The "open-brain injury" caused by skull fracture-induced disruption of the dura will be addressed separately (see Chap. 8, pp. 151 ff). A more common result of skull fracture is hemorrhage into the epidu-ral and/or subdural spaces. Such bleeding itself can lead to intracranial displacement of the brain, generally laterally and/or caudally with consequent direct injury of the cerebral parenchyma and (secondary) herniation syndromes (see Sect. 7.3.3) as demonstrated in Figs. 7.7, 7.8.
Dural hemorrhages can be induced by both contact and non-contact loading. An isolated dural hemorrhage resulting from external mechanical force is not invariably accompanied by additional direct injury of the brain, especially if the hemorrhagic source is not cortical. Although most patients exhib-
it neurological deficits as symptoms of accompanying subarachnoid or cortical hemorrhages, in some instances of mechanical injury there are no apparent clinical, i.e., neurological, symptoms of any kind. Epidural hemorrhages in particular are unlikely to be accompanied by foci of cortical bleeding. If there is a gradual displacement of the brain caused by space-occupying bleeding, secondary clinical symptoms will be delayed, i.e., occur after a symptom-free (lucid) interval, the length of the delay depending on the rate and amount of bleeding. Morphological changes in the brain itself are mainly due to its displacement and compression and are associated with clouding of consciousness and/or hemiparesis.
The findings of microscopic examination of the hematomas are greatly dependent on survival time (see below): signs of coagulation appear first, followed by evidence of a blood cell reaction, and resorption and/or organization (see below). Subdural hemorrhages (SDHs) in particular are likely to involve intradural bleeding but do not involve a complete breach of the dura, as evidenced on histological examination.
Morphologically (and clinically) significant lesions of the brain are secondary in nature and characterized by damage to the brain parenchyma. The sharp edges of the dura mater may cause lacerations if the brain is pressed against them. Two types of influence may cause the brain to be pressed against the dura mater:
1. Acceleration forces may press the brain against the dura, causing cutting or bruising of the brain (median part of the hippocampal area, corpus callosum).
2. A hemorrhage as well as an edema-induced increase in brain volume may force the brain against the dura, resulting in herniation of brain tissue with consequent structural distortion, stretching, and compression injuries (see Sect. 7.3.3 on secondary lesions).
Often - especially after rotational acceleration - a hemorrhage is found in the white matter of the first frontal lobe gyrus, i.e., a so-called gliding contusion injury (see below). Moreover axonal injury can almost always be demonstrated in cases with survival times of >2-3 h (Oehmichen et al. 1997), most frequently in both the corpus callosum and the rostral portion of the brain stem as an indication of diffuse axonal injury (DAI) (Graham and Gennarelli 1987).
Examination of the alcohol concentration (AC) in the dura hematomas in comparison with the peripheral blood will be of special diagnostic value. The AC will give evidence of the time course of the bleeding process and the dying process as demonstrated in Fig. 7.9. In this special case a contact mechanism caused an epidural and subdural hemorrhage. While the blood alcohol concentration (BAC) was 0.05%o at the time of death, the concentration in the SDH was 0.42% and in the epidural hematoma (EDH) 1.00%. These differences give evidence of the velocity of bleeding and some information on the duration of the agony.
The outcome in EDH and SDH was found to be predominantly influenced by the preoperative state of consciousness, associated brain lesions, and, in comatose patients, the duration of the time interval between onset of coma and surgical decompression. When this interval exceeded 2 h, mortality from SDH rose from 47 to 80% (good outcomes 32 and 4%, respectively). In acute EDH an interval under 2 h led to 17% mortality and 67% of good recoveries compared to 65% mortality and 13% of good recoveries after an interval of more than 2 h (Haselsberger et al. 1988).
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