Clinical applications
A number of studies have investigated NIRS in patients with carotid occlusive disease. Vernieri and colleagues used NIRS to measure cerebral carbon dioxide reactivity and found differences between symptomatic and asymptomatic patients. Intraoperative NIRS during carotid endarterectomy demonstrated cerebral desat-uration in 50% of patients after internal carotid artery cross-clamping. Cerebral oxygen saturation has been found to correlate with transcranial Doppler blood flow, EEG and clinical evidence of ischaemia. Sensitivity and specificity vary between studies but may potentially be high: a drop in TOI >13% has been suggested as a threshold for ischaemia.
Use of NIRS to monitor patients with traumatic brain injury has shown similar changes with oxygen-ation status to other monitoring modalities. However, Kirkpatrick and colleagues showed that NIRS was able to detect 97% of cerebral hypoperfusion events compared with only 53% detected by jugular bulb oxim-etry. A small study has shown a correlation between TOI and CPP. Tissue saturation >75% was usual when CPP was > 70 mmHg. Conversely, TOI < 55% was typically associated with CPP < 70 mmHg.
The method of NIRS brain oximetry has been evaluated for preventing cerebral injury during cardiac surgery. he influence of hypothermia, alkalosis and the extracorporeal circulation on the NIRS algorithms is unclear. While episodes of cerebral desaturation correlate with poor neurological outcome, comparisons with SjO2 monitoring have yielded mixed results. his perhaps serves to emphasize that these approaches to cerebral oxygenation measurement are fundamentally distinct and consequently may respond differently in certain circumstances.
Extracerebral signal contamination, changes in the optical properties of injured tissue and the local nature of the technique are all limitations of NIRS as a mature monitoring technology. However, its completely non-invasive nature, portability, real-time temporal resolution and relatively low cost make the technique promising.
Brain tissue oxygen measurement
The flux of oxygen through the extracellular compartment arises from a concentration gradient that is maintained by a balance between supply at the capillaries and consumption within the cells. he average extracellular oxygen tension, therefore, reflects this source-sink equilibrium as well as the nature of the diffusion barrier. Direct measurement of brain tissue oxy-genation (PbrO2) at the bedside is now possible with microsensors introduced directly into the cerebral parenchyma either through a bolt or tunnelled from a craniotomy site.
Technology
The LICOX sensor is a miniature electrochemical sensor based on the Clark polarographic cell. It is contained in a flexible polyethylene microcatheter and has a diameter of <1 mm with a sensitive region approximately 5 mm in length. Oxygen from brain tissue within a few millimetres from the device diffuses into the sensor cell where it accepts electrons on a charged catalytic surface generating an electric current in proportion to the dissolved oxygen tension. Temperature compensation is achieved in the most recent generation of devices by means of an integral sensor, which also allows the instrument to display brain temperature. he device does not require calibration, but results may be unreliable for the first 2 h after insertion as a result of microtrauma in the region immediately adjacent to the surface of the sensor.
Of historical interest is the NeuroTrend monitor, which was able to simultaneously measure PbrO2 , PbrCO2 and brain tissue pH using a bundle of optical fibre sensors. While this monitor is no longer available commercially, a substantial body of research has previously been published using this technology. However, differences in probe geometry mean that absolute comparisons between LICOX and NeuroTrend PbrO2 measurements should be made with caution.
Clinical practice
In health, tissue oxygen tension varies considerably with position depending on local brain activation as well as neuronal and blood vessel density. Measurements are usually made from white matter, which has lower and more stable PbrO2 . Sensor site selection is not a clear-cut decision, particularly where brain injury is extensive or multifocal. With focal brain lesions, two approaches are common. Measurements made in the contralateral hemisphere (or in the less-injured hemisphere) attempt to characterize the oxygenation state of non-contused brain, and such values of PbrOt correlate well with SjOt measurements. Alternatively, the sensor may be placed in perilesional tissue in order to directly optimize oxygenation of this ‘at-risk’ tissue where PbrO2 is typically lower. Placement of the device within either infarcted tissue or a haematoma is clearly unhelpful.
