आईएसएसएन: 2155-6148
Randi Beier-Holgersen
Introduction: Postoperative hyponatremia is still not fully understood. Some of the explanations presented are based on dilutions with low-sodium fluids, the influence of anti-diuretic hormone, the desalination process, and the “sick cell syndrome” with re-distribution of sodium and increased cell membrane permeability, but the authors of these trials are still looking for further evidence. Purpose: To provide information on postoperative hyponatremia in combination with early postoperative enteral nutrition.
Methods: S-sodium, s-potassium, and s-creatinine were analysed daily during a random double blind prospective trial in which 30 patients received Nutridrink® and 30 patients received a placebo (water) through a nasoduodenal tube from the day of the operation to the 4th postoperative day. The patients were mobilised from the 1st postoperative day and weighed every day on the same scales. Twenty-four hour urine was collected one day preoperatively, the day of the operation, and postoperatively on days 1 through 5 and the urinary creatinine was measured. Multivariate analysis of variance for 5-7 related means (MANOVA) was used in a combined design with nutrition and placebo as between-subject factors and combined with univariate F tests.
Results: S-sodium values were significantly lower and s-potassium values significantly higher in the placebo group on postoperative days 2 and 3, although the two groups received the same amount of intravenous sodium, and the placebo group received significantly less potassium.
Conclusions: The result indicates that early postoperative enteral nutrition ensures the energy supply to the cell (Na/K pump) in the postoperative period and prevents sodium being redistributed intracellularly during postoperative stress.