Subarachnoid Hemorrhage—Factors in Prognosis and Management

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Aconsiderable diversity of opinion exists concerning the management of subarachnoid hemorrhage and of its principal cause, ruptured intracranial aneurysms. Moreover, that the controversy transcends disciplinary boundaries is illustrated by the conclusions of McKissock et al.33–35 that“the untreated appear to fare as well as those operated upon” and that “there can be no proof of the value of surgical treatment in this condition.”33 Benson3 concluded that if those patients who terminate fatally in the early danger period are excluded, “conservatively treated aneurysms and surgically treated aneurysms have nearly the same prognosis.” Yet

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    Angiograms made on patient C.Q. showed diffuse angiospasm (A, B and C) of vessels filling or draining an aneurysm of the antsrior communicating artery (arrows). Injection made on the opposite side (D) revealed absence of spasm in visualized vessels which did not communicate with the aneurysm.

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    The carotid angiograms on patient W.C. in the upper pair of photographs (A and B) show advanced vasospasm bilaterally in association with an aneurysm in the anterior communicating artery. The angiograms shown in the lower pair of photographs (C and D) indicate complete resolution of the spasm as the result of 5 weeks of conservative therapy.

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    Angiograms on patients P.H. (A and B) and L.S. (C and D) showed diffuse angiospasm in the vascular tree (A and C) ipsilateral to aneurysms (arrows). Injection of the opposite side made during same procedure (B and D) displayed normal vasculature contralateral to the lesions.

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    Angiograms on patients W.A. (A and B) and G.S. (C and D) displayed severe angiospasm (A and C) of all intracranial arteries both above and below the circle of Willis ipsilateral to the aneurysms (arrows). Contralateral vasculature appeared normal.

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    The graph plots highest recordings of systolic pressure of patient E.B. during the entire course of his illness. Bleedings occurred shortly after admission, on the 20th day and again on the 35th day of hospitalization. On each occasion, the blood pressure rose precipitously, but returned to normal levels, where it remained, upon recovery of the patient.

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    The graph shows observed fatality rates of patients exhibiting various combinations of symptoms found to influence prognosis: cerebral vasospasm; increased lumbar puncture pressure and hypertension. Numbers in the left margin indicate numbers of cases and stippled bars indicate observed mortality rates in each subgroup. Ninety per cent confidence bands are shown for each rate except one where the sample size was too small for accurate comparison. An increase in fatality rate is clearly evident when spasm is present.



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