Clinical experience to date with direct tissue oxygen sensors has mainly been accrued from patients either with severe traumatic brain injuries or undergoing cerebrovascular surgery. Measured values of PbrO2 are accurate to within about 10%, and values of around 22 mmHg are typical in health. his is much lower than the oxygen tension of arterial blood, reflecting the high metabolic requirements of cerebral tissue. hresholds for ischaemia are not yet clearly defined, but a PbrO2 of <8-10 mmHg seems to indicate a high risk of ischae-mia in patients with subarachnoid haemorrhage. Low values of PbrO2 t particularly if they are sustained, are associated with poor outcome after traumatic brain injury, and there is some evidence that brain tissue oxygen-directed therapy may improve outcome in such patients.
Similarly to jugular bulb oximetry and NIRS, measurements of PbrOt are expected to reflect supply-demand imbalances of oxygen. Comparison with positron emission tomography has demonstrated that changes in PbrO2 correlate well with changes in local venous oxygen tension. However, it is also observed that the absolute value of PbrO2 is consistently lower than local venous oxygen tension by an amount that varies from patient to patient. his is unsurprising as the sensor measures an average oxygen tension over a volume containing regions of oxygen supply, diffusion and consumption. For a given oxygen lux, the extracellular oxygen concentration may also be affected by tissue and endothelial oedema, which reduce the facility with which oxygen can diffuse across this barrier. hus, brain tissue oxygen measurements are sensitive to the properties of a tissue compartment to which NIRS and jugular bulb oximetry do not have access but which may be physiologically highly relevant.
In contrast to PbrO2, measured PbrCO2 (40-70 mmHg) is higher than that of the arterial blood, thus providing a concentration gradient favouring the elimination of this highly diffusible metabolic product. Brain tissue pH is typically in the range of 7.05-7.25, again predictably lower than that of arterial blood. hese parameters may have some prognostic significance. It seems that the risk of vasospasm is increased in patients with cerebrovascular disease if the pH is < 7.0 and PbrCO2 is > 60 mmHg. Mortality after severe traumatic brain injury is increased in tissue acidosis when the pH is below 7.0 (Figs 6.6 and 6.7).
Conclusions
The need to maintaining a cerebral oxygen supply sufficient for the metabolic requirements is axiomatic to strategies for cerebral protection. While there is an absence of prospective evidence, it is reasonable to assume that early detection of ischaemia may improve outcome by allowing targeted instigation of corrective therapy. he techniques described aim to provide such an early warning system.
Fig. 6.6. Demonstration that the correlation between changes in jugular venous oxygen saturation (ASjO2) and brain tissue oxygen pressure (APbO2) is dependent on the position of the sensor. There is good correlation when the sensor is in normal brain tissue (a) and poor correlation when the sensor is in an area of focal pathology (b).
Fig. 6.7. The effect of hyperventilation on brain tissue oxygenation in areas of focal pathology and with no pathology.
Fig. 6.8. Asummarydiagramshowing the currently available methods for cerebral oximetry. NIRS, near-infrared spectroscopy; PO2, oxygen pressure.
Although cumbersome and prone to artefact, jugular venous oximetry is the oldest technology and thus a natural benchmark against which to evaluate newer systems. However, it is prone to false positives and is a fundamentally global measure, which also limits its sensitivity. he techniques of NIRS and tissue oxygen measurement are more local probes, but there may be circumstances where this is not necessarily advantageous either: NIRS has a number of other very attractive features but is less well quantified and extracranial signal contamination is a limitation. Experience with brain tissue oxygenation microsensors is increasing and clearly these provide a very direct measurement of tissue metabolism, but their invasive nature precludes their use outside specialist neuroscience centres. To some extent, all these technologies are complementary because of the diversity in the principles and assumptions that underpin their operation. In view of all these strengths and limitations, it is the synthesis of data from multiple modalities that hopefully allows timely and targeted therapy (Fig. 6.8).
