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Anesth Analg 1999;88:549
© 1999 International Anesthesia Research Society

NEUROSURGICAL ANESTHESIA

Measuring Brain Tissue Oxygenation Compared with Jugular Venous Oxygen Saturation for Monitoring Cerebral Oxygenation After Traumatic Brain Injury

Arun K. Gupta, FRCA*,{dagger}, Peter J Hutchinson, FRCS{ddagger}, Pippa Al-Rawi, BSc{ddagger}, Sanjeeva Gupta, FRCA*, Mike Swart, FRCA*, Peter J Kirkpatrick, FRCS{ddagger}, David K. Menon, PhD, FRCA*,{dagger}, and Avijit K Datta, MD, MRCP{dagger}

Departments of *Anesthesia, {dagger}Neurosciences Critical Care, and {ddagger}Neurosurgery, University of Cambridge, Addenbrooke’s Hospital, Cambridge, United Kingdom

Address correspondence and reprint requests to Dr. A. K. Gupta, MBBS, FRCA, Department of Anaesthesia, Level 4, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK. Address e-mail to akg01@ globalnet.co.uk.


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Jugular bulb oximetry is the most widely used method of monitoring cerebral oxygenation. More recently, measurement of brain tissue oxygenation has been reported in head-injured patients. We compared the changes in brain tissue oxygen partial pressure (PbO2) with changes in jugular venous oxygen saturation (SjvO2) in response to hyperventilation in areas of brain with and without focal pathology. Thirteen patients with severe head injuries were studied. A multiparameter sensor was inserted into areas of brain with focal pathology in five patients and outside areas of focal pathology in eight patients. A fiberoptic catheter was inserted into the right jugular bulb. Patients were hyperventilated in a stepwise manner from a PaCO2 of approximately 35 mm Hg to a PaCO2 of 22 mm Hg. There was no significant change in cerebral perfusion pressure or arterial partial pressure of oxygen with hyperventilation. In areas without focal pathology, there was a good correlation between changes in SjvO2 and PbO2 ({Delta}SjvO2 and {Delta}PbO2; r2 = 0.69, P < 0.0001). In areas with focal pathology, there was no correlation between {Delta}SjvO2 and {Delta}PbO2 (r2 =0.07, P = 0.23). In this study, we demonstrated that measurement of local tissue oxygenation can highlight focal differences in regional cerebral oxygenation that are disguised when measuring SjvO2. Thus, monitoring of PbO2 is a useful addition to multimodal monitoring of patients with traumatic head injury.

Implications: Brain oxygenation is currently monitored by using jugular bulb oximetry, which attracts a number of potential artifacts and may not reflect regional changes in oxygenation. We compared this method with measurement of brain tissue oxygenation using a multiparameter sensor inserted into brain tissue. The brain tissue monitor seemed to reflect regional brain oxygenation better than jugular bulb oximetry.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
After severe head injury, patients are at risk of developing secondary cerebral hypoxia and ischemia, which causes additional brain damage (1,2). These insults may occur more frequently than previously assumed and often go undetected (3). Both global and regional cerebral blood flow (CBF) and cerebral metabolism are disturbed during the first few hours and days after injury. This change in CBF is rarely uniform throughout the brain with evidence of profound reductions of flow in pericontusional areas (4). The regional heterogeneity of CBF and metabolism in the brain is now well recognized (5–7).

The primary therapeutic aim in severe head injury is directed at maintaining cerebral perfusion and avoiding tissue hypoxia. Continuous monitoring of jugular venous oxygen saturation (SjvO2) has become an accepted method of monitoring global cerebral oxygenation and metabolism, but it may be difficult to use for continuous monitoring in clinical practice. Catheters require constant care and frequent recalibration if artifactual data are to be excluded. More recently, sensors measuring brain tissue partial pressure of oxygen (PbO2), carbon dioxide (PbCO2), and brain pH have been used to measure regional changes in tissue oxygenation and may provide an alternative, less artifact-prone method of assessing cerebral oxygenation (8–11).

In the context of head injury, the use of tissue oxygen sensors is significantly different from SjvO2 monitoring with respect to one other important attribute. Whereas SjvO2 monitoring provides an assessment of global cerebral oxygenation and metabolism, tissue oxygen sensors reflect metabolic conditions in a much smaller area. Regional changes measured by these multiparameter sensors have the disadvantage that they may not reflect physiology across a metabolically heterogeneous brain. However, the limited field of view may be used to advantage. Careful placement of tissue sensors in structurally normal and abnormal areas may allow us to monitor metabolic conditions in targeted regions, thus providing spatially (and, hence, pathologically) resolved, on-line data concerning brain oxygenation and biochemistry.

