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Successful treatment of cibenzoline succinate poisoning using direct hemoperfusion (DHP)
PosterSession iF. Human Toxicology
74
ment included gastric lavage and activated charcoal. Then, areflectic coma, low blood pressure and oliguria appeared. Biological monitoring revealed metabolic acidosis, liver injury, hyperglycemia and hyperamylasemia. Anemia, leucopenia, thrombocytopenia occurred over days 3 to 5. EEG showed diffuse slow waves activities. EMG revealeda sensorimotor neuropathy. Coma lasted one month but two yrs later, the patient was still tetraplegic. Method: P determination in plasma has been performed using a reverse-phase HPLC with fluorescentdetection. Results: Hours after ingestion
12
16
20
24
32
Plasma concentrations (/LgIL)
115
77
24
2
1.5
P plasma concentrations decay had 2 slopes: phase I, between 12 to 16 h, half-life was 16 hours; phase 2, from 16 to 32 H, half-life was 3 hours. The decrease of P plasma half-life in phase 2 was due to hemodynamic and diuresis improvement, since main elimination of P is through urinary excretion. Conclusion: Immediate treatment of hypotension and oliguria may be usefull for improving P clearance, but the effect of faster P kinetics for reducing toxicity has to be further studied.
IP1 F150 I
INFREQUENT MORPHINE ADVERSE EFFECTS: CASE REPORT OF A PEDIATRIC PATIENT
A young male adult absorbed 150 mgr of yohimbine and has been hospitalisedwithin a delay of one hour. Differentblood samples have been taken in order to evaluate the kinetics of eliminationof the drug in a case of massive intoxication. Clinical manifestations were poor except a certain degree of excitation and tachycardia. Yohimbine is known to induce neurological and psychiatric side effects such as irritability, shakings and insomnia. According to previous studies, the eliminationis very quick and only very low levels of yohimbine have been screened by automated HPLC system with full scan UV detection. No observationhad been reported in such a situation of human voluntary intoxication. A few days after this patient put the fire in his bedroom. We do not know if this act is consecutive to the drug effect. This patient had no previouspsychiatric disease.
IP1F1521 SUCCESSFUL TREATMENTOFCIBENZOLINE SUCCINATE POISONING USING DIRECT HEMOPERFUSION (DHP)
Rumiko Kondo*, Naoyoshi Aoyama, TakeshiSasaki1 , Makoto Yoshida,Keisuke Suzuki, YoshitoKamijo, YasushiAsari, Kazui Soma, Tohru Izumi", TakashiOhwada. Departmentof Emergency & Critical CareMedicine; J intemal Medicine, Kitasato University SchoolofMedicine, Sagamihara, Japan
A 5 yr old male patient, 16 kg body weight, presenting second and third degree burns in 26% of his body (lower part) was first hospitalized at the ICU for two and a half weeks. Then, the patient was transferred to the burned patients unit where he stayed until his release. This patient received usual treatment for his condition, for cleaning and dressing of burns, i.e. 0.15 mglkg morphine iv; however, 2.5 h after morphine administration the patient presented narcosis. Respiratory maneuvers were performed and the patient recovered normal breathing.Four and a half hour after morphine, the patient presented hiccups, cyanosis, apnea, stomach distension and respiratory alkalosis. Patient received naloxone and the condition was reversed. Four days later, patient received 0.1 mg/kg morphine iv when cleaning and dressing his burned skin. Thirty minutes later, patient presented apnea, rigidity of limbs and facial muscles, which lasted about 15 sec. After naloxone administration, patient completely recovered. It is important to notice that patient was conscious at all times, and that he did not have a history of neurological disturbances, nor was he receiving any other medication. None of the other patients in the same unit presented any of the symptoms described when receiving morphine. In a 15 yr literature review of morphine use in patients, includingburned ones, we only found a few cases of rigidity of limbs, hiccups and myoclonus. In these cases the patients also remained conscious. We suggest that patients receiving morphine should be closely observed for respiratory depression but also for neurological signs which may be delayed and seem to be dose independent.
