Hyperkalemia is encountered infrequently in preoperative patients. It is usually associated with renal impairment but can be seen in patients who have adrenal insufficiency, are taking potassium-sparing diuretics, and have marked tissue breakdown such as that occurring with crush injuries, massive gastrointestinal bleeding, or hemolysis. The clinical manifestations are mainly cardiovascular. Marked hyperkalemia (potassium >7 mEq/L) can result in bradycardia, ventricular fibrillation, and cardiac arrest. The treatment chosen depends on the severity of the hyperkalemia and whether there are associated cardiac abnormalities detected with electrocardiography. Calcium gluconate (10 mL of a 10% solution), given intravenously, can offset the toxic effects of hyperkalemia on the heart. One ampule each of sodium bicarbonate and D5W, with or without insulin, will cause a rapid shift of potassium into cells. Over the longer term, cation exchange resins such as sodium polystyrene sulfate (Kayexalate), taken orally or by enema, will bind and decrease total body potassium. Hemodialysis is reserved for emergent conditions in which other measures are not sufficient or have failed (35).
Several hormonal and physiologic alterations in the postoperative period may complicate ﬂuid and electrolyte management. The stress of surgery induces an inappropriately high level of circulating ADH. Circulating aldosterone levels are increased, especially if sustained episodes of hypotension occurred either intraoperatively or postoperatively. The elevated levels of circulating ADH and aldosterone make postoperative patients prone to sodium and water retention.
Total body ﬂuid postoperative volume may be altered significantly. First, 1 mL of free water is released for each gram of fat or tissue that is catabolized and, in the postoperative period, several hundred milliliters of free water are released daily from tissue breakdown, particularly in the patient who has undergone extensive intra-abdominal dissection and who is restricted from ingesting food and ﬂuids by mouth. This free water is often retained in response to the altered levels of ADH and aldosterone. Second, ﬂuid retention is further enhanced by third spacing, or sequestration of ﬂuid in the surgical field. The development of an ileus may result in an additional 1 to3Lof ﬂuid per day being sequestered in the bowel lumen, bowel wall, and peritoneal cavity.
In contrast to renal sodium homeostasis, the kidney lacks the capacity for retention of potassium.
In the postoperative period, the kidneys continue to excrete a minimum of 30 to 60 mEq/L of potassium daily, irrespective of the serum potassium level and total body potassium stores (27). If this potassium is not replaced, hypokalemia may develop. Tissue damage and catabolism during the first postoperative day usually result in the release of sufficient intracellular potassium to meet the daily requirements. Beyond the first postoperative day, potassium supplementation is necessary.