Hypertonic Saline Compared to Mannitol for the Management of Elevated Intracranial Pressure in Traumatic Brain Injury: A Meta-Analysis

Background: We performed a meta-analysis to evaluate the effect of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury.Methods: A systematic literature search up to July 2021 was performed and 17 studies included 1,392 subjects with traumatic brain injury at the start of the study; 708 of them were administered hypertonic saline and 684 were given mannitol. They were reporting relationships between the effects of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury. We calculated the odds ratio (OR) and mean difference (MD) with 95% confidence intervals (CIs) to assess the effect of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury using the dichotomous or continuous method with a random or fixed-effect model.Results: Hypertonic saline had significantly lower treatment failure (OR, 0.38; 95% CI, 0.15–0.98, p = 0.04), lower intracranial pressure 30–60 mins after infusion termination (MD, −1.12; 95% CI, −2.11 to −0.12, p = 0.03), and higher cerebral perfusion pressure 30–60 mins after infusion termination (MD, 5.25; 95% CI, 3.59–6.91, p < 0.001) compared to mannitol in subjects with traumatic brain injury.However, hypertonic saline had no significant effect on favorable outcome (OR, 1.61; 95% CI, 1.01–2.58, p = 0.05), mortality (OR, 0.59; 95% CI, 0.34–1.02, p = 0.06), intracranial pressure 90–120 mins after infusion termination (MD, −0.90; 95% CI, −3.21–1.41, p = 0.45), cerebral perfusion pressure 90–120 mins after infusion termination (MD, 4.28; 95% CI, −0.16–8.72, p = 0.06), and duration of elevated intracranial pressure per day (MD, 2.20; 95% CI, −5.44–1.05, p = 0.18) compared to mannitol in subjects with traumatic brain injury.Conclusions: Hypertonic saline had significantly lower treatment failure, lower intracranial pressure 30–60 mins after infusion termination, and higher cerebral perfusion pressure 30–60 mins after infusion termination compared to mannitol in subjects with traumatic brain injury. However, hypertonic saline had no significant effect on the favorable outcome, mortality, intracranial pressure 90–120 mins after infusion termination, cerebral perfusion pressure 90–120 mins after infusion termination, and duration of elevated intracranial pressure per day compared to mannitol in subjects with traumatic brain injury. Further studies are required to validate these findings.

Different Stratification of Physiological Factors Affecting Cerebral Perfusion Pressure in Hypoxic-Ischemic Brain Injury after Cardiac Arrest According to Visible or Non-Visible Primary Brain Injury: A Retrospective Observational Study

We aimed to explore the stratification of physiological factors affecting cerebral perfusion pressure, including arterial oxygen tension, arterial carbon dioxide tension, mean arterial pressure, intracranial pressure (ICP), and blood-brain barrier (BBB) status, with respect to primary or secondary brain injury (PBI or SBI) after out-of-hospital cardiac arrest (OHCA). Among the retrospectively enrolled 97 comatose OHCA survivors undergoing post-cardiac arrest (PCA) care, 46 (47.4%) with already established PBI (high signal intensity (HSI) on diffusion-weighted imaging (DWI) had higher ICP (p = 0.02) and poorer BBB status (p < 0.01) than the non-HSI group. On subgroup analysis within the non-HSI group to exclude the confounding effect of already established PBI, 40 (78.4%) patients with good neurological outcomes had lower ICP at 24 h (11.0 vs. 16.0 mmHg, p < 0.01) and more stable BBB status (p = 0.17 in pairwise comparison) compared to those with poor neurological outcomes, despite the non-significant differences in other physiological factors. OHCA survivors with HSI on DWI showed significantly higher ICP and poorer BBB status at baseline before PCA care than those without HSI. Despite the negative DWI findings before PCA care, OHCA survivors have a cerebral penumbra at risk for potentially leading the poor neurological outcome from unsuppressed SBI, which may be associated with increased ICP and BBB permeability.

Principles and Management of Increased Intracranial Pressure

Intracranial pressure (ICP) is a reflection of the total volume inside the skull. Normal ICP is 5 to 15 mm Hg. Intracranial hypertension is defined as sustained ICP of more than 20 mm Hg. Increased ICP may lead to a reduction of cerebral perfusion pressure, a shift of brain tissue, and, as a result, secondary brainstem injury. Early recognition and treatment of elevated ICP are needed to prevent irreversible damage.

Optimal Cerebral Perfusion Pressure Guided by Brain Oxygen Pressure Measurement

Background: Although increasing cerebral perfusion pressure (CPP) is commonly accepted to improve brain tissue oxygen pressure (PbtO2), it remains unclear whether recommended CPP targets (i. e., &gt;60 mmHg) would result in adequate brain oxygenation in brain injured patients. The aim of this study was to identify the target of CPP associated with normal brain oxygenation.Methods: Prospectively collected data including patients suffering from acute brain injury and monitored with PbtO2, in whom daily CPP challenge using vasopressors was performed. Initial CPP target was &gt;60 mmHg; norepinephrine infusion was modified to have an increase in CPP of at least 10 mmHg at two different steps above the baseline values. Whenever possible, the same CPP challenge was performed for the following days, for a maximum of 5 days. CPP “responders” were patients with a relative increase in PbtO2 from baseline values &gt; 20%.Results: A total of 53 patients were included. On the first day of assessment, CPP was progressively increased from 73 (70–76) to 83 (80–86), and 92 (90–96) mmHg, which resulted into a significant PbtO2 increase [from 20 (17–23) mmHg to 22 (20–24) mmHg and 24 (22–26) mmHg, respectively; p &lt; 0.001]. Median CPP value corresponding to PbtO2 values &gt; 20 mmHg was 79 (74–87) mmHg, with 2 (4%) patients who never achieved such target. Similar results of CPP targets were observed the following days. A total of 25 (47%) were PbtO2 responders during the CPP challenge on day 1, in particular if low PbtO2 was observed at baseline.Conclusions: PbtO2 monitoring can be an effective way to individualize CPP values to avoid tissue hypoxia. Low PbtO2 values at baseline can identify the responders to the CPP challenge.