Articles: brain-injuries.
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Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. ⋯ Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.
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Eighteen examinations of acute head trauma have been performed using computerized tomography (CT), EMI scanner, before and after operation in our department since September, 1975. Diagnostic findings in CT before emergency operations of 5 cases including epidural hematoma (1), subdural hematoma (2), intracerebral hematoma (1), and combined hematoma (1) were presented and the diagnostic value of this new method was compared with that of cerebral angiography. CT was proved to be highly valuable in the diagnosis of not only intracranial hematomas but also cerebral edema, cerebral contusion and other abnormalities of the brain structures in head injury.
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Acta Anaesthesiol Scand · Jan 1977
Comparative StudyThe cerebrovascular CO2 reactivity during the acute phase of brain injury.
Using the intra-arterial 133xenon (133Xe) method, the cerebrovascular response to acute Paco2 reduction was studied in 26 unconscious, brain-injured patients subjected to controlled ventilation. The CO2 reactivity was calculated as delta in CBF/delta Paco2. The perfusion pressure was defined as the difference between mean arterial pressure and mean intraventricular pressure. ⋯ An increase of the CO2 reactivity with time was observed, indicating normal response after 1-2 weeks. Chronic hypocapnia in six unconscious patients resulted in sustained CSF pH adaptation. The question whether a delay in CSF pH adapation exerts an influence on the CO2 reactivity, and the influence of cerebral lactacidosis on the CO2 response are discussed.