Treatment of Severe Hyponatremia

Abstract

Patients with severe (serum sodium ≤120 mEq/L), symptomatic hyponatremia can develop life-threatening or fatal complications from cerebral edema if treatment is inadequate and permanent neurologic disability from osmotic demyelination if treatment is excessive. Unfortunately, as is true of all electrolyte disturbances, there are no randomized trials to guide the treatment of this challenging disorder. Rather, therapeutic decisions rest on physiologic principles, animal models, observational studies, and single-patient reports. European guidelines and recommendations of an American Expert panel have come to similar conclusions on how much correction of hyponatremia is enough and how much is too much, but there are important differences. We review the evidence supporting these recommendations, identifying areas that rest on relatively solid ground and highlighting areas in greatest need of additional data.

Keywords: Animal; Animals; Brain Edema; Demyelinating Diseases; Models; Osmosis; Sodium; United States; Water-Electrolyte Imbalance; clinical nephrology; electrolytes; humans; hypokalemia; hyponatremia; osmolality.

Figure 1.

In a cohort of chronically hyponatremic patients with serum sodium concentrations ≤105 mEq/L, post-therapeutic (post-Rx) neurological complications occurred after correction by >12 mEq/L in 24 hours and >18 mEq/L in 48 hours. Patients with chronic hyponatremia refers to patients without psychotic polydipsia who became hyponatremic at home. Solid circles represent patients with post-therapeutic neurologic complications, and open triangles represent patients who recovered uneventfully. The dashed lines represent therapeutic limits identified by the study (12 mEq/L in 24 hours and 18 mEq/L in 48 hours). Modified from ref. , with permission.

Figure 2.

Limits for safe correction are difficult to define when the serum sodium concentration is extremely low. This patient presented with mild symptoms despite a serum sodium of 100 mEq/L. Beginning on the third day after correction by 8 mEq/L per day, the patient developed new progressive symptoms, including dysphasia, psychosis, and dyskinetic movements consistent with a diagnosis of osmotic demyelination syndrome. However, the symptoms resolved spontaneously, and magnetic resonance imaging was negative. D, day; GCS, Glascow coma scale. Reprinted from ref. , with permission.

Figure 3.

Most, but not all patients with osmotic demyelination associated with both hypokalemia and hyponatremia and documented by autopsy or magnetic resonance imaging had undergone correction by >10 mEq/L in 24 hours and >18 mEq/L in 48 hours. Patients were identified by a literature review, and they were included if data on sodium correction in the first 24 and 48 hours were provided. Dashed lines represent proposed limits of 10 mEq/L in 24 hours and 18 mEq/L in 48 hours. Modified from ref. , with permission.