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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.

Acute aortic dissection (AAD) is the most common aortic catastrophe. The mortality rate of type A dissection approaches 40% to 50% in 48 hours. Causes of death include rupture, aortic insufficiency, or malperfusion involving the coronary arteries, head vessels, visceral arteries, and lower extremities. Other acute aortic conditions can be confused with AAD. Emergent surgery is usually recommended, although there are some situations in which initial management of malperfusion or conservative therapy can be considered prior to proximal aortic repair. Various surgical techniques are employed to manage AAD. This article reviews the etiology, clinical presentations, and management of patients with type A AAD.

BACKGROUND:Cerebral hyperperfusion syndrome (HS) is presumed to be because of an increase in postendarterectomy flow in patients with fixed cerebral vascular reserve. Severe headache is thought to be an early sign of possible HS. An increase in partial pressure CO₂ (pCO₂) is known to cause cerebral vasodilatation and is used to evaluate the presence of cerebral reserve. METHODS:A total of 45 patients undergoing carotid endarterectomy had internal carotid artery flow measured with a transonic flow probe as follows: F1, immediately after full dissection of the internal carotid artery; F2, after 30 seconds of breath holding; and F3, after restoration of flow. ΔF2-F1 and ΔF3-F2 were also evaluated. A 10% increase between F2 and F1 indicated normal cerebral reserve and between F3 and F2 indicated increased postoperative flow. Age, gender, medical comorbidities, indication for carotid endarterectomy, intraoperative cerebral oximetry values, and percentage of bilateral carotid stenosis were recorded. All patients were contacted after discharge about the presence of postoperative headache or other suggestions of HS. Fisher's exact test was used for categorical predictors and the rank-sum test for continuous predictors. RESULTS:Seven (16%) patients (group A) developed postoperative headache and 38 (group B) did not. No patient developed HS. No variables were associated with postoperative headache except for female gender (p = 0.005). There were no statistically significant differences in F1, F2, F3, and ΔF (F2-F1 or F3-F2) between groups A and B (there was no descriptively significant ΔF2-F1 in 17 patients). Only one of the nine patients who had no change between F2 and F1, who had a significant increase in F3, and who was thought to be at higher risk for HS developed a postoperative headache. CONCLUSIONS:Lack of cerebral reserve is common in patients undergoing endarterectomy. If headache is an early sign of hyperperfusion, it does not seem to be predicted by lack of cerebral reserve and an increase in postendarterectomy flow.

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.

Endovascular repair of aortic dissection is the subject of multiple studies. This article aims to review the current literature on Type B complicated and uncomplicated dissection, including indications for medical therapy, open surgical therapy, and endovascular therapy. The review suggests a benefit for thoracic endovascular aortic repair in complicated dissection and medical therapy for uncomplicated dissection. Upcoming trials may shed more light on this issue.

BACKGROUND:This study evaluated patients undergoing femoropopliteal bypasses using endoscopically harvested vein to treat Trans-Atlantic Inter-Society Consensus (TASC) stage D lesions. Primary patency and primary assisted patency were evaluated, as were perioperative morbidity and mortality and hospital length of stay (LOS). Results for this minimally invasive alternative to femoropopliteal bypass with conventional open vein harvesting were analyzed. METHODS:A retrospective analysis was performed on patients who underwent femoral-popliteal bypass with endoscopic saphenous vein harvest and angiographic TASC D anatomy. Postoperative duplex exams were evaluated, and the study end points of graft thrombosis or the development of a high-grade stenosis prompting reintervention were sought. Patient demographics, morbidity, mortality, and hospital LOS were analyzed. RESULTS:Twenty-seven patients meeting our inclusion criteria underwent surgery between June 2002 and June 2007. Indications for surgery in these patients were claudication (n=10), gangrene or ulceration (n=9), and ischemic rest pain (n=8). Fifty-two percent of the patients were male, 50% had cardiac disease, 65% had hypertension, 54% were diabetic, and 65% had a significant smoking history. Median LOS was 2.5 days in claudicants, 3.0 days in patients with rest pain, and 7.0 days in patients with gangrene or ulceration (p<0.05). Kaplan-Meier primary patency and primary assisted patency rates were 73.2% and 80.8% at 1 year, respectively; and these rates were maintained for 70 months. The only perioperative complication was a superficial wound infection, and two patients died during follow-up from causes unrelated to the surgery. CONCLUSION/CONCLUSIONS:Femoropopliteal bypass using endoscopic vein harvest is a durable reconstructive vascular procedure which can be performed with minimal postoperative morbidity, short LOS, and satisfactory long-term patency.

Portal venous aneurysms are rare and are usually discovered as incidental findings on abdominal imaging studies. Although most are asymptomatic, they may occasionally cause symptoms of compression of an adjacent structure, thrombosis, or bleeding. Treatment is usually not necessary and conservative follow-up is suggested. We present four patients with portal system aneurysms. One patient had a 10.5 cm thrombosed aneurysm, one had a right 3.5 cm intrahepatic portal aneurysm, one patient had a symptomatic 4 cm splenic artery aneurysm, which was repaired, and one patient had a 4 cm aneurysm at the confluence of the splenic and portal veins.

A 42-year-old woman developed right arm and right leg weakness when turning her head to the left. A carotid angiogram, in the neutral position, demonstrated anterior deviation of the left internal carotid artery and complete occlusion of the left internal carotid artery when the head was rotated to the left. During surgery, our patient had redundant left internal carotid artery and was treated by resection and reanastomosis of the internal carotid artery. The patient's Doppler 4 months postoperatively showed widely patent arteries, and she has subsequently been asymptomatic.