Articles: brain-injuries.
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The authors review acute and delayed traumatic intracerebral hemorrhages. Based on recent experimental and clinical data, these injuries' clinical presentation, pathologic characteristics, and treatment are discussed. A description of traumatic hemorrhage based on biomechanics is emphasized.
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Journal of neurotrauma · Mar 1992
ReviewCerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury.
Traumatic brain injury (TBI) often causes disturbances of the cerebrovascular circulation, which contribute to the infliction of secondary injury, although the complex nature of the mechanisms involved is not fully understood. First, the role of ischemia in TBI is still controversial. Despite experimental and pathologic data suggesting important interactions between ischemia and trauma, evidence for posttraumatic ischemia with CBF measurements in patients so far had eluded most investigators. ⋯ Impairment of cerebrovascular CO2 reactivity and autoregulation often occurs after TBI. Although no correlation with the severity of injury or outcome has been established, it is obvious that diminished adaptive responses of the cerebral vasculature render the brain more vulnerable to additional systemic insults, such as derangements of blood pressure, altered rheology, or hypoxia. The posttraumatic status of vascular reactivity and autoregulation also has important implications with regard to the treatment of high ICP, in particular for the use of hyperventilation and pharmacologic management of blood pressure, which are discussed in detail.
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Hounsfield's development of computed tomography (CT) in 1972 revolutionized the care of patients with acute craniocerebral trauma. CT evaluation facilitates early surgical and medical intervention and has significantly improved patient outcome. This review describes the role of CT in assessing acute head trauma. Despite the growing role of magnetic resonance imaging in the acute, subacute, and chronic phases of brain injury as well as in many other central nervous system disorders, CT retains its unique capacity to image acutely ill patients rapidly and accurately.
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Acute management involves triage, well directed investigation and timely surgical intervention when necessary. All are discussed in this review. Cerebral blood flow (CBF) and flow velocity assessment are among the other investigations mentioned. Other topics include paediatric head injury, cerebrospinal fluid (CSF) fistulae, stab wounds and post-traumatic epilepsy.
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We reviewed the records of 253 patients with head injury who required serial computed tomographic (CT) scans; 123 (48.6%) developed delayed brain injury as evidenced by new or progressive lesions after a CT scan. An abnormality in the prothrombin time, partial thromboplastin time, or platelet count at admission was present in 55% of the patients who showed evidence of delayed injury, and only 9% of those whose subsequent CT scans were unchanged or improved from the time of admission (P less than 0.001). Among patients developing delayed injury, mean prothrombin time at admission was significantly longer (14.6 vs. 12.6 s, P less than 0.001) and partial thromboplastin time was significantly longer (36.9 vs. 29.2 s, P less than 0.001) than patients who did not have delayed injury. ⋯ This risk rose to almost 85% if at least one clotting test at admission was abnormal (P less than 0.001). We conclude that clotting studies at admission are of value in predicting the occurrence of delayed injury. If coagulopathy is discovered in the patient with head injury early follow-up CT scanning is advocated to discover progressive and new intracranial lesions that are likely to occur.