General Description

Cerebral arterial vasospasm secondary to aneurysmal subarachnoid hemorrhage (aSAH) is a common complication of a ruptured aneurysm and can lead to severe infarction or even death. Angiographic vasospasm occurs in 30%–70% of aSAH patients. Symptomatic vasospasm with cerebral ischemia occurs in 20%–30% of aSAH patients. The severity of ischemia correlates with the severity of radiographic vasospasm and the need for early and aggressive endovascular treatment. Transcranial Doppler imaging and computed tomography angiography and computed tomography perfusion (CTP) imaging are noninvasive diagnostic tools that can provide early evidence for ongoing cerebral vasospasm, even before any neurological changes are observed. Medical management of vasospasm should always be utilized in addition to any endovascular treatment.

Indications

Endovascular vasospasm treatment is indicated in patients who have either radiographic or symptomatic vasospasm refractory to medical therapy (e.g., the combination of induced hypertension, hypervolemia, and hemodilution [triple-H therapy]). By comparing the percentage of vessel narrowing to that of the initial vessel diameter, we define vasospasm as mild when it is less than 25%, moderate at 50%, and severe when it is more than 75%. The Neurocritical Care Society proposed that invasive management of cerebral vasospasm is indicated in the presence of a new neurological deficit that cannot be completely reversed by maximal medical therapy or when complications associated with medical management become a concern. A literature review made a class IIb recommendation for medical therapy based on level of evidence B according to the American Heart Association guidelines that calcium channel blockers may be beneficial and may be considered for vasospasm refractory to other forms of medical therapy.

Neuroendovascular Anatomy

When considering treatment of vasospasm, it is important to have an initial angiogram available for comparison; otherwise, the contralateral side must be utilized for comparison (e.g., initial vessel diameter). The interventionist must be careful interpreting radiographic vasospasm in vascular territories that could be prone to hypoplasia (i.e., anterior cerebral artery [A1 segment], posterior communicating artery, intradural vertebral artery) because treating these vessel segments with a balloon can have devastating consequences. If stent-assisted coiling or flow-diverter device placement is considered for a ruptured aneurysm with vasospasm, caution is advised in conjunction with the infusion of a vasodilator because this can make the sizing of the device incorrect.

Endovascular Angioplasty Alternatives

The two endovascular treatment options for vasospasm are pharmacological angioplasty (intra-arterial vasodilator therapy) and balloon angioplasty.

Pharmacological Angioplasty

Pharmacological angioplasty or intra-arterial vasodilator therapy refers to direct intra-arterial delivery of vasodilators, including calcium channel blockers (verapamil, nicardipine, nimodipine) and a phosphodiesterase inhibitor (milrinone). Calcium channel blockers have been the most studied and have indicated the most promise. Among all calcium channel blockers, verapamil is the most commonly used

Balloon Angioplasty

The physiology behind balloon angioplasty effectiveness remains unclear. Dilation of smooth muscle in the contractile state stretches and disrupts connective tissue fibers in the extracellular matrix of the vessel wall and in the smooth muscle.

Perioperative Medications

If the patient is awake and not intubated, we usually perform pharmacological and balloon angioplasty without the need for general anesthesia. While the patient is in the neurointensive care unit, intravenous bolus doses of milrinone are administered, typically 8 mg for a duration of 30 min. A milrinone drip can be started intravenously and continued for 14 days in the intensive care unit (ICU), slowly incrementing from 0.5 µg/kg/min to 1.5 µg/kg/min as tolerated. ¹ Milrinone can cause tachycardia and hypotension. Continuous blood pressure monitoring is essential during the endovascular procedure, given the risk of intraoperative hypotension secondary to vasodilator infusion.

Pharmacological Angioplasty—Specific Technique and Key Steps

1. 
   

   After a femoral angiogram has been performed to confirm the absence of any irregularity or dissection, the diagnostic catheter is placed over a curved wire (0.035-inch angled Glidewire, Terumo), and the system is advanced into the aorta under fluoroscopic guidance.

   
   
2. 
   

   We typically utilize a 6 French (F) femoral sheath in the event that balloon angioplasty is needed.

   
   
3. 
   

   The diagnostic catheter is advanced into the internal carotid artery (ICA) of the symptomatic side and cervical anteroposterior and lateral angiographic runs are obtained.

   
   
4. 
   

   Once roadmaps have been obtained to make sure there is no stenosis or dissection in the neck vessels, the diagnostic catheter is placed just below the skull (C2) segment of the ICA or upper V2 segment of the vertebral artery.

   
   
5. 
   

   An intra-arterial bolus of verapamil (10–20 mg in 10–20 mL of normal saline solution) is slowly infused over a period of 2–4 min. It is important to coordinate with an anesthesiologist because verapamil can cause hypotension and a seizure if injected too fast.

   
   
6. 
   

   Once the verapamil is given, we then move to the next vessel territory (contralateral ICA [contralateral hemisphere] and vertebral artery [posterior circulation territory]). Once all three vessels have been accessed and the symptomatic areas infused, we repeat an angiogram to inspect for improvement.

   
   
7. 
   

   If the symptoms resolve and/or the caliber of the vessels improves, the procedure is then terminated.

   
   
8. 
   

   Patients with severe refractory vasospasm need this procedure every 24 hours or even every 12 hours during the vasospasm period.