Predictors of Death and Prolonged Renal Insufficiency in Ethylene Glycol Poisoning.

BACKGROUND: We assessed the predictive value of selected factors on the outcomes of death and prolonged renal insufficiency (RI) from ethylene glycol poisoning. METHODS: Retrospective, observational California Poison Control System study, over a 10-year period (1999-2008). We compared 2 groups. The first group (D/RI) included 59 patients who died (9 patients) or had prolonged RI (50 patients). Prolonged RI was defined as kidney injury in which dialysis was required for greater than 3 days after presentation. The second group (RECOV) of 62 patients had an uncomplicated recovery. Secondarily, we evaluated the association of time to antidote (ethanol and/or fomepizole) and time to dialysis with these outcomes. RESULTS: The D/RI group was more likely than the RECOV group to present comatose, have seizures, and require intubation. The D/RI group had a lower mean initial arterial pH of 7.03 (standard deviation [SD] 0.20), compared to 7.27 (SD 0.14) for the RECOV group. The D/RI group had a higher initial creatinine (1.7 mg/dL, SD 0.71) than that of the RECOV group (1.0 mg/dL, SD 0.33). Patients with a time to antidote greater than 6 hours had a higher odds of dying or having prolonged RI (OR 3.34, 95% CI : 1.21-9.26) Patients with a time to dialysis greater than 6 hours had a lower odds of dying or having prolonged RI (OR 0.36, 95% CI : 0.15-0.87). CONCLUSION: Compared to survivors with an uncomplicated recovery, patients poisoned with ethylene glycol who died or had prolonged RI were more likely to exhibit clinical signs such as coma, seizures, and acidosis. Antidote administration within 6 hours is associated with better outcomes, unlike earlier time to dialysis.

Prolonged ventilatory failure and flaccid quadriparesis after ingestion of poison hemlock.

INTRODUCTION: A 28-year-old man presented with acute flaccid paralysis and respiratory failure that persisted for 2 weeks after suicidal ingestion of unknown substances. METHODS: Extensive clinical, nerve, laboratory, and neuroimaging testing excluded alternative causes of this neuromuscular syndrome. Prompted by clues provided by family members, liquid chromatography time-of-flight mass spectrometry was used to investigate for the presence of poison hemlock. RESULTS: Testing of the residue in a jar used for the ingestion of a poisonous concoction confirmed the presence of the nicotinic alkaloid coniine. Analysis of patient serum suggested the presence of conhydrine. Concentrations of amitriptyline and diazepam were also found to be supratherapeutic, but only through the first few days of hospitalization. CONCLUSIONS: Herein we describe a case of reversible coma, flaccid quadriparesis, and neuromuscular respiratory failure caused by intentional ingestion of poison hemlock.

Cardiotoxicity in a citalopram and olanzapine overdose.

BACKGROUND: This is a case of a citalopram and olanzapine overdose causing seizures and severe cardiotoxicity. CASE REPORT: A 21-year-old man presented unresponsive, with seizures, to an Emergency Department. The patient's initial electrocardiogram demonstrated a widened QRS of 160 ms and a normal QT/QTc interval of 400/487 ms consistent with cardiac sodium channel blockade. Within 30 min of arrival, peak citalopram and olanzapine levels were measured to be 522 ng/mL and 505 ng/mL, respectively. Measured levels remained supratherapeutic until 13.6 h and 42.6 h after arrival for citalopram and olanzapine, respectively. The patient developed bradycardia and hypotension that required multimodal therapies including sodium bicarbonate boluses, vasopressors, and transvenous pacing. Seizures and cardiotoxicity continued while citalopram, but not olanzapine, was supratherapeutic. CONCLUSIONS: This case describes cardiotoxicity directly correlated with supratherapeutic citalopram levels in overdose.

Confirmed glyburide poisoning from ingestion of "street Valium".

BACKGROUND: Pharmaceuticals with little to no abuse potential are often sold surreptitiously as drugs of abuse on the street. Anecdotally, sulfonylureas are suspected to be commonly sold as "street Valium." CASE REPORTS: Two patients presented with altered mental status and persistent hypoglycemia requiring continuous intravenous dextrose, in the context of suspected attempted benzodiazepine abuse. Supratherapeutic glyburide levels of 1198 and 647 ng/mL were measured in these patients. CONCLUSIONS: These are two cases of glyburide poisonings from ingestion of "street Valium" that have been confirmed by laboratory testing.

Hypoglycemia in pediatric sulfonylurea poisoning: an 8-year poison center retrospective study.

OBJECTIVE: The goal of this study was to describe the clinical effects and time of onset of hypoglycemia in pediatric sulfonylurea poisoning. METHODS: This was a retrospective, descriptive study of pediatric (<6 years old) sulfonylurea exposures with hypoglycemia (glucose concentration <60 mg/dL) that were consulted on by the California Poison Control System for the 8-year period between January 1, 2002, and December 31, 2009. RESULTS: Of the 1943 consultations for pediatric sulfonylurea exposure in the study period, 300 children developed hypoglycemia. Ten percent had hypoglycemia occurring or persisting ≥ 12 hours after ingestion despite receiving treatment. All 5 children with seizures experienced these before hospital presentation. The mean (SD) time to onset of hypoglycemia in children not given any prophylactic treatment was 2.0 (1.2) hours. The mean (SD) times in children receiving prophylactic food only, intravenous glucose only, and both food and intravenous glucose were 5.9 (3.9), 5.7 (2.5), and 8.9 (3.6) hours, respectively. Ranges were 1 to 18, 1.5 to 9, and 2.5 to 15 hours. Seven of 40 patients (18%) receiving prophylactic food only had an onset of hypoglycemia >8 hours after sulfonylurea ingestion. CONCLUSIONS: Pediatric sulfonylurea exposure can result in significant poisoning. Severe effects such as seizures occurred only in cases of unrecognized sulfonylurea ingestion. The onset of hypoglycemia after pediatric sulfonylurea ingestion can be delayed by as much as 18 hours by either free access to food or administration of intravenous glucose.