NDT Advance Access originally published online on August 24, 2004
Nephrology Dialysis Transplantation 2004 19(12):3190-3191; doi:10.1093/ndt/gfh232
Nephrol Dial Transplant Vol. 19 No. 12 © ERA-EDTA 2004; all rights reserved
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Charcoal haemoperfusion in a child with amitriptyline poisoning
Ismail Islek1,
Tuncer Degim3,
Cemal Akay4,
Ali Türkay1 and
Tekin Akpolat2
1 Department of Pediatrics and 2 Department of Nephrology, Ondokuz Mayis University, School of Medicine, Samsun, Turkey, 3 Department of Pharmaceutical Technology, Faculty of Pharmacy, Gazi University, Ankara, Turkey and 4 Department of Toxicology, Gülhane Military Medical School, Ankara, Turkey
Correspondence and offprint requests to: Dr Ismail Islek, Department of Pediatrics, School of Medicine, Ondokuz Mayis University, 55139 Samsun, Turkey. Email: iislek{at}omu.edu.tr
Keywords: amitriptyline poisoning; charcoal haemoperfusion; paediatrics
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Introduction
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Tricyclic antidepressant (TCA) overdose is a relatively common
cause of poisoning. According to the American Association of
Poison Control Centers, 7961 patients with amitriptyline poisoning
were reported in 2000. Of these, 958 were under 6 years old,
6388 needed treatment in a health care facility and 68 patients
died [
1]. The current therapy of TCA overdose includes preventive
measures such as gastric lavage, activated charcoal, anticonvulsants,
vasopressors for hypotension, and sodium bicarbonate infusion
for dysrhythmias [
2,
3]. Although charcoal haemoperfusion (CHP)
has been used in the management of amitriptyline overdose, the
data regarding CHP in the management of amitriptyline overdose
is controversial [
3–5]. To our knowledge, there is no
report related to the use of CHP in children with amitriptyline
poisoning in the English literature. Here, we report a child
with amitriptyline poisoning who showed dramatic improvement
after CHP treatment.
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Case report
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A 2.5-year-old, 14 kg male was admitted to our paediatric emergency
department 4 h after ingesting 20 tablets of amitriptyline (25
mg each, totally 500 mg). The parents stated that he ingested
a total of 20 tablets of amitriptyline at 19.00 h, was sleepy,
and minutes later became unresponsive. The parents observed
that he developed tonic–clonic seizures on his way to
hospital. At the local hospital, diazepam was given and he was
referred to our hospital. At presentation in our paediatric
emergency room, he was comatose, and blood pressure was 90/50
mmHg, pulse rate was 110/min and irregular. Respiration rate
was 30 with shallow breathing. He was unconscious with mild
flexion withdrawal to painful stimuli. The Glasgow coma score
was 4 (E1, M2, V1). Pupils were mid-range and non-reactive to
light. Babinsky reflexes were bilaterally unresponsive. Deep
tendon reflexes were negative. Laboratory investigation revealed
Hb 6.5 g/dl, WBC 7300/mm
3, platelet 162 000/mm
3, BUN 10 mg/dl,
serum creatinine 0.3 mg/dl, Na 126 mEq/l, K 3.7 mEq/l, Cl 109
mEq/l, Ca 9 mg/dl, ALT 37 IU/l and AST 20 IU/l. Urinalysis showed
pH 6, specific gravity 1010 without protein or blood. Predialysis
ECG showed diffuse ventricular exstrasystoles, QRS prolongation
(0.12 s), QT prolongation, intraventricular branch blocking,
and diffuse ventricular arrhythmia (
Figure 1). A nasogastric
tube was inserted and gastric lavage was started with normal
saline and activated charcoal (1 g/kg). A Foley catheter was
inserted and an 8-Fr double lumen catheter was placed for dialysis
access. Normal saline was used to treat the hypotension and
intravenous sodium bicarbonate to prevent cardiac toxicity.
Blood samples for amitriptyline level were obtained just before
CHP, at midtime and at the end of the session. Blood amitriptyline
levels were measured using HPLC (Hewlett-Packard Model 1050,
USA). CHP was initiated 7 h after ingestion. A 140 ml CHP cartridge
(Gambro Adsorba 150c; Gambro Dialysatoren, Germany) was used.
