Endovascular Management of Cerebral Vasospasm

Cerebral vasospasm is a cause of significant morbidity and mortality in patients with subarachnoid hemorrhage (SAH). Most cases of vasospasm can be managed medically. Medical strategies for treatment include hemodynamic augmentation to improve cerebral perfusion pressure and medical therapy to prevent or reduce cerebral vasospasm. In patients with acute neurological deterioration, imaging assessment is essential to triage those patients appropriate for aggressive medical or endovascular therapy. Such imaging assessment can be performed with many radiologic techniques such as transcranial Doppler, computed tomography (CT), magnetic resonance imaging, and single-photon emission CT (SPECT). Advanced CT applications like CT angiography and CT perfusion are gaining popularity and playing an increasingly important role in the decision making. Endovascular techniques for treatment of vasospasm include intra-arterial administration of vasodilators and intracranial angioplasty. This article discusses the use of these endovascular techniques in the management of vasospasm and provides a current review of literature. Sustained efficacy of intra-arterial vasodilators is less well established at this time, and repeated treatments may be necessary. Balloon angioplasty is an effective technique in treating vasospasm and results in durable clinical improvement. It should be used judiciously, however, given a small risk of vessel rupture associated with intracranial angioplasty. The goal of angioplasty should be improvement of vessel caliber to augment flow rather than to achieve a picture-perfect result.

Cerebral vasospasm causes significant morbidity and mortality in patients with subarachnoid hemorrhage (SAH). The management of these patients is challenging and requires the multidisciplinary input of intensive care, neurosurgical, and endovascular specialists. Angiographic vasospasm occurs in approximately 70% of all aneurysmal SAH, but clinical neurological manifestations occur in only one third of these cases. Up to 15% of patients surviving the initial subarachnoid hemorrhage will suffer stroke or death as a result of vasospasm. Vasospasm rarely occurs before day 4; it tends to peak at day 7, and it may last up to 2 weeks after the initial hemorrhage.

Most cases of vasospasm can be managed medically. Medical strategies for treating vasospasm include hemodynamic augmentation to improve cerebral perfusion pressure and medical therapy to prevent or reduce cerebral vasospasm. A combination of volume expansion, hemodilution, and induced hypertension (Triple H therapy) has been used extensively, but its value has not been tested rigorously. Currently, oral nimodipine is recommended for patients with aneurysmal SAH. Other, newer agents being evaluated include albumin, statins, magnesium sulphate infusion, and clazosentan (endothelin-1 antagonist). Detailed discussion of medical therapy is beyond the scope of this article. Instead, it will focus on the endovascular therapy of vasospasm and the role of radiological imaging in the appropriate selection of patients who are likely to benefit from this form of treatment.

The clinical diagnosis of vasospasm often is based on detailed neurologic examination. The monitoring of patients at risk for clinical vasospasm requires constant neurological examination by intensive care specialists and the decision making of an experienced, multidisciplinary physician team. The diagnosis of symptomatic vasospasm requires identification of new focal motor deficits or sudden changes in mental status in at-risk patients. These new deficits should not be easily attributed to other causes such as development of hydrocephalus, systemic infection, seizures, or ongoing delirium. Although clinical examination is very useful, it is not always reliable. A significant proportion of patients with SAH may be neurologically impaired or comatose at baseline. In such patients, a meaningful neurological examination may not be obtainable.

Imaging assessment

Diagnostic imaging assessment of a patient with SAH in the vasospasm window serves many functions. These include ruling out other pathologies, detecting the presence of vasospasm, and assessing its severity. In a patient with acute neurological deterioration, imaging assessment is essential to triage those patients appropriate for aggressive medical or endovascular therapy. Many different imaging modalities have been used, including transcranial Doppler (TCD) ultrasound, single photon emission computed tomography (SPECT) cerebral blood flow studies, positron emission tomography (PET), magnetic resonance angiography (MRA), magnetic resonance perfusion, stable xenon-enhanced computed tomography (CT), CT angiography, and CT perfusion. In a patient with suspected symptomatic vasospasm, noncontrast CT is a first-line study at most institutions. It can easily rule out other causes for deterioration such as hydrocephalus and rehemorrhage. In addition, a developing hypodensity in the vascular territory of clinical concern could indicate an established infarction. In such patients, aggressive endovascular therapy would be unlikely to be effective, and, in fact, it can be potentially harmful, as it can cause further morbidity or mortality from reperfusion hemorrhage. Clearly, the relative size of this infarct needs to be weighed against the benefit of intervening to prevent infarction in a larger area of at-risk parenchyma (the so-called penumbra).

TCD is used in many institutions and has the advantage of being a portable noninvasive study that can be performed at the bedside in the intensive care unit (ICU) setting. The TCD results correlate well with angiographic findings if the vessel under investigation is insonated adequately ( Fig. 1 ). Its value, however, is rather limited in patients with poor acoustic windows. The sensitivity of TCD varies depending on the vessel affected by vasospasm, with relatively low sensitivity for supraclinoid internal carotid and anterior cerebral arteries (ACA). TCD has been shown to be specific but not sensitive for vasospasm of the middle cerebral artery (MCA) when compared with angiography, and it is poorly predictive of developing secondary cerebral infarction. In addition to limitations imposed by poor acoustic window, the utility of TCD is hampered further by operator dependence and inability to study the distal vessels.

