By Keiji Sano M.D., D.M.Sc., F.A.C.S. (Hon.), Takao Asano M.D., D.M.Sc., Akira Tamura M.D., D.M.Sc. (auth.)
During contemporary years, significant advances in surgical concepts, diagnostic tools, anesthesia and adjunctive therapy within the care of sufferers with subarachnoid hemorrhage were completed. however, the general final result of sufferers with SAH can't be considered as passable. the 1st a part of the publication concentrates at the pathogenetic mechanisms underlying vasospasm and edema, the primary reasons of bad consequence. contemporary growth within the box of membrane lipid metabolism has allowed the matter to be approached from a completely new standpoint. the prospective participation of loose radicals, membrane lipids and eicosanoids is carefully mentioned. the second one half good points the issues of sensible administration of SAH sufferers. Timing and indication of surgical procedure of aneurysms and the surgical suggestions are defined in detail.
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Extra resources for Acute Aneurysm Surgery: Pathophysiology and Management
1981, Brandt et al. 1981 a, b, Sasaki et al. 1984), no close relationship between vasoconstrictor activity in postoperative CSF samples and the patient's clinical condition or angiographic vasospasm has been found (Boullin et al. 1981). Thirdly, in chamber studies using the rat stomach fundus (Boullin et al. 1981) or the canine basilar artery segment (Sasaki et al. 1984), the vasoconstrictive activity of the CSF obtained from SAH patients was not suppressed to any significant degree by cumulative addition of antagonists to serotonin, histamine, norepinephrine, epinephrine, and angiotensin acetylcholine, (Fig.
The Current Concept of Cerebral Vasospasm 1. The Time Course of Cerebral Vasospasm and Its Relation tc Neurological Deficits The pioneer observation of Kagstrom et al. (1966) that human vasospasm following SAH due to rupture of intracranial aneurysms is delayed in its onset has been supported by succeeding reports. Saito et al. (1977), by repeated angiograms at intervals of a few days, closely studied the time course of vasospasm and its relationship with neurological deficits in 96 consecutive cases of SAH due to aneurysmal rupture.
These findings together founded the clinical concept of cerebral vasospasm as described he low. Robertson (Robertson 1949) reported that focal necrosis can occur in SAH at sites remote from the aneurysmal lesion, without an obvious reason like intracerebral hemorrhage or arterial thrombosis. To explain such a finding, he postulated cerebral vasospasm. This hypothesis was soon supported by the angiographical demonstration of cerebral vasospasm by Ecker and Riemenschneider (1951}, and succeeding autopsy reports (Tomlinson 1959, Birse and Tom 1960, Smith 1963, Crompton 1964 a, b).