IDENTIFICATION OF POSTTRAUMATIC ISCHEMIA AND HYPERPERFUSION BY DETERMINATION OF THE EFFECT OF INDUCED ARTERIAL-HYPERTENSION ON CARBON-DIOXIDE REACTIVITY

Background and Purpose Both ischemia and hyperperfusion are known phen omena that follow traumatic brain injury. Cerebral carbon dioxide reac tivity 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 cerebr al perfusion pressure. Methods The response of transcranial Doppler-ba sed carbon dioxide reactivity to pharmacologically induced hypertensio n 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 arteri al pressure was raised approximately 20 mm HE by means of phenylephrin e (Neosynephrine) infusion, and the carbon dioxide reactivity test was repeated. Results A significant improvement of impaired (<2%/mm Hg) c arbon dioxide reactivity after arterial pressure was raised by 20 mm H g (signaling ischemia) was found in 32 of 124 evaluated middle cerebra l arteries. Further deterioration of impaired reactivity occurred in o nly four tested hemispheres. While ischemic conditions were identified during the entire study period, hyperperfusion was encountered only a fter day 3. Conclusions Ischemia after traumatic brain injury is a fre quent phenomenon, whereas hyperperfusion is rare. Whether therapeutic optimization of carbon dioxide reactivity can improve the outcome of h ead-injury patients needs to be evaluated in further studies.