TRAUMA, THE TRIGGERING FACTOR OF HEPATORENAL SYNDROME DUE TO MYOGLOBIN TOXICITY

2018 
Background: Myoglobin , essentially acytoplasmichemoprotein in striated muscle, expressed solely in cardiac myocytes and oxidative skeletal muscle fibers. The heme residue binds the oxygen reversibly by a porphyrin ring - iron ion complex. Functionally, myoglobin is an oxygen storage protein in muscle, capable of releasing oxygen during hypoxia or anoxia. Apart from this myoglobin provides additional function like scavenging nitric oxide and reactive oxygen species, thus acts like an antioxidant. Myoglobin toxicity is not uncommon with trauma and degenerative muscle pathology. This involves a condition commonly called rhabdomyolysis, which results when the skeletal muscle gets damage due to strenuous exercise.  In majority of cases it is self limiting but when there is intense damage, the muscle proteins gets released into the circulation and gets deposited in the renal tubules resulting in acute tubular necrosis, with subsequent acute renal failure. From the literature survey it is evident that, a high proportion of marathon runners had developed acute rhabdomyolysis. Azotemia, severe metabolic acidosis, disseminated intravascular coagulation and acute liver failure results due to rhabdomyolysis go unnoticed. Methods: A series of cases who succumbed due to rhabdomyolysis due to various etiology were studied after taking the consent. A detailed analysis of cases and the autopsy findings were noted and tabulated in the table 1. Clinical correlation of  the pathophysiology of  hepato-renal syndrome was studied with respect to rhabdomyolysis. Results: As per the table 1 and figures 1-11 Conclusion: Early detection and hemodialysis will be helpful in unnoticed fatal acute tubular necrosis due to rhabdomyolysis. Not only marathon runners suffer muscle damage but also epilepsy and trauma suffer. apart from treating the primary pathology rhabdomyolysis has to be identified and treated promptly.
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