Further Inpatient Care
Patients with hyponatremia from any cause require close attention to their electrolyte and fluid status.
Patients with symptomatic hyponatremia who are being actively treated often require several daily measurements of serum sodium to avoid a rate of correction that is too rapid.
After acute treatment, follow-up generally is dictated by the underlying etiology of the hyponatremia.
Complications
Clinical manifestations include clouding of consciousness, confusion, stupor, or coma. Seizures commonly occur with rapid reductions in serum sodium or with serum sodium concentrations of less than 115-120 mEq/L.
For unknown reasons, premenopausal women seem to have a less efficient osmotic adaptation. This increases their susceptibility to severe hyponatremia and rapid progression from minimal symptoms (eg, headache, nausea) to respiratory arrest. Cerebral edema and herniation have been found at autopsy. [60]
Correction of hyponatremia that is too rapid may cause permanent neurologic impairment. Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM), complications of excessive correction of chronic hyponatremia, are now diagnosed by diffusion-weighted magnetic resonance imaging (MRI). Of note is that conventional computed tomography and MRI scan findings typically lag behind the clinical manifestations of myelinosis by 2-4 weeks. [61]
The clinical course of these patients features initial encephalopathy secondary to hyponatremia, then improvement as the plasma sodium concentration increases, and finally deterioration several days later. The disorder can resolve completely or result in permanent disability or death. This typical clinical course has been called osmotic demyelination syndrome (ODS). The clinical neurologic picture may be confusing, as it may include a variety of findings from psychiatric, behavioral, and movement disorders, such as dysphagia and flaccid or spastic quadriparesis, depending on the involvement of extrapontine or central pontine myelinolysis. Disruption of the blood-brain barrier is presumed to play an important role in the pathogenesis of ODS.
An increased susceptibility to osmotic demyelination is also observed in cirrhotic patients. In this setting, myoinositol, the most abundant organic osmolyte, is depleted because of glutamine- and hyponatremia-induced brain cell swelling. CPM is a common and often fatal complication of orthotopic liver transplantation, affecting up to 10% of patients who are hyponatremic prior to transplant. [62]
Prognosis
The prognosis for patients with hyponatremia is predicated upon the underlying etiology. Hyponatremia in patients with cancer is associated with extended hospital stays and higher mortality rates; however, whether long-term correction of hyponatremia would improve these outcomes is unclear. [63]
In patients with end-stage renal disease who are receiving hemodialysis or peritoneal dialysis, evidence suggests that the risk of death rises with incrementally lower sodium levels. Causes of hyponatremia-related mortality in the dialysis population remain uncertain, but possibilities include central nervous system toxicity, falls and fractures, infection-related complications, and impaired cardiac function. [64]
A meta-analysis of 15 studies encompassing 13,816 patients found that any improvement in hyponatremia was associated with a reduced risk of overall mortality (odds ratio [OR]=0.57). With the eight studies that reported a threshold for serum sodium improvement to > 130 mmol/L, the association was even stronger (OR=0.51). The reduction in mortality risk persisted at 12-month follow-up (OR=0.55). Reduced mortality was more evident in older patients and in patients with lower serum sodium levels at enrollment. [65]
Patient Education
For patient education information, see Hyponatremia (Low Sodium). Patients to be treated with a fluid restriction often require education regarding the free-water content of foods and an explanation of the need to limit the intake of liquids to a predetermined level.
Tables
United States Guidelines |
European Guidelines |
|
Symptomatic Acute Hyponatremia < 24-48 hours |
||
Urgent correction goal to aim to prevent brain herniation |
Increase serum Na+ by 4-6 mmol/L |
Increase serum Na+ by 5 mmol/L |
Treatment based on symptoms |
||
Severe symptoms |
Bolus 100 mL of 3% NaCl over 10 minutes x 3 as needed |
Bolus 150 mL of 3% NaCl over 20 minutes, 2- 3 times as needed, checking Na every 20 minutes (First-hour management, regardless of acute or chronic condition) |
Moderate symptoms with low risk of herniation |
Continuous infusion of 3% NaCl at 0.5-2 mL/kg/h |
Bolus 150 mL 3% NaCl over 20 minutes, x 1 to prevent further decrease in Na |
Limit not to exceed |
None in true acute hyponatremia |
None in true acute hyponatremia |
Chronic Hyponatremia > 48 hours |
||
Correction rate |
||
Goal in symptomatic patients using hypertonic saline |
4-8 mmol/L/d if low risk for ODS 4-6 mmol/L/d if high risk of ODS For patients with severe symptoms, the first day’s increase can be accomplished during first 6 h |
Avoid > 10 mmol/L in the first 24 h And > 8 mmol/l during every 24 h thereafter |
Limit to avoid potential harm in asymptomatic patients |
10-12 mmol/L/d, but max 18 mmol in 48 h if at low risk for ODS 8 mmol/L/d if at high risk of ODS |
10 mmol/L in the first 24 h and 8 mmol/l during every 24 h thereafter |
Managing Overcorrection of Chronic Hyponatremia |
||
Baseline serum Na+ ≥ 120 mmol/L: Intervention probably unnecessary |
Start once above mentioned limits are exceeded |
|
Baseline serum Na+ < 120 mmol/L: Replace water orally or as D5W at 3 mL/kg/h with or without desmopressin (2-4 µg every 8 h parenterally) Withhold any vasopressin receptor antagonists (vaptans) used Consider dexamethasone, 4 mg every 6 hr for 24 hr following excessive correction |
Consult an expert to discuss infusion containing electrolyte-free water (10 mL/kg) over 1 h with or without 2 µg desmopressin IV every 8 h |
|
Other Treatment Options |
||
Hypovolemic hyponatremia |
Isotonic saline |
Isotonic saline or balanced solution at 0.5-1.0 mL/kg/h |
Euvolemic hyponatremia (SIADH) |
Fluid restriction of 500 mL/d below the 24-h urine volume (first-line treatment) Urea, vaptan, or demeclocycline (second-line treatment) |
Fluid restriction (first-line) Urea or loop diuretics + oral NaCl (second-line) Do not recommend vaptans Recommend against lithium or demeclocycline |
Hypervolemic hyponatremia |
Fluid restriction, loop diuretic Vaptans |
Fluid restriction Recommend against vaptans and demeclocycine |
