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Potassium permanganate (KMnO4), a powerful oxidizing agent, is readily available without prescription. Tissue contact produces coagulation necrosis and the lethal consequences of oral ingestion are well described, with most deaths because of airway oedema and obstruction or circulatory collapse. Whilst systemic toxicity is reported, its mechanism is unclear. We describe a case of suicidal ingestion of KMnO4 followed by acute hepatorenal toxicity resulting in the death of the patient. The clinical course bore close resemblance to that of severe paracetamol overdose. We discuss the pathogenesis of the systemic toxicity of KMnO4 and postulate that it is due to oxidative injury from free radicals generated by the absorbed permanganate ion. We recommend that N-acetyl cysteine be given within the first few hours to all patients with potassium permanganate poisoning.

Funding Acknowledgements Type of funding sources: None. Background/Introduction Prior studies have demonstrated abnormalities of diastolic function are independent predictors of heart failure and all-cause mortality. The optimal way to classify diastolic function has continued to evolve over time, particularly in those with preserved left ventricular ejection fraction. A notable change in the 2016 American Society of Echocardiography (ASE)/European Association of Cardiovascular Imaging (EACVI) guidelines is that individuals with impaired myocardial relaxation and normal filling pressure can be classified as normal diastolic function. Purpose To determine whether the association of diastolic dysfunction with increased risk of all-cause mortality is driven by cardiovascular or non-cardiovascular death. Second, to evaluate if the presence of an impaired myocardial relaxation inflow pattern without other diastolic abnormalities conveys a marker of increased risk. Methods This study utilized the Olmsted County Heart Function Study (OCHFS), a well characterized prospective adult community cohort with comprehensive echocardiography between 2001 and 2004 and long-term follow-up. Only individuals with measurable diastolic function were included (n = 1,104). Those with reduced left ventricular ejection fraction, more than moderate valve disease, or a clinical diagnosis of heart failure (n = 52); or indeterminate diastolic function (n = 47) were excluded. Diastolic function was assessed by the current Mayo Clinic diagnostic algorithm (Figure). Results A total of 695 individuals were classified as normal, 265 with impaired myocardial relaxation or grade 1 diastolic dysfunction, and 45 with grade 2-3 diastolic dysfunction. Those with diastolic dysfunction were older and had more comorbidities including diabetes, hypertension and coronary disease (Table). There were 264 deaths in the median follow up period of 15.2 years (IQR 14.4 – 18.0), including 173 non-cardiovascular and 81 cardiovascular deaths. Both cardiovascular and non-cardiovascular mortality were associated with the presence and grade of diastolic dysfunction (Table 1). Individuals classified as normal by 2016 ASE/EACVI criteria, but grade 1 by the Mayo algorithm had an increased risk of all-cause mortality after univariate analysis (HR 4.35, 95% CI (3.35, 5.65), p < 0.0001) compared to normal subjects and remained associated after adjustment for age (HR 1.55, 95% CI (1.15, 2.09), p < 0.0001. Subjects with a grade 1 pattern had a higher rate of cardiovascular mortality (ꭕ2 70.1, p < 0.0001). Conclusions Individuals with diastolic dysfunction, including those with an impaired relaxation mitral inflow, were at increased risk of mortality, particularly cardiovascular mortality. This study highlights the importance of separating grade 1 diastolic dysfunction from normal in the assessment of diastolic function as it represents a clinically significant risk marker of myocardial disease. Abstract Figure.  Abstract Figure.

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