The aim of this study was to measure PbO2 during graded hyperventilation in head-injured patients and to compare changes in PbO2 ({Delta}PbO2) with changes in SjvO2 ({Delta}SjvO2) in areas with and without focal pathology.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After local research ethics committee approval and with written consent from the patients’ next of kin, we studied 13 patients with severe head injuries. All patients were sedated with IV infusions of propofol (2–5 mg · kg-1 · h-1), fentanyl (2–3 µg · kg-1 · h-1) and paralyzed with atracurium (0.5–1.0 mg · kg-1 · h-1). After tracheal intubation, the lungs were mechanically ventilated.

Routine invasive monitoring of these patients included mean arterial pressure (MAP), central venous pressure (CVP), intracranial pressure (ICP), and SjvO2. Pulmonary artery catheters were inserted into those patients requiring inotropic support, those with preexisting cardiac disease, or those with significant myocardial contusion.

A multiparameter sensor (Paratrend 7TM, Diametrics Medical, High Wycombe, UK) was used to measure PbO2, PbCO2, brain pH, and temperature. This sensor, which is 0.5 mm in diameter, contains a miniature Clarke electrode for measuring PbO2, two fiberoptic elements to measure PbCO2 and pH, and a thermocouple to measure temperature. Although this sensor was originally designed for continuous arterial blood gases measurement, its use as a device for brain tissue measurement has been evaluated in animal models (8).

Before insertion, the sensor was calibrated with three precision gases. The first calibration gas contained 2% CO2 and 15% O2, the second contained 5% CO2 and 15% O2, and the third contained 10% CO2 and 15% O2. Two sensors were inserted into each patient. One was inserted through an 18-gauge cannula into a femoral artery for continuous blood gas analysis. The second was inserted into brain tissue through a modified Camino bolt, which was placed adjacent to the ICP monitoring bolt. Subsequent computed tomographic (CT) scans of the head identified whether the sensor was placed in an area of focal pathology (e.g., contusion) or in an area with no focal lesion.

Baseline readings were taken after a 30-min equilibration period. The arterial Paratrend 7TM sensor readings were verified with intermittent arterial blood gas estimations, and SjvO2 readings were calibrated with an aspirated sample before the protocol and again if there was a poor signal quality on the monitor or if artifact was suspected during the course of the protocol. A calibration sample was also taken at the end of the protocol. Patients were then hyperventilated in a stepwise manner by decreasing PaCO2 concentrations by 4-mm Hg increments, down to a level of 22 mm Hg. Readings were taken at each PaCO2 level after stabilization for 15 min. Hyperventilation was abandoned if SjvO2 decreased below 50%.

MAP, ICP, SjvO2, arterial blood gases, PbO2, PbCO2, brain pH, and temperature were measured. Cerebral perfusion pressure (CPP) was calculated by the relationship CPP = MAP - ICP. Signals were time averaged over 4 s, digitized, and collected on a laptop computer using specialized multimodality software (12). Data were analyzed using repeated-measures analysis of variance, and results were considered significant when P < 0.05. Correlation plots were obtained using a commercially available statistics package.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
We studied eight men and five women with a mean age of 50 yr (range 26–78 yr). All patients had Glasgow Coma Scale scores of <8 (median score 5). CT scans after insertion of monitors revealed that the Paratrend 7TM sensors were inserted into areas of focal pathology in five patients and into areas without focal pathology in eight patients. No complications were associated with insertion of the cerebral Paratrend 7TM. Intermittent blood gas analysis demonstrated accurate readings and long-term stability from the femoral artery Paratrend 7TM sensors.

Table 1 shows the variation of CPP and PaO2 at different levels of PaCO2. CPP was maintained at a mean of 81 mm Hg, and there were no significant or systematic changes in CPP or PaO2 with changes in PaCO2. Figure 1 shows representative CT scans of the sensor in "normal" brain (Figure 1a) and in an area of focal pathology (Figure 1b). There was no significant difference among PbO2 values at different PaCO2 levels (P = 0.4). The response of PbO2 to PaCO2 changes in the two groups revealed no significant change in PbO2 with hyperventilation in the areas without pathology (P > 0.49), or in regions with focal pathology (P = 0.12) (Figure 2).


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  		Table 1. Cerebral Perfusion Pressure (CPP) and PaO2 at Different Levels of PaCO2
 


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  		Figure 1. a, Computed tomographic scan of tissue sensor in area of no focal injury. b, Computed tomographic scan of tissue sensor in area of focal pathology (arrow denotes tip of sensor).

