Brain Tissue Oxygen Tension Monitoring Research Articles

Brain tissue oxygen tension monitoring for traumatic brain injury: limitations and alternatives

Brain tissue oxygen tension monitoring for traumatic brain injury: limitations and alternatives

Role of Bedside Multimodality Monitoring in the Detection of Cerebral Vasospasm Following Subarachnoid Hemorrhage.

Detection of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) in patients with a poor clinical exam is challenging. Brain tissue oxygen tension monitoring (PbtO2) and cerebral microdialysis (CMD) can detect ischemia and metabolic derangements. Our aim was to evaluate efficacy of these modalities in real-time detection of DCI. All patients with aSAH who underwent with multimodality monitoring (MMM) with PbtO2 and/or CMD between the years of 2013 and 2015 at our institution were retrospectively studied. Mean PbTO2, lactate to pyruvate ratio (LPR), and glucose over the 24-h period prior to each angiogram for evaluation and treatment of vasospasm were correlated to the extent of vasospasm observed in the hemisphere with the monitors. The average measurements were also compared in the setting of presence and absence of angiographically significant vasospasm. A total of ten patients with aSAH who underwent MMM were identified. PbtO2 decline correlates with severity of proximal vasospasm (r=-0.66). PbtO2 was significantly lower in the setting of vasospasm (17.6 vs. 25.8, p=0.003), but LPR (34.5 vs. 26.8, p=0.1) and glucose (0.8 vs. 1.1, p=0.6) were not significantly different. Proximal vasospasm after aSAH is associated with MMM indicator of tissue ischemia and/or metabolic derangement. PbtO2 and CMD help in real-time detection and management of DCI.

Adjustable and Rigid Fixation of Brain Tissue Oxygenation Probe (Licox) in Neurosurgery: From Bench to Bedside

Multimodal neuromonitoring has become a fundamental part of management for many neurosurgical disorders such as subarachnoid hemorrhage and severe traumatic brain injury. 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, typically using bolts is disadvantageous due to massive metal artifact. Similarly, subcutaneous tunneling is often problematic as suture fixation can loosen over time. We hereby report a new method of fixation of the Licox brain tissue oxygenation probe with 1 or 2 3-way taps that are attached to a standard plastic cannula, resulting in a stable connection with no need for further direct sutures around the probe and above all with no metal artifacts, which negates magnetic resonance imaging. The extended fixation system was first tested with cardiopulmonary resuscitation in a brain injured porcine model. It was thereafter adopted in our daily clinical practice.

Changing trends in monitoring brain ischemia

Cerebral ischemia forms the pathophysiological basis of several acute neurological conditions. Successful management of these conditions depends on early and accurate identification of ischemia and prompt treatment. Several techniques of assessing ischemia have evolved over decades. But their importance in the management of neurological patients remains ambiguous. Current trends in monitoring cerebral ischemia follow two pathways: (1) Indirect methods of assessing global and regional cerebral perfusion [intracranial pressure/cerebral perfusion pressure (ICP/CPP), transcranial Doppler]; and (2) Assessment of adequacy of cerebral blood flow (CBF) at tissue level by monitoring global or regional oxygenation and metabolism (SjvO2, rSO2, PbtO2, microdialysis).Traditional approach to ICP/CPP monitoring has changed to more complex analysis of the ICP waveform to derive variables related to cerebral perfusion and vascular reactivity. Noninvasive techniques of cerebral perfusion pressure assessment are under investigation. Newer methods are being explored to derive indices of CBF autoregulation from various modalities of cerebral monitoring. Direct brain tissue oxygen tension monitoring and microdialysis facilitate regional monitoring of oxidative metabolism. However, there seems to be some complexity in interpreting the results from these monitors. A wide range of options are available for monitoring adequacy of regional and global CBF. But no single monitor per se fulfils the requirements of all clinical situations. Impact of these monitors on clinical outcomes is equivocal. Also, at present, many of these monitors are invasive and not cost-effective.

Fluid Balance, Complications, and Brain Tissue Oxygen Tension Monitoring Following Severe Traumatic Brain Injury

Refractory intracranial hypertension (RIH) frequently complicates severe traumatic brain injury (TBI) and is associated with worse outcomes. Aggressive fluid resuscitation contributes to the development of peripheral and pulmonary edema, but an effect on cerebral edema is not well established. Some clinicians, including advocates of the "Lund Concept", practice fluid restriction as a means of limiting cerebral edema and reducing intracranial pressure (ICP). We performed a retrospective cohort study involving 41 consecutive patients with severe TBI to assess the association between fluid balance and the development of RIH or pulmonary complications. There was no difference in cumulative fluid balance between patients who did, or did not, develop RIH. Patients in the tertile with the largest fluid balance were no more likely to develop RIH than those in the more restrictive groups (HR 1.05, 0.78-1.42, P = 0.73). In contrast, there was a strong association between fluid balance and the development of bilateral pulmonary infiltrates, which persisted even after adjusting for Glasgow Coma Scale and Injury Severity Score (HR 1.69, 1.40-2.04, P < 0.0001). The use of P(bt)O(2) monitors to guide therapy was associated with higher cumulative fluid balance, more vasopressor use, and the development of both pulmonary edema and RIH. We found no association between cumulative fluid balance and the development of RIH. However, more judicious volume management has the potential to reduce the occurrence of pulmonary complications. Further research is needed to clarify optimal approaches to fluid management among patients with severe TBI and to guide the interpretation and integration of information derived from P(bt)O(2) monitors.

