The American journal of medicine
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Consequences of hyponatremia are generally mild and remain unnoticed by both physician and patient. When water restriction, usually prescribed to avoid water intoxication, fails to normalize serum sodium values, clinicians will tolerate mild stable hyponatremia (especially when serum sodium is >125 mEq/L [1 mEq/L = 1 mmol/L]). In a recent study, we observed that mild chronic hyponatremia contributes to an increased rate of falls, probably due to impairment of attention, posture, and gait mechanisms. ⋯ In another series of 122 consecutive patients hospitalized from the emergency room with mild hyponatremia, approximately 21% were admitted for falls. After controlling for age, sex, and other known risk factors for falls, the adjusted odds ratio for falls in patients with hyponatremia was 67, compared with a control group. These data show that the concept of asymptomatic hyponatremia does not withstand a detailed epidemiologic analysis of falls or of sensitive posture, gait, and attention tests.
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Hyponatremia exerts most of its clinical effects on the brain. An acute onset (usually in <24 hours) of hyponatremia causes severe, and sometimes fatal, cerebral edema. Given time, the brain adapts to hyponatremia, permitting survival despite extraordinarily low serum sodium concentrations. ⋯ Areas of the brain that remain most depleted of organic osmolytes are the most severely injured by rapid correction. The brain's reuptake of myoinositol, one of the most abundant osmolytes, occurs much more rapidly in a uremic environment, and patients with uremia are less susceptible to osmotic demyelination. In an experimental model of chronic hyponatremia, exogenous administration of myoinositol speeds the brain's reuptake of the osmolyte and reduces osmotic demyelination and mortality caused by rapid correction.