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ESSENTIALS OF DIAGNOSIS

  • Increased thirst and water intake are the main defense against hypernatremia.

  • Urine osmolality helps differentiate renal from nonrenal water loss.

GENERAL CONSIDERATIONS

Hypernatremia is defined as a sodium concentration greater than 145 mEq/L. All patients with hypernatremia have hyperosmolality, unlike hyponatremic patients who can have a low, normal, or high serum osmolality. The hypernatremic patient is typically hypovolemic due to hypotonic fluid losses, or, less often, hypodipsia or adipsia. Hypotonic fluid losses can be renal (such as with DI or inappropriately dilute urine from diuretics) or nonrenal (such as with gastrointestinal [GI] losses or burns). Hypervolemic hypernatremia is less common but can be an iatrogenic complication in hospitalized patients who receive substantial amounts of intravenous sodium salts, and rarely in other settings as well (such as with sea water ingestion). Hypernatremia in primary aldosteronism is mild and usually does not cause symptoms.

Normally, the hypothalamus senses minimal changes in serum osmolality. High osmolality triggers two responses: the first is to secrete ADH, which acts on the kidney to minimize urinary water losses, and the second is to stimulate thirst. These two mechanisms are complimentary. For example, in DI, where the kidney is inappropriately losing free water either because of impaired ADH secretion or inability of the kidney to sense ADH appropriately, the thirst mechanism is generally sufficient to avoid hypernatremia. Thus, whatever the underlying disorder, excess water loss generally only causes hypernatremia when either the thirst mechanism is not intact or adequate water intake is not possible.

CLINICAL FINDINGS

A. Symptoms and Signs

When the patient is dehydrated, orthostatic hypotension and oliguria are typical findings. Because water shifts from the cells to the intravascular space to protect volume status, these symptoms may be delayed. Lethargy, irritability, and weakness are early signs. Hyperthermia, delirium, seizures, and coma may be seen with severe hypernatremia (ie, sodium greater than 158 mEq/L). In acute hyperosmolality, somnolence and confusion can appear when the osmolality exceeds 320–330 mOsm/kg (320–330 mmol/kg); coma, respiratory arrest, and death can result when osmolality exceeds 340–350 mOsm/kg (340–350 mmol/kg). Symptoms in older adults may not be specific; a recent change in consciousness is associated with a poor prognosis. Osmotic cerebral demyelination is an uncommon but reported consequence of acute severe hypernatremia.

B. Laboratory Findings

1. Urine osmolality greater than 400 mOsm/kg

Renal water-conserving ability is functioning.

A. NONRENAL LOSSES

Hypernatremia will develop if water intake falls behind hypotonic fluid losses from excessive sweating, the respiratory tract, or bowel movements. Lactulose causes an osmotic diarrhea with loss of free water.

B. RENAL LOSSES

While severe hyperglycemia can cause translocational hyponatremia, progressive volume depletion from glucosuria can result in hypernatremia. Osmotic diuresis can occur with ...

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