The effect of blood transfusion on brain oxygenation in children with severe traumatic brain injury*

The indications for blood transfusion in traumatic brain injury are controversial. In particular, little is known about the effect of blood transfusion in childhood traumatic brain injury. This study aimed to examine the influence of blood transfusion on brain tissue oxygen tension in children with severe traumatic brain injury. A retrospective analysis of a prospective observational database of children with severe traumatic brain injury who received brain tissue oxygen tension monitoring and a blood transfusion. University-affiliated pediatric hospital. Children with severe traumatic brain injury and blood transfusion. None. Brain tissue oxygen tension was measured in normal-appearing white matter with a commercially available polarographic Clarke-type electrode. Brain tissue oxygen tension values after blood transfusion were compared with pre-transfusion values in hemodynamically stable patients. Limited interventions were allowed during the studied period. Brain tissue oxygen tension values were examined for early (1-4 hrs) and late (24 hrs) changes after blood transfusion, controlling for multiple clinical and physiologic variables with regression techniques. Further comparison was made with matched non-transfused controls to examine the influence of time after injury. Nineteen blood transfusions in 17 patients were evaluated. Brain tissue oxygen tension increased significantly in the early period after blood transfusion (p = .0018; 79% increased, 21% decreased) in comparison with baseline values and matched controls, but the overall changes were small and, in part, influenced by accompanying cerebral perfusion pressure changes. Also, this effect was limited to the early period after blood transfusion and was not significant after 24 hrs. In general, the brain tissue oxygen tension increase was larger in patients with higher baseline brain tissue oxygen tension and lower initial hemoglobin; however, no factors associated with the magnitude of the brain tissue oxygen tension change were significant in multivariate analysis. Increased age of blood did not appear to impair brain tissue oxygen tension changes, but most blood transfusion were <14 days old. Brain tissue oxygen tension increased transiently in 79% of blood transfusion in pediatric traumatic brain injury patients, and decreased transiently in 21%. Brain tissue oxygen tension returned to baseline within 24 hrs. Reliable predictors of this brain tissue oxygen tension response to blood transfusion, however, remain elusive.

Brain tissue oxygen tension monitoring in pediatric severe traumatic brain injury

Intracranial pressure (ICP) monitoring and cerebral perfusion pressure (CPP) management are the current standards to guide care of severe traumatic brain injury (TBI). However, brain hypoxia and secondary brain injury can occur despite optimal ICP and CPP. In this study, we used brain tissue oxygen tension (PbtO(2)) monitoring to examine the association between multiple patient factors, including PbtO(2), and outcome in pediatric severe TBI. In this prospective observational study, 52 children (less than 15 years) with severe TBI were managed with continuous PbtO(2) and ICP monitoring. The relationships between outcome [Glasgow Outcome Score (GOS) and Pediatric Cerebral Performance Category Scale] and clinical, radiologic, treatment, and physiological variables, including PbtO(2), were examined using multiple logistic regression analysis. Outcome was favorable in 40 patients (77%) and unfavorable (mortality, 9.6%; n = 5) in 12 (23%). In univariate analysis, the following variables had a significant association with unfavorable outcome: initial GCS, computed tomography classification, ICP(peak), mICP(24), mICP, CPP(low), CPP(<40), pupil reactivity, PbtO(2)(low), PbtO(2) < 5 mmHg, PbtO(2) < 10 mmHg, mPbtO(2)(24), and time-severity product. PbtO(2) parameters had the strongest independent association with poor outcome in multiple regression analysis. In particular, when PbtO(2) was <5 mmHg for >1 h, the adjusted OR for poor outcome was 27.4 (95% confidence interval, 1.9-391). No variables apart from PbtO(2) were independently associated with mortality when controlled for PbtO(2). Reduced PbtO(2) is shown to be an independent factor associated with poor outcome in pediatric severe TBI in the largest study to date. It appears to have a stronger association with outcome than conventionally evaluated measures.

