Imaging Evaluation and Endovascular Treatment of Vasospasm

The first angiographic description of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (aSAH) was provided in the 1950s by Ecker and Riemenschneider. and substantial contributions have been made in subsequent decades to the clinical and pathophysiologic understanding of this debilitating condition. The traditional belief has been that subarachnoid blood products trigger vasospasm of the proximal, large-caliber cerebral vessels, which consequently leads to impaired cerebral perfusion and eventual infarction of the affected tissue.

Robertson in 1949 was the first to describe the autopsy findings and the clinical manifestations of delayed cerebral ischemia (DCI) in a series of 93 patients with subarachnoid hemorrhage. He postulated that these findings could be related to spasm of arteries.

While the complete picture of its pathogenesis remains to be fully elucidated, there is strong evidence that the presence of severe vasospasm correlates with the development of DCI and subsequent cerebral infarcts. Oxyhemoglobin released from breakdown of RBCs has been postulated to cause the release of endothelin-1, which is a potent vasoconstricting agent. ^,

Prompt diagnosis and treatment of vasospasm prior to the onset of permanent ischemic damage are therefore essential to improving survival and preventing secondary loss of neurologic function in the aSAH patient population.

Historically, the most common cause of mortality following initial hemorrhage from aSAH was rebleeding. Advancements in surgical and endovascular techniques and a general trend toward more aggressive, early repair of aneurysm have led to a decrease in the incidence of this complication. DCI from vasospasm has thus emerged as the most common cause of secondary morbidity and death. From literature and clinical experience, this reversible narrowing of cerebral vessels typically occurs between 3 and 14 days , , following initial hemorrhage, with a peak incidence around day 7. Up to 70% of patients demonstrate angiographically visible vasospasm within this time window, but only 20% to 30% of these cases develop clinical evidence of cerebral ischemia and consequently require acute therapy. ^{, , ,} Of symptomatic patients, up to 50% suffer devastating neurologic deficits or death as a result of clinically significant vasospasm, highlighting the importance of prompt diagnosis and therapeutic management. ^,

To assess which patients are at highest risk of developing vasospasm, various groups have suggested clinical factors, including Hunt and Hess grading and characteristics of the subarachnoid clot on computed tomography (CT) (i.e., initial presence, volume, density, and duration) that associate with an increased risk of vasospasm. , , Other clinical variables, including young patient age, poor neurologic grade, greater-than-normal thickness of the subarachnoid clot, intraventricular or intracerebral hemorrhage, and history of smoking, have been associated with the development of more severe vasospasm. ^{, ,} While these considerations can aid in the care of aSAH patients, no comprehensive prediction algorithm exists to determine which patients will suffer DCI. Therefore, there continues to be no substitute for vigilant clinical monitoring and careful decision-making by an experienced, multidisciplinary care team to prevent or limit the neurologic injury from vasospasm.

Diagnostic Imaging

Transcranial Doppler Ultrasonography

Transcranial Doppler (TCD) ultrasonography has been widely employed as the first-line modality for monitoring cerebral vasospasm in aSAH patients ( Fig. 67.1 ). It is noninvasive, inexpensive, and easily performed at the bedside, making it particularly appropriate for daily evaluations. The sensitivity of TCD is highest for vasospasm in the proximal middle cerebral artery (MCA) but decreases in other vascular territories. It also varies depending on the adequacy of vessel insonation. The diagnostic value of TCD comes from its high specificity; detection of normal flow velocities can effectively exclude the presence of vasospasm. It is thus an excellent modality for initial patient triage.

Noncontrast Head Computed Tomography

For patients with changes in clinical exam or TCD findings, noncontrast head CT should be performed before any subsequent interventions are considered. This modality offers a rapid survey for infarctions in the territory of suspected vasospasm and rules out other etiologies of neurologic deterioration, including hydrocephalus and rehemorrhage. The identification of developing infarcts has important implications for subsequent treatment decision-making, because the restoration of flow to these areas typically provides minimal recovery of neurologic function and can potentially lead to further decline as a result of reperfusion hemorrhage. ^,

Computed Tomography Angiography and Perfusion

Computed tomography angiography (CTA) and computed tomography perfusion (CTP) imaging have undergone significant advancements in recent years and have emerged as effective modalities for triaging vasospasm patients toward endovascular therapy ( Fig. 67.2 ). CTA has been shown to be highly accurate for detection of severe vasospasm (more than 50% luminal reduction) and has excellent negative predictive value. ^, The severity of vasospasm can be overestimated in certain vascular territories, and metallic artifacts from coils or clips can hinder the assessment of nearby territories. Despite these limitations, CTA provides an informative and practical assessment of cerebral vessel caliber in patients with concerning symptoms. The addition of CTP scans to the vasospasm imaging armamentarium has allowed insight into the hemodynamic implications of CTA findings. Stereotypical patterns of perfusion abnormality can indicate the presence of either reversible ischemia, which should be addressed promptly to maximize penumbral recovery, or irreversible ischemia, which is a contraindication to aggressive therapy. This distinction is essential for the appropriate triage of patients toward endovascular therapy, because the treatment of infarcted territories potentially leads to further morbidity. A combined, multimodality, CT-based approach has been implemented at many institutions, allowing acquisition of conventional CT, CTA, and CTP images in one setting. This protocol is well suited for aSAH patients for whom lengthy transport or imaging studies may be unfeasible. Clinicians need to be wary of radiation exposure when ordering repeated CT studies; there have been reports of associated sequelae in the medical literature and lay press.

Magnetic Resonance Angiography and Perfusion-Weighted Magnetic Resonance Imaging

Magnetic resonance angiography and perfusion-weighted magnetic resonance imaging (MRI) have been used for detecting vasospasm but have failed to achieve wider adoption for vasospasm imaging due to logistical impracticability of MRI in acutely sick patients.

Digital Subtraction Angiography

Digital subtraction angiography (DSA) remains the gold standard for evaluation of cerebral vasospasm and provides the foundation for all endovascular treatments. It is highly sensitive and specific for detection of proximal, as well as distal, lesions and provides real-time assessment of hemodynamic alterations. Because it is a costly and resource-intensive procedure with a small risk of procedural complications, patients should undergo noninvasive imaging first before receiving DSA.