TABLE 236 Clinical Manifestations of Hypernatremic States Related to Serum Osmolality

Virtually all hypernatremia encountered in the ED is related to volume loss, usually severe. There are two potential mechanisms seemingly opposed but having the same result. The first is the ADH response to low volume and hypertonicity. The renal response to ADH, conservation of free water, results in low urine output (less than 20 mL/h) that has a high osmolality (usually greater than 1000 mosm/kg H2O). The second mechanism is failure of ADH response, either central or peripheral

(vide infra). In essence, the patient cannot excrete Na + properly. Urine osmolality is low (200 to 300 mosm/kg with urinary [Na+] of 60 to 100 meq/kg).

Finally, one mechanism of hypernatremia may result in hypervolemia. This is excessive intake of Na +. Usually, the kidney is able to regulate Na + at a very constant level. However, if the kidneys are impaired, then serum [Na+] will increase and a dangerous ECF volume expansion will occur. Note that even large volumes of normal saline administration by itself cannot result in hypernatremia, because the [Na +] is only 154 meq. However, administration of concentrated Na+ solutions (e.g., hypertonic saline, addition of NaHCO3 to normal solution) can result in euvolemic or hypervolemic hypernatremia.

DIABETES INSIPIDUS A particularly interesting cause of hypernatremia is diabetes insipidus (DI), which results in excessive loss of hypotonic urine. Diabetes insipidus may be central in origin (due to a failure of secretion of ADH) or nephrogenic (due to renal unresponsiveness to ADH). About 30 percent of central DI is idiopathic and about 70 percent is secondary to neoplasms (25 percent), pituitary surgery (20 percent), or trauma (15 percent). Most of the remaining 10 percent is due to various granulomas (tuberculosis, sarcoidosis, or eosinophilic granuloma) or local vascular problems (aneurysms, thrombosis, or Sheehan syndrome). Nephrogenic DI may be primary (familial) or secondary to a wide variety of causes, including hypercalcemia, hypokalemia, renal disorders, various drugs (including lithium, demeclocycline, amphotericin B, aminoglycosides, and cisplatin), hematologic disorders (sickle cell disease and myeloma), malnutrition, or amyloidosis.

Traumatic DI is typically triphasic. After an initial polyuria from insufficient ADH secretion by hypothalamic cells, there is a transient second phase lasting 1 to 7 days characterized by release of previously formed hormone from the posterior pituitary and resolution of the polyuria. In the third phase, central DI returns after the released hormone has been utilized. Regeneration of cells that secrete ADH may occur weeks to months after injury. The ADH-secreting cells have their cell bodies in the hypothalamus, and these are not usually completely destroyed by trauma.

Differentiation between central and nephrogenic DI is best achieved by noting (1) the response of serum and urine osmolarity to water deprivation (trying to reach a serum osmolarity greater than 295 mosm/L) and (2) the response to 5 units of subcutaneous aqueous vasopressin. Patients with central DI show little or no response to dehydration but respond well to vasopressin (urine osmolarity of 800 mosm/L or greater). Nephrogenic DI shows little or no response to dehydration or vasopressin.

PATHOPHYSIOLOGY Because Na+ does not freely penetrate tissue cell membranes, ECF and plasma volume tend to be maintained in hypernatremic dehydration until the water loss is greater than 10 percent of body weight. Although there may be rather profound dehydration in some patients with severe hypernatremia, shock is an infrequent occurrence. When the dehydration results in loss of 10 percent of body weight, skin turgor becomes reduced and the skin of the abdomen has a characteristic "doughy" feel when it is pinched between the fingers.

Acute symptomatology is seen in many patients once serum [Na+] exceeds 158 meq/L. Patients tend to become irritable, and infants may also have a high-pitched cry or wail alternating with periods of severe lethargy. As dehydration and hypernatremia become more severe, one may see increased muscle tone or even coma with eventual seizures. Fever can be both a contributing cause and a result of hypernatremic dehydration.

Restlessness and irritability occur when serum osmolality increases to between 350 and 375 mosm/kg, while ataxia and tremulousness tend to occur when osmolality is between 375 and 400 mosm/kg. When serum osmolality rises above 400 mosm/kg, asynchronous jerks and tonic spasms are apt to occur. Death usually occurs at an osmolality above 430 mosm/kg.

Permanent sequelae are not uncommon in children when serum [Na+] exceeds 160 to 165 meq/L. Up to 16 percent of children with hypernatremia develop chronic neurologic deficits as a consequence. The overall mortality rate of hypernatremia is above 10 percent. If the plasma osmolality exceeds 350 mosm/kg, the incidence of severe morbidity or mortality may exceed 25 to 50 percent.

Hypocalcemia, which is frequently seen in patients with hypernatremia, may contribute to the CNS symptomatology. However, the mechanism of the hypocalcemia is unclear.

Massive brain hemorrhage or multiple small hemorrhages and thromboses may occur when hypernatremia causes enough cellular dehydration and resultant brain shrinkage to cause tearing of cerebral blood vessels. This has been observed most frequently in neonates following acute administration of a large Na + load. As a consequence, the amount of sodium bicarbonate administered to acidotic infants must be limited.

If the hypernatremia persists for more than a few days, the brain dehydration may resolve, and brain water content may return to normal or near-normal levels due to accumulation in the brain cells of amino acids known as idiogenic osmoles, particularly taurine. The formation of these idiogenic osmoles increases intracellular osmolality, attracts water back into the brain cells, and restores their cellular volume. If the hypertonicity develops gradually, this protective mechanism tends to prevent severe brain cell shrinkage.

TREATMENT The cornerstone of treatment is volume replacement. There are many opinions regarding appropriate initial fluid and subsequent therapy. Where volume is the issue, we believe volume should be replaced first with either normal saline or Ringer's lactate. Either of these will have, by definition, a lower [Na +] than the patient's serum. Plasma-expanding fluids should continue until tissue perfusion is restored. Once perfusion has been established, the solution should be converted to 0.45% saline or other isotonic solution. This should continue until the urine output is at least 0.5 mL/kg per hour. The reduction in [Na +] should not exceed 10 to 15 meq/L per day. A calculation to estimate free water deficit is

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