**5. Conclusion**

396 Aneurysm

Cerebral vasospasm is the highest contributing factor to morbidity in patients with aneurysmal SAH. Cerebral vasospasm may have evolved as a protective measure to prevent re-rupture of a cerebral aneurysm; however, its diffuse cerebral effects are deleterious and add significant morbidity to aneurysmal SAH. Vasospasm is thought to occur secondary to blood product degradation in the subarachnoid space. Deoxy-hemoglobin and oxyhemoglobin decrease perivascular nitric oxide and increase endothelin-1 respectively. The net result is a pathologic prolongation of calcium in smooth muscle, leading to an increase in

Monitoring for vasospasm is of great value in the management of aneurysmal SAH. TCD, CT Angiography with perfusion imaging, and conventional digital subtraction angiography

The advantages of TCD are its noninvasive low risk profile; however it's sensitivity is variable and dependent on the skill of the ultrasonographer. Many patients have poor transcranial windows, making monitoring with TCD's difficult, if not impossible. Mean flow velocities are typically utilized for detection of vasospasm. Using a mean fellow velocities less than 120cm/s has a 94% negative predictive value for cerebral vasospasm. Mean flow velocities greater than 130cm/s have been proposed as the threshold for mild-moderate vasospasm; this carries a 73% sensitivity and 100% specificity for detecting vasospasm. Mean flow velocities greater than 200cm/s reliably predict moderate to severe angiographic vasospasm. The Lindegaard ratio compares intracranial MCA mean flow velocity to extracranial ICA mean flow velocity; the advantage of a ratio is to distinguish hyperemic states from vasospasm. Ratios greater 4 are suggestive of vasospasm; a ratio greater than 6

CT angiography has a 87-95% percent sensitivity for angiographic vasospasm, but carries a high negative predictive value approaching 99%. However, CT angiography and perfusion are cumbersome and may pose additional risk to the patient secondary to iodinated contrast. CT angiography with perfusion may be a surveillance option for patients who have

Non-interventional strategies to combat cerebral vasospasm include the traditional triple H model. Augmenting MAP has been utilized to decrease DCI associated with cerebral vasospasm [74]. Our practice utilizes MAP goals between 110-140 to treat cerebral

Few centers have utilized intrathecal calcium antagonists. Some have utilized intrathecal nicardapine with success in decreasing flow velocities as measured by TCD's [77]. Multicenter randomized trials utilizing have yet to be completed demonstrating efficacy.

The trigger for intervention varies between centers. Many centers choose an aggressive intervention including endovascular delivery of local intra-arterial verapamil (and other calcium antagonists) that have an immediate effect with resulting local vasodilatation. Specific management of interventional management of vasospasm associated with

spasm, apoptosis, and vascular remodeling [75].

are options for monitoring for cerebral vasospasm.

reliably predicts cerebral vasospasm [76].

poor TCD windows [26].

vasospasm.

Aneurysmal SAH is a complex critical illness with multisystem complications that requires the close attention of a dedicated neurocritical care team. Mortality and morbidity are high; the likelihood of a good outcome depends on presentation grade and careful and diligent management of complications.
