Pediatric Critical Care Medicine:
Chapter 6. Advanced neuromonitoring
Kochanek, Patrick M. MD, FCCM; Carney, Nancy PhD; Adelson, P. David MD, FACS, FAAP; Ashwal, Stephen MD; Bell, Michael J. MD; Bratton, Susan MD, MPH, FAAP; Carson, Susan MPH; Chesnut, Randall M. MD, FCCM, FACS; Ghajar, Jamshid MD, PhD, FACS; Goldstein, Brahm MD, FAAP, FCCM; Grant, Gerald A. MD; Kissoon, Niranjan MD, FAAP, FCCM; Peterson, Kimberly BSc; Selden, Nathan R. MD, PhD, FACS, FAAP; Tong, Karen A. MD; Tasker, Robert C. MBBS, MD, FRCP; Vavilala, Monica S. MD; Wainwright, Mark S. MD, PhD; Warden, Craig R. MD, MPH, FAAP, FACEP
From Critical Care Medicine (PMK, MJB), University of Pittsburgh School of Medicine, Pittsburgh, PA; Department of Medical Informatics and Clinical Epidemiology (NC, SC, KP), Oregon Health & Science University, Portland, OR; Barrow Neurological Institute at Phoenix Children's Hospital (PDA), and Pediatric Neurosurgery/ Children' Neurosciences (PDA), Phoenix, AZ; Division of Child Neurology, Department of Pediatrics (SA) and Section of Neuroradiology (KAT), Loma Linda University School of Medicine, Loma Linda, CA; Pediatric Critical Care Medicine (SB), University of Utah School of Medicine, Salt Lake City, UT; Department of Neurological Surgery (NRS), Oregon Health & Science University, Portland, OR; Orthopedics and Sports Medicine (RMC), University of Washington School of Medicine, Seattle, WA; Neurological Surgery (JG), Weill Cornell Medical College; President of the Brain Trauma Foundation (JG), New York, NY; Translational Science (BG), Ikaria, Inc., Clinton, NJ; Pediatrics (BG), University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ; Surgery and Pediatrics (GAG), Duke University School of Medicine, Durham, NC; Pediatrics and Emergency Medicine (NK), British Columbia's Children's Hospital, University of British Columbia, Vancouver, BC; Neurocritical Care (RCT), Children's Hospital Boston; Neurology and Anesthesia (RCT), Harvard Medical School, Boston, MA; Anesthesiology and Pediatrics (MSV), University of Washington School of Medicine, Seattle, WA; Molecular Pharmacology and Biological Chemistry (MSW), Northwestern University Feinberg School of Medicine, Chicago, IL; Emergency Medicine and Pediatrics (CRW), and Pediatric Emergency Services (CRW), Oregon Health & Science University/Doernbercher Children's Hospital, Portland, OR.
Funding provided by the Brain Trauma Foundation and partial funding from the Charles Maddock Foundation.
The authors have not disclosed any potential conflicts of interest.
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Strength of Recommendation: Weak.
Quality: Low, from one moderate- and one poor-quality class III study.
A. Level I
There are insufficient data to support a level I recommendation for this topic.
B. Level II
There are insufficient data to support a level II recommendation for this topic.
C. Level III
If brain oxygenation monitoring is used, maintenance of partial pressure of brain tissue oxygen (PbtO2) ≥10 mm Hg may be considered.
II. EVIDENCE TABLE (see Table 1)
Children with severe traumatic brain injury (TBI) frequently have abnormal cerebral hemodynamics, including intracranial hypertension, cerebral hypoxia, delayed and/or altered processing of electrophysiological signals, and impaired cerebral autoregulation. In addition to intracranial pressure (ICP) monitoring, advanced neuromonitoring techniques such as microdialysis, electrophysiological assessments, and examination of cerebral autoregulation may help identify and treat patients with these derangements after TBI. The development of advanced monitoring systems to provide information regarding both cerebrovascular and metabolic function after TBI is critical to providing optimal neurocritical care. If treatment preventing unwanted cerebral pathophysiological processes is shown to improve outcome in children with severe TBI, the use of monitoring systems, beyond ICP monitoring, will mark an important advance in the care of patients with TBI. Advanced neuromonitors may provide useful information about derangements in cerebral oxygenation, blood flow and metabolism, autoregulation, and function after severe pediatric TBI.
