Cerebral edema on CT. Diagnosis of hydrocephalus
Acute craniocerebral injury with CT. In addition, it manifests itself as a general or locala decrease in the density of the brain substance due to cerebral edema [New P. Scott W. 1975; Drayer W. 1979]. The density of the brain in the edema zone is 18 - 29 units. H. (normal brain density 29-36 units for white and 33-15 units I. for gray matter). When analyzing CT data, which was produced in patients admitted to the Institute of Neurosurgery, it was revealed that in 85% of patients acute trauma was accompanied by edema, characterized by wide limits of density reduction. In 71% of these patients, there was a zone with fairly clear boundaries (total edema) against a background of general edema. In these cases, the zone of local edema usually corresponded to a foci of bruising or hematoma. Only in white matter, edema was localized in 18% of patients, more often (82%) it spread to both white and gray matter of the brain.
A general CT scan of cerebral edema was a reduction or disappearance of the image of the ventricular system and subarachnoid fissures.
Depending on the prevalence the following types of edema are distinguished: 1) local, occupying a restricted area, more often adjacent to the main focus; 2) generalized, characterized by a large area of low density, against which there are areas of normal-density brain tissue; 3) total, exciting the greater part of the brain or even the entire brain; 4) periventricular, is manifested by low density zones in the brain regions around the anterior and posterior horns of the dilated lateral ventricles.
When comparing the degree manifestations edema in various age groups is established,that diffuse edema is detected in children 3 times more often than in adults. The peculiar dynamics of edema development was observed in children with severe craniocerebral trauma, long-term in coma. During the first 2 days, with obvious signs of severe intracranial hypertension (sharp narrowing of the ventricles, compression of the cisterns, absence of arachioidal gaps), there was an increase in white matter density, which allowed thinking about cerebral hypertension. On the 3rd day after the trauma, the severity of intracranial hypertension was further increased and the cerebrospinal fluid system was practically not determined, which indicated an increase in the degree of its compression. Simultaneously, the increased density of the cortex and white matter began to decrease, which indicated the replacement of the phase of hyperemia with the phase of cerebral edema. The ventricular system began to be determined only at the end of the 2nd pedal after the injury. At that time, all children still had signs of cerebral edema.
J. Bruce et al. consider that half of children develop edemaswelling associated with cerebral hyperemia. We believe that in children, cerebral hyperemia is the initial phase of brain edema development. In a control CT scan 2-3 months later, half of a child, who were in coma for a long time, showed a dropsy and signs of marked brain atrophy.
Should stay another complication - the development of acutehydrocephalus in the first days after a traumatic brain injury. A similar pathology was observed only in 2 patients with craniocerebral trauma: one was diagnosed with neo-oolpai (thickness up to 7-8 mm and an area of about 1500 mm2) subdural hematoma in the occipital region with extensive concomitant edema. the other - occlusion of the hematoma of the IV ventricle and the sylvace of the aqueduct. According to our data, this complication is rare (in 2 out of 11), 6 patients who were examined in an acute period).
Other researchers showed the development of hydrocephalus in the first days after injury much more often.