DOI: 10.1097/01.CCM.0000259172.19375.9F

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PMID: 17413800

Issn Print: 0090-3493

Publication Date: 2007/04/01


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Sleeping Beauty: A tale still with an uncertain happy ending after head trauma*

Nino Stocchetti

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Excerpt

Focal injuries are a mixture of blood, water, and damaged or necrotic tissue that evolves over time. When the volume of this mixture is >20–25 mL, the traditional approach was (and in some institutions still is) unhesitating surgical removal. The contused brain was, in fact, presumed to be dead, so that evacuation would only remove useless tissue. Unfortunately, when surgery is performed, it is impossible to precisely remove only “lost” brain.
In the field of cerebral ischemia, >20 yrs ago, the concept of penumbra was developed: at the border of infarcted tissue, where perfusion was low but not lethal, some cells could survive for some time (1). This tissue, which could be rescued by reperfusion, may be seen as Sleeping Beauty (2): restoration of perfusion could play the role of the Prince’s kiss, and the tale could have a happy ending, at least partially.
When this concept is extended to focal lesions in traumatic brain injury (TBI), a traumatic penumbra has been hypothesized. Although some of the contused tissue is irreversibly destroyed after trauma, other portions, usually peripheral to the core lesion, suffer damage of varying degree that is potentially reversible. In this scenario, the penumbra-like zones are not totally lost, and they deserve exploration and treatment.
Dr. Vespa and coworkers (3) report in this issue of Critical Care Medicine on the neurochemistry of pericontusional tissue with the specific objective of determining neurochemical responses to cerebral perfusion pressure (CPP) changes. They report that the lactate/pyruvate ratio (LPR) is frequently higher surrounding contusions and that this index did not show any relationship with CPP.
A state of metabolic distress is often encountered following TBI, supporting the first conclusion by Dr. Vespa and coworkers (3). In fact, their article also describes normal-appearing tissue that demonstrates profound alterations, with high values of LPR, presumably due to very low levels of pyruvate, since lactate was not markedly altered. The exact significance of such alterations is unclear, as discussed in the article, and does not necessarily imply ischemia. However, the second conclusion of this study, that metabolism appears altered for reasons independent of CPP, should not engender the mistaken conclusion that CPP is irrelevant for supporting cellular metabolism in pericontusional areas of the brain.
This study was conducted at a well-established institution where CPP was, fortunately, stringently preserved. CPP was, in fact, relatively high for the recommended standards (79 mm Hg average, whereas updated guidelines on TBI management recommend 60 mm Hg) (4) and fell below 60 mm Hg only during 7% of the total monitoring time. The study was not designed and powered to identify metabolic responses to CPP manipulations and was observational and not interventional (even if strenuous efforts to preserve CPP, and not to lower it, are very likely).
Was high CPP associated with better LPR? The data are not totally clear on this point, but it does not seem so. Other articles have shown that increased CPP can improve tissue oxygenation in areas of impaired perfusion (5, 6), but that does not automatically translate into improved neurochemistry (5). TBI associated with contusions likely causes a cascade of very complex metabolic alterations, which are not solely resolved by increasing CPP.
A subsequent question appears warranted: Is low CPP as good as normal CPP for the “suffering” brain? Here the data require careful examination. Even if an association between low CPP and metabolic worsening is not apparent, it does not prove that maintenance of low CPP is appropriate.
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