Cerebral Vasospasm After Subarachnoid Hemorrhage Treatment & Management

Updated: Jul 10, 2016
  • Author: William W Ashley, Jr, MD, PhD, MBA; Chief Editor: Brian H Kopell, MD  more...
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Medical Care

Although there is a paucity of class A evidence regarding prevention and treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), a number of therapeutic strategies have been studied and found to have varying degress of utility. [11]

Of the management options currently used, the hemodynamic augmentation strategy known as triple H therapy, which includes hypertension, hemodilution, and hypervolemia, has been an important component. This approach is intended to improve cerebral perfusion by increasing mean arterial pressure (MAP) and reducing blood viscosity. [23]

One study found that approximately 70% of patients with vasospasm experienced improvement in their symptoms after initiation of triple H therapy. [24] It must be kept in mind, however, that triple H therapy can have significant complications, such as pulmonary edema and subsequent hypoxemia, which may be detrimental to an at-risk hypoperfused brain. A 2000 study by Lennihan et al found that hypervolemic therapy had no significant advantage over normovolemic therapy with respect to cerebral blood flow after subarachnoid hemorrhage and that the two therapies yielded similar incidences of symptomatic vasospasm. [25]

Increases in MAP alone have been shown to be beneficial to patients with vasospasm, and a number of medications have been investigated and utilized to achieve this goal. [26] Phenylephrine, norepinephrine, and dopamine are the primary pressors employed in this setting. [27, 28] Phenylephrine appears to have the most evidence to support its use; several trials have suggested that is effective in patients with preserved left ventricular function. [29, 30] Other medications, such as vasopressin, may play adjunctive roles to play in management. [31]

Calcium-channel antagonists have been widely investigated for prevention of vasospasm in aSAH. [32] In particular, nimodipine has been shown to improve neurologic outcomes after aSAH, but it does not decrease radiographic vasospasm and does not significantly reduce mortality. [33] Several studies have shown that nicardipine reduces vasospasm as determined by transcranial Doppler (TCD), but no clear improvements in outcome or mortality have been demonstrated. [34]

A myriad of other drugs, including magnesium oxide, antiplatelet agents, anti-inflammatory drugs, statins, and endothelin receptor antagonists, have been studied in attempts to exploit nuances of the many theories of vasospasm physiology, including inflammatory cascade, heme breakdown product–mediated oxidative injury, spreading depolarization, and potassium channel modulation, but no clinical outcome benefit has yet been shown. [11, 35, 21, 36]  In contrast to nimodipine, the endothelin receptor antagonist clazosentan reduces angiographic spasm but has no effect on outcome, as noted in the CONSCIOUS trials. [37, 38]

Nimodipine is currently recommended as first-line medical treatment for preventing post-aSAH cerebral vasospasm. It is usually given orally at a dosage of 60 mg every 4 hours for 21 days after the initial subarachnoid hemorrhage. [11]  Maintenance of euvolemia and normal circulating blood volume is recommended to prevent vasospasm. [11] In symptomatic vasospasm, induction of hypertension is recommended to achieve increased cerebral blood flow. [11]  Hypervolemia is no longer recommended as a measure to prevent vasospasm. [11]  (See Guidelines.)


Surgical Care

More invasive means of treatment of vasospasm depend on the utilization of cerebral angiography and include the following:

  • Intra-arterial vasodilator administration
  • Balloon angioplasty

Papavarine was one of the drugs initially tried for intra-arterial injection, but it fell out of favor because of (1) the lack of evidence for its efficacy and (2) the possibility of serious side effects, including paradoxical vasospasm. Several studies suggested that intra-arterial verapamil may provide a benefit in terms of neurologic outcome, but the benefit appears not to be obtained via vasodilation. [36]

Angioplasty is an accepted modality for refractory vasospasm, though to date, there have not been any good-quality clinical trials demonstrating its efficacy. Prophylactic angioplasty has not been demonstrated to yield any significant improvements in outcome. [39]

Current guidelines recommend intra-arterial vasodilator therapy and balloon angioplasty as reasonable treatment modalities in symptomatic patients who are not responding to hypertensive therapy. [11]  (See Guidelines and Table 1 below.)

Table 1. Recommendations for Endovascular Treatment of Cerebral Vasospasm (Open Table in a new window)

Degree of Radiographic Vasospasm

Clinical Findings

  Asymptomatic Symptomatic
Mild No intervention Vasodilation (rare)
Moderate Vasodilation Vasodilation ± balloon angioplasty
Severe Vasodilation ± balloon angioplasty (rare) Vasodilation + balloon angioplasty


Prevention of vasospasm after severe aSAH is challenging, in that vasospasm represents a natural progression of this disease process. Use of nimodipine continues to be recommended as a means to improve neurologic outcomes after aSAH, though it has not been shown to exert this effect by decreasing the incidence of vasospasm. [11]

Historically, strategies for preventing vasospasm emphasized triple H therapy (hypervolemia, hemodilution, and hypertension). Systematic reviews of the literature have demonstrated that studies examining triple H therapy are of mostly poor design and quality. There is relatively little compelling evidence to supporting the use of triple H therapy as an effective means of preventing vasospasm. [40, 41]

Currently, the American Heart Association and the American Stroke Association state that euvolemia should be the goal after aSAH and that induction of hypertension may be pursued once symptomatic vasospasm has been diagnosed. [11]  (See Guidelines.)