Pyrethroid poisoning: features and predictors of atypical presentations.

BACKGROUND: Although pyrethroids are known for low toxicity to humans, clinical systemic characteristics of pyrethroid poisoning remain undefined. We investigated atypical presentations of pyrethroid poisoning and the predictors, among those readily assessed in the emergency department. METHODS: 59 pyrethroid poisoning cases that were diagnosed and treated at the emergency department of Wonju Severance Christian Hospital from September 2004 to December 2012 were retrospectively reviewed. RESULTS: Atypical presentations were seen in 22 patients (39.3%). Atypical presentations after pyrethroid poisoning included respiratory failure requiring ventilator care (10 patients, 17.9%), hypotension (systolic blood pressure <90 mm Hg) (6 patients, 10.7%), pneumonia (4 patients, 7.1%), acute kidney injury (6 patients, 10.7%), Glasgow Coma Scale (GCS) <15 (19 patients, 33.9%), seizure (2 patients, 3.6%) and death (2 patients, 3.6%). There were differences between atypical versus typical groups in terms of age (62.1±3.7 vs 51.0±2.9, p=0.020), ingested amounts (300 (IQR 100-338) cc vs 100 (IQR 50-300) cc, p=0.002), and bicarbonate and serum lactate (17.4±1.1 vs 20.5±0.4, p=0.011; and 4.42 (IQR 3.60-7.91) mmol/L vs 3.01 (IQR 2.16-4.73) mmol/L, p=0.010, respectively) in initial arterial blood gas analysis. Predictors of the atypical presentations were ingested amount and serum lactate ((OR 1.004, 95% CI 1.001 to 1.008, p=0.013) and (OR 1.387, CI 1.074 to 1.791, p=0.012), respectively). The optimal points were 250 cc and 3.5 mmol/dL. CONCLUSIONS: 39.3% of pyrethroid poisoned patients had atypical presentations with the most common being respiratory failure requiring ventilator care. Predictors of atypical presentation were ingested amount >250 cc and serum lactate >3.5 mmol/L.

Evaluation of cardiac function using transthoracic echocardiography in patients with myocardial injury secondary to methomyl poisoning.

Generally, the mortality rate for cases of carbamate poisoning is low, but fatalities secondary to methomyl poisoning have been reported including a case report of cardiac toxicity following short-term exposure to methomyl. There have been no reports, however, regarding patterns of cardiac toxicity after exposure to methomyl. Therefore, we investigated the prevalence and patterns of myocardial injury using a biochemical marker, troponin I (TnI), and evaluated cardiac function using transthoracic echocardiography (TTE). We conducted a retrospective review of 14 consecutive methomyl poisoning cases that were diagnosed and treated at the emergency department of the Wonju Severance Christian Hospital between January 2009 and December 2013. On ECG analysis, ST depression and T-wave inversion were seen in five patients (35.7%) and one patient (7.1%), respectively. On cardiac biochemical marker analysis, initial TnI was elevated in 11 patients (78.6%). TTE was performed in nine patients among the 11 patients in whom TnI was found to be elevated. Of the nine patients that underwent TTE, three patients (33.3%) showed a reduced ejection fraction (EF), and RWMA was noted in two patients. There were two patients (22.2%) that had both reduced systolic function and RWMA. One patient did not regain normal systolic function on admission. None of the three patients with reduced EF received any specific treatment to support cardiac function. One patient expired due to pneumonia, and one patient was transferred as moribund. We followed up on 12 patients who survived to discharge for 6-44 months. One patient (8.3%) was died to follow-up, and 11 patients survived without any further complications. Methomyl exposure can cause direct myocardial injury and reversible cardiac dysfunction. Monitoring of TnI levels and TTE for evaluation of cardiac function may be useful in the workup of patients suffering from methomyl poisoning.