Use of imaging modalities such as magnetic resonance imaging (MRI)/MRA/magnetic resonance perfusion, PET, SPECT, and xenon CT that assess cerebral vasculature or brain perfusion often require the patient to remain still for prolonged periods. These techniques are not universally available and are often not practical for routine clinical use in these very sick patients. In recent years, a combination of CT angiography (CTA) and CT perfusion (CTP) has emerged as an important tool. It is very helpful in triaging patients with suspicion of vasospasm into those who should have aggressive medical management and others who should undergo early endovascular therapy. It is an attractive technique as it is a fast, readily available, relatively inexpensive, and practical imaging modality well suited to ICU patients. This can be combined easily with noncontrast head CT and performed on most commercially available scanners. Modern multidetector scanners are capable of rapidly assessing the caliber of the intracranial arteries using CTA and the brain parenchymal perfusion (CTP) with the use of 50 to 100 cc bolus of iodinated contrast ( Figs. 2 and 3 ). Multidetector CTA has a very high accuracy of 98% to 100% for detecting severe vasospasm when compared with digital subtraction angiography. Lower degrees of accuracy for mild–moderate vasospasm (57% to 85%) have been reported. Supraclinoid internal carotid artery (ICA) and very distal intracranial arteries are slightly difficult areas to assess on the CTA studies. The addition of CTP, however, however improves the accuracy of diagnosis of distal vasospasm by demonstrating tissue-level perfusional abnormalities despite the absence of proximal vasospasm on CTA.

CTP provides several quantitative parameters of cerebrovascular hemodynamics. These include MTT, CBV and CBF. MTT is defined as the average transit time of blood through a given brain region, measured in seconds. CBV is defined as the total volume of blood in a given volume of brain, usually measured in milliliters per 100 grams of brain tissue. CBF is the volume of blood moving through a given volume of brain per unit time, measured in milliliters per 100 grams of brain tissue per minute.

MTT or time to peak (TTP) maps have been shown to be the most sensitive in detecting early auto-regulation changes in cerebral ischemia, and these maps should be interrogated first when reading a CTP study. In the authors’ experience, if these maps are normal and symmetrical, then clinically significant vasospasm is highly unlikely. Abnormality on these maps, however, mandates close and careful inspection of the CBV and CBF maps to further characterize the severity of the perfusional defect. Three patterns of CT perfusional abnormality can be identified with progressive severity.

1.

Elevated MTT/TTP with normal CBF and normal-to-increased CBV: indicates perfusional abnormality that is adequately compensated for by auto-regulation
2.

Elevated MTT/TTP with reduced CBF and normal-to-increased CBV: indicates perfusional abnormality with reversible cerebral ischemia (penumbra) (see Figs. 2 and 3 )
3.

Elevated MTT/TTP with reduced CBF and matched reduced CBV: indicates perfusional abnormality with irreversible cerebral ischemia.

This constitutes a relative contraindication to aggressive therapy. Endovascular treatment targeted to this area is not advisable, as this region likely will progress to established cerebral infarction and will be at risk for reperfusion hemorrhage.

MTT and TTP have been shown to be sensitive and early predictors of secondary cerebral infarction in patients with vasospasm. These CT perfusion changes occur a median of 3 days prior to the development of established infarct on noncontrast CT. Wintermark and colleagues found MTT to have a negative predictive value for cerebral vasospasm of 99% and that the combination of CTA with an MTT threshold of greater than 6.4 seconds was the most accurate in the diagnosis of cerebral vasospasm. In addition, a cortical regional CBF value of less than 39.3 mL/100 g/min was the most accurate (95%) indicator for the need for endovascular therapy.

Although CTA and CTP are excellent imaging tools, they also have a few limitations. Current limitations include metallic artifact from coils or clips preventing evaluation, problems with contrast bolus timing, and restricted range of parenchymal coverage on perfusion maps. Although the posterior fossa is usually not included on CTP, a range usually can be selected that includes a large part of all three supratentorial vascular territories. Further widespread availability of the latest multidetector scanner technology (256 and 320 slice scanners) will allow complete brain coverage. In addition, the problem of metallic artifacts is being addressed with new, dual-source CT technology.

Patients that are triaged as candidates for endovascular therapy will undergo initial emergent catheter angiography. Vasospasm found on angiography typically is divided into proximal and distal. Most literature divides severity of vasospasm arbitrarily into mild, moderate, and severe based on varying degrees of stenosis. A useful example is that described by Kassell and colleagues, with four grades: no stenosis or mild (<50%), moderate (50%), and severe (>50%) stenosis. The location of vasospasm determines the method of endovascular treatment employed. Proximal vasospasm should be treated with balloon angioplasty whenever possible. Intra-arterial (IA) vasodilators are used for distal spasm that is not amenable to balloon angioplasty or for vessels considered not safe for angioplasty, for example vasospasm in a vessel segment recently treated with surgical clipping of an aneurysm. The authors also use IA vasodilators as a complement to angioplasty.

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