Treatment Guidelines for Hyponatremia: Stay the Course.

International guidelines designed to minimize the risk of complications that can occur when correcting severe hyponatremia have been widely accepted for a decade. On the basis of the results of a recent large retrospective study of patients hospitalized with hyponatremia, it has been suggested that hyponatremia guidelines have gone too far in limiting the rate of rise of the serum sodium concentration; the need for therapeutic caution and frequent monitoring of the serum sodium concentration has been questioned. These assertions are reminiscent of a controversy that began many years ago.

Estimating urine volume from the urine creatinine concentration.

Spot determinations of the urine creatinine concentration are widely used as a substitute for 24-h urine collections. Expressed as the amount excreted per gram of creatinine, urine concentrations in a single-voided sample are often used to estimate 24-h excretion rates of protein, sodium, potassium, calcium, magnesium, urea and uric acid. These estimates are predicated on the assumption that daily creatinine excretion equals 1 g (and that a urine creatinine concentration of 100 mg/dL reflects a 1 L 24-h urine volume).

Complications and management of hyponatremia.

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.

Urea for hyponatremia?

Once the standard of care for cerebral edema, urea can also be used to treat hyponatremia. The 2014 European Clinical Practice Guidelines recommend urea for the treatment of the syndrome of inappropriate antidiuretic hormone, while discouraging use of vasopressin antagonists. Although there is evidence that urea can diminish hypertonic injury to brain cells caused by rapid correction of hyponatremia, clinical trials are needed that include patients at high risk to develop complications from overcorrection.

Management of hyponatremia in the ICU.

Hyponatremia is common in critical care units. Avoidance of neurologic injury requires a clear understanding of why the serum sodium (Na) concentration falls and why it rises, how the brain responds to a changing serum Na concentration, and what the goals of therapy should be. A 4 to 6 mEq/L increase in serum Na concentration is sufficient to treat life-threatening cerebral edema caused by acute hyponatremia.

Hypertonic saline and desmopressin: a simple strategy for safe correction of severe hyponatremia.

Background: Prompt correction of severe hyponatremia is important, but correction also must be limited to avoid iatrogenic osmotic demyelination. Expert opinion recommends that serum sodium level not be increased by more than 10-12 mEq/L in any 24-hour period and/or 18 mEq/L in any 48-hour period. However, inadvertent overcorrection is common, usually caused by the unexpected emergence of a water diuresis.

DDAVP is effective in preventing and reversing inadvertent overcorrection of hyponatremia.

Background And Objectives: Adherence to therapeutic guidelines for the treatment of hyponatremia becomes difficult when water diuresis emerges during therapy. The objective of this study was to assess the effectiveness and safety of desmopressin acetate as a therapeutic agent to avoid overcorrection of hyponatremia and to lower the plasma sodium concentration again after inadvertent overcorrection.

Design, Setting, Participants, & Measurements: Retrospective chart review was conducted of all patients who were given desmopressin acetate during the treatment of hyponatremia during 6 yr in a 528-bed community teaching hospital.

Cerebral salt wasting versus SIADH: what difference?

The term cerebral salt wasting (CSW) was introduced before the syndrome of inappropriate antidiuretic hormone secretion was described in 1957. Subsequently, CSW virtually vanished, only to reappear a quarter century later in the neurosurgical literature. A valid diagnosis of CSW requires evidence of inappropriate urinary salt losses and reduced "effective arterial blood volume.

Brain volume regulation in response to hypo-osmolality and its correction.

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.

Myoinositol administration improves survival and reduces myelinolysis after rapid correction of chronic hyponatremia in rats.

When chronic hyponatremia is rapidly corrected, reaccumulation of brain organic osmolytes is delayed and brain cell shrinkage occurs, leading to the osmotic demyelination syndrome (ODS). We hypothesized that treatment with myoinositol, a major organic osmolyte, could prevent ODS. Severe hyponatremia was induced in adult male rats by administration of arginine vasopressin and intravenous infusion of dextrose and water.

Brain uptake of myoinositol after exogenous administration.

An acute increase in plasma tonicity results in an adaptive increase in brain organic osmolyte content, but this process requires several days to occur. Slow reaccumulation of brain organic osmolytes may contribute to osmotic demyelination. It was investigated whether administration of intravenous myoinositol in rats could speed entry of the osmolyte into the brain.