Brain tissue oxygen tension monitoring
Partial pressure of oxygen in brain tissue
Abbreviation: PbtO2
The oxygen content of the white matter of the brain. It is determined by inserting a small monitor directly into the brain parenchyma. Normal values are > 20 mm Hg.
Low brain tissue oxygen tension (PbtO2), or brain hypoxia, is an independent predictor of poor outcome 1)
PbtO2 monitoring
see PbtO2 monitoring.
Systematic review and meta-analysis
Cerebral tissue oxygenation monitoring (PbtO2) may detect neuronal tissue infarction thresholds, enhancing neuroprotection. We performed a systematic review and meta-analysis to evaluate the effects of combined cerebral tissue oxygenation (PbtO2) and ICP compared to isolated ICP monitoring in patients with TBI. PubMed, Embase, Cochrane, and Web of Sciences databases were searched for trials published up to June 2023. A total of 16 studies comprising 37,820 patients were included. ICP monitoring was universal, with the additional placement of PbtO2 in 2222 individuals (5.8%). The meta-analysis revealed a reduction in mortality (OR 0.57, 95% CI 0.37-0.89, p = 0.01), a greater likelihood of favorable outcomes (OR 2.28, 95% CI 1.66-3.14, p < 0.01), and a lower chance of poor outcomes (OR 0.51, 95% CI 0.34-0.79, p < 0.01) at 6 months for the PbtO2 plus ICP group. However, these patients experienced a longer length of hospital stay (MD 2.35, 95% CI 0.50-4.20, p = 0.01). No significant difference was found in-hospital mortality rates (OR 0.81, 95% CI 0.61-1.08, p = 0.16) or intensive care unit length of stay (MD 2.46, 95% CI - 0.11-5.04, p = 0.06). The integration of PbtO2 to ICP monitoring improved mortality outcomes and functional recovery at 6 months in patients with TBI. PROSPERO (International Prospective Register of Systematic Reviews) CRD42022383937; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=383937 2).
Indications for SjVO2 or PbtO2 monitoring include the need for augmented hyperventilation (pCO2 = 20–25) to control ICP. Monitored e.g., with Licox® probe. The likelihood of death increases with longer times of brain tissue oxygen tension (pBtO2) < 15 mm Hg or even a brief drop of PbtO2 < 6.
Initial pBtO2 < 10 mm Hg for > 30 minutes correlates with an increased risk of death or bad outcome.
Probe placement: 1. TBI: assumed to be a diffuse process, often placed on the least injured side
2. SAH: placed in vascular distributions at greatest risk of vasospasm
a) ACA (with ACA or AComA aneurysm): standard frontal placement (≈ 2–3 cm off midline on appropriate side)
b) MCA (with ICA or MCA aneurysm): 4.5–5.5 cm off midline
c) ACA-MCA watershed area: 3 cm lateral to the midline
3. ICH: usually placed near the site of the hemorrhage
Brain tissue oxygen tension monitoring requires insertion of a probe into the brain parenchyma through a single multiple-lumen bolt, or in a subcutaneously tunneled fashion. As those patients often require early magnetic resonance imaging(MRI), typically used bolts are disadvantageous due to massive metal artifacts. Similarly, subcutaneous tunneling is often problematic as suture fixation can loosen over time.
One physiological parameter of particular interest is brain tissue oxygenation (PbtO2) since the brain depends on an uninterrupted supply of oxygen and glucose to maintain cellular metabolism and viability. Additionally, observational studies demonstrate that brain tissue hypoxia may occur even when ICP or cerebral perfusion pressure (CPP) is normal and result from diffusion rather than perfusion defects 3) 4).
The Level III recommendation about brain tissue oxygen monitoring has been removed because of higher-quality, contradictory evidence acquired since the 3rd Edition of severe traumatic brain injury guidelines.
Past indications for SjVOs or PbtO2 monitoring include the need for augmented hyperventilation (pCO2 = 20–25) to control ICP. Monitored e.g. with Licox® probe. The likelihood of death increases with longer times of brain tissue oxygen tension (pBtO2) < 15mm Hg or even a brief drop of PbtO2 < 6.48 Initial pBtO2 < 10mm Hg for > 30 minutes correlates with increased risk of death or bad outcome.
Management suggestions for pBtO2 < 15–20mm Hg:
1. consider jugular venous O2 saturation monitor or lactate microdialysis monitor for confirmation
2. consider CBF study to determine generalizability of pBtO2 monitor reading
3. treatment: proceed to each tier as needed
Case series
A cohort study comprised 629 patients admitted to a Level I trauma center with a diagnosis of severe traumatic brain injury over a period of 3 years. Hospital mortality rate, neurological outcome, and resource utilization of 123 patients who underwent both Brain tissue oxygen partial pressure (PbO2) and intracranial pressure monitoring were compared with the same measures in 506 patients who underwent ICP monitoring only. The main outcomes were Hospital mortality rate, functional independence at hospital discharge, duration of mechanical ventilation, hospital length of stay, and hospital cost. Multivariable regression with robust variance was used to estimate the adjusted differences in the main outcome measures between patient groups. The models were adjusted for patient age, severity of injury, and pathological features seen on head CT scan at admission.
