Snakebite, Antivenom and Mitochondrial Toxicity

How to Cite this Article: Kohli S, Bhatia S, Sexana K, Kalsi R, Rajeshwari K, Arora M. Discolouration of Polymethyl Methacrylate versus bis‐acrylic based Provisional Crown and Bridge Dental Resins: Effect of Storage Me‐ dia and Duration. Ann Med Health Sci Res. 2017; 7: 200‐202 This is an open access article distributed under the terms of the Creative Commons Attribution‐NonCommercial‐ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non‐commercially, as long as the author is credited and the new creations are licensed under the identical terms. Abstract Background: Snake bites are common in underdeveloped countries and produces generally cardiac, renal and neuromuscular complications. Common side effect of antivenom is anaphylaxis. Snake poison is the most complex natural poison which acts on the victim by the multiple components present in it. Apart from supportive treatment polyvalent antivenom is used in treatment. Neither the snake venom nor the antivenom is reported to have mitochondrial toxicity so far in literature. Subject and Methods: A 10-year-old male child presented with cardiovascular collapse following snake bite and treated with polyvalent antivenom. Following a brief period of recovery, patient presented with features of acute mitochondrial encephalopathy which was confirmed by T2 changes and lactate peak in MR spectroscopy. Child made complete recovery with mitochondrial cocktail. Investigation for mitochondrial Cytopathy with muscle biopsy was normal. However, mitochondrial genetics for primary mitochondrial disease was not done. Discussion and Conclusion: It is possible that some of the substances present in the snake venom, antivenom might have mitochondrial toxicity and this should be considered as a possibility when a second encephalopathy occurs following treatment for snakebite.