A 80-year-old woman was admitted to our hospital for general fatigue. Three years ago, the patient had been implanted permanent right ventricular pacing because of bradycardia-tachycardia syndrome with taking cibenzorine succinate (300 mglday) for one month before this admission.The patient when brought to our hospital was clouding of consciousness(GCS: 13), covered with a profuse clammy sweat and was clearly in shock. Her height was 143 em, weight 38 kg, blood pressure 58 mmHg, heart rate 54 beats/min, temperature 34.8 C and respiratory rate 26/min. ECG showed prolongation of QRS duration and QTc interval, and pacing failure. Furthermore, the pacing threshold was increased. The chest radiograph revealed slight cardiomegalyand lung congestion. Laboratory results showed liver and renal failure. Continuous administration of dopamine and norepinephrine were initiated. Pacing amplitude increased from 2.5 V to 7.5 V, the pacing failure was disappear. The hemodynamics was stable after that. Plasma concentrations of cibenzoline succinate on admission were 2580 nglmI. The hemodynamic failure, ECG abnormality including pacing failure, liver and renal dysfunctioncaused by cibenzoline succinate poisoning.On day 3, to stabilize the hemodynamicsituation and increase urine out put, catecholamines were tapered. On day 5, hypoglycemiaappeared (fasting blood sugar: 52 mgldl) and the plasma concentrations of cibenzoline succinatewere 1710 nglmI.DHP therapy was done for fivehours because cibenzolinesuccinatewas reported to not removeeffectivelyby hemodialysis. After the therapy, prolongationof QRS duration, QTc intervaland pacing thresholdwas improved.The hemodynamicswas stable without inotropic agents. Liver and renal dysfunction was improved gradually. On day 50, she was discharge with taking digoxin. We report the DHP therapy is available for the treatment of cibenzolinesuccinate poisoning.
IP1 F151 I CASE REPORT OF A MASSIVE INTOXICATION BY
IP1 F1531 THE POSSIBLEWAYOF DECREASE OF
A.F. Y Pasqualatto Abbinante*, D. Pasqualatto. Centro de informacion y Asesoramiento Toxicologico (CiATO). Facultad de Farmacia. UCv. Caracas. Venezuela
YOHIMBINE
G. Mignot *, I. Le Normand, A. Caubet, J.Y. Breurec, A. Feuillu, J.P. Curtes, J. Krebs. PoisonControl Center; Rennes, France We report the case of a massive voluntary intoxication with yohimbine hydrochloride, in a context of suicide attempt. This type of intoxication is quite rare. Yohimbine is a drug used for treatment of sexual impotence. It belongs to the group of the alpha receptor antagonists. It has a direct effect on the spongy body.
CONDITIONING REGIMEN TOXICITY IN BONE MARROW TRANSPLANTATION PEDIATRIC PATIENTS
E. Pachanov *, E. Skorobogatova, O. Kryzhanovsky, A. Maschan. RussianCentral Children Hospital, Russianinstitute ofPediatric Hematology, BMT Department, Moscow, Russia Bone marrow transplantation (BMT) has proved to be capable of treatment of severe aplastic anaemia (SAA) and Fanconi anaemia
74
ment included gastric lavage and activated charcoal. Then, areflectic coma, low blood pressure and oliguria appeared. Biological monitoring revealed metabolic acidosis, liver injury, hyperglycemia and hyperamylasemia. Anemia, leucopenia, thrombocytopenia occurred over days 3 to 5. EEG showed diffuse slow waves activities. EMG revealeda sensorimotor neuropathy. Coma lasted one month but two yrs later, the patient was still tetraplegic. Method: P determination in plasma has been performed using a reverse-phase HPLC with fluorescentdetection. Results: Hours after ingestion
12
16
20
24
32
Plasma concentrations (/LgIL)
115
77
24
2
1.5
P plasma concentrations decay had 2 slopes: phase I, between 12 to 16 h, half-life was 16 hours; phase 2, from 16 to 32 H, half-life was 3 hours. The decrease of P plasma half-life in phase 2 was due to hemodynamic and diuresis improvement, since main elimination of P is through urinary excretion. Conclusion: Immediate treatment of hypotension and oliguria may be usefull for improving P clearance, but the effect of faster P kinetics for reducing toxicity has to be further studied.
IP1 F150 I
INFREQUENT MORPHINE ADVERSE EFFECTS: CASE REPORT OF A PEDIATRIC PATIENT
A young male adult absorbed 150 mgr of yohimbine and has been hospitalisedwithin a delay of one hour. Differentblood samples have been taken in order to evaluate the kinetics of eliminationof the drug in a case of massive intoxication. Clinical manifestations were poor except a certain degree of excitation and tachycardia. Yohimbine is known to induce neurological and psychiatric side effects such as irritability, shakings and insomnia. According to previous studies, the eliminationis very quick and only very low levels of yohimbine have been screened by automated HPLC system with full scan UV detection. No observationhad been reported in such a situation of human voluntary intoxication. A few days after this patient put the fire in his bedroom. We do not know if this act is consecutive to the drug effect. This patient had no previouspsychiatric disease.
