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Introduction and importance: Stroke, a global health concern, often results from embolic events of cardiac origin. Coxsackie B virus (CBV) myocarditis, a common cause of viral heart infections, can lead to cardiac thrombi formation, subsequently causing devastating complications such as embolic stroke. The authors present a rare case of a 26-year-old male who experienced an embolic stroke following CBV myocarditis and cardiomyopathy. Case presentation: The patient exhibited left-sided weakness, facial droop, and respiratory distress. Laboratory findings indicated leukocytosis, hyponatremia, and elevated troponin I. Imaging revealed an acute right basal ganglia infarct and multifocal pulmonary embolism. The diagnosis involved positive CBV serology, severely reduced left ventricular function, and a large apical thrombus. Discussion: Cardioembolic strokes, often attributable to atrial fibrillation, can also result from intracardiac thrombosis associated with myocarditis. CBV, implicated in up to 40% of acute myocarditis cases, binds to cardiac myocytes, triggering inflammation and potential thrombus formation. Myocarditis-induced hypercoagulability increases the risk of thromboembolic events, complicating the clinical course. Conclusion: CBV myocarditis poses a risk of heart failure, cardiomyopathy, and thromboembolic complications such as embolic stroke. Vigilant monitoring for complications and prompt management is crucial, as primary disease treatment remains primarily supportive. This case highlights the need for increased awareness and further studies to understand the intricate relationship between viral myocarditis and embolic strokes.
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Introduction: Acute oral intoxication of pretilachlor, a synthetic chloroacetanilide herbicide, can present similar clinical manifestations of organophosphorus toxicity in humans. Case presentation: A 15-year-old male was admitted after suicidal ingestion of pretilachlor poison, with decreased consciousness and blood-mixed vomiting. Discussion: Pretilachlor is a colorless and odorless liquid that can cause neurotoxicity and carcinogenicity due to its prolonged exposure. The effects of acute oral exposure are mild and may differ from chronic exposure. Individuals exposed to chloroacetanilides may not show symptoms or experience vomiting and neurological issues. Clinical manifestations such as vomiting, excessive lacrimation, bowel and bladder incontinence, bradycardia, and hypotension can be observed in both organophosphate poisoning and pretilachlor poisoning, making accurate diagnosis challenging, particularly in resource-limited settings like ours. There is no specific antidote for pretilachlor poisoning. Treatment focuses on symptomatic care and monitoring the patient's hemodynamics as per standard protocol. Conclusion: This case underscores the need for prompt stabilization, vigilant monitoring, and supportive care to ensure timely recovery in pretilachlor poisoning cases despite similarities with organophosphate poisoning. It emphasizes the importance of educating and raising awareness among physicians about potential mimickers like organophosphates.