A conversation about hypophosphatemia after a recent liver resection elicited a literature search on the subject. A paucity of material in the pediatric surgical literature (a quick search yielded only one case report) prompted a move to the adult literature (yes, I know, they are not just small adults!).
A retrospective study by Salem et al looked at post operative phosphate levels in 20 patients who underwent major liver resection. The authors confirmed the known association between hypophosphatemia and major liver resection with a drop in phosphate levels of an average of 1.1 mg/dl and a nadir at post operative day 2.
They discussed several potential explanations, including the common assumption that the drop in phosphate levels is due to the consumption of phosphate ions by the aggressively regenerating liver, but noted that these patients also experience hyperphosphaturea. This finding contradicted what would be expected in the setting of phosphate ion depletion by the liver.
Their alternate explanation involved some form of messenger molecule controlled by the liver, and depleted with a major liver resection. They described this as a disruption in normal hepatorenal messaging that results in phosphate ion wasting by the kidney. This starts immediately postoperatively, peaks at 2 days post operatively, and usually resolves by post op day 5.
A retrospective study by Salem et al looked at post operative phosphate levels in 20 patients who underwent major liver resection. The authors confirmed the known association between hypophosphatemia and major liver resection with a drop in phosphate levels of an average of 1.1 mg/dl and a nadir at post operative day 2.
They discussed several potential explanations, including the common assumption that the drop in phosphate levels is due to the consumption of phosphate ions by the aggressively regenerating liver, but noted that these patients also experience hyperphosphaturea. This finding contradicted what would be expected in the setting of phosphate ion depletion by the liver.
Their alternate explanation involved some form of messenger molecule controlled by the liver, and depleted with a major liver resection. They described this as a disruption in normal hepatorenal messaging that results in phosphate ion wasting by the kidney. This starts immediately postoperatively, peaks at 2 days post operatively, and usually resolves by post op day 5.
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