Treatment Strategy for Hyponatremia
ABSTRACT & COMMENTARY
Source: Ayus JC, Arieff AI. Chronic hyponatremic encephalopathy in postmenopausal women. JAMA 1999;281:2299-2304.
In a nonrandomized, prospective study, 53 encephalopathic postmenopausal women with symptomatic, chronic hyponatremia (Na+ < 130 mmol/L) were treated in one of three ways: intravenous sodium chloride before respiratory insufficiency (n = 17); intravenous sodium chloride after respiratory insufficiency (n = 22); or fluid restriction only (n = 14). Treatment approach was determined by when the authors were consulted to guide therapy. They were directly involved in the treatment of the first group; whereas in the other two groups, they were not involved until the patients had developed respiratory insufficiency (defined as either respiratory arrest or p02 < 50 mmHg). Chronicity of hyponatremia was defined as either a documented duration of 48 hours or longer or a rate of decrease of less than 0.5 mmol/L per hour over at least 48 hours. Intravenous sodium chloride therapy involved both "normal" and hypertonic saline.
Neurological outcome, initially and at follow-up, did not correlate with initial plasma sodium concentration or rate of correction of the hyponatremic state. The neurologic outcome was dramatically better in the first group, as was the mortality data. All patients without hypoxia experienced full recovery. The authors conclude that chronic, symptomatic hyponatremia in postmenopausal women is not a benign entity, and that intravenous sodium chloride therapy is both safe and effective.
Comment by Richard Harrigan, MD, FAAEM, FACEP
The treatment of serious hyponatremia has been a subject of debate in the literature, as researchers try to determine predictors of morbidity and mortality and balance the benefits of aggressive therapy with the risks, most notably myelinolysis (formerly central pontine myelinolysis).1 Acute hyponatremia has been regarded as more malignant than chronic, although this has been questioned,2 and the current study certainly casts some doubt on this position. As the accompanying editorial highlights, hypoxia seems to be operative in the determination of morbidity and mortality in these patients.3 It seems to be important to be aggressive with these patients—if they have mental status changes attributable to the low sodium—regardless of the acuity/chronicity of the hyponatremic state. Although chronic hyponatremia is a risk factor for the development of myelinolysis,1 the rate of correction is probably more important—overly rapid correction leads to an increased likelihood of myelinolysis.1-3 It is also important to note that none of the patients in this study had "hypervolemic hyponatremia," wherein the low sodium is attributable to underlying cirrhosis, nephrosis, or heart failure; these patients had either hypovolemic or euvolemic hyponatremia.
1. Laureno R, Karp BH. Myelinolysis after correction of hyponatremia. Ann Intern Med 1997;126:57-62.
2. Votey SR, et al. Disorders of water metabolism: Hyponatremia and hypernatremia. Emerg Med Clin North Am 1989;7:749-769.
3. Knochel JP. Hypoxia is the cause of brain damage in hyponatremia (editorial). JAMA 1999;281:2342-2343.
When treating an elderly, dehydrated woman on thiazides in the ED with a sodium of 110 mEq/L and obtundation, it is probably reasonable to:
a. recommend her for emergent hemodialysis to correct the sodium.
b. administer intravenous sodium chloride at a controlled rate and admit her.
c. admit her with fluid restriction if the hyponatremia is chronic.
d. perform a head CT and continue the thiazide if there is no evidence of cerebral edema.