Aneurysmal subarachnoid hemorrhage

Autoregulatory responses are known to be impaired following acute subarachnoid hemorrhage, and hypovolemia and hypotension are poorly tolerated. Disturbances of fluid and electrolyte balance, in the form of cerebral salt wasting, the syndrome of inappropriate ADH secretion, or diabetes insipidus, are also common. Therefore adequate hydration, careful volume assessment including central venous pressure measurement, and maintenance of a normal mean arterial pressure (80-100 mmHg) are mandatory following acute subarachnoid hemorrhage. Specific hemodynamic management following aneurysmal subarachnoid hemorrhage is governed by whether vasospasm is present, whether the aneurysm has been clipped, and the hemodynamic response to nimodipine therapy ( Fig 2).

Fig. 2 Flowchart for hemodynamic management in aneurysmal subarachnoid hemorrhage: CVP, central venous pressure; SBP, systolic blood pressure; Hct, hematocrit; PAWP, pulmonary artery wedge pressure; CI, cardiac index.

*Triple-H therapy should be used with caution in the presence of myocardial ischemia or established cerebral infarction, and may need to be withdrawn if fluid overload results in pulmonary edema.

Many patients with aneurysmal subarachnoid hemorrhage develop delayed neurological deficits, typically between 4 and 10 days following hemorrhage, often associated with angiographic evidence of vasospasm and reductions in cerebral blood flow. These delayed ischemic neurological deficits may be prevented or reduced by Ca2+-channel blockers such as nimodipine. Established delayed ischemic neurological deficits have been successfully treated with a combination of induced hypervolemia, hemodilution, and hypertension (triple-H therapy) ( M,c.G,r.a.t.h...§.L§L 1995). Hypervolemia is typically achieved by crystalloid and colloid loading to achieve central venous pressure levels of 8 to 12 mmHg, or pulmonary artery wedge pressure levels of 12 to 16 mmHg, and a hematocrit of 30 to 35 per cent. Depending on plasma sodium levels, either desmopressin or fludrocortisone can be used to assist volume loading by preventing diuresis while maintaining normal plasma sodium levels. Phlebotomy may be needed in addition to volume loading to achieve hematocrit targets in some polycythemic patients. Most reports describe systolic blood pressure targets of 160 to 240 mmHg, but hypertension may be titrated to reversal of delayed ischemic neurological deficits (which may not be immediate). Phenylephrine, norepinephrine, and dopamine have commonly been used as adjuncts to volume loading to achieve hypertension (occasionally along with atropine). Dobutamine has also been used to maintain a high cardiac index (approximately 5.0 l/m 2/min).

The presence of an unclipped recently ruptured aneurysm is a self-evident contraindication to aggressive triple-H therapy, and maintenance of a systolic blood pressure of 140 to 150 mmHg is more appropriate in such patients. Indeed, the ability to treat delayed ischemic neurological deficits effectively with triple-H therapy provides one major justification for early clipping in subarachnoid hemorrhage. Complications of aggressive triple-H therapy include pulmonary edema, myocardial ischemia and infarction, and, particularly in patients with an established low-density lesion on CT scanning, intracranial hemorrhage into an established infarction. Therefore special care is required in patients with myocardial ischemia, cardiac decompensation, or established cerebral infarction. Such patients, and those who fail triple-H therapy, are early candidates for balloon angioplasty or selective pharmacological vasodilatation of vasospastic lesions. The use of nimodipine, particularly by the intravenous route, can result in profound vasodilatation, but this response is inconsistent, and comprehensive hemodynamic monitoring is mandatory in these patients before norepinephrine or other vasopressors are employed ( Fig 2).

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