Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3742_Библиотеки_им_академика_М_И_Перельмана

Most nerve injuries associated with carotid endarterectomy affect the hypoglossal or vagus nerves, and a vast majority of nerve injuries are transient. Data from the European Carotid Surgery Trial (ECST) were gathered on the largest series of patients undergoing CEA in which neurological assessment was performed before and after surgery. The study revealed that a 4% risk of moderate cranial nerve injury persisted beyond hospital discharge. A meta-anal­ysis of 26 articles published between 1972 and 2015 corresponding to 20,860 CEAs revealed the vagus nerve is the most frequent nerve injured (3.99%) followed by the hypoglossal nerve (3.79%). Some variations in reporting may reflect temporary weakness being permanent nerve injury, thus accounting for a higher incidence of hypoglossal nerve palsy. Cranial nerve injury is more common in patients undergoing repeat carotid endarterectomy and CEA for high plaque.

Patch graft closure with CEA is almost universally performed. The most common patches used are bovine pericardial patch, Dacron PTFE, and autologous vein patch. Carotid vein patch blowout has been reported in the past. At present, the autologous vein patch is not as commonly used. Approximately 0.25%–0.5% of all synthetic patches appear to get infected following CEA. Patch graft infection may appear early or late and has a bimodal distribution depending on the virulence of the microorganism. Postoperative hematoma is associated with late development of infection. Most patients with patch graft infections present with neck swelling, pseudoaneurysm, or a draining sinus at the time of the incision. CT angiography of the neck is necessary for com­plete evaluation. Complete excision of the infected tissue and arterial reconstruction with autolo­gous interposition vein graft should be considered. In patients with a history of neck radiation with poorly vascularized tissues such as the sternocleidomastoid muscle (if present) or pectoralis major, a myocutaneous flap should be performed. An interposition vein graft tends to develop myointimal hyperplasia at follow-up. The site of myointimal hyperplasia is usually at the site of the valves. Carotid stenting is an option for carotid restenosis due to myointimal hyperplasia. Long-term results of carotid stenting for carotid interposition graft stenosis are not well defined.

In a small number of patients, opening a high-grade stenosis in the CCA/ICA can result in a significant increase in regional cerebral blood flow with loss of autoregulation resulting in hyperperfusion and intracerebral hemorrhage. In its milder form, hyperperfusion syndrome manifests as headaches or seizures, which are the result of cerebral edema. Following CEA/ CAS, intracerebral hemorrhage occurs in less than 1% of patients with a mortality of approxi­mately 50%, with associated significant morbidity in most survivors. There is a higher risk of postoperative intracerebral hemorrhage among patients undergoing CAS as compared to patients undergoing CEA. Intracerebral hemorrhage occurs in the first 24 hours following CAS and 2–7 days following CEA. Systemic hypertension, if not controlled, is an important risk factor for intracerebral hemorrhage. Intracerebral hemorrhage, if localized to the frontal lobe, can be treated urgently by a neurosurgeon with craniotomy. However, a large intrace­rebral hemorrhage in the parietal lobe with midline shift requires reversal of anticoagula­tion, modest blood pressure reduction, and in some cases intracranial pressure monitoring. Treatment options are limited. Ipsilateral CEA should preferably be delayed for at least 3 months after contralateral CEA for asymptomatic stenosis in order to reduce the risk of hyperperfusion syndrome.

In patients undergoing CEA for high plaque mobilization of the internal carotid artery, divi­sion of the sternocleidomastoid branch of the occipital artery and often the occipital artery itself is required. This maneuver helps to mobilize the hypoglossal nerve cephalad. The posterior belly of the digestive muscle is retracted cephalad, or it may have to be divided to gain distal exposure of the internal carotid artery. For the hypoglossal nerve to be mobi­lized, the ansa hypoglossi may need to be divided. The hypoglossal nerve is gently looped with a silastic vessel loop and retracted cephalad.1 Following endarterectomy, the distal intima is inspected. If there is any question about the smooth tapering of the intima and hence its complete removal, completion operative arteriogram via a microcatheter in the CCA or via catheter in the superior thyroid artery is performed, and carotid stenting may be necessary (rarely). If there is any concern that the distal intima is not adequately removed to its distal feathery end with difficulty in visualizing the endpoint of endarterectomy, intraoperative carotid stenting is performed via a 6 or 7 Fr sheath inserted into the common carotid artery just above the clavicle with a micro puncture technique and a 0.014 microw­ire advanced cranially.