Brain tissue oxygen tension monitoring in pediatric severe traumatic brain injury

Brain tissue oxygen tension (PbtO(2)) monitoring is used increasingly in adult severe traumatic brain injury (TBI) management. Several factors are known to influence PbtO(2) in adults, but the variables that affect PbtO(2) in pediatric TBI are not well described. This study examines the relationships between PbtO(2) and (1) physiological markers of potential secondary insults commonly used in pediatric TBI, in particular intracranial pressure (ICP), cerebral perfusion pressure (CPP), and systemic hypoxia, and (2) other clinical factors and treatment received that may influence PbtO(2). In this prospective observational study, 52 children (mean age, 6.5 +/- 3.4 years; range, 9 months to 14 years old) with severe TBI and a median post-resuscitation Glasgow Coma Score (GCS) of 5 were managed with continuous PbtO(2) monitoring. The relationships between PbtO(2) parameters (Pbt)(2)(low), PbtO(2) < 5, PbtO(2) < 10, and mPbtAO(2)(24)) and clinical, physiological, and treatment factors were explored using time-linked data and Spearman's correlation coefficients. No clinical, physiological, or treatment variable was significantly associated with all PbtO(2) parameters, but individual associations were found with initial GCS (PbtO(2) < 5, p = 0.0113), admission Pediatric Trauma Score (PbtO(2) < 10, 0.0175), mICP > 20 (mPbtO(2)(24), p = 0.0377), CPP(low) (PbtO(2)(low), p = 0.0065), CPP < 40 (PbtO(2)(low), p = 0.0269; PbtO(2) < 5, p = 0.0212), P(a)O(2) < 60 (mPbtO(2)(24), p = 0.0037), S(a)O(2) < 90 (PbtO(2)(low), p = 0.0438), and use of inotropes during ICU care (PbtO(2)(low), p = 0.0276; PbtO(2) < 10, p = 0.0277; p = mPbtO(2)(24)). Delivery of oxygen to the brain is important to limit secondary neuronal injury after severe TBI. Our data show that PbtO(2) is poorly predicted by clinical and physiological factors commonly measured in the pediatric ICU. Multimodality monitoring may be needed to detect all secondary cerebral insults in pediatric TBI.

Future of Brain Support: Multimodality Monitoring

Multimodality monitoring of cerebral physiology encompasses the application of different monitoring techniques and integration of several measured physiological and biochemical variables into the assessment of brain metabolism, structure, perfusion and oxygenation status, in addition to clinical evaluation. Novel monitoring techniques include transcranial Doppler ultrasonography, neuroimaging, intracranial pressure, cerebral perfusion and cerebral blood flow monitors, brain tissue oxygen tension monitoring, microdialysis, evoked potentials and continuous electroencephalography. Multimodality monitoring enables the immediate detection and prevention of acute neurological events, as well as appropriate intervention based on a patient’s individual disease state in the neurocritical care unit. Simultaneous real-time analysis of cerebral physiological, metabolic and cardiovascular parameters has broadened knowledge regarding complex brain pathophysiology and cerebral hemodynamics. Integration of this information allows for a more precise diagnosis and optimization of management of patients with brain injury.

Multimodal Brain Monitoring in the Neurological Intensive Care Unit: Where Does Continuous EEG Fit In?

Continuous EEG (cEEG) is a vital component of patient monitoring in the neurologic intensive care unit, allowing the intensivist to diagnose nonconvulsive seizure activity. Though still in its infancy, Fourier-transformed cEEG data are also increasingly being used in ICUs to monitor global cerebral activity and cortical function. In conjunction with other components of multimodality neurologic monitoring, including intracranial pressure, cerebral blood flow, brain tissue oxygen tension monitoring, transcranial Doppler, and microdialysis monitoring, cEEG provides unique data regarding the electrical activity of the brain. The main challenge for clinicians and researchers will be to understand how these different aspects of multimodality monitoring relate to each other, and how physiologic variables such as blood pressure, osmolality, and temperature can be manipulated to optimize cerebral function and tissue survival in the setting of acute injury.

Multimodal Monitoring in the Neurological Intensive Care Unit

Neurocritical care is a specialty that focuses on the critical care management of patients with catastrophic neurologic diseases. Brain ischemia and hypoxia are often central causes of brain damage in these patients. Until recently, the only methods widely accepted for monitoring in the neurological intensive care unit have been intracranial pressure and cerebral perfusion pressure monitoring. Recent developments in technology have resulted in several new monitoring techniques that can provide the neurointensivist with information, at the cellular level, that can help guide management. The brain requires a continuous blood-borne supply of oxygen and glucose for normal metabolism. Ischemia occurs when supply is insufficient to meet the metabolic demand. Cerebral blood flow can now be directly monitored using laser Doppler or thermal diffusion techniques. Transcranial cerebral oximetry can estimate regional cerebral oxygen saturation, although the reliability is questionable. Jugular bulb oximetry can provide a global assessment of oxygen delivery, and consumption and brain tissue oxygen tension monitoring can provide a focal measurement of cerebral oxygenation. Intracerebral microdialysis can provide information about glucose metabolism and the overall health of the neuron. New monitoring techniques can provide the neurointensivist with crucial information about brain physiology and metabolism. Combining these techniques ("multimodal monitoring") can produce a more accurate overall picture. This approach, along with new computer systems for integrating data at the bedside, may change the way patients with brain injury are monitored and treated in the future.