For this new topic, MEDLINE was searched from 1950 through 2010 (Appendix B for search strategy), and results were supplemented with literature recommended by peers or identified from reference lists. Of 44 potentially relevant studies, two were included as evidence for this topic.
V. SCIENTIFIC FOUNDATION
Two class III publications met the inclusion criteria for this topic and provide evidence to support the recommendations (1, 2). The recommendations on the use of advanced neuromonitoring in this chapter are for patients with no contraindications for neuromonitoring such as coagulopathy (brain oxygenation) and for patients who do not have a diagnosis of brain death.
In 2009, a study by Figaji et al (1) reported the relationship between PbtO2 and long-term outcome in 52 children with severe TBI. Patients with compromised PbtO2 were treated to a threshold ≥20 mm Hg. Overall mortality was nearly 10%. After considering other conventional predictors, authors reported that PbtO2 <5 mm Hg for >1 hr or <10 mm Hg for >2 hrs were associated with a significantly increased risk of unfavorable outcome (Glasgow Outcome Scale and Pediatric Cerebral Performance Category scores) and mortality, independent of other factors that were also significant (e.g., ICP, cerebral perfusion pressure, Glasgow Come Scale, computed tomography classification, and systemic hypoxia). This study provided no comparison group. All patients with compromised PbtO2 were treated to maintain the targeted threshold, and at the same time they may have received various treatments depending on other physiological variables such as ICP, cerebral perfusion pressure, systemic oxygen, and hemoglobin. What can be inferred is that in this sample of patients, those with higher PbtO2 and fewer episodes of PbtO2 <10 mm Hg had better outcomes. We cannot say that this relationship is a direct response to treatment.
In 2006, a study by Narotam et al (2) described changes in PbtO2 in relation to changes in cerebral perfusion pressure, FIO2, and PaO2 in 15 children ranging from 1.5 to 18 yrs and Glasgow Coma Scale score ≤8. Like with the previous study, patients were managed to maintain a PbtO2 level ≥20 mm Hg. In addition, the authors aimed to assess a treatment protocol (Critical Care Guide) for manipulation of physiological factors that influence oxygen delivery to the brain. Survival was associated with normal initial PbtO2 (≥10 mm Hg). There was no difference in the mean initial PbtO2 among the ten survivors and six deaths at 3 months. Final PbtO2 in survivors was higher than that in nonsurvivors (mean PbtO2, 22.7 ± 9.05 vs. 7.2 ± 7.85 mm Hg; p = .0045). However, only six patients had elevated ICP, making the relationship between ICP and PbtO2 difficult to interpret. Like with the previous study, we cannot infer from this study that response to treatment influenced outcome.
In these two studies, a treatment threshold for PbtO2 of 20 mm Hg was used; however, they both reported an association between unfavorable outcome and PbtO2 <10 mm Hg. Although the study by Figaji et al (1) reported an even stronger association between PbtO2 <5 mm Hg and unfavorable outcome, until proven otherwise, if this advanced monitoring modality is used, it would be prudent to target the more conservative threshold of >10 mm Hg.
VI. INFORMATION FROM OTHER SOURCES
Several articles on advanced neuromonitoring in the pediatric TBI literature were identified in the search but excluded from the evidentiary table because they simply described use of a given advanced neuromonitoring device rather than targeting a treatment value for that monitor (i.e., a threshold parameter on the advanced monitoring device was not specifically manipulated). Given that this guidelines document is focused on treatment, for these reports, a treatment recommendation regarding the monitoring device could not be given. The devices in those studies included brain microdialysis (3), cerebral blood flow and autoregulation monitors (4–7), signal processing of hemodynamic and hydrostatic signals (8), and jugular venous oxygen saturation monitoring (9).
