Fig. 20.1
The NASCET method of measuring internal carotid stenosis. The internal carotid artery distal to the stenosis is used as the reference vessel diameter (A). The minimal lumen diameter is measured in the proximal internal carotid artery (B). The percent stenosis is calculated as % diameter stenosis = (1 − [B/A]) × 100
As an invasive exam, carotid DSA carries the risk of complications. Catheterization of the aortic arch, aortic branches, and common carotid arteries can dislodge atherosclerotic plaque or generate thromboemboli resulting in a stroke. Other risks common to all forms of angiography include bleeding, pseudoaneurysm, dissection, and contrast reaction. Although the potential risks of carotid DSA have discouraged its use as a purely diagnostic exam, it still plays a role in the management of patients with carotid stenosis. Treatment decisions for carotid disease are now usually based on the results of duplex ultrasonography, CT angiography (CTA), or magnetic resonance angiography. Ensuring the accuracy and reliability of these noninvasive exams requires regular audits to validate and correlate their findings with DSA images. Beyond quality assurance, carotid DSA is also essential for planning and performing carotid artery stenting. Angiographic findings, including aortic arch morphology, vessel tortuosity, plaque ulceration, and angulation, kinking, or coils within the inflow, bifurcation, or outflow vessels of the carotid system have implications for both endovascular and surgical intervention. Cerebral angiography which is usually performed in conjunction with carotid DSA provides information regarding the status of the intracranial circulation.
CTA and MRA provide detailed imaging of the carotid and cerebral circulations and have been increasingly used prior to carotid interventions. The NASCET methodology for determining carotid stenosis (percentage by diameter) should be applied for both CTA and MRA. As previously discussed, validating these imaging modalities requires correlation with the gold standard, i.e., diagnostic angiography including intra- and interobserver variability [15, 16]. Anatomic assessment of the aortic arch, carotid tortuosity and morphology, status of the intracranial circulation, and morphologic characterization of the carotid lesions using CTA and MRA is useful for planning carotid interventions, particularly carotid stenting [15, 16].
Treatment
All patients with carotid stenosis, irrespective of degree of stenosis, symptomatic status, or surgical risk should receive best medical therapy for atherosclerotic disease including risk factor reduction, antiplatelet therapy, and lifestyle modification [1]. The goals of medical treatment should be optimization of both primary risk factors, namely, high systolic blood pressure and elevated low-density lipoprotein (LDL) cholesterol, and secondary risk factors, including diabetes, high non-high-density lipoprotein (non-HDL) cholesterol, smoking, excess weight, and insufficient exercise. Systolic blood pressure should be ideally maintained below 140 mmHg (<130 mmHg in the case of patients with diabetes) and LDL cholesterol levels below 70 mg/dL.
Intervening for carotid stenosis now involves choosing between surgical repair in the form of a carotid endarterectomy (CEA) or endovascular therapy involving carotid angioplasty/stent (CAS). In the past, CEA was considered the treatment of choice for appropriately selected patients with low to moderate surgical risk while CAS was reserved for patients at high surgical risk due to either medical comorbidites or hostile anatomy. Recent evidence suggests that CAS is a feasible form of treatment for patients with carotid stenosis regardless of risk status. Although CEA remains one of the most well studied and widely performed vascular procedures, practice patterns may begin to shift toward endovascular therapy with more patients eligible to receive CAS.
Treatment indications for performing a carotid endarterectomy (CEA) or carotid angioplasty/stent (CAS) vary according to the severity of stenosis and surgical risk. For moderate- and low-risk patients, CAS has the same indications as CEA for both symptomatic and asymptomatic patients. These indications are based on the CREST trial [7] and include:
Symptomatic carotid stenosis ≥50 % by angiography, ≥70 % by duplex ultrasound, or ≥70 % by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) if the stenosis on ultrasonography was 50–69 %.
Asymptomatic carotid stenosis ≥60 % by angiography, ≥70 % by ultrasound, or ≥80 % by CTA or MRA if the stenosis on ultrasonography was 50–69 %.
In practice, the decision to intervene for asymptomatic carotid stenosis is not always as straightforward as these guidelines imply. Medical therapy may be the most appropriate treatment in patients older than 75 or 80 who have stable, asymptomatic carotid stenosis. At the other end of the spectrum, younger patients with more rapidly progressive internal carotid stenosis or an ulcerated plaque usually benefit from an intervention.
