In diabetic ketoacidosis the excretion of phosphate leads to phosphate depletion, which can, comparable to the situation with potassium, be manifested during rehydration and insulin therapy of diabetic ketoacidosis. Possibly the increased uptake of phosphate by skeletal muscles via carbohydrate assimilation might play a role. Since the concentration within the erythrocytes of 2.3 diphosphoglycerate is lowered in diabetic ketoacidosis this leads to a decrease of tissue oxygenation. This was the reason why there was hope that substitution of phosphate might alleviate the clinical course of diabetic coma. However, most of the studies have shown no significant effect on the clinical course by phosphate substitution in diabetic ketoacidosis with or without coma. In cases of severe hypophoshatemia a low dose of phosphate repletion is recommended, e.g., using sodium glycerol phosphate (20 mL infusion additive contain 20 mmol) in a dose of 10 to 20 mmol/L (without calcium). Higher doses such as 50 mmol phosphate per day can lead to hypocalcemia and hypomagnesemia. A dose of 20 mmol/hr and a total dose of 100mmol/day should be the limit even in cases of severe phosphate deficiency. The control of calcium and phosphate under therapy is recommended at least every 12 hours (30,31).
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