USA Surgery Today

Hyponatremia is a common postoperative electrolyte disturbance and usually results from administration of hypotonic fluids or large volume resuscitation with lactated Ringer’s, which has a sodium concentration of 130 meq per L. Although the strict definition of hyponatremia is a serum sodium of less than 135 meq per L, symptoms are unlikely to be present unless the concentration is below 120 meq per L. However, symptoms may occur at higher serum sodium levels if the fall in sodium is more acute (less than 24 hours:Avapro). The most common symptoms are central nervous system irregularities, although cardiovascular and musculoskeletal symptoms may also occur. When the serum sodium is low, free water crosses the blood brain barrier and results in excess water in the brain parenchyma. Nausea, emesis, headache, seizures, lethargy, and even coma may ensue in the acute setting. Weakness and ataxia are more common in cases of chronic hyponatremia. Rapid correction of the serum electrolyte imbalance may actually exacerbate these symptoms. This is because rapid alterations in serum osmolality may occur before the slower correction in the brain parenchyma, and further cellular dehydration is a possible result. Thus, it is preferable to correct major serum sodium deficits over a 24- to 48-hour period unless serious symptoms are present.

Although hyperkalemia is the most life-threatening disorder of potassium balance, hypokalemia is much more common, especially in the postsurgical patient. It most commonly results from fluid resuscitation after trauma or operative intervention without potassium supplementation. Another common cause is prolonged emesis seen in pyloric stenosis, which classically results in hyporchloremic hypokalemic metabolic alkalosis as potassium is excreted in exchange for sodium in the renal tubules. Vomiting and diarrhea from other reasons, as well as gastrointestinal losses from high output stomas or fistulae, can also lead to hypokalemia. Less commonly in the surgical patient, diuretic administration without potassium replacement may lead to hypokalemia. Diuretics induce sodium wasting and overall volume depletion, which may trigger aldosterone secretion and potentially worsen the hypokalemia. Intrinsic kidney disease may also result in potassium wasting and hypokalemia.

Signs and symptoms of hypokalemia are often subtle and may not be apparent unless there is an acute change in serum potassium concentration. Muscle weakness and ileus are the most commonly encountered and result from hyperpolarization of the muscle cells. Cardiac arrhythmias can occur, especially in patients taking digoxin. The U wave on electrocardiogram (ECG:Cardizem) is a classical sign of hypokalemia and is accompanied by low amplitude T waves. The urine potassium concentration may be useful in distinguishing among the causes of hypokalemia. In cases of hypokalemia where the urine concentration of potassium is less than 15 meq per L, appropriate conservation is being accomplished and thus losses are not due to renal dysfunction.

The appropriate distribution of water in the intracellular and extracellular spaces is regulated by osmotic gradients. Because the cell wall is a semipermeable membrane, it allows for the free passage of water in response to changes in ion concentration on either side of the membrane. The major extracellular cation is sodium; potassium is the major intracellular cation. The major extracellular anions are chloride and bicarbonate; phosphates and nondiffusable proteins predominate intracellularly. Thus, significant changes to any one of the principle ions, most commonly the extracellular ions, may cause alterations in fluid distribution and subsequently cell and organ function.

Sodium balance is the key regulator of ECF volume. However, it is the total body sodium, not merely the serum sodium, that is responsible. The majority of total body sodium is in the bone, which usually contains nearly 25 meq per kg. In addition, there is approximately 17 meq per kg of sodium in the interstitial fluid, 6.5 meq per kg in plasma, and about 1.5 meq per kg intracellularly. The rest of the total body sodium is located within connective tissue and cartilage, totaling about 10 meq per kg. Thus, the sodium content for the entire body approaches 60 meq per kg. The fetus has a higher proportion of ECF than the adult and, therefore, the total body sodium is closer to 90 meq per kg. The body strives to keep intracellular sodium constant, using active transport of sodium out of the cells via a sodium-potassium ATPase. This pump keeps intracellular sodium close to 10 meq per L at the expense of extracellular sodium. Changes in extracellular sodium may or may not be reflected in serum levels, which are usually 135 to 145 meq per L regardless of patient age.

Water is the major contributor to total body weight and accounts for nearly 60% of body weight in adults. However, total body water (TBW) comprises a much higher proportion of the total body weight in neonates. Estimates for fetal TBW are greater than 90% of total body weight early in gestation, close to 80% at 32 weeks’ gestation, and approximately 75% at term (1). There is an additional decrease in TBW over the first few days of life in the term infant, and adult levels are generally reached by 1 year of age. However, the premature infant has a TBW similar to that of the fetus and must accomplish fluid redistribution and diuresis in a short period (days to weeks) after birth rather than more gradually (weeks to months) in utero. Neonates with intrauterine growth retardation (IUGR) have similar body water distribution as premature infants of similar birthweight (2) (Fig. 6-1). Infants who fail to unload fluid effectively or who receive excess fluid during normal postnatal diuresis may be at increased risk for developing a patent ductus arteriosus, chronic lung disease, and even necrotizing enterocolitis (3,4).