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Background: Hyponatremia develops in approximately a third of patients with aneurysmal subarachnoid hemorrhage (SAH). Studies have been conflicting about the association between hyponatremia and cerebrovascular spasm (CVS).Aims: To investigate whether hyponatremia can signal the onset of CVS.Settings and Design: Retrospective chart review of all patients with SAH treated at a tertiary-care university hospital from January to May 2002.Materials and Methods: 106 patients were included in the study. Serum sodium levels were recorded from days 1 to 14 of hospitalization. Hyponatremia was defined as serum sodium level<135 meq/l and a fall in sodium level of >4 meq/l from the admission sodium level. The presence of CVS was determined by transcranial doppler sonography. Patients were assigned to one of four groups based on the presence or absence of CVS and hyponatremia.Statistical Analysis: Student's t-test was used for comparison of means. A logistical regression model was constructed and odds ratios (OR) were calculated.Results: 41 patients developed hyponatremia and 44 developed CVS. Among the 41 with hyponatremia, 22 (54%) had evidence of CVS, whereas among the 65 patients without hyponatremia, 22 (34%) had evidence of CVS (P=0.023). Among those with hyponatremia, the mean sodium drop was 7.9 meq/L in those with CVS compared to 7.0 meq/L in those without CVS (P=0.068). More than half of those with hyponatremia and CVS (13/22) developed hyponatremia at least a day before CVS was diagnosed.Conclusion: In patients with SAH, hyponatremia is associated with a significantly greater risk of developing CVS and may precede CVS by at least one day. [ABSTRACT FROM AUTHOR]

An abstract of the study "Hyponatremia and Cerebrovascular Spasm in Aneurysmal Subarachnoid Hemorrhage" by Dipak Chandy and Vidya Ramachandraiah is presented.

Intrathecal (IT), intraventricular (IVt), and intracisternal administration of nicardipine deliver treatment directly into the central nervous system. This route of drug delivery is being investigated as a potential treatment of vasospasm following aneurysmal subarachnoid hemorrhage (aSAH). The authors reviewed the existing literature regarding the direct administration of nicardipine into the intracranial space for the treatment of vasospasm following aSAH. An electronic search of literature published between 1994 and 2018 was performed using PubMed in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis guidelines. A variety of combinations of the search terms "intrathecal nicardipine," "intraventricular nicardipine," and "nicardipine prolonged-release" were used. A total of 17 studies were included in this systematic review, 3 of which were studies in animals. The studies consistently demonstrated that IT nicardipine successfully reverses vasospasm, but the effect, as shown in some studies, was limited to the immediate vicinity of drug release. The data regarding long-term clinical outcomes are variable, with some studies demonstrating marked improvement whereas others fail to demonstrate improved outcomes when compared with patients who receive standard of care. Although adverse sequalae were uncommon, IT and IVt administration and therapy were associated with adverse effects including headache, meningitis, and hydrocephalus. Given the findings presented in these studies, IT, IVt, and intracisternal (pellet) nicardipine administration can be useful treatment adjuncts for vasospasm following aSAH, especially in cases refractory to conventional forms of treatment. However, larger, controlled clinical trials are warranted. [ABSTRACT FROM AUTHOR]