The Impact of Fluid Balance on Acute Kidney Injury in Nontraumatic Subarachnoid Hemorrhage.

Nontraumatic subarachnoid hemorrhage (SAH) can lead to poor neurologic outcomes, particularly when delayed cerebral ischemia (DCI) occurs. Maintenance of euvolemia following SAH is thought to reduce the risk of DCI. However, attempts at maintaining euvolemia often err on the side of hypervolemia. In this study, we assessed the relationship between fluid balance and acute kidney injury (AKI) in SAH patients, assessing hypervolemia versus euvolemia and their impact on AKI. In a quaternary care center, neuroscience intensive care unit we conducted a retrospective longitudinal analysis in adult patients who suffered a nontraumatic SAH. Out of 139 patients, 15 (10.8%) patients developed an AKI while hospitalized, with 7 stage I, 3 stage II, and 5 stage III injuries. Acute kidney injury patients had higher peak sodium (150.1 mEq/L vs 142.7 mEq/L, 95% confidence interval [CI]: [2.7-12.1 mEq/L]), higher discharge chloride (109.1 mEq/L vs 104.9 mEq/L, 95% CI: [0.7-7.6 mEq/L]), and lower hemoglobin at discharge (9.3 g/dL vs 11.3 g/dL, 95% CI: [1.0-2.9 g/dL]). At 7 days, AKI patients had a fluid balance that was 1.82 L higher ( = .04), and 3.38 L higher at 14 days ( = .02), in comparison to day 3. Acute kidney injury was associated with significant mortality increases. This increase in mortality was found at 30 days from admission with a 9.52-fold increase, and at 60 days with a 6.25-fold increase. As a secondary outcome, vasospasm (19 patients, 13.7%) showed no association with AKI. Acute kidney injury following SAH is correlated with clinically significant hypervolemia, elevated sodium, elevated chloride, decreased urine output, and decreased hemoglobin at discharge-risk factors for all SAH patients. This study further elucidates the harm of hypervolemia and gives greater practical evidence to physicians attempting to balance the dangers of vasospasm and AKI.