Potassium permanganate toxicity: A rare case with difficult airway management and hepatic damage.

Abstract

Sir, We read case report “potassium permanganate (KMnO4) toxicity: A rare case with difficult airway management and hepatic damage” by Agrawal et al.[1] with great interest. We would like to discuss some points regarding the management of the patient. Potassium permanganate is a powerful oxidizing agent. Free radicals generated due to absorbed permanganate ion overwhelm reduced tissue glutathione stores and causes liver injury. Its clinical course closely resembles that of paracetamol poisoning.[2] Hepatic injury due to a similar mechanism is also seen in toxicities due to carbon tetrachloride, chloroform, clove oil and amanita mushroom. N-acetylcysteine (NAC) acts as an antioxidant, both directly as a glutathione substitute and indirectly as a precursor for glutathione. It also causes vasodilatation by increasing cyclic guanosine monophosphate level, inhibits platelet aggregation, acts as a sulfydryl donor to regenerate endothelial derived relaxing factor and reduce interleukin-8 and tumor necrosis factor-alpha production.[3] It improves transplant free survival in early stage nonacetaminophen acute liver failure[4] and also of great benefit in centers without facility for liver transplantation.[5] Use of NAC has shown good outcome in above mentioned toxicities, which are oxidizing agents like KMnO4. Hence, we suggest an early use of NAC in KMnO4 poisoning to prevent or reduce hepatic injury as also suggested by Young et al.[2]