Hypervolemic hyponatremia is described as TBW in great excess. These patients present with manifestations of volume overload, such as peripheral and/or pulmonary edema. They usually have impaired ability to excrete a water load. This allows for water retention in excess of Na + retention. These patients can be further categorized into two groups (Iabje,,2..3.:.3): The first of these is generalized edematous states without advanced renal insufficiency. These patients have urinary [Na +] of less than 20 meq/L. They include patients with cirrhosis and/or ascites, congestive heart failure, and nephrotic syndrome. The second category is advanced acute or chronic renal insufficiency. These patients have urinary [Na +] in excess of 20 meq/L.
Management of patients with hypervolemic hyponatremia includes optimizing treatment for the underlying disorder coupled with judicious salt and water restriction. Often diuretics are required to aid in management. Dialysis may be necessary.
EMERGENCY TREATMENT OF SEVERE HYPONATREMIA While specific or general treatment of hyponatremia for the condition discussed may be initiated in the ED, there is little urgency to address the hyponatremia itself immediately when [Na +] is above 120 meq/L. In cases where hyponatremia is severe (less than 120 meq/L), develops rapidly (a greater than 0.5-meq/L decrease in serum [Na+] per hour), or is associated with a patient in extremis (i.e., coma or seizures), administration of 3% saline solution (513 meq/L) is usually indicated. This can be administered at 25 to 100 mL/h, with careful observation for fluid overload and the rise in serum [Na+] levels. The rise in [Na+] should be no greater than 0.5 to 1.0 meq/L per hour. In the face of seizures, this can be increased to 1 to 2 meq/L per hour. It is sometimes necessary to administer concomitant furosemide to reduce the amount of water present in the body, allowing more rapid correction of plasma [Na+].4
CALCULATION OF SODIUM DEFICIT In hypovolemic patients, the Na+ deficit should be calculated and replaced with normal saline solution. The formula is
I desired plasma |Na] - actual plasma fSaF|) * (TBW)
COMPLICATIONS OF THERAPY Complications with the treatment of acute hyponatremia, especially when there is no underlying CNS, hepatic, or renal disorder, are uncommon and occur in fewer than 2 percent of patients. In chronic hyponatremia, brain edema is usually not severe, and little evidence exists that chronic hyponatremia itself causes brain damage. Nevertheless, these patients appear to be at greater risk for brain injury (CPM) during the correction process. The injury reportedly occurs after the hyponatremia has been corrected and progresses in a predictable manner. These neurologic changes are believed to be due to correction of the serum [Na+] at a rate faster than the brain can adapt to the higher osmolality. In patients with chronic hyponatremia, other factors contributing to the CPM may include alcoholism, malnutrition, toxins, and metabolic imbalance.
Brain histology in fatal cases shows myelinolysis and demyelination of central pontine and extrapontine myelin-bearing neurons. In typical cases, the neurologic findings include fluctuating levels of consciousness, behavioral disturbances, dysarthria, dysphagia, or convulsions progressing to pseudobulbar palsy and quadriparesis. Improvement may occur after several weeks of severe debilitation, but some patients are permanently impaired.
In patients with chronic severe hyponatremia, the threshold for the production of CPM is a rate of correction of Na + levels faster than 0.5 meq/L per hour (12 meq/L per day). In patients with acute severe hyponatremia, correction at rates exceeding 0.5 to 1.0 meq/L per hour, with or without diuretics, does not usually cause any problems. Severe neurologic complications have occurred almost exclusively in clinically hypernatremic patients treated with hypertonic or isotonic saline without the addition of furosemide or an osmotic diuretic. Similar patients treated with the same fluids but with furosemide almost uniformly have done well. Patients with chronic hyponatremia corrected at a rate less than 0.5 meq/L per hour have also done well.
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