Acute Pseudoaneurysms and Hemorrhage After Transcarotid Artery Revascularization

PRACTICAL IMPLICATIONS

Consider the rapid formation of pseudoaneurysm(s) after carotid artery revascularization as a potential function of hyperperfusion syndrome, leading to acute postprocedural intracerebral hemorrhage.

Case

A 60-year-old woman with lung adenocarcinoma and previous right carotid artery endarterectomy with patching presented with left hand paresis and left facial droop, then was confirmed to have a right middle cerebral artery (MCA) stroke at an outside institution on a brain MRI; no intervention was performed. MR angiogram showed high-grade restenosis of the right internal carotid artery with increased T1 signal suggestive of intraplaque hemorrhage. No intracranial pseudoaneurysms were visualized. She was referred to our institution and then eventually underwent transcarotid artery revascularization with balloon angioplasty and carotid artery stenting (CAS). The open transcarotid vs transfemoral approach was deemed as preferable by the surgeon so as to avoid the aortic arch and to allow for flow reversal with a distal cerebral protection device. During the reversal of flow (by placing a clamp across the common carotid artery), she was noted to be hypertensive (systolic blood pressure >200 mm Hg). Her systolic blood pressure was titrated to 140–160 mm Hg, and the wire was advanced beyond the lesion. The patient was noted to not follow commands at this point. Given that the lesion was crossed and the carotid was clamped, angioplasty was quickly pursued and the stent was deployed. Completion of cerebral angiogram showed no contrast extravasation, carotid dissection, stenosis, or any apparent abnormality (figure 2A). She subsequently grew more alert but was still unable to follow commands, and additionally had left-sided weakness.

Figure 2. Sagittal Views of Cerebral Angiograms.

(A) At completion of carotid artery stenting that looks to be normal and (B) 2 hours after stenting showing the formation of 2 new pseudoaneurysms (arrows). (C) Reconstructed image.

Emergent CT head showed acute right temporal intracerebral hemorrhage (ICH) and subarachnoid hemorrhage, and CT angiogram showed possible extravasation just lateral to the right MCA bifurcation (figure 1). Repeat cerebral angiogram 2 hours after the previous angiogram showed 2 tiny MCA pseudoaneurysms (figure 2, B and C). Owing to the high risk of occluding the M2 to endovascularly treat the aneurysms, medical management with blood pressure control was pursued. On examination, she had right gaze deviation, dysarthria, and left-sided hemineglect with hemiparesis. Radiographically, her hemorrhages remained stable the following few days. She then had acute hypoxemia and ongoing agitation. Due to overall debility and suspected recurrence of lung cancer, the family decided to withdraw life-sustaining treatments consistent with the patient's wishes, and she died the following day.

Figure 1. Axial Views of CT and CT Angiogram of the Head.

(A) Right temporal intraparenchymal hemorrhage with subarachnoid hemorrhage in and around the Sylvian fissure and (B) contrast extravasation emanating from near the right MCA bifurcation. MCA = middle cerebral artery.

Discussion

We demonstrate the rapid formation of pseudoaneurysms ipsilateral to the revascularized territory and suggest this to be the cause of the rare but catastrophic complication of ICH. The mechanism is postulated to be hyperperfusion syndrome. The revascularization of severe stenosis may have caused a sudden increase in intraluminal pressure then hemorrhage through fragile dilated vessels, consistent with initial theories of chronic miliary aneurysm formation.¹ The hemorrhage caused the patient's left-sided hemiparesis (although the decreased level of alertness was most likely due to hypoperfusion during flow reversal). Acute pseudoaneurysm formation is rare in a patient with postprocedural hemorrhage and in the context of a transcarotid approach.

Hyperperfusion syndrome as the cause for ICH after transfemoral carotid revascularization is a well-described phenomenon in up to 25% of patients after CAS.^2,3 The main proposed mechanism of ICH involves the combination of increased cerebral perfusion with impaired autoregulation as a function of chronic hypoperfusion ipsilateral to the side of carotid stenosis. This may then result in ICH. Although difficult to predict preoperatively, high-grade ipsilateral and concomitant contralateral carotid stenosis, recent stroke, and female sex are potential risk factors for hyperperfusion.³

Perhaps what we witnessed in this case is real-time angiographic documentation of the pathophysiologic mechanism of reperfusion hemorrhage. There are a few case reports describing delayed pseudoaneurysm formation after CAS in the area of stenting a few days up to years after the initial procedure.^4,5 Early pathophysiologic theories include the formation of “fibrin globes” as small secondary extravasations from torn arteries and a functional circulatory disturbance causing arterial necrosis and bleeding. When massive, an “avalanche” of hemorrhage arises from the simultaneous rupture of many small adjacent necrotic segments.⁶

This is a rare case of rapid pseudoaneurysm formation after transcarotid CAS. It remains unclear as to how the aneurysms formed as quickly as they did. We hypothesize that sudden high pressure from hypertension in low-pressure-adjusted arteries led to rupture and hemorrhage. Although unproven, avoidance of blood pressure surges without aggressive lowering that can be harmful in poorly autoregulated vessels may limit the formation of these aneurysms. Charcot and Bouchard demonstrated chronic miliary aneurysms—we demonstrate an acute form may exist.

Appendix. Authors

Study Funding

No targeted funding reported.

Disclosure

T. Chakraborty and W. Brinjikji report no disclosures. G. Lanzino is a shareholder of Marblehead and a consultant for Superior Medical Editing. R.R. DeMartino and E.F. Wijdicks report no disclosures. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.