The concept of the high-risk CEA must be critically reexamined. Although 29% of patients for CEA were high risk as defined by others, we found no evidence that this influenced the results after CEA. Patients with significant medical comorbidities, contralateral carotid occlusion, and high carotid lesions can undergo operation without increased complications. If a high-risk group exists, it is small and restricted to reoperation or radiated neck (4% in this series). With this possible exception, carotid angioplasty stenting should be restricted to randomized clinical trials.
Cerebral hyperperfusion syndrome (CHS) after carotid surgery, although rare, is a well-described phenomenon. Although originally described after carotid endarterectomy, it has now also been described after carotid artery stenting. It is classically described as an acute neurologic deficit occurring several days after a carotid procedure, associated with severe hypertension and preceded by a severe headache. CHS represents a spectrum of clinical symptoms ranging from severe unilateral headache, to seizures and focal neurologic defects, to intracerebral hemorrhage in its most severe form. The exact mechanism leading to CHS is unknown; however, it seems to be related to increased regional cerebral blood flow secondary to loss of cerebrovascular autoregulation. Given the significant morbidity associated with CHS, researchers have been trying to identify which patients are most at risk. This is a difficult task given the rarity of the disease and the multiple confounding factors in the patient population who undergo carotid intervention. The goal was to determine those patients most at risk preoperatively, so that they may be more closely monitored postoperatively to prevent the development of CHS and its associated morbidity. The purpose of this review was to summarize the data currently available in the literature on CHS, with emphasis on pathophysiology, risk factor assessment, diagnostic modalities, and disease management, to provide insight for future research to better elucidate how to reduce the morbidity and mortality caused by CHS.
Splenic vein aneurysms are rare and are usually caused by portal hypertension. Symptoms are unusual, but may include rupture or abdominal pain. Diagnosis can usually be made either by means of duplex ultrasonography or computed tomography scanning. Treatment varies from noninvasive follow-up to aneurysm excision. We report an expanding splenic vein aneurysm in a young woman with abdominal and back pain and no history of portal hypertension. She was treated with aneurysm excision and splenectomy.
Spontaneous recanalization of a chronically occluded internal carotid artery (ICA) is a rare occurrence. The authors report 3 patients who had documented total occlusion of the ICA followed by late spontaneous recanalization with subsequent high-grade stenosis. The patients in this series had occlusions for 11 months, 36 months, and 39 months, respectively. One patient had symptoms ipsilateral to the recanalized vessel, and 2 patients were asymptomatic. Endarterectomy was performed uneventfully in 2 patients and pathologic specimens demonstrated typical atherosclerotic plaque with patent lumens. Our experience demonstrates that although chronic recanalizations of occluded ICAs are rare, this does occur. Pathology demonstrates typical atherosclerotic plaque which appeared to have been recanalized by lysis of thrombus. The natural history of this condition is not well known and indications for intervention are not well established.
Cerebral oximetry is a simple method of measuring regional cerebral oxygen saturation (rSO(2)). One promising application is its use during carotid endarterectomy (CEA) to help minimize the risk of perioperative stroke. The authors used the INVOS-4100 cerebral oximeter at several steps during CEA to measure the effect of carotid clamping and shunting on rSO(2). The authors prospectively evaluated 42 consecutive CEAs in 40 patients. All had CEA under general anesthesia with the routine use of a Javid shunt. The INVOS-4100 oximeter was used to measure rSO(2) before clamping (t1), after clamping but before shunting (t2), 5 minutes after shunt insertion (t3), and after patch closure with reestablished flow (t4). The Wilcoxon signed-rank and rank-sum tests were used for analysis. Clamping of the internal carotid artery (t1 vs t2) resulted in a drop of ipsilateral rSO(2) by -12.3% (p < 0.001). Shunt insertion (t2 vs t3) increased rSO(2) by 10.9% (p < 0.001). Contralateral rSO(2) for the same time periods was insignificant. Patients with preoperative neurologic symptoms had a greater decrease in rSO(2) after clamping (-18.4%) compared with a decrease of -10.4% in asymptomatic patients (p = 0.037). Cerebral oximetry monitoring is simple and inexpensive. The study showed statistically significant changes in rSO(2) as a result of clamping and shunting of the carotid artery. Symptomatic patients had a greater drop in rSO(2).
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