Cerebral pressure autoregulation in traumatic brain injury (original) (raw)

The Relationship Between Cerebral Blood Flow Autoregulation and Cerebrovascular Pressure Reactivity After Traumatic Brain Injury

Neurosurgery, 2012

BACKGROUND: Cerebrovascular pressure reactivity is the principal mechanism of cerebral autoregulation. Assessment of cerebral autoregulation can be performed by using the mean flow index (Mx) based on transcranial Doppler ultrasonography. Cerebrovascular pressure reactivity can be monitored by using the pressure reactivity index (PRx), which is based on intracranial pressure monitoring. From a practical point of view, PRx can be monitored continuously, whereas Mx can only be monitored in short periods when transcranial Doppler probes can be applied. OBJECTIVE: To assess to what degree impairment in pressure reactivity (PRx) is associated with impairment in cerebral autoregulation (Mx). METHODS: A database of 345 patients with traumatic brain injury was screened for data availability including simultaneous Mx and PRx monitoring. Absolute differences, temporal changes, and association with outcome of the 2 indices were analyzed. RESULTS: A total of 486 recording sessions obtained from 201 patients were available for analysis. Overall a moderate correlation between Mx and PRx was found (r = 0.58; P , .001). The area under the receiver operator characteristic curve designed to detect the ability of PRx to predict impaired cerebral autoregulation was 0.700 (95% confidence interval: 0.607-0.880). Discrepancies between Mx and PRx were most pronounced at an intracranial pressure of 30 mm Hg and they were significantly larger for patients who died (P = .026). Both Mx and PRx were significantly lower at day 1 postadmission in patients who survived than in those who died (P , .01). CONCLUSION: There is moderate agreement between Mx and PRx. Discrepancies between Mx and PRx are particularly significant in patients with sustained intracranial hypertension. However, for clinical purposes, there is only limited interchangeability between indices.

Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury*

Critical Care Medicine, 2002

Background: Impaired cerebral autoregulation is frequent after severe traumatic head injury. This could result in intracranial pressure fluctuating passively with the mean arterial pressure. Objective: This study examines the influence of autoregulation on the amplitude and direction of changes in intracranial pressure in patients with severe head injuries during the management of cerebral perfusion pressure. Design: Prospective study. Setting: Neurosurgical intensive care unit Patients: A total of 42 patients with severe head injuries. Interventions: Continuous recording of cerebral blood flow velocity, intracranial pressure, and mean arterial pressure during the start or change of continuous norepinephrine infusion. Measurements and Main Results: Cerebrovascular resistance was calculated from the cerebral perfusion pressure and middle cerebral artery blood flow velocity. The strength of autoregulation index was calculated as the ratio of the percentage of change in cerebrovascular resistance by the percentage of change in cerebral perfusion pressure before and after 121 changes in mean arterial pressure at constant ventilation between day 1 and day 18 after trauma. The strength of autoregulation index varied widely, indicating either preserved or severely perturbed autoregulation during hypotensive or hypertensive challenge in patients with or without intracranial hypertension at the basal state (strength of autoregulation index, 0.51 ؎ 0.32 to 0.71 ؎ 0.25). The change in intracranial pressure varied linearly with the strength of autoregulation index. There was a clinically significant change in intracranial pressure (>5 mm Hg) in the same direction as the change in mean arterial pressure in five tracings of three patients. This was caused by the mean arterial pressure dropping below the identified lower limit of autoregulation in three tracings for two patients. It seemed to be caused by a loss of cerebral autoregulation in the remaining two tracings for one patient. Conclusion: Cerebral perfusion pressure-oriented therapy can be a safe way to reduce intracranial pressure, whatever the status of autoregulation, in almost all patients with severe head injuries.

Noninvasive Cerebrovascular Autoregulation Assessment in Traumatic Brain Injury: Validation and Utility

