Managing critically ill patients with severe traumatic brain injury: How should we season the recipe?

Abstract

Maintaining adequate cerebral perfusion remains the overarching objective in the management of critically ill patients with severe traumatic brain injury. Despite limited evidence, the concept of maintaining normal intracranial pressure has been the driving force behind most interventions over the last few decades. The current guidelines for the management of severe traumatic brain injury advocate limiting brain edema using hyperosmolar therapy with mannitol to control elevated intracranial pressure.1 Nevertheless, concerns that the diuretic effect of mannitol induces hypovolemia have led to the popularity of using hypertonic saline solutions as an alternative optionthis despite limited evidence.2,3 Moreover, concerns that hyponatremia may lead to increased cerebral edema have led to a broader use of hypertonic saline as a continuous infusion with the goal of either normalizing or obtaining a greater than normal serum sodium. 4 In this issue of the Journal, Griesdale et al. publish the results of a retrospective cohort study (two centres, n = 231 patients) that aimed to evaluate the effect of a continuous 3% hypertonic saline infusion on the incidence of hypernatremia and mortality in patients with severe traumatic brain injury.5 This study provides new insights into this important topic in neurocritical care with findings that are not in agreement with the previous literature. The authors considered many relevant confounders in the adjusted analyses, including markers of trauma severity (abnormal pupillary reactivity, hypotension upon admission, and use of mannitol) and diabetes insipidus (use of desmopressin). Moreover, the multivariable stratified Cox regression analysis allowed consideration of the effect of time-since hypertonic saline solutions and hypernatremia were modelled as time-dependent variables. The investigators found no association between hospital mortality and continuous hypertonic saline infusion (hazard ratio [HR], 1.07; 95% confidence interval [CI], 0.56 to 2.05; P = 0.84) or hypernatremia (HR, 1.31; 95% CI, 0.68 to 2.55; P = 0.42). Additionally, they observed that hypertonic saline did not modify the relationship between hypernatremia and death-i.e., among patients who received hypertonic saline, the occurrence of hypernatremia was not associated with increased mortality (HR, 1.52; 95% CI, 0.16 to 14.7; P = 0.79). Due to the nature of the intervention and the study design, the presence of residual confounding cannot be excluded, and the authors did not account for several other cointerventions. For example, patients who received hypertonic saline infusion seemed to have experienced a decrease in intracranial pressure, but other co-interventions that may impact on the control of intracranial pressure, such as sedatives, neuromuscular blockade, and therapeutic hypothermia (or controlled normothermia), were not measured. Also, the analysis of the impact of hypertonic saline infusion on the control of intracranial pressure was

Impact of Altered Airway Pressure on Intracranial Pressure, Perfusion, and Oxygenation: A Narrative Review

“…Hyperosmolar agents (e.g. mannitol) acutely increase intravascular Chen, Menon & Kavanagh 9 volume, but subsequent diuresis causes hypovolemia, which can amplify the depressant effects of positive-pressure ventilation on hemodynamics and cerebral perfusion (68).…”