Complications
Generally caused by thrombosis of the endarterectomy site with intracranial embolism; or by embolization of atheromatous debris from the endarterectomized arterial surface.
Intraoperative anticoagulation with heparin and meticulous surgical technique are the best forms of prevention.
If a neurologic deficit is observed in the immediate postoperative period, this may be secondary to technical error. In this event, patients should be returned immediately to the operating room for re-exploration. Perioperative thromboembolic or atheroembolic strokes may prompt endovascular rescue attempts in the form of thrombectomy or thrombolysis.
Generally caused by thrombosis of the stent with intracranial embolism; or by embolization of atheromatous debris generated during delivery or deployment of the stent.
Preoperative dual antiplatelet therapy with aspirin and clopidogrel once daily along with intraoperative anticoagulation with heparin to maintain activated clotting times of 250 to 300 milliseconds is the best form of prevention. Dual antiplatelet therapy is used for 1 to 3 months following stenting, followed by aspirin alone.[25]
The risk of myocardial infarction is as high as 2.3% after carotid endarterectomy and 1.1% after carotid artery stenting, and depends on the cardiac status of the patient. The risk is concentrated within the first few days of the procedure.[32]
Aspirin before carotid endarterectomy, and aspirin plus clopidogrel before carotid artery stenting are the optimal methods of prevention.
Incisional hematomas (carotid endarterectomy) or puncture site hematomas (carotid artery stenting) are infrequent and best managed expectantly.
Rarely, expansile hematomas from continued active bleeding require operative intervention and blood transfusions.
Injuries to the hypoglossal, vagus, and glossopharyngeal nerves occur in about 6% of patients after surgery.[57]
They are most commonly a result of traction; rarely from a complete transection.
Most deficits will recover within 6 months of the surgery.
The risk of postoperative cerebral hemorrhage and cerebral hyperperfusion syndrome is highest in the first 72 hours after revascularization.
Neurologic symptoms (e.g., unilateral headache, stroke, seizure) occurring within hours, or sometimes days, after carotid artery revascularization.
This is a rare complication. It is more frequently associated with revascularization of an extremely tight stenosis and with a concomitant occlusion or tight stenosis in the opposite (contralateral) carotid artery. It is believed to occur slightly more frequently after carotid artery stenting compared to carotid endarterectomy because of the more aggressive intraprocedural anticoagulation used during carotid artery stenting.
Patients often present with nonspecific headaches and difficult to control hypertension postoperatively. Other symptoms include unilateral headaches, strokes, or seizures.
Brain imaging may reveal cerebral edema with or without frank hemorrhage. Severe instances may be associated with a midline shift.
Management is essentially supportive and includes control of blood pressure, reduction of anticoagulation (if any is being used), head elevation, and surgical decompression in the worst instances.
This is a rare complication of endarterectomy and carotid artery stenting and is generally associated with the aggressive anticoagulation and antiplatelet therapy utilized during the procedure or hypertension in the postoperative phase.
When part of the cerebral hyperperfusion syndrome, symptoms include unilateral headaches, seizures, or strokes.
Treatment is guided by the severity of the complication and is generally supportive. It may include management of blood pressure, head elevation, and surgical decompression in severe cases.
In patients with asymptomatic carotid stenosis, the annual stroke rate ranges from 1% to 5%.[55][56] The risk rises if a prior transient ischemic attack or stroke has already occurred and approaches 10% per year.[24]
The etiology is usually atherosclerotic plaque disruption and embolization with ischemic brain infarction.
For asymptomatic stenoses <70%, optimal pharmacologic therapy is the mainstay of stroke prevention, while revascularization is reserved for selected patients with high-grade stenoses ≥70%.
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