The CHP session lasted 3 h. No adverse effect related to CHP
treatment was seen.
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Fig. 1. Predialysis ECG showed diffuse ventricular exstrasystoles, QRS prolongation (0.12 s), QT prolongation, intraventricular branch blocking, and diffuse ventricular arrhythmia (the top ECG line). Three hours after the CHP session ECG showed normal QRS tracing (the bottom ECG line).
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After the CHP session, the child began to respond, showing extremity
flexion withdrawal and eye movement (opening) to painful stimuli.
The Glasgow coma score was 7 (E2, M3, V2) and the ECG became
normal 3 h after the first CHP session (
Figure 1). He was still
unconscious with mild flexion withdrawal to painful stimuli
24 h after admission. The second CHP session was done on the
second day. The serum amitriptyline levels are given in
Table 1.
In the follow-up, the patient improved completely and was
discharged after 5 days of admission. On control examinations,
the patient was healthy.
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Discussion
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Amitriptyline poisoning was the cause of coma in our patient.
Although the beneficial effects of haemoperfusion in the management
of amitriptyline overdose have been reported, the experience
with the dialysis modality in the treatment of amitriptyline
overdose is limited and contradictory. Neither textbooks nor
reference books recommend haemoperfusion for the treatment of
amitriptyline overdose [
2,
4–7]. In our patient, the response
to CHP treatment was excellent and this case is the first reporting
beneficial effects of CHP in the management of amitriptyline
overdose in a young child. The administration of other preventive
measures does not eliminate the beneficial effect of these measures
in addition to CHP. Some authors state that haemoperfusion is
unnecessary in the management of amitriptyline overdose [
2,
4,
5].
However, the recommendation of haemoperfusion in the management
of amitriptyline overdose is based on (i) its effectiveness
for shortening the coma, (ii) its stability to severity of complications
due to prolonged therapy and to the cost of hospital admission,
(iii) the prevention of the broad QRS complexes in the ECG during
treatment [
5–7]. It has been reported that the QRS interval
and the clinical manifestations of overdose were reliable and
more readily available indicators of toxicity than serum concentrations
of TCA [
2,
3]. Our indications for CHP treatment in our patient
were deep coma, generalized seizures, shallow breathing and
prolonged QRS complex. The Glasgow coma scores increased from
4 to 7 after CHP treatment, the coma disappeared gradually over
1–3 days [
2,
3] and our patient was fully awake and conscious
after the second CHP session.
In conclusion, our experience showed a dramatic improvement of an amitriptyline overdose with CHP treatment in a very young child but controlled studies are needed to clarify the indication of CHP treatment in the management of this intoxication.
Conflict of interest statement. None declared.
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References
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- Litovitz TL, Klein-Schwartz W, White S et al. 2000 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance system. Am J Emerg Med 2001; 19: 337–395[CrossRef][ISI][Medline]
- Benowitz NL. Tricyclic-antidepressants. In: Olson KR, ed. Poisoning and Drug Overdose. Appleton and Lange, Stanford, CT, 1999: 310–312
- Baldessarini RJ. Drugs and the treatment of psychiatric disorders. In: Hardman JG, Limbird LE, Gilman AG, eds. Goodman and Gilman's The Pharmalogical Basis of Therapeutics, 10th Edn. McGraw-Hill, New York, 2001: 447–520
- Comstock TJ, Watson WA, Jennison TA. Severe amitriptyline intoxication and use of charcoal hemoperfusion. Clin Pharm 1983; 2: 85–88[Medline]
- McAlpine SB, Calabro JJ, Robinson MD, Burkle FM. Late death in tricyclic-antidepressant overdose revisited. Ann Emerg Med 1986; 15: 1349–1352[Medline]
- Pedersen RS. Hemoperfusion in tricyclic-antidepressant poisoning. Lancet 1980; 1: 154–155[Medline]
- Trafford A, Sharpstone P, O'Neal H. Hemoperfusion in tricyclic-antidepressant poisoning. Lancet 1980; 1: 155[Medline]
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