12.1.7\ Carotid Endarterectomy

12.1.7.1\ Discussion

Carotid endarterectomy (CEA) is considered the treatment of choice for symptomatic and asymptomatic patients with high-grade carotid artery stenosis. In order to appropriately interpret imaging studies obtained following CEA, it is helpful to be familiar with the surgical techniques involved.

CEA can be performed through an incision made anterior to the sternocleidomastoid and ligation of the facial vein in order to expose the carotid bifurcation and clamping of the carotid artery distal to the endarterectomy. Consequently, a small hematoma within or adjacent to the sternocleidomastoid and mild circumferential narrowing of the carotid artery resulting from clamp placement during surgery can be appreciated on follow-up CT (Fig. 12.25). These findings are usually self-limited.

CEA involves opening the carotid artery, removing the plaque and associated endothelium, and suturing the vessel wall closed with or without an enlargement patch. The patch is usually composed of Dacron, which is not readily visible on CT, but can appear as a thin hyperechoic mesh on ultrasound (Fig. 12.26). Alternatively, the section of carotid artery that is resected can be reconstructed using a saphenous vein graft. This has a distinct patulous or bulbous appearance on imaging (Fig. 12.27).

Complications related to CEA include localized intimal flap or dissection, reperfusion syndrome, patch infection, restenosis, cerebral infarction, and cranial nerve injury, usually facial and hypoglossal (Figs. 12.28, 12.29, 12.30, 12.31, 12.32, and 12.33).

Wound infection following carotid endarterectomy occurs in about 2% of cases. Staphylococcus

species are the most common causative organisms. Patients typically present with wound swelling, drainage, and fever. On imaging, abscess appears as a fluid collection that abuts the surgical site. Characteristic rim enhancement and cellulitis are often present. There may also be debris, septations, and draining sinus that extends from the operative bed to the incision. Wound abscesses usually resolve with antibiotics and debridement. However, periarterial abscess or patch infection may predispose to dehiscence of the suture line, resulting in pseudoaneurysm formation.

Hyperperfusion or reperfusion syndrome is an unusual complication of carotid endarterectomy or carotid artery stenting, occurring in 0.3–1.2% of cases. A possible etiology for this condition is impaired cerebrovascular autoregulation. Predisposing factors include severe underlying cerebrovascular disease, diabetes mellitus, long-­ standing hypertension, prolonged cross clamping during endarterectomy, and a greater than 100% increase in the degree of reestablished cerebral blood flow, which is usually associated with greater than 90% carotid artery stenosis. Patients may present with headaches, seizures, focal ­neurological deficits, or confusion within several days after surgery. Patients may recover completely if the diagnosis is made promptly. However, in some series, there is a mortality rate of up to 50%. The diagnosis of cerebral hyperperfusion syndrome can be suggested on CT in the proper setting by noting the presence of edema, often in the watershed zones ipsilateral to the side of surgery. On MRI, focal ipsilateral vasogenic edema is apparent. Diffusion-weighted imaging and apparent diffusion coefficient maps help confirm the presence of vasogenic edema. On MRA, prominent vessels on the affected side may be apparent. Similarly, perfusion-weighted imaging

can depict the relative increased flow to the affected side. The finding of hemorrhage portends a poor prognosis. Imaging can help identify hyperperfusion syndrome before serious sequelae result. Differential considerations for the imaging appearance of cerebral hyperperfusion syndrome include hypertensive encephalopathy, cyclosporine toxicity, and eclampsia. The lack of restricted diffusion helps exclude cerebral ischemia.

Recurrent stenosis after carotid endarterectomy occurs at the rate of about 1% per year. This complication is the main limitation of carotid endarterectomy and predisposes to cerebrovascular ischemia. Acute thrombotic occlusion is much less common and is a potentially devastating complication that can result in cerebral infection. Conventional carotid end-

arterectomy with patch angioplasty and the use of lipid-lowering pharmaceuticals are associated with lower rates of restenosis. Risk factors for restenosis include female gender and renal failure. CTA, MRA, and Doppler ultrasound are all appropriate for evaluation of suspected restenosis or occlusion after carotid endarterectomy. Each of these modalities has advantages and disadvantages. CTA with reformats, especially the curved planar reformats, is useful for studying stenoses. In the setting of carotid endarterectomy with patching, the internal carotid artery velocities on Doppler ultrasound must be interpreted with caution, since these are normally higher than in the nonoperated counterparts. MRA is best suited for identifying pseudo-occlusions.

Fig. 12.25  Expected carotid endarterectomy early postoperative changes. Axial contrast CT after recent CEA demonstrates several foci of air scattered within and adjacent to the surgical bed, left sternocleidomastoid swelling, and edema in the fat planes

Fig. 12.26  Patch endarterectomy ultrasound image shows the echogenic Dacron patch (arrow) in the proximal internal carotid artery

Fig. 12.29  Reperfusion syndrome. The patient presented with acute onset of seizures 1 week status post left carotid endarterectomy . Axial FLAIR MRI (a) and ADC map (b) show areas of high T2 signal with elevated diffusivity in

the left cerebral hemisphere watershed zones. CTA MIP image (c) shows asymmetrically prominent left middle cerebral artery branches diffusely

Fig. 12.31  Carotid artery restenosis. Initial postoperative axial CTA image (a) shows a patent proximal left internal carotid artery. Axial (b) and curved planar reformatted (c) CTA images obtained 6 months later now show focal high-grade stenosis at the origin of the left internal

carotid artery due to low-density plaque at the site of reanastomosis (arrows). Doppler ultrasound (d) confirms the presence of high-grade stenosis of the proximal internal carotid artery with turbulent flow and velocities surpassing 500 cm/s

Fig. 12.32  Post-endarterectomy carotid artery occlusion and cerebral infarction. Delayed phase axial CTA image (a) shows occlusion of the CCA at the site of recent CEA

(arrow). The diffusion-weighted image (b) shows an associated left internal capsule/insula infarction (arrow)

Fig. 12.33  Cranial nerve injury. The patient presented with right cranial nerve XII deficit after right internal carotid endarterectomy. Initial postoperative axial CT image (a) shows that the endarterectomy was performed

at the expected level of the right hypoglossal nerve (arrow). A subsequent axial CT image (b) shows prolapse and fatty infiltration of the right hemi-tongue (encircled)