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INTRODUCTIONThe inorganic electrolytes i.e. sodium, potassium, chloride, calcium etc. are important constituents of body fluid as they play a vital role in cellular function and survival, in regulating fluid balance in respective zones, excitability of tissues and acid base equilibrium and other manifestations associated with life.1 Changes in both fluid volume and electrolyte composition occur preoperatively, intraoperatively and postoperatively. Operative trauma imposes a great impact in the physiology of fluid and electrolytes within the body, which is greater than the changes associated with a simple lack of alimentation. Apart from blood loss, there is sequence of events consisting of increased loss of fluid through lungs along with pooling of plasma and ECF in ABSTRACT Background: Operative trauma is followed by a series of changes collectively referred to as metabolic response to injury, the magnitude and duration of the response being directly proportional to the severity of the trauma. Operative trauma imposes a great impact in the physiology of fluid and electrolytes within the body. Fluid and electrolyte management has thus been an integral part of care of each and every surgical patient. In the present study, an attempt has been made to study the electrolyte changes, especially that of sodium and potassium following surgical trauma due to various surgical procedures and its implication in the principles of replacement therapy. Methods:The present study is being carried out in 50 surgical patients both male and female, of age group of 18-70 years. Serum electrolytes (Na, K, Cl, Ca and Mg) of each patient was estimated one day before operation (-1), on the day of operation (0) after surgery, next consecutive 4 postoperative days (+1, +2, +3, +4) and on 7th postoperative day (+7).Results: There occur a fall in serum sodium and chloride level on the day of operation in all cases which attain a still lower level in 1 st postoperative day. Then from 2 nd postoperative day onwards, there occur a gradual rise and attain preoperative value by 4 th postoperative day in most cases and by 7 th postoperative day in all cases. There occurs an elevation on serum potassium level from the day of operation, which becomes highest in 1 st postoperative day. This follows a gradual fall in from 2 nd postoperative day onwards and attains preoperative level in most cases by 4

In chronic renal failure there is a steady and continued decrease in renal clearance or glomerular filtration rate (GFR), which leads to the gathering of urea, creatinine and other waste metabolites in the blood. Haemodialysis is considered as a good therapeutic option in the context of the renal replacement therapies in which different body waste products including urea, creatinine and free water are removed from the blood. In view of that, the present study was conducted to evaluate the effect of haemodialysis on different renal biochemical parameter in CRF patients. Materials and Methods: The present study was a hospital based study including 84 chronic renal failure patients on haemodialysis attending a tertiary care hospital in Bihar. Blood samples were collected before and four hours after haemodialysis and serum urea, creatinine, uric acid, potassium, sodium and calcium were estimated. Results: Our results revealed that there was significant decrease in the serum level of urea, creatinine, uric acid and potassium in post dialysis samples with p-value (<0.001, 0.001 0.003 and 0.001) respectively when compared to pre dialysis samples, while showed significant increase of sodium and calcium level in post dialysis samples with p-value (<0.004 and 0.005) Conclusion: The Study concludes that, haemodialysis increase serum sodium and calcium level and decrease serum urea, creatinine, uric acid and potassium level.

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Recent studies in India shows that about one third of urban population in major cities has metabolic syndrome. 3 The majority of persons with metabolic syndrome have insulin resistance. Insulin resistance and/or associated hyperinsulinemia are believed to be the direct cause of other metabolic syndrome risk factors. 4 Insulin resistance is usually caused by a defect in insulin action within target organs and tissues that result in compensatory hyperinsulinemia. 5 It has been proved that insulin resistance and hyperinsulinemia are closely linked. 6 Although hyperinsulinemia may compensate for insulin resistance to some biological actions of insulin,