Ischaemia

Oxygen Secondary ischaemic damage has been shown, time and again, after TBI. Therefore a monitor that provides an early warning of impending ischaemia should offer promise. However, increasingly we believe that the pathophysiological process that leads to neuronal death is mitochondria failure. This will not be detected by any monitor of the adequacy of global oxygen delivery (jugular bulb oxygen saturation Sjvo2) or regional brain tissue oxygen tension (Ptio2).64 There are data to show a relationship between both these variables and outcome in a small number of patients but both lack sensitivity and specificity.

Cerebral blood flow Measurements of CBF, regional (PET, Xe133, MRI-PWI) or global (Kety Schmidt), cannot predict what level of oxygen delivery is required to meet metabolic demand and, sadly, PET lacks the refinement of double labelling and flow and metabolism cannot be simultaneously recorded. There is increasing evidence that metabolic requirements for oxygen are extremely low after TBI and previously recognised thresholds may not equate with neuronal damage after TBI. Hyperglycolysis may be an example of mitochondria adapting to failure of oxidative metabolism.

Intermediate metabolites Intermediate metabolites of oxidative metabolism can be assessed by brain microdialysis fluid, chemical shift imaging (CSI-MRS), and sampling of the jugular venous blood. Glucose, lactate, pyruvate, their ratio, and byproducts of membrane breakdown (glycerol) have all been assessed, and phenomenology that supports current thinking has been reported.

There are few randomised trials that have compared therapy to treat therapeutic goals generated by such monitors. Robertson et al. conducted a pilot study in which patients were block randomised to be treated according to an Sjvo2 endpoint or an ICP threshold. The result was a trend to more favourable outcomes and less intractable ICP problems in the ICP treatment cohort.65

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