Cerebral perfusion pressure and brain ischaemia: can one size fit all?
Critical Care volume 9, Article number: 638 (2005)
Current recommendations regarding the management of patients after traumatic brain injury include reduction in brain tissue pressure (i.e. intracranial pressure) and maintenance of an adequate arterial pressure; these measures combined should result in cerebral perfusion pressure sufficient to achieve adequate oxygen delivery. After almost 20 years of observational studies comparing cerebral perfusion pressure and indices of cerebral oxygenation, it is apparent that there is no single value for cerebral perfusion pressure that, if achieved, will provide adequate cerebral oxygen delivery in all patients. Traumatic brain injury remains a common problem, and this should encourage researchers and clinicians to design better and adequately powered trials of monitors and associated interventions.
In this issue of Critical Care, Marin-Caballas and coworkers  investigate the relationship between cerebral perfusion pressure (CPP) and brain tissue oxygen tension (PtiO2). Identifying the optimal CPP following traumatic brain injury (TBI) is as crucial to best care for this vulnerable patient population as determining what is the best parameter (with acceptable sensitivity and specificity) for detecting impending brain ischaemia.
Marin-Caballas and coworkers investigated the relationship between CPP and PtiO2 using an observational study design. The patients enrolled had suffered varying degrees of diffuse axonal injury, and six of the 22 patients underwent surgical evacuation of a mass lesion. Observation is always a good place to start exploring a research question when little is known about the subject. However, there are many data already available on PtiO2 monitoring after TBI, and the relationship between PtiO2 and physiological variables has been extensively investigated [2, 3]. A randomized controlled trial could have been performed, because there is equipoise among clinicians and guideline authors as to what is the optimal CPP, and this might have allowed standardization of other patient parameters. It is not possible to address the relationship between CPP and PtiO2 in only 22 patients, in whom spontaneous fluctuations in CPP (but mostly intracranial pressure [ICP]) were related to PtiO2 measurements. An important confounding factor in this observational study is the patient management protocol, which mandates that when a low PtiO2 is detected, all causes of this possible impending ischaemia should be corrected and CPP increased. Thus, low PtiO2 is likely to be associated with lower CPPs, and higher PtiO2 will be associated with higher CPPs solely because of the management protocol.
Although an impressive 1672 data points were recorded, these should have been analyzed per patient and summary data subsequently analyzed for all 22 patients combined or with all data presented for each individual participant. Many factors can influence PtiO2, and many of them are documented in Table 1 of the report by Marin-Caballas and coworkers. There appears to have been little physiological stability in the patient cohort, making any interpretation of the relationship between CPP and PtiO2 impossible; for instance, the core temperature ranged between 31°C and 39°C [4, 5], ICP between 0 mmHg and 69 mmHg [6, 7], and haemoglobin between 6.7 g/dl and 14 g/dl. With large fluctuations in ICP documented and relative arterial pressure stability described, the authors might have considered looking at the relationship between ICP and PtiO2 rather than that between CPP and PtiO2.
This commentary may appear somewhat critical, but it is worth emphasizing the potential for successful intervention to prevent critical reductions in PtiO2, and Marin-Caballas and coworkers describe a protocol with the potential to achieve this aim. Mixenberger and colleagues  showed that, in patients who had suffered TBI, low brain tissue oxygenation was associated with a worse outcome on neuropsychological testing, especially with respect to executive function and memory. These patients also exhibited reduced ability to work compared with their preinjury level. These data suggest that there is possible predictive value of brain tissue oxygen for global functional recovery after head injury.
No clinical index will improve outcome on its own. The data generated by clinical indices must be incorporated into treatment protocols, which require development adhering to evidence-based medicine guidelines and then tested in a rigorous way. To date there has been no adequately powered intervention study (powered for outcome ) in TBI with which to modulate a monitored physiological variable that is closely associated with outcome, with outcome assessed as the primary end-point.
Current recommendations regarding the management of patients after traumatic brain injury include reduction in brain tissue pressure (i.e. ICP) and maintenance of an adequate arterial pressure; these measures combined should result in CPP sufficient to achieve adequate oxygen delivery. After almost 20 years of observational studies comparing CPP and indices of cerebral oxygenation, it is apparent that there is no single value for CPP that, if achieved, will provide adequate cerebral oxygen delivery in all patients. Thus, in order to minimize exposure to the risks associated with CPP interventions and to maximize benefit, clinicians must measure or assess cerebral oxygen delivery. PtiO2 can provide this information and allows titration of ICP and mean arterial pressure interventions to a directly measured endpoint and not a surrogate (i.e. ICP/CPP). TBI remains a common problem, and this should encourage us to design better and adequately powered trials of monitors and their associated interventions.
cerebral perfusion pressure
brain tissue oxygen tension
raumatic brain injury.
Marín-Caballos AJ, Murillo-Cabezas F, Cayuela-Domínguez A, Domínguez-Roldán JM, Rincón-Ferrari MD, Valencia-Anguita J, Flores-Cordero JM, Muñoz-Sánchez MA: Cerebral perfusion pressure and risk of brain hypoxia in severe head injury: a prospective observational study. Crit Care 2005, 9: R670-R676. 10.1186/cc3822
Stevens WJ: Multimodal monitoring: head injury management using SjvO2 and LICOX. J Neurosci Nursing 2004, 36: 332-339.
Coles JP: Regional ischemia after head injury. Curr Opin Crit Care 2004, 10: 120-125. 10.1097/00075198-200404000-00008
Andrews P: Effect of hypothermia on brain tissue oxygenation in patients with severe head injury. Br J Anaesth 2003, 90: 251-252. 10.1093/bja/aeg517
Gupta AK, Al Rawi PG, Hutchinson PJ, Kirkpatrick PJ: Effect of hypothermia on brain tissue oxygenation in patients with severe head injury. Br J Anaesth 2002, 88: 188-192. 10.1093/bja/88.2.188
Kiening KL, Schoening WN, Stover JF, Unterberg AW: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO2. Br J Neurosurg 2003, 17: 311-318. 10.1080/02688690310001601199
Lang EW, Czosnyka M, Mehdorn HM: Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain injury. Crit Care Med 2003, 31: 267-271. 10.1097/00003246-200301000-00042
Meixensberger J, Renner C, Simanowski R, Schmidtke A, Dings J, Roosen K: Influence of cerebral oxygenation following severe head injury on neuropsychological testing. Neurol Res 2004, 26: 414-417. 10.1179/016164104225014094
Contant CF, Valadka AB, Gopinath SP, Hannay HJ, Robertson CS: Adult respiratory distress syndrome: a complication of induced hypertension after severe head injury. J Neurosurg 2001, 95: 560-568.
The author(s) declare that they have no competing interests.
About this article
Cite this article
Andrews, P.J. Cerebral perfusion pressure and brain ischaemia: can one size fit all?. Crit Care 9, 638 (2005). https://doi.org/10.1186/cc3922
- Traumatic Brain Injury
- Cerebral Perfusion Pressure
- Diffuse Axonal Injury
- Tissue Oxygen Tension
- Brain Tissue Oxygen