Hyponatremia in the Patient With Subarachnoid Hemorrhage

Ellen Dooling; Chris Winkelman


J Neurosci Nurs. 2004;36(3) 

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Hyponatremia is a serum sodium concentration level of less than 135 mEq/L (< 135 mmole/L, SI) for at least 1 day (Kurokawa et al., 1996). A value of less than 120 mEq/L is considered a critical value requiring immediate intervention (Larsen, Kronenberg, Melmed, & Polonsky, 2003; Nicoll, McPhee, Pignone, Detmer, & Chou, 2001). Signs and symptoms associated with hyponatremia are secondary to cellular hypo-osmolality. Fever, headache, nausea and vomiting, muscle cramps weakness, and confusion occur when serum sodium values are 115-120 mEq/L. Stupor, seizures and coma are more typically associated with serum sodium values of less than 110 mEq/L (Andreoli, Carpenter, Griggs, & Loscalzo, 2001; Diringer, 2001). Sudden decrements in serum sodium are more likely to elicit severe symptoms than a gradual decrease over days to weeks. In the presence of SAH, hyponatremia can be especially dangerous to patients since low serum sodium has been linked to decreased intravascular volume and vasospasm, one of the leading causes of morbidity and mortality in SAH (Suarez, 2004; Wijdicks, Ropper, Hunnicut, Richardson, & Nathanson, 1991).

Hyponatremia usually occurs several days post-hemorrhage (Mayberg et al., 1994). The incidence is increased in patients with a poor clinical grade of SAH (i.e., a Hunt-Hess grade of 3 or more, indicating severe neurological symptoms at the onset of SAH) and hydrocephalus (Mayberg et al.). The etiology of SAH-related hyponatremia has been controversial for decades. The two most common causal hypotheses are cerebral salt wasting (CSW) and syndrome of inappropriate antidiuretic hormone (SIADH).