Guidelines for Treating Cardiac Manifestations of Organophosphates Poisoning with Special Emphasis on Long QT and Torsades De Pointes

Bar-Meir, Eran; Schein, Ophir; Eisenkraft, Arik; Rubinshtein, Ronen; Grubstein, Ahuva; Militianu, Arie; Glikson, Michael

doi:10.1080/10408440601177855

Cited by 44 publications

(17 citation statements)

References 27 publications

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“…53,54 QT prolongation and Torsades de pointes is reported with relative frequency. 49,55 Pancreatitis and hyperamylasemia have been reported 56 and has a reported incidence of 12% of OP-poisoned patients in 1 case series. 57 Hyperglycemia and hypokalemia are the most common metabolic abnormalities.…”

Section: Clinical Manifestationsmentioning

confidence: 98%

Organophosphate and Carbamate Poisoning

King

Aaron

2015

Emergency Medicine Clinics of North America

226

147

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Section: Clinical Manifestationsmentioning

confidence: 98%

Organophosphate and Carbamate Poisoning

King

Aaron

2015

Emergency Medicine Clinics of North America

226

147

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“…Organophosphate poisoning may precipitate complex ventricular arrhythmias, a frequently overlooked and potentially lethal aspect of this condition [5]. The mechanism by which organophosphates induce cardiotoxicity is still uncertain.…”

Section: Introductionmentioning

confidence: 99%

Heart Rate-Corrected QT Interval Helps Predict Mortality after Intentional Organophosphate Poisoning

et al. 2012

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IntroductionIn this study, we investigated the outcomes for patients with intentional organophosphate poisoning. Previous reports indicate that in contrast to normal heart rate-corrected QT intervals (QTc), QTc prolongation might be indicative of a poor prognosis for patients exposed to organophosphates.MethodsWe analyzed the records of 118 patients who were referred to Chang Gung Memorial Hospital for management of organophosphate poisoning between 2000 and 2011. Patients were grouped according to their initial QTc interval, i.e., normal (<0.44 s) or prolonged (>0.44 s). Demographic, clinical, laboratory, and mortality data were obtained for analysis.ResultsThe incidence of hypotension in patients with prolonged QTc intervals was higher than that in the patients with normal QTc intervals (P = 0.019). By the end of the study, 18 of 118 (15.2%) patients had died, including 3 of 75 (4.0%) patients with normal QTc intervals and 15 of 43 (34.9%) patients with prolonged QTc intervals. Using multivariate-Cox-regression analysis, we found that hypotension (OR = 10.930, 95% CI = 2.961–40.345, P = 0.000), respiratory failure (OR = 4.867, 95% CI = 1.062–22.301, P = 0.042), coma (OR = 3.482, 95% CI = 1.184–10.238, P = 0.023), and QTc prolongation (OR = 7.459, 95% CI = 2.053–27.099, P = 0.002) were significant risk factors for mortality. Furthermore, it was revealed that non-survivors not only had longer QTc interval (503.00±41.56 versus 432.71±51.21 ms, P = 0.002), but also suffered higher incidences of hypotension (83.3 versus 12.0%, P = 0.000), shortness of breath (64 versus 94.4%, P = 0.010), bronchorrhea (55 versus 94.4%, P = 0.002), bronchospasm (50.0 versus 94.4%, P = 0.000), respiratory failure (94.4 versus 43.0%, P = 0.000) and coma (66.7 versus 11.0%, P = 0.000) than survivors. Finally, Kaplan-Meier analysis demonstrated that cumulative mortality was higher among patients with prolonged QTc intervals than among those with normal QTc intervals (Log-rank test, Chi-square test = 20.36, P<0.001).ConclusionsQTc interval helps predict mortality after intentional organophosphate poisoning.

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“…However, in a large cohort of OP pesticide-poisoned patients (5), we have noted patients with dimethoate poisoning on adequate ventilatory support dying from cardiovascular complications, in particular severe hypotension. Previous reports on cardiac complications of OP poisoning have focused on dysrhythmias (6)(7)(8)(9)(10)(11) and hypertension (12,13) with hypotensive effects being relatively less frequently reported (14)(15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Hypotension in severe dimethoate self-poisoning

Davies

Roberts

Eyer³

et al. 2008

Clinical Toxicology

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Introduction. Acute self-poisoning with the organophosphorus (OP) pesticide dimethoate has a human case fatality three-fold higher than poisoning with chlorpyrifos despite similar animal toxicity. The typical clinical presentation of severe dimethoate poisoning is quite distinct from that of chlorpyrifos and other OP pesticides: many patients present with hypotension that progresses to shock and death within 12-48 h post-ingestion. The pathophysiology of this syndrome is not clear. Case reports. We present here three patients with proven severe dimethoate poisoning. Clinically, all had inappropriate peripheral vasodilatation and profound hypotension on presentation, which progressed despite treatment with atropine, i.v. fluids, pralidoxime chloride, and inotropes. All died 2.5-32 h post-admission. Continuous cardiac monitoring and quantification of troponin T provided little evidence for a primary cardiotoxic effect of dimethoate. Conclusion. Severe dimethoate self-poisoning causes a syndrome characterized by marked hypotension with progression to distributive shock and death despite standard treatments. A lack of cardiotoxicity until just before death suggests that the mechanism is of OP-induced low systemic vascular resistance (SVR). Further invasive studies of cardiac function and SVR, and post-mortem histology, are required to better describe this syndrome and to establish the role of vasopressors and high-dose atropine in therapy.

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Guidelines for Treating Cardiac Manifestations of Organophosphates Poisoning with Special Emphasis on Long QT and Torsades De Pointes

Cited by 44 publications

References 27 publications

Organophosphate and Carbamate Poisoning

Organophosphate and Carbamate Poisoning

Heart Rate-Corrected QT Interval Helps Predict Mortality after Intentional Organophosphate Poisoning

Hypotension in severe dimethoate self-poisoning

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