Electrolyte disorders in surgical patients can be confusing but a simple algorithm for identification and treatment of the common problems should be part of the skill set of the pediatric surgeon. The most common imbalances seen in clinical practice involve sodium and potassium. Since most mild abnormalities are self-correcting, it is rarely necessary to even check electrolytes after an uncomplicated procedure in a healthy patient who resumes normal oral intake within 2–3 days of the operation. Patients who need regular routine monitoring of electrolytes include those who are NPO for several days, have high GI fluid losses, are being provided nutrition parenterally, or have another specific risk factor. Even these patients rarely need to have labs checked more than twice weekly unless there is a potentially dangerous value that is being actively corrected. It is still common to see daily or twice daily labs being drawn, especially in ICU patients, despite the values being minimally aberrant or entirely normal for days on end – this is a wasteful and potentially dangerous practice that should be abolished.
Mild hyponatremia is common in pediatric general practice due to a combination of factors: GI losses, over-resuscitation in the OR and postoperative period with hypotonic solutions, and a surgical stress-induced SIADH. Our current protocols for fluid resuscitation tend to err on the side of excess, which contributes to hyponatremia, dilutional anemia, and bowel edema/ ileus. Some fast-track protocols recommend a slightly lower calculation for “maintenance” fluids, a preference for crystalloid boluses as needed, and early reliance on oral intake and thirst to guide fluid management. It is also common for surgical residents to mistakenly use the fluid replacement strategy recommended for gastric fluid losses (½mL per mL of D5½NS + 20 mEq/L KCl) for other GI losses (ileostomy output, diarrhea, biliary drainage), which are all isotonic and have higher concentrations of potassium. Hypernatremia is less common and the cause is usually obvious, although insensible losses in infants can be more than expected. The most serious cases of hypernatremia (serum sodium >200) have occurred when parents are instructed to supplement their infant’s formula with a pinch of salt. Regardless of the cause, correction of hypo- and hypernatremia should be gradual to prevent brain injury related to rapid fluid shifts.
Hyperkalemia can be dangerous but is very uncommon in the setting of normal renal function. It is much more commonly spurious, especially in infants, due to hemolysis of the specimen. Nevertheless, having to prove that it is normal is time-consuming (delays induction of anesthesia) and potentially dangerous in that potassium is withheld from an infant who more likely has hypokalemia (pyloric stenosis). Hypokalemia must be profound to have clinical effects but is dangerous because of the excitement it causes for nurses and physicians, who tend to overreact by giving large doses of potassium intravenously, which is hazardous, or orally, which induces vomiting and can make the problem worse. Calmly correcting acid-base imbalances, replacing potassium losses in GI fluids, and providing moderate concentrations of potassium in the maintenance fluids or parenteral nutrition solutions are usually all that is required.
Mild hypocalcemia is relatively common but is more often spuriously due to hypoalbuminemia. Patients who are risk (thyroidectomy) and symptomatic should be treated with oral calcium carbonate and calciferol. Rarely, intravenous calcium gluconate or calcium chloride is needed and should be administered according to institutional guidelines for rate and cardiac monitoring. Hypomagnesemia can be seen in patients with malnutrition or excessive GI fluid losses, often in conjunction with hypocalcemia. Oral magnesium supplements usually work best but intravenous replacement is occasionally necessary. Hypophosphatemia occurs commonly after massive hepatic resection and is due to a transient hyperphosphaturia rather than consumption by the regenerating liver. It typically peaks on postoperative day two and resolves by day 5. Supplementation is necessary to prevent life-threatening hypophosphatemia but will not prevent the underlying parathyroid hormone spike that is the likely cause.