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  • Title: [A case of traumatic subacute subdural hematoma presenting symptoms arising from cerebral hemispheric edema].
    Author: Nishio M, Akagi K, Abekura M, Maeda Y, Matsumoto K.
    Journal: No Shinkei Geka; 1998 May; 26(5):425-9. PubMed ID: 9621356.
    Abstract:
    Traumatic subacute subdural hematoma is a condition in which the major symptoms affecting prognosis most appear in the subacute stage after head trauma, while traumatic acute subdural hematoma is treated conservatively when the symptoms are mild. The cause of the major symptoms occurring in the subacute stage is mostly expansion of the subdural hematoma volume. The authors report a case of traumatic subacute subdural hematoma in which the cause of the major symptoms was cerebral hemispheric edema instead of expansion of the subdural hematoma volume. To our knowledge, only one similar case to the present case has been previously reported. A 44-year-old female fell from the stairs on July 21, 1995 and was suffering from headache. On July 23, she was admitted to our hospital because of generalized convulsion. On admission, she was drowsy but showed no convulsion. Head CT showed an acute subdural hematoma on the right side with a slight midline shift and no other abnormalities. She was treated conservatively because of the mildness of the symptoms and two days later became alert with no symptoms. Thereafter she only complained of occasional headache which was controlled with medicine. On August 3, she suddenly fell into coma. Head CT showed severe cerebral hemispheric edema on the right side without change of the subdural hematoma size. Emergency cerebral angiography showed no definitive abnormalities such as occlusion of the arteries or of the venous sinuses. Craniotomy associated with external decompression was performed. The hematoma was composed of red-brown jelly accompanied with some liquid component and had a thin black-brown outer membrane. While removing the hematoma, bleeding from a vein on the cerebral surface around the sylvian fissure was observed and this location was suspected to be the sources of the bleeding point. Postoperatively, she received steroid and barbiturate therapy associated with moderate hypothermia under hyperventilation. She tolerated this treatment well and left the hospital, on September 26, 1995 with only diplopia during downward gaze. Although the mechanisms of the cerebral hemispheric edema occurring in the subacute stage was unclear, a failure in the cerebral venous circulation arising from compression to the bridging veins, which may be hypoplastic, by the subdural hematoma was suspected to have been the cause.
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