Initial Stabilization

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Patient's clinical condition must be carefully assessed and stabilized prior to diagnostic testing. If the patient is lethargic or agitated, management of the airway should be addressed first. During angiography, sedation is frequently used, which could lead to airway obstruction in lethargic patients. To facilitate a safe and rapid study for agitated patients, elective endotracheal intubation should be considered.

Generalized sympathetic activation with high catecholamine levels, as well as pain and anxiety, generally cause elevated blood pressure after SAH. Because hypertension is associated with aneurysmal rerupture, it requires prompt treatment; however, headache should be addressed first. Nimodipine, used routinely for prevention of vasospasm, and analgesics may be sufficient for blood pressure control in some patients, whereas others may require the administration of additional antihypertensive medications. The most widely employed agents are combined a-1 and P-blocker labetalol or other general P-blockers, none of which raises ICP.

In the presence of a mass lesion or elevated ICP, the use of vasodilators engenders concern, especially venous dilators, such as sodium nitroprusside, which can raise ICP to a significant degree (16). Debate is ongoing regarding the appropriateness of administering agents that are pure arterial dilators, e.g., hydralazine, nicardipine, and angiotensin-converting enzyme inhibitors; yet many centers routinely use them (17). One trial demonstrated an improved outcome after SAH with the use of high doses of P-blockers (18). A notable exception to vigorous management of hypertension is made when patients develop hydrocephalus with potentially higher ICP, in which case, elevated blood pressure helps to maintain adequate cerebral perfusion. Only after the treatment of hydrocephalus should hypertension be addressed.

Cardiac abnormalities are common in the first 24 to 48 hr following SAH, and they are almost always completely reversible. Electrocardiographic alterations, including tall-peaked T-waves ("cerebral T-waves"), QT segment prolongation, and ST segment elevation/depression, are frequent; they have been linked to excessive levels of circulating catecholamines (19). Cardiac enzymes may be elevated in up to one-third of patients and are variably associated with echocardiographic abnormalities. These disturbances may occur in the absence of coronary artery disease. Myocardial lesions (mainly contraction band necrosis) that have been reported in cases of SAH are pathologically distinct from ischemic lesions (20). Arrhythmias are frequently seen; however, life-threatening arrhythmias such as ventricular tachycardia have been only rarely noted (21). Cardiac wall motion abnormalities have also been detected in up to one-third of patients (22). In rare cases, a picture of a "stunned myocardium" develops, with severe pump

Table 3 Fisher Scale (Based on Initial CT Appearance and Quantification of Subarachnoid Blood)

Grade CT Description

1 No subarachnoid blood on CT

2 Broad diffusion of subarachnoid blood, no clots, and no layers of blood greater than 1 mm

3 Either localized blood clots in the subarachnoid space or layers of blood greater than 1 mm

4 Intraventricular and intracerebral blood present, in the absence of significant subarachnoid blood

Abbreviation: CT, computed tomography.

failure, poor cardiac output, pulmonary edema, and hypotension. The most important predictors of cardiac dysfunction are those that reflect the severity of the hemorrhage.

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