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Abnormal serum sodium levels are markers for impaired water balance. The reference range for serum sodium concentration is 135 to 145 mmol/L. In the evaluation of abnormal

Table 15-24 Classification of Hypernatremia

Table 15-23 Classification of Hyponatremia

Clinical Findings


Volume depletion



Urine sodium <10 mEq/L

Increased urine osmolarity

Volume overload


Urine sodium <10 mEq/L Urine osmolarity high

Gastrointestinal losses: vomiting, diarrhea

Renal losses: diuretics, chronic renal failure, salt-wasting nephropathies

Skin losses: burns

Third-space losses: pancreatitis

Congestive heart failure, nephrotic syndrome, cirrhosis


No evidence of dehydration

Urine sodium >20mEq/L (unless Na-restricted diet)

Urine osmolality > serum osmolality

Normal thyroid and adrenal function

CNS disorders: infection, mass lesion, head trauma, acute intermittent porphyria Pulmonary: lung cancer, infection

Drugs: chlorpropamide, opiates, nicotine, diuretics, phenothiazines, vincristine, carbamazepine, SSRIs

Psychogenic polydipsia

CNS, Central nervous system; SSRis, selective serotonin reuptake inhibitors.

Table 15-24 Classification of Hypernatremia

Total Body Sodium (Na)


Urine Measurements

Reduced total body sodium (both Na and water losses, but relatively more loss of water)

Gastrointestinal losses: diarrhea, lactulose

Skin losses: excess sweating

Renal losses: loop diuretics, osmotic diuretics

Urine Na <10 mEq/L Hypertonic urine Urine Na >20 mEq/L Hypotonic or isotonic urine

Normal total body Na (loss of water)

Renal losses: central or nephrogenic diabetes insipidus, lithium, demeclocycline, hypercalcemia, hypokalemia

Nonrenal losses: insensible losses from skin or respiratory tract

Variable urine Na Variable urine tonicity Urine Na variable Hypertonic urine

Increased total body Na (addition of sodium)

Hypertonic intravenous fluids Hypertonic dialysate Saltwater drownings

Urine Na >20 mEq/L Hypertonic or isotonic urine

Modified from Schrier RW. Renal and Electrolyte Disorders, 4th ed. Boston, Little, Brown, 1992, p 43.

sodium levels, it is helpful to measure or calculate the plasma osmolarity, which typically has a range of 280 to 295 mOsm/ kg H2O.

Calculated osmolarity = (2 x Na) + (BUN / 2.8) + (Glucose /18)

In most cases, hyponatremia is associated with hypo-osmo-lality. Pseudohyponatremia can occur in the presence of other osmotically active substances, such as ethanol, methanol, mannitol, and glucose. Pseudohyponatremia is associated with an osmolar gap, which means the laboratory's measured osmolarity is greater than the calculated osmolar-ity by 10. In the setting of hyperglycemia, every 100-mg/dL rise in glucose lowers serum sodium by 1.6 mmol/L.

In hyponatremia associated with hypo-osmolarity, the determination of the patient's volume status is essential to determine the cause of hyponatremia (Verbalis, 2007).

Hyponatremia can occur in states of volume deficiency, euvolemic states, or hypervolemic conditions (Table 15-23). The clinical significance of hyponatremia depends on the severity and rate of development. In general, symptoms are seen when sodium levels are less than 120 mmol/L.

Hypovolemic hyponatremia is associated with low total-body sodium. The most common sources of sodium loss are the GI tract or kidney and, less often, third-space losses. With nonrenal losses, the kidney responds by reducing sodium and water excretion in the urine. In the absence of diuretic therapy, the urine sodium concentration is usually less than 30 mmol/L, and urine osmolarity is high. Hypovolemic hyponatremia responds readily to isotonic fluid replacement.

Hypervolemic hyponatremia can occur with advanced congestive heart failure, cirrhosis, nephrotic syndrome, and renal failure in the presence of total-body sodium overload and edema. In these disorders, effective renal blood flow is reduced, thus stimulating the release of antidiuretic hormone

Table 15-25 Causes of Hyperuricemia*


Myeloproliferative disorders

Polycythemia vera

Hemolytic anemia



Toxemia of pregnancy


Decreased Excretion

Renal failure

Volume depletion



Diabetic ketoacidosis




Aspirin (low dose)





Vitamin B12 therapy

(ADH), which reduces renal excretion of water. Both sodium and water are increased, but water is increased proportionally more than sodium. In the absence of diuretic therapy, urine sodium is generally less than 30 mmol/L, and urine osmolarity is increased.

The most common cause of euvolemic hyponatremia is the syndrome of inappropriate ADH secretion (SIADH), which occurs when the stimulus for ADH secretion is not related to osmolarity or reduced renal blood flow. No edema is present, although mild volume expansion and a modest increase in weight are seen. Continued release of ADH occurs despite low plasma osmolarity. SIADH should be considered a cause of hyponatremia in the absence of evidence of volume loss, edema, and adrenal insufficiency or hypothyroidism. The major laboratory finding, in addition to hyponatremia, is urine that is not maximally dilute (i.e., urine osmolarity >100 mOsm/kg H2O). The urine sodium level is greater than 30 mmol/L, assuming adequate sodium intake. Other clinical findings that suggest SIADH include a uric acid level less than 3 mEq/dL and BUN less than 10 mg/dL. Serum ADH

levels are not helpful because most causes of hyponatremia are associated with elevated ADH levels. The major causes of SIADH are drugs and pulmonary and central nervous system diseases. SIADH can respond to fluid restriction or correction of the underlying disorder. Another cause of euvolemic hyponatremia is called primary polydipsia, which occurs in people who consume massive amounts of water and have very large volumes of urine. In general, plasma osmolarity is mildly decreased. These individuals have low urine sodium and dilute urine. The hyponatremia readily responds to a reduction in fluid intake.

Hypernatremia is a serious electrolyte abnormality, but it generally occurs in the setting of a significant underlying medical illness (Table 15-24). Determination of the patient's volume status is also critical in the evaluation of hypernatre-mia (Schrier, 1992). Hypernatremia can occur in the setting of reduced total-body sodium, normal total-body sodium, and increased total-body sodium. Hypernatremia is seen with reduced total-body sodium when sodium and water losses occur but more water than sodium is lost. For example, when a patient has significant diarrhea, hypernatremia can develop when the patient cannot ingest enough water to compensate for the loss. Clinical evidence of dehydration is noted, urine osmolarity is high, and the urine sodium level is low.

Water loss not connected with sodium loss is associated with hypernatremia and normal total-body sodium. Inadequate ADH secretion (central diabetes insipidus) or renal tubules unresponsive to ADH (nephrogenic diabetes insipi-dus) can lead to hypernatremia because of an inability to concentrate the urine. Uncommon disorders of the hypothalamus and pituitary can cause a high-set osmoreceptor in which osmotic, but not volume, regulation is impaired. The trigger for the release of ADH may be closer to 300 instead of the normal 285 mOsm/kg.

Less frequently, hypernatremia can occur in a setting of increased total-body sodium from an excessive exogenous sodium load. Hypertonic intravenous fluids, saltwater near-drowning, and hypertonic dialysis can cause hypernatremia.

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