A. Indications From the Adult Guidelines
Evidence from the adult guidelines (10) supported a level III recommendation for use of jugular venous saturation and PbtO2 monitoring, in addition to standard ICP monitors, in the management of adults with severe TBI. Evidence suggests that episodes of jugular venous desaturation (saturation <50%) are associated with poor outcome and that this value represents a treatment threshold when using this monitoring technique. Similarly, low values of PbtO2 (<15 mm Hg) and the extent of their duration (>30 mins) are associated with high rates of mortality and that 15 mm Hg represents a treatment threshold value for PbtO2. However, the accuracy of jugular venous saturation and PbtO2 monitoring was not evaluated. Although many technologies including cerebral microdialysis, thermal diffusion probes, transcranial Doppler, and near-infrared spectroscopy were recognized to hold promise in advancing the care of adults with severe TBI, there was insufficient evidence to comment on the use of these advanced neuromonitors in this population.
Overall, advanced neuromonitors have been subjected to very limited clinical investigation in pediatric TBI, particularly study of their use specifically to guide therapy. Most of the medical literature on these agents is composed of observational studies on relatively small numbers and case series receiving some form of local standard TBI care. The lack of sufficient high-quality pediatric studies limits the conclusions that can be made and differences between study centers in the treatment of TBI and inpatient populations limit the generalizability of findings.
VIII. KEY ISSUES FOR FUTURE INVESTIGATION
* Examine critical thresholds for each neuromonitoring modality and determine the risk-benefit ratio, cost-effectiveness, comparative effectiveness, and impact of neuromonitors on patient long-term functional outcomes.
* Address issues of single vs. multimodal neuromonitoring, reliability of technology, optimal combination of monitors, location of neuromonitor vs. site of injury (hemispheric, pericontusional), relationship between neuromonitor data and imaging data, neuromonitor use for optimization of treatment and patient prognosis as well as optimal duration of advanced monitoring.
* Evaluate the role of advanced neuromonitoring on clinical decision-making and patient outcomes.
* Develop additional bedside and noninvasive advanced neuromonitors.
1. Figaji AA, Zwane E, Thompson C, et al.: Brain tissue oxygen tension monitoring in pediatric severe traumatic brain injury. Part 1: Relationship with outcome. Childs Nerv Syst 2009; 25:1325–1333
2. Narotam PK, Burjonrappa SC, Raynor SC, et al.: Cerebral oxygenation in major pediatric trauma: its relevance to trauma severity and outcome. J Pediatr Surg 2006; 41:505–513
3. Tolias CM, Richards DA, Bowery NG, et al.: Extracellular glutamate in the brains of children with severe head injuries: A pilot microdialysis study. Childs Nerv Syst 2002; 18:368–374
4. Brady KM, Shaffner DH, Lee JK, et al.: Continuous monitoring of cerebrovascular pressure reactivity after traumatic brain injury in children. Pediatrics 2009; 124:e1205–1212
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6. Vavilala MS, Tontisirin N, Udomphorn Y, et al.: Hemispheric differences in cerebral autoregulation in children with moderate and severe traumatic brain injury. Neurocrit Care 2008; 9:45–54
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8. Shapiro K, Marmarou A: Clinical applications of the pressure–volume index in treatment of pediatric head injuries. J Neurosurg 1982; 56:819–825
9. Perez A, Minces PG, Schnitzler EJ, et al.: Jugular venous oxygen saturation or arteriovenous difference of lactate content and outcome in children with severe traumatic brain injury. Pediatr Crit Care Med 2003; 4:33–38
10. Bratton SL, Chestnut RM, Ghajar J, et al.: Guidelines for the management of severe traumatic brain injury. X. Brain oxygen monitoring and thresholds. J Neurotrauma 2007; 24(Suppl 1):S65–70
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