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We thank Poignant and Laffon (1) for their letter outlining where they feel our research contributes to patient care. As the authors mention, current research has demonstrated variable benefits related to the use of continuous infusion 3% hypertonic saline (HTS) in neurocritical care. They have raised several valid points that we feel require further commentary.
Overall, the current body of evidence evaluating continuous infusion HTS is mainly limited to single-center studies with small patient samples. Although the randomized, double-blind study referenced by Poignant did demonstrate a potential benefit of an induced hyperosmolar hypernatremic state, it included only 30 patients receiving this intervention. Patients in this study received a half-molar sodium lactate infusion and had lower serum chloride levels than the control group (2). Notably, our study of intracerebral hemorrhage (ICH) patients found no association, positive or negative, with hypernatremia and mortality (3). Wagner et al (4) retrospectively reported that the use of continuous 3% HTS significantly decreased cerebral edema volume and occurrences of intracranial pressure crisis, but only 26 patients received continuous 3% HTS. In the referenced study by Qureshi et al (5), use of continuous HTS was a positive predictor of in-hospital mortality in 36 head trauma patients. An earlier study by the same authors evaluated the use of a mixed HTS/acetate continuous infusion on a cohort of 27 patients that included those with head trauma, ICH, ischemic stroke, and postoperative cerebral edema. It revealed possible benefits in those with head trauma and postoperative edema, but these data are even more limited considering only 13 patients had these types of injuries (6). While there have been several other studies on the subject, there still remains a paucity of data showing benefits of this therapy, yet the practice seems to be one that is widely used to reduce cerebral edema and limit episodes of intracranial hypertension across a broad range of neurologic injuries. In fact, no major guideline related to neurocritical care recommends this therapy with even a moderate level of evidence.
While this practice requires further study, we also feel that studies are needed regarding hyperchloremia in those with severe neurologic injuries. Our analysis of patients with ICH supports a recent publication that demonstrated an association between hyperchloremia and increased rates of acute kidney in subarachnoid hemorrhage (7). The impact of hyperchloremia on acute ischemic stroke and traumatic brain injury are of equal interest and currently lack sufficient evaluations. Additionally, clinicians would benefit from studies aimed at identifying predictors of hyperchloremia in all the aforementioned populations. Does the use of continuous infusion 3% HTS increase the likelihood of hyperchloremia? Is hyperchloremia an indicator of disease severity or prescribing bias? Does the use of balanced mixtures of HTS lead to less hyperchloremia and reduced adverse effects? Should total volume of chloride-based fluids be monitored, including fluids from medication admixtures? All these questions remain unanswered based upon the current available evidence and require further evaluation.
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