Abstract and Introduction
Purpose of review Hyponatremia causes significant morbidity, mortality, and disability. This review considers the literature of the past 18 months to improve understanding of these complications and to identify therapeutic strategies to prevent them.
Recent findings Acute hyponatremia causes serious brain swelling that can lead to permanent disability or death. A 4–6 mEq/l increase in serum sodium is sufficient to reverse impending herniation. Brain swelling is minimal in chronic hyponatremia, and to avoid osmotic demyelination, correction should not exceed 8 mEq/l/day. In high-risk patients, correction should not exceed 4–6 mEq/l/day. Inadvertent overcorrection of hyponatremia is common and preventable by controlling unwanted urinary water losses with desmopressin. Even mild chronic hyponatremia is associated with increased mortality, attention deficit, gait instability, osteoporosis, and fractures, but it is not known if the correction of mild hyponatremia improves outcomes.
Summary Controlled trials are needed to identify affordable treatments for hyponatremia that reduce the need for hospitalization, decrease hospital length of stay, and decrease morbidity. Such trials could also help answer the question of whether hyponatremia causes excess mortality or whether it is simply a marker for severe, lethal, underlying disease
Hyponatremia is associated with significant morbidity, mortality, and disability. Acute hyponatremia causes serious brain swelling that can lead to permanent disability or death. Chronic hyponatremia causes attention deficit, gait instability, and osteoporosis, and it increases the risk of falls and fractures. Overly rapid correction of chronic hyponatremia causes osmotic demyelination, which can lead to irreversible brain damage. Many of these complications can be avoided with proper therapy. This review will highlight the major contributions to our understanding of hyponatremia that have been published in the last 18 months.
Curr Opin Nephrol Hypertens. 2016;25(2):114-119. © 2016 Lippincott Williams & Wilkins