Under Pressure: Defining Management Goals for Pediatric Traumatic Brain Injury.

Unauthorized reproduction of this article is prohibited Pediatric Critical Care Medicine www.pccmjournal. org 777 In this “Era of Goal-Directed Therapy,” scientifically based goals for management of traumatic brain injury (TBI)—the leading cause of childhood death in many countries (1)—are woefully sparse. In fact, one could argue that they are nonexistent. Intracranial pressure (ICP) monitoring is the current mainstay of contemporary management. However, despite being considered “standard of care,” there is controversy over whether ICP-directed management is warranted in TBI. This is partly based on the fact that there are no preclinical studies that show that intracranial hypertension exacerbates damage to injured brain in a causeand-effect manner; and further based on a lack of clinical studies to definitively support or refute ICP-directed therapy in this spectrum of diseases. Indeed, current published guidelines for the monitoring and management of ICP and cerebral perfusion pressure (CPP) in both adult and pediatric patients cite level II evidence for ICP control at best (2, 3). In fact, only recently level I evidence has been published. The results of this randomized clinical trial performed in Bolivia and Ecuador do not support ICP monitoring in adults with TBI; however, ICP-directed treatments were more heavily used in the empiric versus ICP-guided cohort (4). This argues for a more rigorous scientific approach to determine and refine clinical guidelines and—perhaps more importantly, identification of better “goals” for goal-directed management of children with TBI. In this issue of Pediatric Critical Care Medicine, Lewis et al (5) attempt to tackle this as yet elusive component of TBI management via individual optimization of CPP in the setting of disturbed cerebrovascular autoregulation through the use of the pressure reactivity index (PRx). The PRx is has been evaluated in adults with severe TBI; however, few studies have examined the PRx in pediatric TBI. Briefly, the PRx correlates temporally linked changes in mean arterial blood pressure (MAP) and ICP. If the PRx is positive, then changes in MAP are associated with changes in ICP, generally reflecting impaired autoregulation; if the PRx is negative, then changes in MAP are not associated with ICP, generally reflecting intact autoregulation. The PRx can be averaged across levels of CPP or ICP, to infer patient-specific “optimal CPP” (CPPopt) and ICP thresholds, respectively (6). The PRx has potential to better inform critical bedside decisions, and nowhere are those decisions felt as keenly as the bedside of a child. As the authors point out, very little data exist to guide CPP management for patients whose brain and brain vasculature are still in development. The most recent guidelines provide an age-adjusted sliding scale ranging from 40 to 60 mm Hg (3) although much work is needed to better understand developmental changes in cerebrovascular autoregulation in healthy children let alone those with brain injury. It is logical to posit that there is a “sweet spot” for CPP after TBI, and that this varies on a case-by-case basis, and with age in general. The study by Lewis et al (5) uses the PRx in pediatric TBI and examines associations with patient outcomes, age, and CPP. The authors prospectively enrolled 36 patients over the course of 6 years at the Royal Children’s Hospital who met the inclusion criteria of a documented TBI and the need for invasive MAP and ICP monitoring. Their clinical protocol included age-based criteria for defining increased ICP (> 15 mm Hg for < 5 yr and > 20 mm Hg for ≥ 5 yr), and the duration required for defining increased ICP was threshold dependent (2 min for ICP > 25 mm Hg and 5 min for ICP > 20 mm Hg). Because the study was performed at a single center following an institutional TBI protocol, it seems reasonable to assume that patients were managed similarly, with limited interprovider variability. The main findings of the study were that PRx correlated with outcome assessed at 6 months (modified Glasgow outcome score); that CPP plotted against PRx resulted in a U-shaped curve, with a positive PRx observed when CPP less than 45 and greater than 75 mm Hg; and that CPPopt increased with patient age. Perhaps the most intriguing finding is shown in Figure 4B in (5), where PRx averaged within 5 mm Hg CPP bins was plotted for all patients. PRx signifying impaired autoregulation was seen with a CPP below 45, and somewhat surprisingly, above 75 mm Hg. The lower CPP threshold would be consistent with what is generally considered to be the lower limit of autoregulation; however, the higher CPP threshold is far below what is generally considered to be the upper limit of autoregulation Copyright © 2015 by the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies DOI: 10.1097/PCC.0000000000000501 Megan K. Browning, MD University of Pittsburgh School of Medicine Pittsburgh, PA