If hypovolemia is present or suspected, 0.9 % saline infusion should be administered. For patients with severe acute or symptomatic hyponatremia, hypertonic (3 %) saline should be infused at a rate of 1–2 ml/kg actual body weight [2]. Correction of serum sodium concentration by 4–6 meq/L in the first 2–3 h is sufficient to significantly reduce intracranial pressure and increase cerebral perfusion pressure [4]. Serum sodium should be monitored hourly and infusion stopped when symptoms resolve. For patients who do not require emergent rapid correction of serum sodium concentration, management should be tailored to the underlying condition. Management of the hypervolemic hyponatremias requires addressing underlying organ dysfunction (Table 46.2). Glucocorticoid or thyroid hormone deficiency, discussed elsewhere, can be treated by supplementing these hormones. Severe hyponatremia from CSW may initially require hypertonic saline, though in most cases volume expansion with isotonic saline is sufficient [2]. SIADH is managed with fluid restriction and ensuring adequate dietary sodium and protein intake. In the ICU, total fluid intake should be limited to 500 mL less than daily urinary output, and should account for oral fluids, solid foods, and IV medications [5].

In patients with asymptomatic chronic hyponatremia, there is virtually no risk of death from cerebral edema. Accordingly, guidelines and expert opinion recommend that correction be limited to 6–8 meq/L per day, with serum sodium checks every 2–4 h. During correction of hypovolemic hyponatremia, urinary output must be monitored closely, for which a urinary catheter is helpful. Once the hypovolemic stimulus for ADH secretion has been relieved, ADH levels will drop, urinary output will increase, and serum sodium concentration will increase rapidly. At this point the isotonic saline solution should be stopped and serum sodium monitored carefully. If correction proceeds at a rate greater than 0.5 meq/L/h for more than 4 h, rate of rise can be slowed by administering hypotonic fluids or IV desmopressin 2–4 micrograms [5].

In the setting of serum hyponatremia, brain cells extrude organic solutes, which prevents cerebral swelling. This process takes about 2 days, but when hyponatremia is corrected, it can take up to a week for cells to recapture lost osmolytes. If serum sodium correction outpaces solute recapture, central pontine or extrapontine myelinolysis results. ODS classically has a biphasic presentation: the patient’s neurologic status initially improves with serum sodium correction, but days later, pseudobulbar palsy and quadriparesis develop. Most described cases of ODS resulted from serum sodium correction greater than 10–12 mmol/L in 24 h or 18 mmol/L in 48 h, though slower rates of correction have been associated with this syndrome in high-risk patients including those with alcoholism, cirrhosis and severe malnutrition [5].