Pathology and Differential Diagnosis
SAH have three main localizations (Courville 1962):
1. Diffuse basilar SAH
2. Diffuse dorsolateral SAH
3. Focal (localized anywhere) SAH
Although dorsolateral and localized SAH are usually a supplementary finding, they can provide information on the biomechanics of the traumatic event(s) that can be valuable in its reconstruction. Basilar SAH with massive bleeding in the large basal cisterns, and possibly spilling over into the ventricular system (also retrograde), are usually fatal.
The morphology of basilar SAH is said to be crucial for distinguishing between a mechanically induced hemorrhage and a spontaneous aneurysmal hemorrhage (Avdeef 1974; Krauland 1982). The morphology holds the key to whether an intact artery or an altered vessel, i.e., a preexisting aneurysm, could have ruptured as a result of impact. In cases of presumed mechanical loading, the large basal arteries should be carefully prepared. To ensure disclosure of vessel tears, the arterial vessels must be dissected using a microscope or magnifying glass at autopsy (and not on the formalin-fixed brain). In 8-27% of cases of spontaneous rupture an aneurysm cannot be demonstrated (Lange-Cosack 1966; Krauland 1982), making accurate reconstruction of the traumatic event indispensable for determination of the cause.
As already stated, a preexisting aneurysm has to be excluded even in apparent cases of mechanical loading. Other types of preexisting vessel disease or damage to the vessel should also be ruled out. Thus, for example, a hyalinosis, amyloidosis, arteritis and an idiopathic cystic medial necrosis need to be excluded before any inferences can be made regarding the external event. By demonstrating hemosidero-phages (Fe-containing macrophages), microscopic examination can confirm the occurrence of repeated hemorrhages. It must also be ascertained whether the mechanical impact was of sufficient violence to cause the SAH.
In an investigation of 31 cases of mechanically induced SAH of the large basal arteries not involving aneurysms, 27 from the literature (for a more recent review see Bunai et al. 2000), Krauland (1982) found the large majority to be located in the area of the basilar artery and the vertebral arteries. Of the 250 cases of ruptured aneurysm examined by Freytag (1966), a traumatic event was associated with the acute hemorrhage and was considered to have caused the rupture in 16 cases (6.4%). But cortical hemorrhages were discovered in none of the cases. Richardson and Hyland (1941) found a mechanical loading to be the cause of the rupture in only 2 of 108 cases they investigated.
The following relationships between mechanical injury and aneurysms were described by Newbarr and Courville (1958) for their own material:
1. A preexisting aneurysm that did not rupture despite severe impact (n=1)
2. A preexisting aneurysm that ruptured immediately upon impact(n=6)
3. A preexisting aneurysm that ruptured some time after impact (n=9)
In contrast several recent investigations give no evidence of a causal relationship between mechanical loading and rupture of an aneurysm (Asari and Ohmoto 1993; Rinkel et al. 1998; Cummings et al. 2000; Juvela et al. 2000). These authors suggest that the hemorrhage of the ruptured aneurysm will cause an impact, e.g., by spontaneous breakdown.
The cytological response to SAH is comparable with the morphology mentioned in association with dural hemorrhages (p. 135), but the timetable is different (see Oehmichen 1976, 1990): leukocytes in the subarachnoid space will increase within 1 h, macrophages will be seen within 7-15 h, erythrocyte-con-taining macrophages are observed after 17 h, and siderin-containing macrophages are not described before 72 h. The time dependence of a mesenchymal reaction is not evaluated.
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