Cardiac and neuromuscular effects of acute organophosphate poisoning

ABSTRACTCardiac And Neuromuscular Effects Of Acute Organophosphate PoisoningAim: The knowledge about cardiac and neuromuscular effects of organophosphatepoisoning depends on limited publications and case reports. In thıs study, we aimed todetermine the agent type, cardiac and neuromuscular effects of organophosphate poisoningand the influence of these information in clinical approach and treatment modalities that willguide further studies to prement complications, disability and death.Materials and methods: In this prospective study conducted for 2 years with theapproval of ethical comittee, 46 patients older than 15 years old who were admitted withcholinergic complaints with suspected organophosphate poisoning were evaluated. Thedemographic properties of the patients (age, gender), comorbitidies, the route of exposure, thetype of agent, serum pseuducholinesterase levels and cardiac markers ( Electrocardiographicfindings, Creatine kinase, Creatine kinase-MB, Troponin-T ) on admission, 6th and 12thhours were recorded. After proper primary assesment and treatment Electromyography,Visuel evoked potential, Somatosensory evoked potential were performed to evaluate theneuromuscular affect.Results: Forty six patients, 27 (58,7%) females and 19 (41,3) males were included inour study. Of this 91,3% was suicidal where 8,7% was accidental exposure. The mostcommon Electrocardiographic finding was sinus tachycardia (30,4%). While long QT interval(15,2%), negative T wave (4,3%), left bundle branch block (2,2%), rigth bundle branch block(2,2%), nodal extra systole (2,2%) were ather common findings. The elevated Creatine kinasewas 65,2%, Creatine kinase-MB 52,2% and Troponin-T 4,3% as cardiac biomarkers, 76,1%of patients had decresed pseudocholinesterase levels supporting organophosphate poisoning.Electromyograhy of 20 patients were normal with normal neuromuscular junction functions.Latacy and/or amplitude asymmetry were found in 4 (20%) patients in Visuel evokedpotential and 3 (15%) patients in Somatosensory evoked potential. All of the patients weredischarged without sequela.Conclusion: All though the mechanism of cardiac affects of organophosphate poisoningis still adilemma, this is an important clinical entity. There is no evoked potential studiesperformed in organophosphate poisoning althoung electroneurography repotitive and P300studies exist in literatüre. More further studies are needed to evaluate the cardiac andneuromuscular effects of organophosphate poisoning.Keywords: Organophosphate poisoning, cardiac effects, neuromuscular effects