[Cerebral oxygen consumption and ischemia in traumatic brain injury]. / Consumo cerebrale di ossigeno e ischemia nel danno cerebrale traumatico.

AIM: Clinical and experimental studies have shown a reduction of cerebral blood flow (CBF) and metabolic alterations following traumatic brain injury (TBI). The incidence of ischemia and the meaning of post-traumatic metabolic alterations are still unclear. METHODS: Revision of CBF and metabolic changes following TBI based on the literature and on our clinical experience. RESULTS: Cerebral ischemia and metabolic alterations are part of the secondary insults/damage leading to an increased damage following TBI. Global ischemia occurs early following TBI as shown by CBF measurements and by greater values of arterio-jugular difference of oxygen (AJDO(2)) during the 1(st) 24 hours postinjury. Post-traumatic ischemia should be defined based on the relationships between CBF and on the metabolic requirements of the brain. Regional ischemia occurs more frequently than global ischemia as shown by regional monitoring of cerebral oxygenation. Following TBI there is a transient phase of increased glycolitic activity followed by a more prolonged phase of reduced metabolic rate of glucose (CMRglc) and oxygen (CMRO(2)). The extent of CMRO(2) reduction is a marker of injury severity and it is associated with unfavorable outcome. CONCLUSION: Cerebral ischemia occurs following TBI and should be defined based on CBF value and the metabolic needs of the brain. Global monitoring of cerebral oxygenation adequacy should be combined with regional monitoring. The meaning of high AJDO(2) values should be reconsidered: if they can highlights potential ischemia they are also showing a still living brain with a partially preserved oxygen extraction capability.

Head injury, subarachnoid hemorrhage and intracranial pressure monitoring in Italy.

BACKGROUND: Intracranial pressure monitoring is recommended for the management of severe head injury and is increasingly used during intensive care for other pathologies, such as subarachnoid hemorrhage. However, it is still not uniformly applied in different centers. The objectives of this paper are to summarize the frequency and the modalities of intracranial pressure (ICP) monitoring in different centers in Italy; to describe its use in traumatic brain injury (TBI) and in subarachnoid hemorrhage (SAH); and to identify areas for improvement. METHODS: The medical directors of either the neurosurgical department or the intensive care unit, or both, of every Italian neurosurgical center were personally interviewed. They answered specific questions about TBI and SAH patients admitted, and ICP monitoring used, in their units. Data were cleared of any obvious inconsistencies and entered in a database for analysis. All analyses were based simply on the data declared. FINDINGS: The clinical information was obtained from 9137 TBI cases, of whom 4240 severe, and 3151 SAH patients. Among the 106 participating centers, 15 did not use ICP monitoring at all. The remaining 91 had used 3293 ICP devices during the year 2001; 146 were used in tumor cases, 2009 in TBI, and 1138 in SAH. Twenty-two percent of TBI cases admitted to centers with ICP equipment were monitored. Restricting this analysis to severe cases, 47% of TBI with a GCS <8 had ICP. On average, 36% of SAH underwent ICP monitoring. The proportions of head injury and SAH cases who underwent ICP monitoring varied widely in the different centers. Dividing the country into three main areas (north, center and south), there were considerable differences both in the rate of admissions per million inhabitants and in the frequency of ICP monitoring. INTERPRETATION: ICP monitoring in Italy is used in most, but not all, centers. ICP is measured fairly extensively in head injury cases, but a significant proportion of SAH patients is monitored as well. There are substantial differences in the frequency of ICP monitoring in different parts of the country. The use of ICP for both these indications, and the rates of admission to specialized centers, could be improved.

[Brain vulnerability and its modulation]. / Vulnerabilità del cervello e suo adattamento.

Clinical and experimental studies revealed that the injured brain is highly vulnerable to a subsequent insult. Surfery of the literature pertinent to clinical and experimental traumatic brain injury (TBI) is made. Increased vulnerability of the traumatically injured brain to an additional sub lethal ischemic, hypoxic, excitotoxic, or mechanical insult has been clearly demonstrated. Compared to traumatic brain injury alone, the double insult paradigm dramatically increases the brain damage. Brain vulnerability following TBI can be explained by a reduced ability to compensate for a reduction of cerebral blood flow (CBF) and oxygen (O(2)) delivery to the brain or inability to meet an increased metabolic demand. In addition, there is a specific increased sensitivity to delayed insults induced by the first injury. Potential mechanisms of the increased sensitivity to a second insult might be related to post-traumatic gene expression alterations leading to changes in neurotransmitters release, density of receptors and reduced thresholds for activation of pathways leading to delayed cell death. The brain is vulnerable to repetitive injuries. Derangements of compensatory mechanisms are responsible, in part, for this vulnerability. Additional work is needed to better understand the molecular pathways leading to secondary damage and to find novel therapeutic strategies to modulate the brain response to TBI.