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Future studies that further elucidate the pathophysiology of hypophosphatemia after hepatic resection might lead to better management. Universally accepted method for investigation, optimal replacement and target serum levels are lacking. In summary, hypophosphatemia after hepatic resection can lead to deleterious consequences and should be properly addressed. Further validation studies are needed to assess the clinical utility of these measures in the management of hypophosphatemia. Persistently low serum 2,3-DPG levels and high nucleotide breakdown products in the urine would potentially indicate inadequate intracellular phosphate replenishment ( 7). Alternatively, measurements of serum 2,3- diphosphoglycerol (DPG) and nucleotide breakdown products in the urine have been reported to be more sensitive physiologic markers of hypophosphatemia-related cellular stress. Acidosis can cause a shift of intracellular phosphate to extracellular space resulting in normalization of extracellular phosphate levels.
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Currently, management of hypophosphatemia relies on serum phosphate measurements, which may not be an accurate measure of actual intracellular phosphate levels due to intra-extracellular shifts. Standard liver resection management includes adequate replacement of phosphate with supplementation of maintenance fluids with potassium phosphate and oral/parenteral replacement. Hypophosphatemia results in impaired energy metabolism, leading to cellular dysfunction in many organ systems including respiratory failure, cardiac arrhythmias, hematologic dysfunction, insulin resistance, and neuromuscular dysfunction ( 8, 9). Whether this reflects an increased production of phosphaturic mediators by the injured liver versus decreased clearance of a circulating mediator by the remnant liver is unclear. However, recent work by several investigators has suggested that excessive urinary losses mediated by phosphaturic mediators termed phosphatonins might be responsible for post-hepatic resection hypophosphatemia ( 6, 7). The pathogenesis of hypophosphatemia after hepatic resection is poorly understood and is generally believed to be due to increased phosphate uptake by regenerating hepatocytes. Hypophosphatemia is encountered in nearly all patients after major hepatic resection. Due to the additive effects of lactate-containing intravenous solution, non-lactate containing solutions are recommended for postoperative use ( 5). The initial arterial plasma lactate concentration was significantly higher in non-survivors than in survivors, and correlated with bilirubin levels and was an excellent independent predictor of morbidity and mortality. Watanabe, et al., examined the relationship between lactate and base excess with clinical outcomes in 151 hepatic resection patients. When the liver is damaged or stressed, it produces lactate rather than metabolizing it. Gluconeogenesis carried out by the liver normally consumes 40-60% of lactate. Hyperlactemia and hypophosphatemia are common derangements in patients undergoing liver resection. Paracentesis may be necessary to prevent tense ascites. Management with sodium restriction and judicious use of diuretic therapy is recommended. New onset postoperative ascites frequently occurs in cirrhotic patients. In this setting, colloids rather than crystalloids should be administered to restore intravascular volume. Cirrhotics are prone to fluid shifts, vasodilation and resultant hypotension. Maintenance of adequate fluid balance and normal renal function is critical. The immediate postoperative period after hepatic resection is characterized by fluid and electrolyte imbalances that are further accentuated by derangements of liver function. The purpose of this review is to elaborate on specific early postoperative management issues after liver resection, examine current evidence and present the management options. Majority of postoperative management issues after liver resection are unique and require a thorough understanding of liver metabolism and the pathophysiology of liver disease. Although, no single factor is solely responsible, overall advances in surgical and anesthetic techniques, better understanding of hepatic physiology and improvement in perioperative management have all been contributory. Outcomes after hepatic resection have significantly improved over the last few decades ( 1- 4). Keywords: Management postoperative hepatic resection liver resection