Dynamic changes in regional CBF, intraventricular pressure, CSF pH and lactate levels during the acute phase of head injury

Abstract

The authors measured regional cerebral 133xenon (133Xe) blood flow (rCBF), intraventricular pressure (IVP), cerebrospinal fluid (CSF) pH and lactate, systemic arterial blood pressure (SAP), and arterial blood gases during the acute phase in 23 comatose patients with severe head injuries. The IVP was kept below 45 mm Hg. The rCBF was measured repeatedly, and the response to induced hypertension and hyperventilation was tested. Most patients had reduced rCBF. No correlation was found between average CBF and clinical condition, and neither global nor regional ischemia contributed significantly to the reduced brain function. No correlation was found between CBF and IVP or CBF and cerebral perfusion pressure (CPP). The CSF lactate was elevated significantly in patients with brain-stem lesions, but not in patients with "pure" cortical lesiosn. The 133Xe clearance curves from areas of severe cortical lesions had very fast initial components called tissue peaks. The tissue peak areas correlated with areas of early veins in the angiograms, indicating a state of relative hyperemia, referred to as tissue-peak hyperemia. Tissue-peak hyperemia was found in all patients with cortical laceration or severe contusion but not in patients with brain-stem lesions without such cortical lesions. The peaks increased in number during clinical deterioration and disappeared during improvement. They could be provoked by induced hypertension and disappeared during hyperventilation. The changes in the tissue-peak areas appeared to be related to the clinical course of the cortical lesion.

Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury

“…These elevated cerebral levels of lactate may contribute to brain acidosis after' trauma, which has been implicated by several authors as a causative factor in injury to the central nervous system [20,26,28,32,35,38]. Additionally, a correlation of CSF lactate levels to posttraumatic cerebral hyperaemia has been shown [3,12]. For others, however, brain acidosis is only an epiphenomenon associated with tissue injury [1,23,40].…”

Does an Increase in Cerebral Perfusion Pressure Always Mean a Better Oxygenated Brain? A Study in Head-Injured Patients

“…Some authors have suggested that to induce the physiological vasoconstrictory cascade, MABP should be increased above supranormallevels by inotropic support or by vasoactive drugs [9]. However, for many, autoregulation is a very sensitive property of the cerebrovascular bed that is impaired or abolished in many patients after severe head injury [5].…”

Chronic Trigeminal Ganglionectomy or Topical Capsaicin Application to Pial Vessels Attenuates Postocclusive Cortical Hyperemia but Does Not Influence Postischemic Hypoperfusion

“…Blood flow during reperfusion greatly exceeds tissue demands for ox ygen (Gourley and Heistad, 1984), and in the brain this may lead to hemorrhage or swelling, thereby exacerbating the ischemic insult (Reigel et aI., 1987;Batjer et aI., 1989;Powers and Smith, 1990). Hyper emia may also exacerbate cerebral edema accom panying acute head injury (Enevoldsen et al, 1976).…”