Impact of Moderate Hyperchloremia on Clinical Outcomes in Intracerebral Hemorrhage Patients. Is There Still Room for Continuous Infusion of 3% Hypertonic Saline?
The study by Riha et al (1) emphasizes the preponderant role of electrolytic homeostasis in brain injury patients but provocatively raises the question of the role of continuous perfusion of hypertonic serum in such patients.
Several studies (2) in neuro-ICUs have concluded that hyperchloremia is the result of continuous IV infusion of hypertonic saline. In this study (1), the duration of 3% hypertonic saline administration in a propensity-matched cohort was 2.2 (1.3–3.3 d) days for the nonhyperchloremia group versus 3.3 (2.1–4.4 d) days for the hyperchloremia group, p value equals to 0.005.
Qureshi et al (3) showed that infusion of hypertonic saline was associated with higher in-hospital mortality (OR, 3.1; 95% CI, 1.1–10.2) in traumatic brain injury patients who received 2% or 3% hypertonic saline/acetate versus isotonic saline, after adjusting for differences between both groups. However, Roquilly et al (2) showed that continuous infusion of 20% hypertonic saline may decrease intracranial pressure in traumatic brain injury patients with refractory intracranial hypertension using a strict protocol in patients. In the study by Riha et al (1), a 20% saline infusion was used to decrease the risk of fluid overload, and no pulmonary edema or acute kidney injury was recorded, contrary to the study by Qureshi et al (3). This issue is still debated in the literature.
The interesting physiopathologic concept of using the hyperosmolar hypernatremic effect to prevent edema has not been a major focus of studies on the consequences of electrolytic disorders in brain injury patients. Hypernatremia can be an important independent risk factor for death in patients with traumatic brain injury (4) if not controlled, as can hyperchloremia? The difficulty is to know whether they are just a severity marker. In their study, Riha et al (1) reported 26% of patients with hypernatremia greater than 155 mmol/L (p = 0.006) in the hyperchloremia group of the propensity-matched cohort of whom 30% had acute kidney injury. Patients received approximately 1,500 mL of 3% hypertonic saline. We do not have information about their respiratory tolerance.
The benefit of the hyperosmolar hypernatremic effect has been illustrated in part by Ichai et al (5). They tested continuous infusion of half molar sodium lactate during 48 hours versus 0.9% saline solution. The results showed a reduction in the number of elevated intracranial pressure episodes in the sodium lactate group. The cumulative sodium levels in this group were significantly higher than in the saline group while reducing fluid and chloride balances.
Finally, the study by Riha et al (1) highlights the difficulty in maintaining electrolytic homeostasis in brain injury patients and shows the role of continuous infusion of hypertonic saline in the induction of hyperchloremia.
If these results implicating hyperchloremia in mortality are confirmed by data from randomized trials, hyperchloremia may become another indicator to guide the choice between mannitol and hypertonic saline for the treatment of acute intracranial hypertension.