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Association between blood pressure augmentation and brain tissue oxygenation in severe pediatric traumatic brain
Ali Abu-Alya1, Thitikan Kunapaisal2, Abhijit V Lele3,4
1Department of Neurology, University of Washington, Seattle, WA, USA. aliabualya@icloud.com.
Insights
Blood pressure augmentation in pediatric traumatic brain injury (TBI) can increase cerebral perfusion pressure (CPP) and brain tissue oxygenation (PbtO₂). However, patient responses vary, highlighting the need to consider cerebral autoregulation status in TBI management.
Area of Science:
- Pediatric critical care medicine
- Neurotrauma research
- Cerebrovascular physiology
Background:
- Pediatric traumatic brain injury (TBI) carries a high risk of poor outcomes, particularly when associated with brain tissue hypoxia.
- Optimizing blood pressure management is crucial, but data on identifying pediatric TBI patients who benefit most from blood pressure augmentation for cerebral hypoxia is limited.
Purpose of the Study:
- To investigate the association between blood pressure augmentation and brain tissue oxygenation (PbtO₂) in children with severe TBI.
- To explore the impact of cerebral autoregulation on the PbtO₂ response to blood pressure augmentation.
Main Methods:
- Retrospective review of prospectively collected data from severe pediatric TBI patients (<18 years).
- Inclusion criteria: severe TBI (Glasgow Coma Scale score <9) and cerebral autoregulation testing using the autoregulation index (ARI).
- Analysis of changes in mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and PbtO₂ following blood pressure augmentation.
Main Results:
- Blood pressure augmentation (mean MAP increase of 22.8%) led to increased CPP (32.5%) and PbtO₂ (23%).
- A significant correlation was found between PbtO₂ increase and CPP increase (R²=0.36, p=0.024), but not directly with MAP change alone (R²=0.27, p=0.057).
- Four distinct PbtO₂ response patterns were observed, indicating heterogeneous patient responses.
- In patients with intact cerebral autoregulation (n=7), PbtO₂ changes were significantly associated with both MAP and CPP changes.
Conclusions:
- Mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) augmentation can increase PbtO₂ in severe pediatric TBI.
- Patient response to MAP augmentation is heterogeneous, with cerebral autoregulation status potentially influencing outcomes.
- MAP and CPP augmentation strategies may be beneficial for improving PbtO₂ in this vulnerable population.
Background:
Brain tissue hypoxia has poor outcomes in pediatric traumatic brain injury (TBI). However, more data is needed on how to determine which patients benefit the most from blood pressure augmentation as a treatment for cerebral hypoxia in pediatric TBI. We examined the association between blood pressure augmentation and brain tissue oxygenation (PbtO₂) in children with severe TBI.
Methods:
We performed a retrospective review of prospectively collected data at Harborview Medical Center. We included patients < 18 years admitted from January 2014 to July 2021 with severe (admission Glasgow coma scale score [GCS] < 9) TBI who underwent static transcranial doppler cerebral autoregulatory testing using the autoregulation index (ARI), derived from transcranial doppler ultrasonography measures.
Results:
We evaluated 14 patients (median age 13 [IQR 6-15 years], 78.6% male, median admission GCS 3 [IQR 3-4]) between intensive care unit admission days 2-11. Starting MAP was mean 81 mmHg (SD 9.2, range 63-97) and ending MAP was mean 99.3 mmHg (SD 14.7, range 62-115), starting CPP was mean 69 mmHg (SD 8.2, range 58-84) and ending CPP was mean 91 mm, starting PbtO2 was mean 25 (SD 12, range 11-64), and ending PbtO2 was mean 29 (SD 13.1, range 10 to 62). A 22.8% MAP increase resulted in a 32.5% CPP and 23% PbtO₂ increase, respectively. Overall, percent PbtO₂ increased with percent CPP increase (R2 = 0.36, p = 0.024) but not with percent MAP change (R2 = 0.27, p = 0.057). However, PbtO₂ response to MAP augmentation was heterogeneous, resulting in four PbtO₂ response groups (Group 1, normal and maintained [n = 9, 64.3%]); Group 2, normal and deteriorated [n = 1, 7.1%]); Group 3, low and improved [n = 1, 7.1%]); and Group 4, low and not improved [n = 3, 21.4%]). Stratified by cerebral autoregulation status, percent PbtO₂ change was only associated with percent MAP change (R2 = 0.59, p = 0.045) and percent CPP change (R2 = 0.64, p = 0.032) in patients with intact cerebral autoregulation (n = 7).
Conclusions:
MAP augmentation resulted in higher CPP and four distinct PbtO₂ response patterns, including PbtO₂ improvement and cerebral hypoxia. Cerebral autoregulation status and PbtO₂ response status may impact blood pressure augmentation effects. MAP and CPP augmentation may be a desirable strategy to improve PbtO₂ in severe pediatric TBI.
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01:28Traumatic Brain Injury l: Introduction
01:29Increased Intracranial Pressure ll: Pathophysiology