36 Management of Vessel Perforation during Stroke Intervention
36.1 Case Description:
36.1.1 Clinical Presentation
A 55-year-old male presented to the emergency department (ED) at 3 p.m. with onset of left-sided hemiparesis and mild left sensory loss which began at 10 a.m. He was awake, although moderately drowsy, and able to follow basic commands. The patient’s National Institutes of Health Stroke Scale (NIHSS) score was 16.
Past medical history is significant for coronary artery disease, hypertension, hyperlipidemia, and sleep apnea. He has known intracranial atherosclerosis with a prior MRI demonstrating mild right M1 stenosis.
36.1.2 Imaging Workup and Investigations
Noncontrast CT (NCCT) of the head demonstrated mild hyperdensity in the right middle cerebral artery (MCA). His ASPECTS score was 10.
CTA demonstrated an occlusive clot in the right M1 (Fig. 36.1).
Acute ischemic stroke secondary to right MCA M1 occlusion, possibly secondary to intracranial atherosclerosis.
Patient is not a tissue plasminogen activator (tPA) candidate due to time of onset.
The patient was immediately transferred to the angio suite for endovascular intervention. Anesthesia was administered using conscious sedation.
5-Fr Simmons 2 catheter.
8-Fr balloon guide catheter (BGC).
Avigo guidewire (0.014 in).
Rebar 18 (0.021 microcatheter).
Solitaire 4 × 20 device.
Micropuncture was set to access the right common femoral artery and a 5-Fr sheath was placed in it.
5-Fr Simmons 2 catheter was then placed in the right common carotid artery where digital subtraction angiography (DSA) was performed. The Simmons catheter was used due to the patient’s tortuous aortic arch.
Angiography demonstrated a patent right internal carotid artery (ICA) and occlusion of the proximal right M1 (Fig. 36.2).
Using exchange technique, the Simmons catheter was exchanged for an 8-Fr BGC. The catheter tip was placed in the distal cervical ICA.
The Rebar 18 microcatheter was advanced over an Avigo guidewire to the location of the occlusion in the M1. Multiple attempts were made to cross the lesion but were unsuccessful. A microcatheter injection demonstrated extravasation of contrast into the subarachnoid space and into the sylvian fissure. The findings were consistent with a vessel perforation (Fig. 36.3).
Anticoagulation was reversed with 25 mg of protamine. Following this, the BGC was inflated for approximately 1 minute. Repeat angiography demonstrated no more extravasation of contrast (Fig. 36.4). The procedure was ended at this time due to risk of further perforation.
Iodine subtracted dual energy CT demonstrated a small amount of subarachnoid hemorrhage (Fig. 36.5); no acute infarct was present immediately after the procedure.
At 24 hours, the patient’s NIHSS score was 2. The improvement in NIHSS was likely due to spontaneous recanalization of the M1 occlusion. The patient had no evidence of infarct on follow-up imaging. This is likely secondary to the fact that the patient had robust collaterals due to a long-standing M1 stenotic lesion.
36.2 Companion Case
36.2.1 Clinical Presentation
A 59-year-old woman from home presented with right temporal headache and collapse. Her husband noted a left hemiparesis. She was transferred to the ED by ambulance, arriving 3 hours following symptom onset.
Her past history included Meniere’s disease and migraine. Examination at presentation revealed a left gaze palsy, left hemianopia, left facial weakness, and a dense left hemiparesis. Dysarthria and neglect were also present. New atrial fibrillation was noted. Initial NIHSS score was 14.
36.2.2 Imaging Workup and Investigations
NCCT, performed at 3 hours 50 minutes, demonstrated a subtle low density in the right lentiform nucleus, with an ASPECTS score of 9 (Fig. 36.6a).
CTA showed a right M1 occlusion with reduced arborization of the right MCA cortical vessels and left M3 occlusion (Fig. 36.6b).
Perfusion imaging revealed a large region of increased mean transit time (MTT) and decreased cerebral blood flow involving the right lentiform nucleus, insular cortex, and right posterior frontoparietal region. Cerebral blood volume suggested a small area of core infarct in the right lentiform nucleus (Fig. 36.6c, d).