Subarachnoid Hemorrhage—Factors in Prognosis and Management

Abstract

CONSIDERABLE 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. ~-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. ''3a Benson ~ 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 many reports 1,1~176 have emphasized the poor outlook offered by conservative management, and the advocates of surgical therapy are many. 5,9,14Ag,2a,25,31,as,42,45' 5~ Among the proponents of surgical therapy, however, the relative merits of different therapeutic approaches are contested. Direct attack, 39,42,52 as in clipping 9 or reinforcement 5~ of the lesion, is recommended by some, while others prefer indirect measures, 2,6,s,~6,2s,29,46 such as ligation of the carotid artery in the neck or "trapping" procedures. The timing of surgical intervention also evokes controversy. 12Ag,22,3~ Norl~n and Olivecrona 39 concluded that direct attack upon the lesion or ligation of the carotid artery in the neck was extremely dangerous during the acute phase of the illness and advised delay of surgical intervention until after the third week of the acute illness; Pool 42 recommended that direct surgical attack should be carried out between the 7th and 9th day after the initial hemor

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

“…A retrospective review of the influence of rebleeding showed that it occurred less frequently in patients treated with antihypertensive medication, yet blood pressures were still higher in the treated group. 143 Alternately, rebleeding may be related to variations or changes in blood pressure rather than to absolute blood pressure 245 ; 1 report found an increase in blood pressure before rebleeding. 141 In a retrospective review of 179 patients admitted within 24 hours of SAH, 17% experienced rehemorrhage that was associated with a systolic blood pressure Ͼ150 mm Hg.…”

Are We Barking Up the Wrong Vessels?

“…Поскольку в 1950-е и 1960-е гг. в многочисленных клинических [13] и экспе-риментальных [14] исследованиях приводили данные о развитии спазма крупных артерий в течение 7-10 дней после первичного кровоизлияния, было высказа-но предположение, что этот спазм, встречающийся у 40-60% пациентов с САК, является основной при-чиной развития ишемического инсульта [15]. Однако на сегодняшний день при использовании стратегий по лечению отсроченного вазоспазма не удалось улуч-шить исход после САК, о чем свидетельствуют резуль-таты недавно опубликованного испытания Clazosentan to Overcome Neurological Ischemia and Infarct Occurring After Subarachnoid Hemorrhage (CONCIOUS-2) [16].…”

“…As more clinical 13 and experimental 14 studies reported the presence of large artery spasms occurring 7 to 10 days after the initial hemorrhage in the 1950s and 1960s, it was assumed that these spasms, which are present in 40% to 60% of SAH patients, were primarily responsible for the observed infarctions. 15 To date, however, no treatment strategy targeting delayed vasospasm was able to improve outcome after SAH as also evidenced by the recently published Clazosentan to Overcome Neurological Ischemia and Infarct Occurring After Subarachnoid Hemorrhage (CONCIOUS-2) trial. 16 These results suggest that posthemorrhagic ischemia is caused by mechanisms different from large artery spasms, a phenomenon which was the focus of most research efforts trying to understand the pathogenesis of SAH in the past decades.…”

20-HETE contributes to the acute fall in cerebral blood flow after subarachnoid hemorrhage in the rat

“…In humans, an early phase of cerebral vasospasm has been documented as early as 4 h after the onset of SAH (6,40), and this is associated with neurological deficits and a high mortality (4,7,34).…”