 


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  		Figure 2. Effect of decreasing PaCO2 on the change in tissue oxygen partial pressure ({Delta}PbO2) in the groups with focal pathology and with no focal pathology.

 
Although there was a trend for SjvO2 values to decrease with hyperventilation, these changes did not reach significance within the range of PaCO2 values studied (P = 0.19).

We compared changes in PbO2 and SjvO2 produced by hyperventilation. For all patients there was a poor correlation between {Delta}SjvO2 and {Delta}PbO2 (r2 = 0.274, P < 0.0001). However, there were clear differences in the {Delta}SjvO2/{Delta}PbO2 relationship in the two patient groups (Figures 3 and 4). There was little correlation between {Delta}SjvO2 and {Delta}PbO2 in the focal group (r2 = 0.07, P = 0.23), whereas there was a strong correlation between these variables in the nonfocal group (r2 = 0.69, P < 0.0001).



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  		Figure 3. Change in jugular venous oxygen saturation ({Delta}SjO2) plotted against change in tissue oxygen partial pressure ({Delta}PbO2) with the sensor in an area of focal pathology (r2 = 0.07, P = 0.23).

 


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  		Figure 4. Change in jugular venous oxygen saturation ({Delta}SjO2) plotted against change in tissue oxygen partial pressure ({Delta}PbO2) with the sensor not in an area of focal pathology (r2 = 0.69, P < 0.0001).

 

   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The findings of this study show that as PaCO2 decreases PbO2 does not change significantly. However, when the patients were separated by sensor site pathology, there was a gradual decrease in {Delta}PbO2 in the areas with no focal pathology, whereas there was an increase in {Delta}PbO2 in areas of focal pathology as PaCO2 decreased. The decrease in {Delta}PbO2 in areas without focal pathology concurs with findings of other investigators who used brain tissue probes during hyperventilation therapy (8,13–15). The increase in PbO2 in areas of focal pathology may reflect disturbed vascular reactivity in these areas. Indeed, Marion and Bouma (16) suggested that regional heterogeneity of CO2 vasoresponsivity is much more common than global estimates have suggested.

The limitations of SjvO2 monitoring are well recognized. Continuous SjvO2 monitoring has a number of technical difficulties, whereas intermittent sampling only gives a "snapshot" of the state of cerebral oxygenation. Aspiration of blood from the jugular bulb should ideally be representative of mixed cerebral blood. Stocchetti et al. (17). attempted to identify the most appropriate side for catheterization of the jugular bulb by simultaneously sampling both jugular veins. The variation between the two sides was insignificant; thus, neither side was shown to be more appropriate.

Our results suggest a further drawback of SjvO2 monitoring. The lack of correlation between changes in SjvO2 and PbO2 in regions of focal pathology implies that SjvO2 monitoring is poor at assessing the adequacy of oxygenation in areas that are most at risk from secondary physiological insults. These findings add weight to suggestions from Andrews et al. (18) and Chieregato et al. (19) that SjvO2 alone should not be relied on when assessing cerebral oxygenation in the brain injured patient. Indeed, Keining et al. (20) suggested that measurement of brain tissue PO2 is more suitable than SjvO2 in head-injured patients. Adverse changes in cerebral oxygenation in a head-injured patient detected by a brain tissue sensor but not identified by jugular venous bulb oximetry indicate that a normal SjvO2 does not guarantee against regional ischemia (21).

These data confirm regional heterogeneity in physiological responses between injured and noninjured brain. They also underline the value of targeted tissue PO2 monitoring for following such physiology. When the well-being of the noninjured brain is in question, the placement of a tissue PO2 sensor in noninjured areas can provide a method of monitoring cerebral oxygenation that may be more invasive, but that is more reliable and technically easier to maintain. Conversely, placement of probes in injured regions may allow the selective monitoring of tissue most at risk. These considerations may prompt the placement of multiple PO2 sensors in selected patients. Furthermore, the strong correlation between the recordings of changes in SjvO2 and PbO2 indicate that the tissue sensor reflects changes in tissue oxygenation in a wider compartment of brain tissue, rather than a smaller area resulting from local trauma due to probe insertion and disruption of the blood-brain barrier. The in vivo validation of the tissue sensor against a "gold standard" is presently underway.

