symptom-tic treatment was given to our patient consistent with theiterature, and there was no need to perform more invasivereatment modalities like hemodialysis or albumin-en-anced continuous venovenous hemodialysis.

In summary, we present the case of a 7-year-old boyith epilepsy who had a significant carbamazepine tablet

ntake, equal to 100 mg/kg, and presented with coma butventually was discharged neurologically intact.

Murat Dogan, MD

Department of Pediatric EndocrinologyFaculty of Medicine

Yuzuncu Yil UniversityVan, Turkey

Cahide Yılmaz, MD

Department of Pediatric NeurologyFaculty of Medicine

Yuzuncu Yil UniversityVan, Turkey

Hayrettin Temel, MD

Department of PediatricsFaculty of Medicine

Yuzuncu Yil UniversityVan, Turkey

Hüseyin Çaksen, MD

Department of Pediatric NeurologyFaculty of Medicine

Yuzuncu Yil UniversityVan, Turkey

Gökmen Taskın, MD

Department of PediatricsFaculty of Medicine

Yuzuncu Yil UniversityVan, Turkey

doi:10.1016/j.jemermed.2008.10.007 f

REFERENCES

. Spiller HA. Management of carbamazepine overdose. Pediatr EmergCare 2001;17:452–6.

. Cohen H, Howland MA, Luciano DJ, et al. Feasibility and pharma-cokinetics of carbamazepine oral loading does. Am J Health SystPharm 1998;55:1134–40.

. Perez A, Wiley JF. Pediatric carbamazepine suspension overdose—clinical manifestations and toxicokinetics. Pediatr Emerg Care2005;21:252–4.

. Hojer J, Malmlund HO, Berg A. Clinical features in 28 consecutivecases of laboratory confirmed massive poisoning with carbamaz-epine alone. J Toxicol Clin Toxicol 1993;31(3):449–8.

. Macnab AJ, Birch P, Maccready J. Carbamazepine poisoning inchildren. Pediatr Emerg Care 1993;9:195–8.

. Miles MV, Lawless ST, Tennison MB, et al. Rapid loading ofcritically ill patients with carbamazepine suspension. Pediatrics1990;86:263–6.

. Weaver DF, Camfield P, Fraser A. Massive carbamazepine over-dose: clinical and pharmacological observations in five episodes.Neurology 1988;38:755–9.

. Position statement and practice guidelines on the use of multi-doseactivated charcoal in the treatment of acute poisoning. AmericanAcademy of Clinical Toxicology; European Association of PoisonsCentres and Clinical Toxicologists. J Toxicol Clin Toxicol 1999;37:731–51.

. Askenazi DJ, Goldstein SL, Chang IF, Elenberg E, Feig DI.Management of a severe carbamazepine overdose using albumin-enhanced continuous venovenous hemodialysis. Pediatrics2004;113:407–9.

A RARE CAUSE OF JUNCTIONALHYTHM CAUSING SYNCOPE; MADONEY INTOXICATION

To the Editor:

50-year-old man was admitted to our Emergency De-artment (ED) with complaints of blurred vision, dizzi-ess, and a syncopal event 30 min prior without chestain, palpitation, or dyspnea. He did not have any car-iovascular or systemic illnesses and was not taking anyedication or herbal products. In his past medical his-

ory, he described a syncopal attack 6 months before thatccurred after a meal and his cardiovascular evaluationas reported normal at that time. The patient had eaten areakfast that included two bowls of honey 3 h beforerrival. Physical examination revealed a pulse rate of 44eats/min and a blood pressure of 80/55 mm Hg. Anlectrocardiogram (ECG) showed junctional rhythm with

ventricular rate of 44 beats/min (Figure 1). Bloodhemistry and complete blood count were within normalimits.

Atropine sulfate 3 mg was administered intravenouslyithin 10 min but sinus rhythm was not restored. Theatient became more hypotensive and the pulse rateecreased to 36 beats/min. Due to the ongoing symptomsnd worsening clinical condition, intravenous saline in-

usion was started with boluses and a temporary trans-