Charcoal haemoperfusion in Amitriptyline poisoning: Experience in 20 children

Bek, Kenan; Özkaya, Ozan; Mutlu, Birgül; Dağdemir, Ayhan; Sungur, Metin; Acikgoz, Yonca; İşlek, İsmail; Baysal, Kemal

doi:10.1111/j.1440-1797.2008.00922.x

Cited by 23 publications

(21 citation statements)

References 24 publications

(43 reference statements)

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“…In this experiment, CAC-HP had no ameliorating effect on AT-induced ECG changes. This is not consistent with published reports [4,44] that suggest that the treatment with CAC-HP improves recovery and survival of AT-poisoned patients. In the published papers, however, the influence of pH alterations during the initial admittance and during treatment is not taken into consideration.…”

Section: Discussioncontrasting

confidence: 99%

Advanced Electrocardiogram Analysis in the Amitriptyline‐poisoned Pig Treated with Activated Charcoal Haemoperfusion

Jansen

Hoegberg

Eriksen

et al. 2017

Basic Clin Pharma Tox

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Coated activated charcoal haemoperfusion (CAC-HP) does not reduce the plasma concentration in amitriptyline (AT)-poisoned pigs. The aim of this non-blinded, randomized, controlled animal trial was to determine if CAC-HP reduces the pathological ECG changes caused by AT poisoning. Fourteen female Danish Landrace pigs (mean weight 27.7 kg, range 20-35 kg (CAC-HP) and 24.4 kg, range 18-30 kg (control group, CG), n = 7 in each group) were included. After randomization, the pigs were anaesthetized and intravenously poisoned with AT. The intervention group underwent 4 hr of CAC-HP plus standard care (oral activated charcoal). Intervention was compared to standard care alone. From each pig, a 12-lead ECG and haemodynamic variables were obtained at baseline, at full AT loading dose, before and during CAC-HP. Baseline ECG variables (RR, PR, QRS, QTc, QTp, QTe, TpTe and TpTe/QT) for lead II, v2 and v5 were not significantly different (F = 0.035-0.297, p-values 0.421-0.919). Differences within groups over time and between groups were tested by anova repeated measures. For all variables, the time-plus-group level of significance revealed a p-value > 0.05. Severe cardiovascular arrhythmias occurred in both groups with 3 in the CAC-HP group versus 1 incident with premature death in the CG. The attenuating effect of CAC-HP to orally instilled activated charcoal alone on AT-induced ECG alterations did not differ significantly. We conclude that the use of modern CAC-HP as an adjunctive treatment modality in AT-poisoned pigs is inadequate.

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Section: Discussioncontrasting

confidence: 99%

Advanced Electrocardiogram Analysis in the Amitriptyline‐poisoned Pig Treated with Activated Charcoal Haemoperfusion

Jansen

Hoegberg

Eriksen

et al. 2017

Basic Clin Pharma Tox

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“…Several case reports and case series regarding the use of CAC‐HP involve the treatment of human intoxication with AT and other tricyclic antidepressants (TCA) . The authors sometimes state remarkable patient recovery in circulatory and cerebral performance and contribute this to the use of CAC‐HP, although no serum AT samples were collected to quantify the effect of CAC‐HP in these cases.…”

Section: Discussionmentioning

confidence: 99%

“…The use of activated charcoal filters (coated and non‐coated) as an adjunct to the extracorporeal treatment (ECT) of AT intoxications is not widely applied, and only few cases are reported with varying degree of effect . Likewise, we find the indication for initiating treatment involving ECT including coated activated charcoal filters (CAC‐HP) vague and the evidence low .…”

mentioning

confidence: 95%

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Activated Charcoal Haemoperfusion in the Treatment of Experimental Amitriptyline Poisoning in Pigs – The Effect on Amitriptyline Plasma Concentration and Haemodynamic Parameters

