Euvolemic: prostate resection, hysteroscopy [transurethral resection of prostate (TURP) and female TURP syndromes], syndrome of inappropriate antidiuretic hormone (SIADH) (pain, mechanical ventilation, oxytocin), cerebral salt wasting
Hypervolemic: congestive heart failure, cirrhosis
Medications: angiotensin-converting enzyme inhibitor, angiotensin receptor blockers, potassium-sparing diuretics, non-steroidal anti-inflammatory drugs, selective cyclooxygenase-2 (COX-2) inhibitors, some immunosuppressants (cyclosporine and tacrolimus)
Cushing’s syndrome, insulin, epinephrine, surgical stress
Sodium
Sodium is the most abundant cation in the extracellular fluid and is important in the generation of action potentials of neurological and cardiac tissue. In addition, it is important in the determination of plasma osmolality, along with glucose and urea. Hypothalamic osmoreceptors can detect small changes in serum osmolality and will secrete antidiuretic hormone (ADH) in response to an elevated serum osmolality. Control of sodium balance also occurs with atrial natriuretic peptide (ANP) and aldosterone through the renin–angiotensin system. The renin–angiotensin system serves to conserve sodium and can be activated by the sympathetic nervous system, by decreases of sodium delivery to the macula densa, or by decreases in blood pressure to the renal artery, all factors which can be seen in surgical stress.
Hypernatremia
Hypernatremia is defined as a serum sodium of 145 mEq/l or greater. The process is primarily thought of as an absolute or relative inadequate amount of free water for the amount of electrolyte content of plasma.[1] Normally, the osmolality of plasma is tightly regulated between 275 and 290 mOsm/kg by the renal effects of ADH and a normal physiological thirst mechanism. With hypovolemia or an increase of plasma osmolality, increased ADH secretion and thirst come into play to restore the body’s plasma volume and osmolality.
Hypernatremia can be seen with conditions where thirst is impaired, access to water is restricted, or in conditions where there is increased loss of hypotonic fluid such as gastrointestinal (GI) losses and burns. This could easily develop in the elderly, infants, or patients in intensive care units. Solute loading with continuing doses of sodium bicarbonate can lead to hypernatremia. Another cause of hypernatremia could be the lack of ADH secretion seen after pituitary surgery or head injury such as a basilar skull fracture. This condition is known as central diabetes insipidus or DI. Nephrogenic DI is caused by the kidney’s inability to generate a hypertonic urinary output. This could be seen after ureteral obstruction is relieved, in medullary cyst disease, or after the use of various pharmacological agents such as lithium, glyburide, demeclocycline, or amphotericin B. Markedly increased levels of plasma vasopressin are seen with nephrogenic DI, owing to the kidney’s inability to respond to this hormone.
Signs of hypernatremia depend on the rate of serum sodium increase. Acute hypernatremia can produce severe thirst, shock due to hypovolemia, coma, or convulsions. Most concerning is brain shrinkage that occurs when water follows the osmotic gradient and moves out of the intracellular volume; this could lead to tearing of meningeal vessels, producing intracranial or extracranial hemorrhage.
Determination of the cause of hypernatremia is by evaluation of the extracellular fluid volume, thereby separating patients into hypovolemic, euvolemic, or hypervolemic hypernatremia. Next, measurement of plasma and urine sodium concentration along with urine osmolality will determine non-renal or renal losses. A urine osmolality of greater than 400 mOsm/kg with low urine sodium concentration suggests non-renal causes of hypernatremia: that is, loss of water that is non-renal in cause. If a patient’s urine output is greater than 1.5 cc/kg/hr along with the presence of hypernatremia, DI should be suspected. DI is likely with a urine mOsm of less than 300 and a serum sodium of greater than 150 mEq/l.
Management of hypernatremia consists of restoring the amount of free water loss by using hypotonic crystalloid solutions. One first measures the amount of free water deficit using the formula given below (TBW, total body water).
Once the amount of deficit is calculated, the serum sodium should be corrected at a rate of 10% of the offset from normal or about 0.7 mEq/l/hr.[1] This represents a replacement of water deficit over 24 to 48 hours. It is best to avoid rapid correction of this abnormality as it can cause possible brain edema and offers no real advantage in a patient with a chronic hypernatremia. If DI is the cause, additional use of DDAVP or vasopressin acetate is necessary for central DI. DDAVP is given subcutaneously in a dose of 1 to 2 mcg every 12 hours, or intranasally in a dose of 5 to 20 mcg, every 24 hours. In nephrogenic DI, the course is salt and water restriction, enhancing tubular water reabsorption, along with thiazide diuretics and treatment of the underlying cause of nephrogenic DI.
Hyponatremia
Hyponatremia is the most common electrolyte abnormality in hospitalized patients and exists when the level of serum sodium is less than 135 mEq/l. A mid-1980 study found that 4.4% of postoperative patients developed a serum sodium concentration of less than 130 mEq/l.[2]
In evaluating the cause of hyponatremia, one must first measure the serum osmolality. When osmolality is measured as normal or high, one should look for a cause of dilutional hyponatremia caused by another solute which brings water into the extracellular plasma, such as glucose or mannitol. For each 100 mg/dl rise in glucose, the serum sodium can decrease by approximately 2.4 mEq/l.[3] Another common cause of hyponatremia with a normal osmolality is in the TURP (transurethral resection of prostate) syndrome where amounts of sodium-free glycine or sorbitol irrigating solutions are used during resection of the prostate.[4]
If the serum osmolality is low, the total body sodium might still be high, as in various edematous states (congestive heart failure, cirrhosis, nephritis), which will be reflected in a urine sodium concentration of less than 15 mEq/l. Total body sodium is typically low in situations due to excess sodium loss with water replacement (GI losses, skin losses, peritonitis, renal failure, diuretic use). Finally, one of the most common causes of hyponatremia on the postoperative surgical arena is SIADH, which can be present with a normal total body sodium.
SIADH can occur after general surgery, opiate administration, CNS disorders, and various cancerous diseases. Urine osmolality in SIADH with normal renal function is greater than 300 to 400 mOsm/kg with a urinary sodium concentration of greater than 30 mEq/l in a euvolemic patient. Cardiac, renal, and hepatic functions should also be normal to avoid misdiagnosis of an edematous state as noted above.
Symptoms of hyponatremia are dependent on both the acuteness of sodium drop and on the absolute level of sodium concentration. Mostly this relates to brain swelling from water shifting into the brain owing to differences in extra and intracellular osmolality. Patients may initially complain of muscle weakness, but as the severity of hyponatremia progresses, seizures or coma may ensue once the serum sodium level drops to 120 mEq/l or less.
Management of hyponatremia with high serum osmolality consists of reducing the concentration of the responsible solute. Treatment of high glucose concentration requires insulin or dialysis with a high concentration of urea. With low serum osmolality, as in edematous states, restriction of sodium and water are required. SIADH management is restriction of free water administration and treatment of the inciting cause. Administration of furosemide will increase the amount of free water excretion. Severe hyponatremia with seizures may be treated with 3% saline to increase sodium concentration and furosemide to facilitate free water clearance. Aggressive treatment should only continue for one to two hours to avoid abrupt CNS dehydration with shrinkage or central pontine myelinolysis.[5] Ideally, sodium concentration should be increased at a rate of only 10 mEq/l/24 hours.
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