Articles: brain-injuries.
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Five patients with traumatic pneumocephalus are reported. A case with traumatic ventricular and subarachnoidal pneumocephalus resulting from damage to the sphenoidal sinus is described. Treatment of traumatic pneumocephalus is nonoperative is nonoperative in most cases.
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Because of the large numbers of head injuries, physicians are frequently called upon to evaluate and initiate treatment in these acute emergencies. Deterioration of such patients results from direct injury to the brain tissue and a subsequent increase in the intracranial pressure. The pathophysiology of brain injury is manifested in a cycle of detrimental events with increased tissue damage and progressive neurological deficit. Current concepts in management of head injuries aimed at interrupting this cycle of events are discussed in detail.
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Journal of neurosurgery · Apr 1979
Detailed monitoring of the effects of mannitol following experimental head injury.
The experimental model of a cerebral missile injury developed by Crockard was used in three groups of Rhesus monkeys treated with mannitol. One group received mannitol 15 minutes after being injured with a BB pellet at 90 m/sec impact. Another group was wounded identically, but mannitol treatment was delayed until 1 hour after injury. ⋯ The data were contrasted with the results from the original model. After receiving mannitol, all groups showed marked improvement in mean blood pressure, cerebral perfusion pressure, cerebral blood flow, and cerebral metabolic rate of oxygen consumption out of proportion to the degree of reduction in intracranial pressure (ICP). The authors conclude that the therapeutic value of mannitol may, in some injuries, be directly related to its effects on blood flow and metabolism, as well as to its better known effects upon ICP.
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The release of tissue thromboplastin after a severe brain injury can lead to a consumption coagulopathy. In a group of 83 patients with severe brain injury, platelet count, fibrinogen, prothrombin, partial thromboplastin time and thrombin time were investigated. The pathological laboratory findings in 14 were compatible with a consumption coagulopathy. These alterations were demonstrated during the first hours following trauma and represented an extra handicap for the patients who had to be treated surgically.