Journal of Neurotrauma, 2003

A moving correlation index (Mx-CPP) of cerebral perfusion pressure (CPP) and mean middle cerebral artery blood flow velocity (CBFV) allows continuous monitoring of dynamic cerebral autoregulation (CA) in patients with severe traumatic brain injury (TBI). In this study we validated Mx-CPP for TBI, examined its prognostic relevance, and assessed its relationship with arterial blood pressure (ABP), CPP, intracranial pressure (ICP), and CBFV. We tested whether using ABP instead of CPP for Mx calculation (Mx-ABP) produces similar results. Mx was calculated for each hemisphere in 37 TBI patients during the first 5 days of treatment. All patients received sedation and analgesia. CPP and bilateral CBFV were recorded, and GOS was estimated at discharge. Both Mx indices were calculated from 10,000 data points sampled at 57.4Hz. Mx-CPP. 0.3 indicates impaired CA; in these patients CPP had a significant positive correlation with CBFV, confirming failure of CA, while in those with Mx , 0.3, CPP was not correlated with CBFV, indicating intact CA. These findings were confirmed for Mx-ABP. We found a significant correlation between impaired CA, indicated by Mx-CPP and Mx-ABP, and poor outcome for TBI patients. ABP, CPP, ICP, and CBFV were not correlated with CA but it must be noted that our average CPP was considerably higher than in other studies. This study confirms the validity of this index to demonstrate CA preservation or failure in TBI. This index is also valid if ABP is used instead of CPP, which eliminates the need for invasive ICP measurements for CA assessment. An unfavorable outcome is associated with early CA failure. Further studies using the Mx-ABP will reveal whether CA improves along with patients' clinical improvement.

2008 Puppo et al. One-minute dynamic cerebral autoregulation in severe head injury patients and its comparison with static autoregul

Objective To compare dynamic and static responses of cerebral blood flow to sudden or slow changes in arterial pressure in severe traumatic brain injury (TBI) patients. Design Prospective study. Patients and Methods We studied 12 severe TBI patients, age 16-63 years, and median GCS 6. We determined the dynamic cerebral autoregulation: response of cerebral blood flow velocity to a step blood pressure drop, and the static cerebral autoregulation: change in cerebral blood flow velocity after a slow hypertensive challenge. Results During the dynamic response, the median drop in arterial pressure was 21 mm Hg. Dynamic response was graded between 9 (best) and 0 (worst). The median value was 5; four patients showed high values, (8-9), five patients showed intermediate values (4-6). In three patients (value = 0), the CBFV drop was greater than the cerebral perfusion pressure drop, and maintained through 60 s. The static cerebral autoregulation was preserved in 6/11 patients. The comparison between the two showed four different combinations. The five patients with impaired static cerebral autoregulation showed unfavorable outcome. Conclusions A sharp dynamic vasodilator response could not be sustained, and a slow or absent reaction to a sudden hypotensive challenge could show an acceptable cerebral autoregulation in the steady state. We found that patients with impaired static cerebral autoregulation had a poor outcome, whereas those with preserved static cerebral autoregulation experience favorable outcomes.

Pressure autoregulation, intracranial pressure, and brain tissue oxygenation in children with severe traumatic brain injury

Journal of Neurosurgery: Pediatrics, 2009

Object Cerebral pressure autoregulation is an important neuroprotective mechanism that stabilizes cerebral blood flow when blood pressure (BP) changes. In this study the authors examined the association between autoregulation and clinical factors, BP, intracranial pressure (ICP), brain tissue oxygen tension (PbtO2), and outcome after pediatric severe traumatic brain injury (TBI). In particular we examined how the status of autoregulation influenced the effect of BP changes on ICP and PbtO2. Methods In this prospective observational study, 52 autoregulation tests were performed in 24 patients with severe TBI. The patients had a mean age of 6.3 ± 3.2 years, and a postresuscitation Glasgow Coma Scale score of 6 (range 3–8). All patients underwent continuous ICP and PbtO2 monitoring, and transcranial Doppler ultrasonography was used to examine the autoregulatory index (ARI) based on blood flow velocity of the middle cerebral artery after increasing mean arterial pressure by 20% of the b...

Experience with clinical cerebral autoregulation testing in children hospitalized with traumatic brain injury: Translating research to bedside

Frontiers in Pediatrics, 2023

Objective: To report our institutional experience with implementing a clinical cerebral autoregulation testing order set with protocol in children hospitalized with traumatic brain injury (TBI). Methods: After IRB approval, we examined clinical use, patient characteristics, feasibility, and safety of cerebral autoregulation testing in children aged <18 years between 2014 and 2021. A clinical order set with a protocol for cerebral autoregulation testing was introduced in 2018. Results: 25 (24 severe TBI and 1 mild TBI) children, median age 13 years [IQR 4.5; 15] and median admission GCS 3[IQR 3; 3.5]) underwent 61 cerebral autoregulation tests during the first 16 days after admission [IQR1.5; 7; range 0-16]. Testing was more common after implementation of the order set (n = 16, 64% after the order set vs. n = 9, 36% before the order set) and initiated during the first 2 days. During testing, patients were mechanically ventilated (n = 60, 98.4%), had invasive arterial blood pressure monitoring (n = 60, 98.4%), had intracranial pressure monitoring (n = 56, 90.3%), braintissue oxygenation monitoring (n = 56, 90.3%), and external ventricular drain (n = 13, 25.5%). Most patients received sedation and analgesia for intracranial pressure control (n = 52; 83.8%) and vasoactive support (n = 55, 90.2%) during testing. Cerebral autoregulation testing was completed in 82% (n = 50 tests); 11 tests were not completed [high intracranial pressure (n = 5), high blood pressure (n = 2), bradycardia (n = 2), low cerebral perfusion pressure (n = 1), or intolerance to blood pressure cuff inflation (n = 1)]. Impaired cerebral autoregulation on first assessment resulted in repeat testing (80% impaired vs. 23% intact, RR 2.93, 95% CI 1.06:8.08, p = 0.03). Seven out of 50 tests (14%) resulted in a change in cerebral hemodynamic targets.

Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury

Critical Care Medicine, 2002

C erebrovasCular pressure reactivity reflects the capability of smooth muscle tone in the walls of cerebral arteries and arterioles to react to changes in transmural pressure (cerebral vessels constrict in response to an increase in CPP, and vice versa). Cerebro-vascular pressure reactivity represents a key element of cerebral autoregulation, although the two terms should not be used interchangeably because vascular responses can occur outside the range of cerebral autoregulation. 7,25 With increasing ABP, intact cerebrovascular pressure reactivity will lead to vasoconstriction and a reduction of cerebral blood volume. Under the condition of a finite pressure-volume compensatory reserve, this reduction of cerebral blood volume will produce a decrease in ICP, a condition that is usually not met in patients after a decompressive craniectomy or in those with an external ventricular drain. When cerebrovascular pressure reac

Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury*

Critical Care Medicine, 2012

S urvival after traumatic brain injury (TBI) is dependent on the control of intracranial hypertension and the provision of hemodynamic support to achieve an "adequate" cerebral perfusion pressure (CPP). However, the idea of a single value (or even a single range) of CPP being adequate for the diverse group of TBI patients is an oversimplification (1-3). Age and premorbid arterial blood pressure (ABP) are examples of factors likely to influence individual CPP targets, with elderly, hypertensive patients requiring a higher CPP compared with young, normotensive patients. Although multimodal brain monitoring, including continuous brain-tissue oxygenation, near infrared spectroscopy, transcranial Doppler ultrasonography, and microdialysis provide valuable information at the bedside regarding the adequacy of CPP, these technologies are costly and restricted to a relatively small number of specialized neurocritical care units. The 2007 Brain Trauma Foundation guidelines advocated randomized controlled trials to verify the feasibility and the impact on outcome of strategies based on individualized CPP management following severe TBI (4). A method for individualization of CPPoriented management based on determination of cerebrovascular reactivity Objectives: We have sought to develop an automated methodology for the continuous updating of optimal cerebral perfusion pressure (CPP opt ) for patients after severe traumatic head injury, using continuous monitoring of cerebrovascular pressure reactivity. We then validated the CPP opt algorithm by determining the association between outcome and the deviation of actual CPP from CPP opt .

Alternative continuous intracranial pressure-derived cerebrovascular reactivity metrics in traumatic brain injury: a scoping overview

Acta Neurochirurgica, 2020

Background Pressure reactivity index (PRx) has emerged as a means to continuously monitor cerebrovascular reactivity in traumatic brain injury (TBI). However, other intracranial pressure (ICP)-based continuous metrics exist, and may have advantages over PRx. The goal of this study was to perform a scoping overview of the literature on non-PRx ICP-based continuous cerebrovascular reactivity metrics in adult TBI. Methods We searched MEDLINE, BIOSIS, EMBASE, Global Health, SCOPUS, and Cochrane Library from inception to December 2019. Using a two-stage filtering of title/abstract, and then full manuscript, we identified pertinent articles. Data was abstracted to tables and each technique summarized, including pulse amplitude index (PAx), correlation between pulse amplitude of ICP and cerebral perfusion pressure (RAC), PRx 55-15 , and low-resolution metrics LAx and L-PRx. Results A total of 23 articles met the inclusion criteria, with the vast majority being retrospective in nature and based out of European centers. Sixteen articles focused on high-resolution metrics PAx, RAC, and PRx 55-15 , with 6 articles focusing on LAx and L-PRx. PAx may have a role in low ICP situations, where it appears to perform superior to PRx. RAC displays similar behavior to PRx, with a trend to stronger associations with favorable/unfavorable outcome at 6 months, and stronger parabolic relationship with CPP. PRx 55-15 provides a focused assessment on the vasogenic frequency range associated with cerebral autoregulation, with preliminary data supporting a strong association with outcome in TBI. LAx and L-PRx display varying This article is part of the Topical Collection on Brain trauma Electronic supplementary material The online version of this article (