Hyponatremia in the Patient With Subarachnoid Hemorrhage

Ellen Dooling; Chris Winkelman


J Neurosci Nurs. 2004;36(3) 

In This Article


Once the differential diagnosis is made, treatment can be initiated. While many may believe it is the sole responsibility of the physician or APN to diagnose the hyponatremic patient, it is important for nurses at the bedside to understand and recognize when the diagnosis is not consistent with the clinical picture. Though nurses may not be responsible for ordering the treatment, they are responsible for implementing orders. Failure to recognize the appropriate diagnosis and instituting contraindicated treatments could have calamitous results.

In this scenario C.L. was experiencing CSW. Employing fluid restriction measures, as is sometimes utilized in the SIADH patient, could not only worsen her symptoms of hypovolemia, but also could increase the risk of cerebral vasospasm (Palmer, 2000; Suarez, 2003). In contrast, treating someone with SIADH with normal saline could create a symptomatic lowering of the serum sodium concentration (Palmer, 2000).

Overall, the treatment for hyponatremia after SAH is aimed at restoring normovolemia with normal serum sodium levels. Often if the patient is without symptoms, aggressive treatment is unnecessary, and if it is employed, it could have adverse outcomes (Mayberg et al., 1994; Suarez, 2004). If treatment is warranted, the serum sodium concentration level and the duration of time necessary for a safe decrease will determine the measures taken. Kurokawa et al. (1996) utilized a treatment approach based on the daily balances of fluid and sodium and found that by doing this, there were very few neurological deficits related to ischemia.

In general, patients with CSW will receive an order for intravenous normal saline. Depending on the sodium and fluid balance and the patient's symptoms, hypertonic 3% saline at an initial rate of 25-50 ml/hour, 325 mg salt tablets, and/or 1-2 mg daily of oral fludrocortisone (Florinef) may also be used (Palmer, 2000). Fludrocortisone (Florinef Acetate) treatment is sometimes difficult to use because of slow onset and long duration of action (Diringer, 2001). However, if this treatment option is chosen, careful monitoring is paramount because it has been linked with decreased serum potassium levels, hypertension, and pulmonary edema (Suarez, 2004).

In SIADH, the preferred treatment in the general population is fluid restriction (Palmer, 2000). However, in patients with aneurysmal SAH, great care must be taken because of the risk of vasospasm in these patients. One study found an increased incidence of infarction in patients treated for supposed SIADH with fluid restriction (Wijdicks, Vermulean, Hijdra, & van Gijn, 1985). Other types of treatment include the infusion of hypertonic saline in conjunction with loop diuretics.

Regardless of the disorder and the treatment to be used, serum sodium levels should be corrected slowly. If too rapid correction of serum sodium occurs, the patient is placed at risk for developing central pontine myelinolysis (Braunwald et al., 2001, Suarez, 2004). Central pontine myelinolysis is a disorder in which the patient may present with confusion, dysarthria, gaze disturbances, quadriplegia, and pseudobulbar palsy as a result of demyelination in the base of the pons (Braunwald et al., 2001). To prevent this complication, serum sodium concentration levels should not be corrected at a rate exceeding 1.3 mEq/L/hour with a total correction of no more than 10 mEq/L in 24 hours, and sodium levels should be checked frequently throughout treatment. In this scenario, C.L. was treated initially 3% hypertonic saline at 30 ml/hr for 12 hours and then with normal saline at 125 ml/hr. Since C.L. was not yet experiencing neurological deficits related to the sodium deficit, an assessment alone would not be helpful in determining improvement. Also, due to the danger of central pontine myelinolysis, this would not be a safe approach. Therefore, serum sodium levels were checked every 6 hours for the first 24 hours and then every 12 hours until the sodium level was within normal levels. For this patient, the sodium gradually increased to normal levels over a period of 48 hours. The patient did not experience any side effects from the treatment prescribed. The sodium did decrease slightly before it began to improve; however, the patient remained without neurological deficits. If C.L. had been symptomatic, the frequency of laboratory assessment would be every 4 hours for 24 hours or until the symptoms resolved. Then monitoring would be every 6 hours for the next day and then every 12 hours until normalized.