Posters IV - The American Academy of Clinical Toxicology

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life-threatening bleeding. Case Report: A 34 year-old Chinese female attempted suicide by ingesting 7 boxes of d-Con while 33 weeks pregnant. She was treated with oral phytonadione (up to a maximum dose of 40 mg twice daily) and experienced no hemorrhage or complications. Her PT/INR peaked on day 3 post-ingestion at 87.1/7.14. She was released from the hospital on day 43 with a normal PT/INR, and continued to take phytonadione. On day 8 post-ingestion, the fetus was delivered emergently by c-section after experiencing decelerations and had APGARs of 1 and 7 at delivery. The female baby began seizing and required intubation. She bled significantly from the cord and endotracheal tube. Coagulation studies showed a PTT >225, PT >140, and INR >11.4 with a hematocrit of 25. Vitamin K IV and FFP were given to correct anticoagulation and control bleeding. A CT scan of the head showed intraventricular subarachnoid, subdural hemorrhages, and diffuse cerebral edema. Despite aggressive medical treatment, including ventricular drainage, the infant's condition deteriorated, and life support was withdrawn resulting in death 3 days after delivery. Case Discussion: Warfarin crosses the placenta freely but it is unclear how well brodifacoum crosses. Vitamin K1 has been shown in human studies to poorly cross the placenta, including one study in 1982 that found no detectable levels in the cord blood of term infants although adequate levels were present in mothers. Vitamin K1 during pregnancy is generally indicated for maternal hypoprothrombinemia and for prevention of hemorrhagic disease of the newborn induced by maternal drugs. There is only one documented case report of a pregnant poisoning with brodifacoum (at 22 weeks gestation) and there were no fetal complications. Conclusions: This is the first case report of infant demise after maternal ingestion of brodifacoum. Brodifacoum in high doses significantly crosses the placenta, and phytonadione orally in standard doses does not cross the placenta enough to reverse anticoagulation. 303 Comparative electrocardiographic effects of antipsychotic drugs after overdose Salem M Fathalla 2 , Janine Gray 1 , Simon H Thomas 2 1 Janine Gray Statistical Consultancy, East Bolden UK 2 Newcastle University, Newcastle UK Background: Antipsychotic drugs are commonly involved in episodes of drug overdose. Some antipsychotics may delay cardiac repolarisation, leading to QT prolongation and an increased risk of torsade de pointes. Effects on the QRS interval, reflecting sodium channel function and conduction velocity, have also been reported.This study was performed to compare EKG effects of individual antipsychotic drugs after overdose. Methods: Observational cohort study using EKGs collected at 25 mm/s from all adult patients with first presentation of antipsychotic drug overdose in Newcastle between 2000 and 2008. EKGs were analysed blind to patient characteristics and exposure using a digitizer. Relationships between antipsychotic drugs and QT and QRS intervals were examined by multivariate analysis. Results: Of 443 first presentations with reported antipsychotic overdose, 364 had at least one EKG available. In 46 (12.6%) episodes QTc prolongation (>450 ms in males, >470 ms females) was demonstrated but there were no QTc intervals > 500 ms. QT intervals were correlated with RR interval and age, inversely correlated with plasma potassium concentration and were longer in females and those taking thioridazine in overdose (Regression coefficient 16.25, 95% CI 7.7, 24.7 ms). No significantly different QT effects were detected for other individual antipsychotics. There was a weak positive relationship between QRS interval and age. QRS intervals were shorter with haloperidol (Regression coefficient -7.0, 95% CI -12.4 to -1.6, ms) and longer with quetiapine (Regression coefficient 6.0, 95% CI 2.2 to 9.8, ms). Conclusions: Severe QTc prolongation is uncommon after antipsychotic overdose. Lengthening of the QT prolongation was associated with thioridazine overdose, which has also been linked with QT prolongation and torsade de points in normal therapeutic use. The apparent link between
haloperidol and quetiapine overdose and QRS interval changes merits further research. Study shortcomings include limited statistical power, retrospective methodology with incomplete availably of data, lack of analytical confirmation and of doses taken and often absence of baseline EKGs. 304 Massive Amantadine Overdose Resulting in Status Epilepticus and Death Shin K Kwon 1 , Heather Ellsworth 1 , Christian P Lintner 1 , Samuel J Stellpflug 1 , Jon B Cole 1 1 Hennepin Regional Poison Center, Minneapolis MN USA Background: Amantadine has been used in the treatment of the influenza virus, Parkinson's disease, and drug-induced extrapyramidal symptoms. Toxic doses have produced cardiac arrhythmias and neuropsychiatric effects in animal studies and have also been demonstrated in human case reports. We report a case of amantadine toxicity resulting in ventricular tachycardia, status epilepticus, and death. Case Report: An asymptomatic 33 year-old woman with a history of bipolar disorder and multiple sclerosis presented to the ED 1.5 hours after ingesting 6.2 g of amantadine in an attempt at self-harm. Four hours post-ingestion, she became acutely disoriented, developed ventricular tachycardia, seized, and had a cardiac arrest treated successfully with CPR, intubation, lidocaine and amiodarone. Her potassium was 2.5 mEq/L, sodium 135 mEq/L, glucose 88 mg/dL, bicarbonate 26 mEq/L, and creatinine 0.58 mg/dL. Supplemental magnesium and potassium were administered. Her amantadine concentration 1.5 hours postingestion was 3,960 ng/mL, 10.5 hours post-ingestion was 20,508 ng/mL, and 21.8 hours post-ingestion was 15,508 ng/mL. She was extubated on hospital day (HD) 2, but remained confused and was hallucinating. Due to hypoxia and concern for airway compromise, she was re-intubated on HD 3. She developed acute respiratory distress syndrome and septic shock with positive urine (Escherichia coli), blood (Staphylococcus epidermidis), and sputum (Haemophilus influenza) cultures. Levofloxacin and continuous infusions of norepinephrine, propofol, midazolam and vecuronium were administered during hospitalization. Due to refractory seizure activity confirmed by electroencephalogram (EEG), pentobarbital was administered on HD 14. On HD 21 life support was withdrawn after EEG monitoring revealed 252 hours of persistent seizure activity. Discussion: A therapeutic range of amantadine has not been established, however the expected steady state concentration in patients receiving therapeutic doses is thought to be 200-1,000 ng/mL. Time to peak serum concentrations is 3.3 hours, which approximated the onset of toxicity in this case. Reported effects in overdose are cardiac dysrhythmias (including arrest), hypertension, and CNS toxicity. Much of the acute toxicity is attributed to antimuscarinic effects and usually observed when serum concentrations exceed 2,000 ng/mL. This case highlights the rare occurrence of refractory status epilepticus following an acute overdose of amantadine. Conclusion: Toxicologists and emergency providers should be aware that amantadine toxicity may result in lethal cardiac dysrhythmias and refractory seizure activity. 305 Acidosis and prolonged ataxia following massive ibuprofen overdose Ronald I Kirschner 2 , Karah M Debroux 1 1 University of Nebraska Medical Center, Omaha NE 2 Nebraska Regional Poison Center, Omaha NE USA Background: Coma, acidosis, and seizures are sometimes seen with large ibuprofen overdoses. We report a patient who had persistent ataxia until 5 days after ingestion, followed by full recovery. Case presentation: A healthy17 year old female was found unresponsive by family, with seizure-like activity. Initial vital signs were normal except for a heart rate of 127. In the Emergency Department, she had tonic
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Posters IV - The American Academy of Clinical Toxicology

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