Jansen

Petersen

Malskær

et al. 2017

Basic Clin Pharma Tox

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Coated activated charcoal haemoperfusion (CAC-HP) is a well-known treatment modality. Case reports have revealed conflicting results about the efficacy of CAC-HP in the treatment of amitriptyline (AT) poisoning, and no randomized clinical trials have been identified in the literature. This study aimed at quantifying the efficacy of modern CAC-HP as an adjunctive treatment of AT intoxication compared with standard care alone. Fourteen female Danish landrace pigs were randomized to either standard care or standard care plus 4 hr of CAC-HP. The pigs were anaesthetized, and vital parameters were continuously recorded. Amitriptyline infusion (7.5 mg/kg) was completed in 20 min. Thirty minutes after AT infusion, activated charcoal was instilled orally in both groups. In the intervention group, CAC-HP was initiated 60 min. after AT infusion. Blood and urine samples were collected as were vital parameters at specific time intervals. The protocol was approved by the Danish Experimental Animal Expectorate and complied with the NIH guide for care and use of laboratory animals. Data were managed according to the ARRIVE guidelines. No statistical significant differences between intervention and control groups were found when analysing for differences in AT levels in plasma at any time-point. Furthermore, significant differences between the control and intervention groups in regard to vital parameters could not be found either. In our animal model, the addition of CAC-HP did not improve the clearance of AT compared with standard treatment alone. We suggest that the effect of modern CAC-HP as a treatment modality in AT-poisoned human patients may be inadequate.

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“…However, Bek and others paradoxically reported charcoal hemoperfusion as an effective treatment modality for amitriptyline poisoning. 6 They speculated that the toxicokinetics of Tricyclic antidepressant (TCA) might differ from usual pharmacokinetics and may be substantially altered during severe intoxication, which favors extracorporeal removal. Marked elevated drug level above therapeutic range probably decreased both the volume of distribution and degree of protein binding by TCA.…”

mentioning

confidence: 99%

Charcoal hemoperfusion for bupropion overdose with ventricular tachycardia and status epilepticus

Chao¹,

Wu²,

Wang³

2012

Journal of the Formosan Medical Association

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A woman aged 18 years of age was brought to the emergency department due to an acute change in mental status after taking 2.85 g sustained release bupropion 1.5 hours earlier. On presentation, she was disoriented and could not follow verbal orders. The other neurologic and physical examinations were unremarkable. Initial blood pressure was 84/36 mm Hg, heart rate was 121 beats per minute, respiration rate was 19 breaths per minute, and her body temperate was 36.8 C. Electrocardiography (ECG) revealed sinus tachycardia with QRS duration of 100 ms and corrected QT interval of 550 ms. Serum biochemistry showed severe metabolic acidosis (pH 6.82; PaCO 2 54.8 kPa; PaO 2 85 kPa; HCO 3 9.2 mmol/l). Intravenous saline with sodium bicarbonate (50 mEq) was given, and gastric lavage found no pill fragment returned. Four episodes of generalized tonic-clonic seizure occurred, lasting for 15w60 seconds, and we gave multiple doses of diazepam and phenytoin for control. Brain computed tomography did not find any structural abnormality or hemorrhage. At 5 hours postingestion, bradycardia occurred after the fifth seizure episode, with degeneration to pulseless ventricular tachycardia, and she recovered after 10 minutes of cardiopulmonary resuscitation. She was admitted to an intensive care unit and had two additional seizure attacks. We started charcoal hemoperfusion at 9 hours postingestion, and her status epilepticus resolved with regained consciousness within 8 hours of therapy. QTc prolongation also recovered at about 16 hours postingestion (450 ms). She was extubated the same day and discharged on Day 9 of hospitalization after undergoing psychiatric consultation, and she did not have any further seizures or cardiovascular events.QTc prolongation is gradually recognized as a rare presentation of bupropion intoxication. There are several case reports of bupropion overdose associated QTc prolongation (Table 1), 1e5 and the duration of prolongation in most cases exceeds 48 hours after supportive management (gastric lavage and sodium bicarbonate). A 20-year MEDLINE search reveals only two bupropion poisoning cases with status epilepticus and concurrent QTc prolongation. 1,2 Both of them received supportive management only and had longer duration of QTc prolongation than our patient, despite lower dose ingested in one case. 1 In our patient, the QTc prolongation recovered at 16 hours postingestion after charcoal hemoperfusion, which had not been reported previously as a therapeutic option. As a lipid soluble

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Charcoal haemoperfusion in Amitriptyline poisoning: Experience in 20 children

Cited by 23 publications

References 24 publications

Advanced Electrocardiogram Analysis in the Amitriptyline‐poisoned Pig Treated with Activated Charcoal Haemoperfusion

Advanced Electrocardiogram Analysis in the Amitriptyline‐poisoned Pig Treated with Activated Charcoal Haemoperfusion

Activated Charcoal Haemoperfusion in the Treatment of Experimental Amitriptyline Poisoning in Pigs – The Effect on Amitriptyline Plasma Concentration and Haemodynamic Parameters

Charcoal hemoperfusion for bupropion overdose with ventricular tachycardia and status epilepticus

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