Neuromonitoring in Children with Traumatic Brain Injury

Abstract

Traumatic brain injury remains a major cause of mortality and morbidity in children across the world. Current management based on international guidelines focuses on a fixed therapeutic target of less than 20 mm Hg for managing intracranial pressure and 40-50 mm Hg for cerebral perfusion pressure across the pediatric age group. To improve outcome from this complex disease, it is essential to understand the pathophysiological mechanisms responsible for disease evolution by using different monitoring tools. In this narrative review, we discuss the neuromonitoring tools available for use to help guide management of severe traumatic brain injury in children and some of the techniques that can in future help with individualizing treatment targets based on advanced cerebral physiology monitoring.

Keywords: Brain chemistry; Cerebral autoregulation; Cerebral oxygenation; Intracranial pressure; Neuromonitoring; Pediatric traumatic brain injury; Transcranial Doppler.

Fig. 1

CPPopt calculation in real time in a child with sTBI. Real-time in-vivo calculation of CPPopt in a patient recruited to STARSHIP in an 8-h recording window. Top panel displays ABP, followed by ICP, and then CPP (CPPopt in the light gray line and lower limit of autoregulation in dark gray line). The bottom panel shows calculation of CPPopt. CPPopt is continuously calculated using a 5-min median CPP time trend alongside PRx. These PRx values are divided and averaged into CPP bins spanning 5 mm Hg. An automatic curve fitting method is applied to the binned data to determine the CPP value with the lowest associated PRx value. (Author’s own work). ICP intracranial pressure, CPP cerebral perfusion pressure, ABP arterial blood pressure, CPPopt optimum cerebral perfusion pressure, PRx pressure reactivity index, sTBI severe traumatic brain injury, STARSHIP Studying Trends of Auto-Regulation in Severe Head Injury in Paediatrics

Fig. 2

Clinical monitoring schema and protocol. Three intraparenchymal monitors are placed in the sedated, ventilated traumatic brain injury patient, via a cranial access device into the right frontal lobe. a Intracranial pressure is measured using a piezoelectric strain gauge (Codman). b Brain tissue oxygen is measured using a modified Clark electrode (Licox). c The cerebral microdialysis catheter (M Dialysis AB) consists of a double lumen catheter with a semipermeable membrane. A microfluidic pump perfuses the catheter with artificial brain extracellular fluid at 0.3 mL/h. The fluid recovered is collected in a microvial and assayed for lactate, pyruvate, glucose, and glycerol (bedside ISCUSflex analyzer). d Signals from intracranial pressure and brain tissue oxygen monitors are streamed in real time to a bedside computer with a multimodality data acquisition and processing software (ICM+) for analysis. e Study protocol for patients with raised LPR. Patients with cerebral LPR > 25 were treated in a staged fashion with the interventions within this flowchart. The neurometabolic state was classified in any given hourly time epoch, depending on the abnormalities defined above. CPP cerebral perfusion pressure; FiO₂ fraction of inspired oxygen; ICP intracranial pressure; LPR lactate/pyruvate ratio; NMS neurometabolic state; PbtO₂ brain tissue oxygen tension; PRx pressure reactivity index. Adapted from Khellaf et al. [110] under Creative Commons License (CC BY), published by SAGE, copyright the authors.