What types of vascular neurointerventional procedures are available?
- • Cerebral catheter angiography: Assessment for cerebral aneurysm, stenosis (atherosclerosis or vasculitis/vasculopathy), or vascular malformation.
- • Cervical catheter angiography: Assessment for carotid artery stenosis or traumatic cervical vascular injury.
- • Inferior petrosal sinus sampling: Measurement of adrenocorticotropic hormone (ACTH) levels from the pituitary gland in selected patients with Cushing’s syndrome.
- • Cerebral artery aneurysm: Saccular aneurysms are the most common morphologic subtype of cerebral artery aneurysms. They are outpouchings of the intima and adventitia caused by degeneration of the media. Aneurysms may be symptomatic related to mass effect (e.g., compression of cranial nerves with associated neuropathy) or rupture leading to subarachnoid hemorrhage (SAH). The clinical presentation of SAH may range from “the worst headache of one’s life” to sudden death. The long-term prognosis of patients who survive the initial rupture correlates with clinical status on presentation, such as that based on the Hunt and Hess clinical grading scale. The patient workup for SAH includes noncontrast head computed tomography (NCCT) and CT angiography (CTA). Detection of an aneurysm on CTA requires careful assessment of the pattern of SAH, the source (axial) CTA images, maximum intensity projection (MIP) images, and volume-rendered (VR) images. Cerebral artery aneurysms can be treated with detachable platinum coils (which can be performed in conjunction with balloon or stent assistance) or a flow diversion device
Hunt and Hess Clinical Grading Scale for Prediction of Clinical Outcome in Patients with SAH
|1||Asymptomatic, or minimal headache and slight nuchal rigidity||1%|
|2||Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy||5%|
|3||Drowsiness, confusion, or mild focal neurologic deficit||19%|
|4||Stupor, moderate-severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances||42%|
|5||Deep coma, decerebrate rigidity, moribund appearance|
Cerebral arteriovenous malformation (AVM): A cerebral AVM is an abnormal collection (nidus) of vessels between arterial and venous vasculatures without an intervening capillary bed or brain parenchyma, leading to arteriovenous shunting. Half of symptomatic cerebral AVMs present with cerebral hemorrhage. AVM is typically treated with a liquid embolic agent such as n-butyl cyanoacrylate (n-BCA) glue or Onyx (ethylene vinyl alcohol). This is usually performed prior to microsurgical resection to reduce intraoperative bleeding. A liquid embolic cast also serves as a direct visual marker for the surgeon to localize the AVM nidus. Embolization can also be performed prior to radiosurgery.
Cerebral dural arteriovenous fistula (dural AVF): A dural AVF is an abnormal connection between arteries and veins via a network of tiny vessels in the wall of the dural venous sinus. If the transverse sinus is involved, dural AVF patients typically present with pulsatile tinnitus, whereas pulsatile exophthalmos and cranial nerve 3, 4, and 6 neuropathy are more common with cavernous sinus involvement. Dural AVF is typically treated with a liquid embolic agent such as n-BCA glue or Onyx, although particles are sometimes also used. Endovascular treatment can be employed as the primary treatment modality or in conjunction with microsurgical resection.
- • Spinal vascular malformation: Similar to cerebral vascular malformations, spinal vascular malformations are a heterogeneous group of conditions including both AVF and AVM. The spinal cord may or may not be involved. There are several classification schemes, which are beyond of the scope of this chapter. Spinal catheter angiography is the reference standard test for detection of a spinal vascular malformation. Endovascular treatment can be used as the primary treatment modality or in conjunction with microsurgical resection. Spinal dural AVF, the most common type of spinal vascular malformation, is typically treated endovascularly with n-BCA glue or Onyx.
- • Preoperative embolization of tumors: Intracranial tumors (e.g., meningioma), head and neck tumors (e.g., juvenile angiofibroma, paraganglioma), and hypervascular vertebral metastases (e.g., renal cell carcinoma metastases) can be embolized with particles preoperatively to reduce bleeding at surgery.
- • Epistaxis: Embolotherapy is indicated in patients with persistent epistaxis after conservative treatment with packing.
- • Cervical dissection: Vessel sacrifice in patients with pseudoaneurysms (grade 3 injury) or transection (grade 5 injury) can be performed. Endovascular stenting is another option for grade 3 injuries.
- • Acute ischemic stroke: Stroke is a clinical diagnosis, not an imaging one. Time is BRAIN (i.e., brain tissue is rapidly lost as stroke progresses), and therefore rapid diagnosis and initiation of treatment are critical for a good clinical outcome. The standard treatment for acute ischemic stroke is intravenous (IV) tissue plasminogen activator (tPA) within 4.5 hours of onset. Intraarterial (IA) tPA administration and mechanical thrombectomy can be offered as adjunct therapy to IV tPA. Data from the MR CLEAN trial show that IV tPA together with IA mechanical thrombectomy are superior to IV tPA alone. NCCT is the study of choice for initial assessment for acute stroke due to its speed and widespread availability. The primary purpose of a noncontrast head CT in the setting of acute stroke is to exclude contraindications to IV tPA and IA treatment (i.e., intracranial hemorrhage and large infarct [>1/3 MCA vascular territory]). CTA can be used to confirm large vessel occlusion (i.e., carotid terminus, M1 segment, A1 segment, etc.) in which adjunctive IA treatment is most helpful. The role of magnetic resonance imaging (MRI), MR perfusion imaging, and CT perfusion imaging in acute ischemic stroke assessment is not clearly delineated at this point.
- • Dural sinus thrombosis: Symptoms of cerebral venous thrombosis, such as headaches, nausea, vomiting, and seizures, are nonspecific, and therefore this diagnosis is easily overlooked both clinically and on imaging. First-line treatment for cerebral venous thrombosis is anticoagulation. Endovascular thrombectomy is a second-line treatment in patients with dural sinus thrombosis who fail medical management with anticoagulation.
- • Vasospasm is the most common cause of morbidity and mortality in SAH patients. The typical vasospasm window is between days 5 and 14 following hemorrhage, but vasospasm can occur anytime between days 3 and 21. The risk of vasospasm correlates with the modified Fisher scale. Vasospasm can present as worsening headaches, change in mental status, stroke symptoms (e.g., hemiparesis and aphasia), seizures, and elevated cerebral arterial blood flow velocities on transcranial Doppler ultrasonography (US). If vasospasm is suspected clinically, head CTA is a reasonable initial imaging study to obtain. Induced hypertension (systolic blood pressure [SBP] >20% above baseline or SBP 180 to 200) is the most effective treatment for symptomatic vasospasm, and if the patient does not respond to induced hypertension, IA calcium channel blockers and/or balloon angioplasty can be offered as adjunctive therapy
Modified Fisher CT Grading Scale of SAH
|GRADE||CT FINDINGS||SYMPTOMATIC VASOSPASM RISK|
|0||No SAH or IVH||0%|
|1||Focal or diffuse thin ( < 5 mm) SAH, no IVH||24%|
|2||Focal or diffuse thin ( < 5 mm) SAH, with IVH||33%|
|3||Thick SAH (>5 mm), no IVH||33%|
|4||Thick SAH (>5 mm), with IVH||40%|
- • Carotid artery angioplasty/stenting is indicated in symptomatic (i.e., transient ischemic attack [TIA] or stroke) patients with >50% stenosis, or in asymptomatic patients with >70% stenosis who have high surgical risk (i.e., high carotid bifurcation, severe cardiopulmonary disease, etc.).