The Science of Medical Care
Epidemiology, Pathophysiology, and Management of Hyponatremic Encephalopathy

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Pathogenesis of Hyponatremia and Hyponatremic Encephalopathy

To understand the pathophysiology of hyponatremic encephalopathy, there are some basic concepts relating to sodium and water homeostasis that must be understood. These include concepts of free water clearance, osmolality, tonicity, and thirst regulation, and their relationships to the release of antidiuretic hormone (ADH). It is also important to understand the role played by osmolality, tonicity, and thirst in the regulation of cell volume and the distribution of body water.

Clinical Manifestations of Hyponatremia

The clinical signs and symptoms of hyponatremia are directly related to the development of cerebral edema, increased intracellular pressure and cerebral hypoxia (Table 0). Early symptoms of hyponatremia from any cause may include apathy, weakness, muscular cramps, nausea, vomiting, and headache.1, 2, 3 More advanced clinical manifestations include impaired response to verbal and painful stimuli, hallucinations, urinary incontinence, and pulmonary edema. As edema worsens, clinical manifestations

Clinical Settings Associated with Brain Damage from Hyponatremia

The incidence of hyponatremia is similar among men and women, but brain damage occurs predominantly in young (menstruant) females and prepubertal individuals of either gender.4, 21, 24 Brain damage from hyponatremia is generally uncommon in men and older (postmenopausal) women (Fig. 1).

It is now clear that brain damage from hyponatremia can be associated with either hyponatremic encephalopathy or improper therapy of symptomatic hyponatremia. Clinical evidence suggests that the vast majority of

Hypoxia and Hyponatremic Encephalopathy

Hypoxemia is a major factor contributing to brain damage in patients with hyponatremia.5, 48 Hypoxia leads to a failure of homeostatic brain ion transport, which allows the brain to adapt to increases in cell water. The adaptive increase of Na+-K+-ATPase transport activity, which is initiated by hyponatremia, is severely blunted by hypoxia, thus causing a net increase in brain sodium and resulting in brain edema.[39] Among patients with hyponatremic encephalopathy, the progression to death or

The Asymptomatic Patient

In patients with asymptomatic hyponatremia, aggressive therapy with hypertonic NaCl is not indicated. If the patient is volume depleted, isotonic (154 mM) NaCl is usually the fluid of choice. If there is a hormone deficiency (adrenal insufficiency, hypothyroidism), appropriate hormone replacement is indicated in addition to volume repletion. If the patient has received a drug that may interfere with renal handling of sodium or water, the drug should be discontinued whenever possible. Although

Hyponatremia and Cerebral Demyelinating Lesions

There has been some controversy concerning the rate at which hyponatremia should be corrected. Some authors have suggested that the development of a rare neurologic syndrome, central pontine myelinolysis (CPM), is somehow related to the rapid correction of hyponatremia.[57] However, a number of studies have shown that cerebral demyelinating lesions develop only when patients with hyponatremia (a) are inadvertently made hyponatremic during treatment; (b) have an absolute increase in plasma

Summary

Hyponatremia is the most common electrolyte abnormality among hospitalized patients. Death or brain damage associated with hyponatremia has been described since 1935, and it is now evident that hyponatremia can lead to death in otherwise healthy individuals. In the past, it had been assumed that the likelihood of brain damage from hyponatremia was directly related to either a rapid decline in plasma sodium or a particularly low level of plasma sodium. Recent studies have demonstrated that other

Acknowledgements

Supported by a grant RO1 AG 08575 from the National Institute on Aging, Department of Health and Human Services, Bethesda, Maryland, and by the Research Service of the Veterans Affairs Medical Center, San Francisco, California.

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