George L. Hines

Cerebral hyperperfusion syndrome after carotid intervention: a review.

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.

Cerebral Oximetry Monitoring During Carotid Endarterectomy: Effect of Carotid Clamping and Shunting

Cerebral oximetry is a simple method of measuring regional cerebral oxygen saturation (rSO2). 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 rSO2. 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 rSO2 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 rSO2 by –12.3% (p<0.001). Shunt insertion (t2 vs t3) increased rSO2 by 10.9% (p< 0.001). Contralateral rSO2 for the same time periods was insignificant. Patients with preoperative neurologic symptoms had a greater decrease in rSO2 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 rSO2 as a result of clamping and shunting of the carotid artery. Symptomatic patients had a greater drop in rSO2.

A contemporary review of popliteal artery aneurysms.

Popliteal artery aneurysms account for 85% of all peripheral aneurysms and are frequently associated with abdominal aortic aneurysms. Up to 75% of all popliteal artery aneurysms are discovered in symptomatic patients who present with arterial insufficiency, leg swelling, or pain. Popliteal artery aneurysms can be diagnosed with duplex ultrasonography. Aneurysm repair should be considered for all symptomatic patients with rest pain or limb-threatening symptoms. Asymptomatic aneurysms larger than 2 cm should also be treated to prevent the development of limb-threatening ischemia and assure better surgical bypass graft patency and longer freedom from amputation. Conventional aneurysm repair consists of either opening the aneurysm sac and interposing a bypass graft or aneurysm ligation combined with bypass grafting. If the aneurysm sac is left intact, side branch perfusion may persist and the aneurysm may continue to enlarge and can rupture. Endovascular popliteal aneurysm repair has not demonstrated clinical equipoise to standard surgery but may be advantageous in select high-risk patients.

Cerebral Embolic Stroke and Arm Ischemia in a Teenager With Arterial Thoracic Outlet Syndrome: A Case Report

A rare presentation of arterial thoracic outlet syndrome (TOS) is described in a young woman. Arterial TOS caused by a cervical rib produced acute upper extremity ischemia due to subclavian artery aneurysm formation. Clinical presentation also included left hemiparesis caused by right subclavian artery thrombosis and retrograde embolization of thrombus via the common carotid artery to the right middle cerebral artery distribution. Surgical repair of the subclavian artery was performed, but permanent neurologic deficit remained. Acute thrombosis of the right subclavian artery can produce cerebrovascular complication. The assessment of such risk in patients with arterial TOS is warranted and the arterial lesion corrected surgically.

Splenic vein aneurysm: Is it a surgical indication?

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 Dissection of the Abdominal Aorta: Experience With Five Patients

Spontaneous dissection of the infradiaphragmatic abdominal aorta is a rare form of aortic dissection. Its natural history and management are not well defined. We have recently treated five patients with spontaneous aortic dissection. Two patients had acute dissections and three had chronic dissections. Three patients developed saccular aneurysms and underwent resection. Two patients had stable dissections and were treated medically. All patients are alive and well at 6 months to 5 years. We think that spontaneous aortic dissection can be treated as a variant of type III dissection with initial medical management, reserving surgery for those patients in whom a saccular aneurysm or a complication of the dissection develops.

Diagnosis and management of acute type A aortic dissection.

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.

Surgical Intervention for Acute Intestinal lschemia: Experience in a Community Teaching Hospital

The aim of this study was to evaluate the current management of acute mesenteric ischemia secondary to thrombotic or embolic occlusion of visceral vessels in a community teaching hospital. Between October 1997 and July 2000, a review of all hospital discharges revealed 83 patients with a discharge diagnosis of “acute vascular insufficiency-intestine.” Among these 83 patients, 22 cases of acute mesenteric ischemia were confirmed. Management of these 22 patients was divided into 2 groups for analysis. In Group A, 14 patients were aggressively treated with visceral angiography (n = 10), visceral artery bypass (n = 8), visceral embolectomy (n = 4), and bowel resection (n = 7). In 8 of 14 of these patients, surgical intervention occurred in less than 24 hours from presentation. In Group B, 8 patients were managed with supportive care because of advanced age (mean age = 86 ±7 years), comorbid conditions, or patient and family preference. Postoperative morbidity in Group A consisted of cardiac events (n = 3), pulmonary insufficiency (n = 5), and prolonged gastrointestinal tract dysfunction (n = 3). Twelve of 14 patients in Group A survived and were discharged, whereas only 2 of 8 patients in Group B survived and were discharged from the hospital. Although the literature suggests that there can be a significant delay in the diagnosis and treatment of acute mesenteric ischemia, the early recognition and aggressive treatment of acute mesenteric ischemia resulted in a good survival rate. Supportive management of very elderly and debilitated patients needs to be considered on a case-by-case basis. Although the outlook for such patients is dismal, survivors are possible as demonstrated by this series.

Chronic mesenteric ischemia: diagnosis and treatment.

Chronic mesenteric ischemia is an uncommon manifestation of atherosclerotic disease. The presentation of chronic mesenteric ischemia is often confusing and the diagnosis is usually not made until late in the course of the disease. Selective angiography is considered the gold standard for establishing the diagnosis of chronic mesenteric ischemia. The treatment options for patients presenting with symptomatic chronic mesenteric ischemia include various surgical approaches to revascularization and catheter-based interventions.

Surgical management of mesenteric occlusive disease: a contemporary review of invasive and minimally invasive techniques.

Mesenteric ischemia (MI) is caused by compromised blood flow to the arteries supplying the small and large intestine. Acute occlusive mesenteric ischemia (AMI) presents with the abrupt onset of severe abdominal pain, which if not diagnosed and treated immediately can cause bowel necrosis and prove fatal. Chronic occlusive mesenteric ischemia (CMI) is usually a longstanding process characterized by postprandial abdominal pain, progressive food intolerance, and weight loss. If untreated, CMI can lead to progressive disability and failure to thrive. This review article highlights the clinical and radiologic diagnosis of acute mesenteric ischemia and CMI and compares their treatment with surgical revascularization and the less invasive alternative of mesenteric artery angioplasty and stenting.