IP1F1521 SUCCESSFUL TREATMENTOFCIBENZOLINE SUCCINATE POISONING USING DIRECT HEMOPERFUSION (DHP)
Rumiko Kondo*, Naoyoshi Aoyama, TakeshiSasaki1 , Makoto Yoshida,Keisuke Suzuki, YoshitoKamijo, YasushiAsari, Kazui Soma, Tohru Izumi", TakashiOhwada. Departmentof Emergency & Critical CareMedicine; J intemal Medicine, Kitasato University SchoolofMedicine, Sagamihara, Japan
A 5 yr old male patient, 16 kg body weight, presenting second and third degree burns in 26% of his body (lower part) was first hospitalized at the ICU for two and a half weeks. Then, the patient was transferred to the burned patients unit where he stayed until his release. This patient received usual treatment for his condition, for cleaning and dressing of burns, i.e. 0.15 mglkg morphine iv; however, 2.5 h after morphine administration the patient presented narcosis. Respiratory maneuvers were performed and the patient recovered normal breathing.Four and a half hour after morphine, the patient presented hiccups, cyanosis, apnea, stomach distension and respiratory alkalosis. Patient received naloxone and the condition was reversed. Four days later, patient received 0.1 mg/kg morphine iv when cleaning and dressing his burned skin. Thirty minutes later, patient presented apnea, rigidity of limbs and facial muscles, which lasted about 15 sec. After naloxone administration, patient completely recovered. It is important to notice that patient was conscious at all times, and that he did not have a history of neurological disturbances, nor was he receiving any other medication. None of the other patients in the same unit presented any of the symptoms described when receiving morphine. In a 15 yr literature review of morphine use in patients, includingburned ones, we only found a few cases of rigidity of limbs, hiccups and myoclonus. In these cases the patients also remained conscious. We suggest that patients receiving morphine should be closely observed for respiratory depression but also for neurological signs which may be delayed and seem to be dose independent.
A 80-year-old woman was admitted to our hospital for general fatigue. Three years ago, the patient had been implanted permanent right ventricular pacing because of bradycardia-tachycardia syndrome with taking cibenzorine succinate (300 mglday) for one month before this admission.The patient when brought to our hospital was clouding of consciousness(GCS: 13), covered with a profuse clammy sweat and was clearly in shock. Her height was 143 em, weight 38 kg, blood pressure 58 mmHg, heart rate 54 beats/min, temperature 34.8 C and respiratory rate 26/min. ECG showed prolongation of QRS duration and QTc interval, and pacing failure. Furthermore, the pacing threshold was increased. The chest radiograph revealed slight cardiomegalyand lung congestion. Laboratory results showed liver and renal failure. Continuous administration of dopamine and norepinephrine were initiated. Pacing amplitude increased from 2.5 V to 7.5 V, the pacing failure was disappear. The hemodynamics was stable after that. Plasma concentrations of cibenzoline succinate on admission were 2580 nglmI. The hemodynamic failure, ECG abnormality including pacing failure, liver and renal dysfunctioncaused by cibenzoline succinate poisoning.On day 3, to stabilize the hemodynamicsituation and increase urine out put, catecholamines were tapered. On day 5, hypoglycemiaappeared (fasting blood sugar: 52 mgldl) and the plasma concentrations of cibenzoline succinatewere 1710 nglmI.DHP therapy was done for fivehours because cibenzolinesuccinatewas reported to not removeeffectivelyby hemodialysis. After the therapy, prolongationof QRS duration, QTc intervaland pacing thresholdwas improved.The hemodynamicswas stable without inotropic agents. Liver and renal dysfunction was improved gradually. On day 50, she was discharge with taking digoxin. We report the DHP therapy is available for the treatment of cibenzolinesuccinate poisoning.
IP1 F151 I CASE REPORT OF A MASSIVE INTOXICATION BY
IP1 F1531 THE POSSIBLEWAYOF DECREASE OF
A.F. Y Pasqualatto Abbinante*, D. Pasqualatto. Centro de informacion y Asesoramiento Toxicologico (CiATO). Facultad de Farmacia. UCv. Caracas. Venezuela
YOHIMBINE
G. Mignot *, I. Le Normand, A. Caubet, J.Y. Breurec, A. Feuillu, J.P. Curtes, J. Krebs. PoisonControl Center; Rennes, France We report the case of a massive voluntary intoxication with yohimbine hydrochloride, in a context of suicide attempt. This type of intoxication is quite rare. Yohimbine is a drug used for treatment of sexual impotence. It belongs to the group of the alpha receptor antagonists. It has a direct effect on the spongy body.
CONDITIONING REGIMEN TOXICITY IN BONE MARROW TRANSPLANTATION PEDIATRIC PATIENTS
E. Pachanov *, E. Skorobogatova, O. Kryzhanovsky, A. Maschan. RussianCentral Children Hospital, Russianinstitute ofPediatric Hematology, BMT Department, Moscow, Russia Bone marrow transplantation (BMT) has proved to be capable of treatment of severe aplastic anaemia (SAA) and Fanconi anaemia