On average, patients who underwent ICP/PbO(2) monitoring were younger and had more severe injuries than patients who received ICP monitoring alone. Relatively more patients treated with PbO(2) monitoring received osmotic therapy, vasopressors, and prolonged sedation. After adjustment for baseline characteristics, the Hospital mortality rate was, if anything, slightly higher in patients undergoing PbO(2)-guided management than in patients monitored with ICP only (Risk adjusted mortality rate difference 4.4%, 95% CI -3.9 to 13%). Patients who underwent PbO(2)-guided management also had lower adjusted functional independence scores at hospital discharge (adjusted score difference -0.75, 95% CI -1.41 to -0.09). There was a 27% relative increase (95% CI 6-53%) in the median hospital length of stay when the PbO(2) group was compared with the ICP-only group.
The mortality rate in patients with traumatic brain injury whose clinical management was guided by PbO(2) monitoring was not reduced in comparison with that in patients who received ICP monitoring alone. Brain tissue oxygen monitoring was associated with worse neurological outcome and increased hospital resource utilization 5).
One of the main causes of secondary cerebral injury is cerebral hypoxia, basically of ischemic origin. However, cerebral tissue oxygenation depends on multiple physiological variables and cerebral hypoxia may be caused by an alteration of any one of them.
Although several methods of continuous cerebral oxygenation monitoring of neurocritical patients have been developed, direct and continuous measurement of the oxygen pressure in the cerebral tissue (PbtO2) has been a reality in the handling of the neurocritical patients over recent years. This technique is highlighted by its reliability and value of the information that it provides. This present article presents a review of the most outstanding aspects of the PtiO2 monitoring and proposes a protocol for the interpretation of this monitoring technique. This algorithm attempts to facilitate the identification of the different types of different cerebral hypoxia and of the correct therapeutic choice in the complex decision making process in neurocritical patients at risk of cerebral hypoxia 6).
Recent advances in brain tissue monitoring in the intensive care unit and operating room have made it possible to continuously measure tissue oxygen tension and temperature, as well as certain aspects of brain metabolism and neurochemistry. Therefore, it is important to understand the physiological process and the pathophysiology produced by these events. This is Part I of a two-part review that analyzes the physiology of cerebral oxygenation and metabolism as well as some of the pathological mechanisms involved in ischemic and traumatic brain injuries. Brain tissue monitoring techniques will be examined in the second article of this two-part series. To understand cerebral oxygenation, it is important to understand cerebral blood flow, energy production, ischemia, acidosis, generation of reactive oxygen species, and mitochondrial failure. These issues provide the basis of knowledge regarding brain bioenergetics and are important topics to understand when developing new approaches to patient care 7).
Avalanche patients who are completely buried but still able to breathe are exposed to hypothermia, hypoxia and hypercapnia (triple H syndrome). Little is known about how these pathologic changes affect brain physiology. A study aimed to investigate the effect of hypothermia, hypoxia and hypercapnia on brain oxygenation and systemic and cerebral haemodynamics. Anaesthetised pigs were surface-cooled to 28°C. Inspiratory oxygen (FiO2) was reduced to17% and hypercapnia induced. Haemodynamic parameters and blood gas values were monitored. Cerebral measurements included cerebral perfusion pressure (CPP), brain tissue oxygen tension (PbtO2), cerebral venous oxygen saturation (ScvO2) and regional cerebral oxygenation saturation (rSO2). Tests were interrupted when haemodynamic instability occurred or 60 min after hypercapnia induction. ANOVA for repeated measures was used to compare values across phases. There was no clinically relevant reduction in cerebral oxygenation (PbtO2, ScvO2, rSO2) during hypothermia and initial FiO2 reduction. Hypercapnia was associated with an increase in pulmonary resistance followed by a decrease in cardiac output and CPP, resulting in haemodynamic instability and cerebral desaturation (decrease in PbtO2, ScvO2, rSO2). Hypercapnia may be the main cause of cardiovascular instability, which seems to be the major trigger for a decrease in cerebral oxygenation in triple H syndrome despite severe hypothermia 8).
Placement
In order to monitor tissue oxygenation in patients with acute neurological disorders, probes for measurement of brain tissue oxygen tension (pbtO2) are often placed non-specifically in a right frontal lobe location. To improve the value of ptO2 monitoring, placement of the probe into a specific area of interest is desirable. Häni et al presented a technique using CT-guidance to place the pbtO2 probe in a particular area of interest based on the individual patient's pathology.
In this retrospective cohort study, they analyzed imaging and clinical data from all patients who underwent CT-guided ptO2 probe placement between October 2017 and April 2019. Primary endpoint was successful placement of the probe in a particular area of interest rated by two independent reviewers. Secondary outcomes were complications from probe insertion, clinical consequences from ptO2 measurements, clinical outcome according to the modified Rankin Scale (mRS) as well as development of ischemia on follow-up imaging. A historical control group was selected from patients who underwent conventional ptO2 probe placement between January 2010 and October 2017.
Eleven patients had 16 CT-guided probes inserted. In 15 (93.75%) probes, both raters agreed on the correct placement in the area of interest. Each probe triggered on average 0.48 diagnostic or therapeutic adjustments per day. Only one infarction within the vascular territory of a probe was found on follow-up imaging. Eight out of eleven patients (72.73%) reached a good outcome (mRS ≤ 3). In comparison, conventionally placed probes triggered less diagnostic and therapeutic adjustment per day (p = 0.007). Outcome was worse in the control group (p = 0.024).
CT-guided probe insertion is a reliable and easy technique to place a pbtO2 probe in a particular area of interest in patients with potentially reduced cerebral oxygen supply. By adjusting treatment aggressively according to this individualized monitoring data, clinical outcome may improve 9).