Acute regional cerebral blood flow changes caused by severe head injuries.

To evaluate the changes in cerebral blood flow (CBF) that occur immediately after head injury and the effects of different posttraumatic lesions on CBF, 61 CBF studies were obtained using the xenon-computerized tomography method in 32 severely head-injured adults (Glasgow Coma Scale score (GCS) less than or equal to 7). The measurements were made within 7 days after injury, 43% in the first 24 hours. During the 1st day, patients with an initial GCS score of 3 or 4 and no surgical mass had significantly lower flows than did those with a higher GCS score or mass lesions (p less than 0.05): in the first 1 to 4 hours, those without surgical mass lesions had a mean CBF of 27 cc/100 gm/min, which rose to 44 cc/100 gm/min by 24 hours. Patients without surgical mass lesions who died tended to have a lower global CBF than did those with better outcomes. Mass lesions were associated with a high global CBF and bihemispheric contusions with the lowest flows. By 24 hours after injury, global blood flow increased in groups that originally had low flows and decreased in those with very high initial flows, such that by 36 to 48 hours, most patients had CBF values between 32 and 55 cc/100 gm/min. Lobar, basal ganglion, and brain-stem blood flow values frequently differed by 25% or more from global averages. Brain-stem CBF varied the most but did not correlate with clinical signs of brain-stem dysfunction. Double studies were performed at two different pCO2 values in 10 patients with various posttraumatic lesions, and the CO2 vasoresponsivity was calculated. Abnormal CO2 vasoresponsivity was found with acute subdural hematomas and defuse cerebral swelling but not with epidural hematomas. In patients without surgical mass lesions, the findings suggest that CBF in the first few hours after injury is often low, followed by a hyperemic phase that peaks at 24 hours. Global CBF values vary widely depending on the type of traumatic brain injury, and brain-stem flow is often not accurately reflected by global CBF values. These findings underscore the need to define regional CBF abnormalities in victims of severe head injury if treatment is intended to prevent regional ischemia.

[1]  A A DeSalles,et al.  Cerebral blood flow and metabolism in severely head-injured children. Part 1: Relationship with GCS score, outcome, ICP, and PVI. , 1989, Journal of neurosurgery.

[2]  A. Marmarou,et al.  Effect of Prophylactic Hyperventilation on Outcome in Patients with Severe Head Injury , 1989 .

[3]  E. Enevoldsen,et al.  Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury. , 1978, Journal of neurosurgery.

[4]  W. Tweed,et al.  Cerebral circulation after head injury. Part 3: Does reduced regional cerebral blood flow determine recovery of brain function after blunt head injury? , 1981, Journal of neurosurgery.

[5]  T. Gennarelli,et al.  Relation of cerebral blood flow to neurological status and outcome in head-injured patients. , 1979, Journal of neurosurgery.

[6]  J. Blass,et al.  Cerebral blood flow decrements in chronic head injury syndrome , 1985, Biological Psychiatry.

[7]  T A Gennarelli,et al.  Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension. , 1984, Journal of neurosurgery.

[8]  R. Sarabia,et al.  Posttraumatic cerebral hemispheric swelling. Analysis of 55 cases studied with computerized tomography. , 1988, Journal of neurosurgery.

[9]  J. Holaday,et al.  Comparison of thyrotropin‐releasing hormone (TRH), naloxone, and dexamethasone treatments in experimental spinal injury , 1983, Neurology.

[10]  Progress in cerebrovascular disease: local cerebral blood flow by xenon enhanced CT. , 1982 .

[11]  L. Hayman,et al.  Local cerebral blood flow measured by CT after stable xenon inhalation. , 1980, AJR. American journal of roentgenology.

[12]  J. Osterholm,et al.  Altered norepinephrine metabolism, following experimental spinal cord injury. 2. Protection against traumatic spinal cord hemorrhagic necrosis by norepinephrine synthesis blockade with alpha methyl tyrosine. , 1972, Journal of neurosurgery.

[13]  D. Rottenberg,et al.  The effects of CT drift on xenon/CT measurement of regional cerebral blood flow. , 1984, Medical physics.

[14]  N. Lassen,et al.  The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. , 1966, Lancet.

[15]  J. Miller,et al.  Regional cerebral blood flow, intracranial pressure, and brain metabolism in comatose patients. , 1973, Journal of neurosurgery.

[16]  J. Adams,et al.  Ischaemic brain damage in fatal non-missile head injuries , 1978, Journal of the Neurological Sciences.

[17]  D. Gur,et al.  Adverse reactions to xenon-enhanced CT cerebral blood flow determination. , 1987, Radiology.

[18]  David Gur,et al.  In vivo mapping of local cerebral blood flow by xenon-enhanced computed tomography. , 1982, Science.

[19]  J. Jaggi,et al.  Relationship of early cerebral blood flow and metabolism to outcome in acute head injury. , 1990, Journal of neurosurgery.

[20]  Simultaneous mass spectrometry and thermoconductivity measurements of end-tidal xenon concentrations: a comparison. , 1984, Medical physics.

[21]  R. Grossman,et al.  Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatose patients. , 1989, Journal of neurosurgery.

[22]  J. Hodak,et al.  Local Basal Ganglia and Brain Stem Blood Flow in the Head Injured Patient Using Stable Xenon Enhanced CT Scanning , 1986 .

[23]  J. Miller,et al.  Head injury and brain ischaemia--implications for therapy. , 1985, British journal of anaesthesia.

[24]  J. Jaggi,et al.  Factors Relating to Intracranial Hypertension in Acute Head Injury , 1983 .

[25]  G. Murray,et al.  Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury. , 1985, Journal of neurosurgery.

[26]  D. Marion,et al.  Effect of Stable Xenon Inhalation on ICP in Head Injury , 1989 .

[27]  F. Gibbs,et al.  BILATERAL INTERNAL JUGULAR BLOOD , 1945 .

[28]  V. Haughton,et al.  Comparison of Single-Photon Emission Computed Tomography with [123I]Iodoamphetamine and Xenon-Enhanced Computed Tomography for Assessing Regional Cerebral Blood Flow , 1986, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[29]  G. Cold,et al.  The Effects of PaCO2 Reduction on Regional Cerebral Blood Flow in the Acute Phase of Brain Injury , 1977, Acta anaesthesiologica Scandinavica.

[30]  G. Cold,et al.  Dynamic changes in regional CBF, intraventricular pressure, CSF pH and lactate levels during the acute phase of head injury. , 1976, Journal of neurosurgery.

[31]  M. Rosner,et al.  Mechanical brain injury: the sympathoadrenal response. , 1984, Journal of neurosurgery.

[32]  E. Ryding,et al.  Cerebral blood flow, vasoreactivity, and oxygen consumption during barbiturate therapy in severe traumatic brain lesions. , 1988, Journal of neurosurgery.

[33]  M. Fehlings,et al.  The relationships among the severity of spinal cord injury, motor and somatosensory evoked potentials and spinal cord blood flow. , 1989, Electroencephalography and clinical neurophysiology.