Identification of posttraumatic ischemia and hyperperfusion by determination of the effect of induced arterial hypertension on carbon dioxide reactivity.

Abstract

Both ischemia and hyperperfusion are known phenomena that follow traumatic brain injury. Cerebral carbon dioxide reactivity is diminished in both conditions. Differentiation is important because ischemia is thought to be a major factor of secondary neuronal loss and is potentially amenable to therapy by manipulation of cerebral perfusion pressure. The response of transcranial Doppler-based carbon dioxide reactivity to pharmacologically induced hypertension was studied sequentially in 29 patients with severe to moderate head injury to identify ischemia and luxury perfusion. After simultaneous baseline registration of the carbon dioxide reactivity of both middle cerebral arteries by two-channel transcranial Doppler, systolic arterial pressure was raised approximately 20 mm Hg by means of phenylephrine (Neosynephrine) infusion, and the carbon dioxide reactivity test was repeated. A significant improvement of impaired (< 2%/mm Hg) carbon dioxide reactivity after arterial pressure was raised by 20 mm Hg (signaling ischemia) was found in 32 of 124 evaluated middle cerebral arteries. Further deterioration of impaired reactivity occurred in only four tested hemispheres. While ischemic conditions were identified during the entire study period, hyperperfusion was encountered only after day 3. Ischemia after traumatic brain injury is a frequent phenomenon, whereas hyperperfusion is rare. Whether therapeutic optimization of carbon dioxide reactivity can improve the outcome of head-injury patients needs to be evaluated in further studies.