Following rupture of an aneurysm, extravasated blood and its degradation products accumulate subarachnoidally/perivascularly and are thought to be responsible for the development of CVS
Multivariate analysis showed that SAH Fisher scale III-IV was the most important risk factor for vasospasm followed by left ventricular hypertrophy (LVH), on electrocardiogram, cigarette smoking, and hypertension. angiographic vasospasm (AV) grade III-IV, symptomatic vasospasm (SV), and cerebral infarction occurred in 57%, 54%, and 39% of the 46 smokers with LVH, and in 43%, 49%, and 35% of the 68 patients who had both LVH and hypertension, respectively. CT-evident SAH, LVH, cigarette smoking, and hypertension are associated with vasospasm. In smokers or hypertensive patients, premorbid LVH appears to predict much more severe vasospasm 1).
Risk factors for vasospasm include Fischer grade and volume of blood.
The impact of age on the incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) is a matter of ongoing discussion. The aim of a study was to identify age groups with a higher risk for developing vasospasm, delayed ischemic neurological deficit (DIND), or delayed infarction (DI) and to identify a cut-off age for a better risk stratification. We defined six age groups (<30, 30-39, 40-49, 50-59, 60-69, and >70 years). ROC analysis was performed to determine a cutoff age with the highest positive predictive value (PPV) for developing vasospasm, defined as a blood-flow-velocity-increase >120 cm/s in transcranial-Doppler-sonography (TCD). Multivariate binary-logistic-regression-analysis was then performed to evaluate differences in the incidence of cerebral vasospasm, DIND, and DI among the different age groups. A total of 753 patients were included in the study. The highest incidence (70 %) of TCD-vasospasm was found in patients between 30 and 39 years of age. The cutoff age with the highest PPV (65 %) for developing TCD-vasospasm was 38 years. Multivariate analysis revealed that age <38 years (OR 3.6; CI 95 % 2.1-6.1; p < 0.001) best predicted vasospasm, followed by the need for cerebrospinal fluid drainage (OR 1.5; CI 95 % 1.0-2.3; p = 0.04). However, lower age did not correlate with higher rates of DIND or infarcts. The overall vasospasm-incidence after aSAH is age-dependent and highest in the age group <38 years. Surprisingly, the higher incidence in the younger age group does not translate into a higher rate of DIND/DI. This finding may hint towards age-related biological factors influencing the association between arterial narrowing and cerebral ischemia 2).
Vasospasm should be suspected when there is neurological deterioration (headache, new/worsening focal deficits or decline in sensorium).
Serial transcranial doppler (TCD) examination is a noninvasive, repeatable bedside tool to predict vasospasm before clinical presentation. It also helps in assessing effect of therapeutic interventions. Mean cerebral blood flow velocity (CBFV) in anterior circulation of >120 cm/s and >60 cm/s in posterior circulation is suggestive of vasospasm. A Lindegaard ratio (ratio of middle cerebral artery to extracranial ICA) of >3 and >6 is indicative of mild-moderate and severe vasospasm respectively and differentiates vasospasm from hyperperfusion. An increase in CBFV of >50% in 24 h is also predictive of vasospasm 3).
Despite recent advances, cerebral vasospasm and delayed cerebral ischemia (DCI) still represent a major cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (aSAH). Although a significant portion of the morbidity and mortality associated with aSAH is related to the initial hemorrhagic ictus, cerebral vasospasm and DCI are still the leading cause of poor outcomes and death in the acute posthemorrhage period, causing long-term disability or death in more than one in five of all patients who have suffered aSAH and initially survived.
The risk is reduced with oral nimodipine and probably by maintaining circulatory volume 4).
The classic idea that arterial narrowing, called vasospasm (VSP), represents the hallmark of secondary injury after subarachnoid hemorrhage, has been challenged. The more complex and pleiotropic pathophysiological repercussions from the irruption of arterial blood into the subarachnoid layers go beyond the ascribed VSP. Putting adjectives in front of this term, such as “symptomatic,” “microdialytic,” or “angiographic” VSP, is misleading.
Delayed cerebral ischemia (DCI) is a better term but remains restrictive to severe hypoperfusive injury and neglects oligemia, edema, and metabolic nonischemic injuries. In recognition of these issues, the international conference on VSP integrated “neurovascular events” into its name ( www.vasospasm2013.com ) and a multidisciplinary research group was formed in 2010 to study subgroups of DCI/VSP and their respective significance.In three parts, a tiered article provides a broader definitional envelope for DCI and secondary neurovascular insults after SAH, with a rubric for each subtype of delayed neuronal dysfunction. First, it pinpoints the need for nosologic precision and covers current terminological inconsistency. Then, it highlights the input of neuroimaging and neuromonitoring in defining secondary injurious processes. Finally, a new categorization of deteriorating patients is proposed, going beyond a hierarchical or dichotomized definition of VSP/DCI, and common data elements are suggested for future trials 5).
Natriuretic states can herald the onset or worsening of clinical vasospasm as the renin-angiotensin-aldosterone system is activated in a delayed manner 6).