In summary, in this study, we demonstrated a difference in the response of brain tissue oxygen with changes in PaCO2 in areas of brain with focal pathology compared with areas without focal pathology. Furthermore, changes in SjvO2 did not correlate with changes in PbO2 when patients’ data were pooled, which implies that measurement of brain tissue oxygenation may be a more sensitive measure of regional oxygenation than jugular bulb oxygen saturation.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Chestnut RM, Marshall SB, Piek J, et al. Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia after severe brain injury in the Traumatic Coma Data Bank. (Wien) 1993;59 (Suppl):121–5.
  2. Miller JD. Head injury and brain ischaemia: implications for therapy. Br J Anaesth 1985;57:120–30.[Free Full Text]
  3. Jones PA, Andrews PJD, Midgley S, et al. Measuring the burden of secondary insults in head injured patients during intensive care. J Neurosurg Anesthesiol 1994;6:4–14.[Web of Science][Medline]
  4. Bouma JG, Muizelaar JP. Cerebral blood flow in severe clinical head injury. New Horizons 1995;3:384–94.[Medline]
  5. Marion DW, Darby J, Yonas H. Acute regional cerebral blood flow changes caused by severe head injuries. J Neurosurg 1991;74:407–14.[Web of Science][Medline]
  6. Salvant JB, Muizelaar JP. Changes in cerebral blood flow and metabolism related to the presence of subdural hemotoma. Neurosurgery 1993;33:387–93.[Web of Science][Medline]
  7. Bergsneider M, Hovda DA, Shalmon E, et al. Cerebral hyperglycolysis after severe traumatic brain injury in humans: a positron emission tomography study. J Neurosurg 1997;86:241–51.[Web of Science][Medline]
  8. Zauner A, Bullock MR, Di X, Young HF. Brain oxygen CO2, pH, and temperature monitoring: evaluation in the feline brain. Neurosurgery 1995;37:1168–77.[Web of Science][Medline]
  9. Hoffman WE, Charbel FT, Edelman G, Ausman JI. Brain tissue acid-base response to hypercapnia in neurosurgical patients. Neurol Res 1995;17:417–20.[Web of Science][Medline]
  10. Zauner A, Doppenberg E, Woodward JJ, et al. Multiparametric continuous monitoring of brain metabolism and substrate delivery in neurosurgical patients. Neurol Res 1997;19:265–73.[Web of Science][Medline]
  11. Gupta AK, Gupta S, Al-Rawi P, et al. The effect of hyperventilation on brain tissue oxygen and CO2 in severely head injured patients measured by a new multiparameter sensor [abstract]. J Neurosurg Anesthesiol 1997;8:325.
  12. Czosnyka M, Whitehouse H, Smielewski P, et al. Computer supported multimodal bed-side monitoring for neuro intensive care. Monit Comput 1994;11:223–32.
  13. Meixensberger J, Dings J, Kuhnigk H, Roosen K. Studies of tissue pO2 in normal and pathological human brain cortex. Acta Neurochir (Wien) 1993;59:58–63.
  14. Maas AIR, Fleckenstein W, de Jong A, van Santbrink H. Monitoring cerebral oxygenation: experimental studies and preliminary clinical results of continuous monitoring of cerebrospinal fluid and brain tissue oxygen tension. (Wien) 1993;59:50–7.
  15. Van Santbrink H, Maas AIR, Avezaat CJJ. Continuous monitoring of partial pressure of brain tissue oxygen in patients with severe head injury. Neurosurgery 1996;38:21–31.[Web of Science][Medline]
  16. Marion DW, Bouma GJ. The use of stable xenon-enhanced computed tomographic studies of cerebral blood flow to define changes in cerebral carbon dioxide vasoresponsivity caused by a severe head injury. Neurosurgery 1991;29:869–73.[Web of Science][Medline]
  17. Stocchetti N, Paparella A, Bridelli F, et al. Cerebral venous oxygen saturation studied with bilateral samples in the internal jugular veins. Neurosurgery 1994;34:38–44.[Web of Science][Medline]
  18. Andrews PJD, Murugavel S, Deehan S. Conventional multimodality monitoring and failure to detect ischemic cerebral blood flow. J Neurosurg Anesthesiol 1996;8:220–6.[Web of Science][Medline]
  19. Chieregato A, Targa L, Zatelli R. Limitations of jugular bulb oxyhemoglobin saturation without intracranial pressure monitoring in subarachnoid hemorrhage. Anesthesiol 1996;8:21–5.
  20. Keining KL, Unterberg AW, Bardt TF, et al. Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 versus jugular vein oxygen saturation. J Neurosurg 1996;85:751–7.[Web of Science][Medline]
  21. Heath K, Gupta AK, Matta BF. Brain microprobe electrodes: a case for monitoring regional cerebral oxygenation in the severely head injured patient. J Neurosurg Anesthesiol 1998;10:22–4.[Web of Science][Medline]
Accepted for publication November 30, 1998.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 1999 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press