Articles: brain-injuries.
-
Morbidity and mortality are doubled when hemorrhagic hypotension (HEM) accompanies a traumatic brain injury (TBI). Hemorrhagic hypotension initiates a "secondary" injury (SI) that has been attributed to ischemia, but this has not been confirmed in the laboratory. All previous studies have been of relatively short duration (less than 6 hours), allowing insufficient time to study the pathophysiology of SI, since maximal intracranial pressure (ICP) elevations may occur 16 to 20 hours after injury. ⋯ Hemorrhagic hypotension following TBI produced a significant and sustained reduction in cO2del associated with a lower cMRO2 and cO2ER, and higher ICP and CWC, than seen with lesion alone. This occurred despite adequate early restoration of sO2del. This confirms that cerebral ischemia is ongoing despite restoration of systemic hemodynamics.
-
The recent finding that small variations in brain temperature can critically determine the extent of histopathological injury in animal models of brain injury has generated renewed interest in hypothermic brain protection. Whereas mild hypothermia protects the brain from ischemic and traumatic brain injury, mild hyperthermia worsens ischemic outcome. ⋯ The purpose of this article is to review and discuss recent findings demonstrating the importance of brain temperature in ischemic and traumatic brain injury. Potential mechanisms by which mild hypothermia may attenuate and mild hyperthermia accentuate the detrimental consequences of brain injury are reviewed.
-
Using transcranial doppler ultrasonography, cerebral blood flow velocity was measured daily from both middle cerebral arteries in 121 patients who had suffered minor (n = 55), moderate (n = 16), or severe (n = 50) brain injury. Serial computed tomographic scans were performed to identify noncontusion-related infarction (NCI). Cerebral perfusion pressure was monitored continuously in 41 patients who had severe head injury; of these, 22 had continuous measurement of arterial and jugular bulb venous oxygen (SJO2) saturation. ⋯ Four of the 23 patients with increased MFV developed NCI, as compared with none of the patients without elevated MFV (P = 0.015). All patients with NCI had suffered severe brain injury, had unilateral elevation of MFV in the terriory of the relevant cerebral vessel, and had received therapy to correct reduced cerebral perfusion pressure (P = 0.008). NCI did not occur in any patient with increased MFV that was associated with global hyperemia.
-
Critical care medicine · May 1992
Use of brainstem auditory-evoked response testing to assess neurologic outcome following near drowning in children.
To determine a correlation between serial brainstem auditory-evoked response measurements and ultimate neurologic outcome in pediatric patients who suffered a cardiac arrest resulting from a submersion accident. ⋯ Brainstem auditory-evoked response testing is useful as an aid in the assessment of neurologic outcome following submersion-induced cardiac arrest. However, standardization of brainstem auditory-evoked response testing and production of normative data are required before this modality can be more widely studied and applied.
-
Journal of neurosurgery · May 1992
Reduced cerebral blood flow, oxygen delivery, and electroencephalographic activity after traumatic brain injury and mild hemorrhage in cats.
The authors investigated the effects of transient, mild hemorrhagic hypotension after fluid-percussion traumatic brain injury on intracranial pressure, cerebral blood flow (CBF), cerebral oxygen delivery (CBF x arterial O2 content), and electroencephalographic (EEG) activity. Adult mongrel cats were anesthetized with 1.6% isoflurane in N2O:O2 (70:30) and prepared for trauma and for radioactive microsphere CBF measurement. Isoflurane concentration was decreased to 0.8%, and the cats were randomly assigned to one of four control groups or to an experimental group. ⋯ Following resuscitation from mild hemorrhage, mean arterial blood pressure, cardiac output, renal blood flow, and CBF were not significantly different from baseline; cardiac output and renal blood flow did not differ significantly from baseline 2 hours after Hetastarch resuscitation. Neither hemorrhage nor trauma alone produced significant decreases in CBF or in EEG activity, but trauma followed by hemorrhage and resuscitation produced significant (p less than 0.01) decreases in CBF, cerebral oxygen delivery, and EEG score. These data demonstrate that, following traumatic brain injury, even mild hemorrhagic hypotension is associated with significant deficits in cerebral oxygen availability and neurological function.