High-risk, symptomatic patients have the same treatment indications as conventional risk patients (previously cited), whereas asymptomatic, high-risk patients require greater than 80 % stenosis based on angiography to be considered for treatment with CAS. The higher degree of stenosis required for asymptomatic high-risk patients is solely based on the arbitrary inclusion criteria of the clinical trials and observational studies that the FDA used for the approval of CAS devices in the United States [1, 9, 17]. Most of these studies assumed that CAS was only justified in high-risk patients with severe stenosis even though this has never been assessed or proven by any solid evidence or device trials. The criteria of greater than 80 % stenosis for asymptomatic patients to be considered for CAS will continue because it has been incorporated into the regulatory policies that still dictate reimbursement for CAS.
For patients with carotid stenosis who pose a high risk for surgery, CAS offers an interventional alternative that avoids the morbidity and mortality associated with CEA. High-surgical-risk status can be classified as relating to anatomic factors or medical comorbidities [9]. Anatomic high-risk criteria include restenosis after previous CEA or in-stent restenosis; high or low lesions defined as those superior to the second cervical vertebra or inferior to the clavicle; previous cranial nerve injury (ipsilateral or contralateral); “hostile neck” because of previous radical neck dissection, radiation, presence of a permanent tracheostomy, or a frozen neck; and other associated carotid lesions such as tandem lesions within the same carotid artery or stenosis or occlusion of the contralateral internal carotid artery (ICA). Medical high-risk criteria include class III or IV angina or congestive heart failure, coronary artery disease necessitating revascularization within 4 weeks, and severe chronic obstructive pulmonary disease defined as a forced expiratory volume ≤30 % of predicted or <1 L or the need for home oxygen.
Based on the results of the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST), the FDA recently approved carotid stenting devices for conventional surgical risk patients with carotid stenosis [7, 18]. Although any patient with severe carotid stenosis can now be treated with CAS, reimbursement constraints limit the wide application of CAS. The debate continues as to whether CAS should be considered as a treatment alternative on equal footing with CEA for all patients with carotid stenosis. Recent improvement and refinement in best medical therapies for atherosclerotic diseases have also questioned the benefit of carotid interventions, particularly among asymptomatic high-risk patients. Future clinical trials will help define which patient populations benefit the most from each form of carotid intervention and/or medical therapy. Clinicians will make the most appropriate treatment decisions if they can classify patients with carotid stenosis into one of three categories: patients at high risk for CEA who would benefit from CAS, patients at high risk for CAS that should be treated with CEA, or patients for whom best medical therapy alone may be sufficient.
Mesenteric Ischemia
Mesenteric ischemia results from atherosclerotic stenosis or embolic occlusion of the celiac, superior mesenteric, or inferior mesenteric arteries. Acute mesenteric ischemia (AMI) can result from abrupt embolic occlusion of the superior mesenteric artery (SMA), while chronic mesenteric ischemia usually requires stenosis or occlusion of two of the three arteries supplying the gastrointestinal tract. Mesenteric venous thrombosis and nonocclusive vasospasm can also cause acute mesenteric ischemia.
Multilevel atherosclerotic disease, cardiac arrhythmias, female sex, advanced age, and recent vascular interventions are the most common risk factors for AMI. Despite advances in endovascular therapy and critical care, AMI still has an in-hospital mortality rate as high as 80 % [19]. Several characteristics and conditions conspire to make AMI such a deadly condition including: an ambiguous clinical presentation, delayed diagnosis, long-duration ischemia, reperfusion injury, and medical comorbidities. Chronic mesenteric ischemia (CMI) typically occurs in elderly, frail patients with extensive atherosclerotic disease who present with significant weight loss and malnutrition because of “food fear.” Successful management for both acute and chronic mesenteric ischemia requires tailoring the treatment plan to match the severity of ischemia and the patient’s coexisting medical problems.
The two mechanisms of AMI are embolism and thrombosis [20]. The most common sources of emboli are cardiac lesions, including left atrial or ventricular mural thrombus, and lesions of the aortic or mitral valves that occur in the setting of atrial fibrillation or myocardial infarction. The embolus usually lodges a few centimeters distal to the ostium of the SMA near the origin of the middle colic artery. In contrast, SMA thrombosis occurs when clot forms within an existing atherosclerotic plaque usually located in the proximal segment of the vessel. Making the clinical distinction between an embolus to the SMA and an SMA thrombosis can be challenging.
Diagnosis
Prompt diagnosis and treatment play an important role in improving the clinical outcome of patients with AMI. Unfortunately, the vague and nonspecific initial clinical presentation of AMI often prevents clinicians from recognizing and treating AMI early in its course. Patients with AMI often present with complaints of abdominal pain that appears to be out of proportion to findings on physical exam. As ischemia progresses, the pain becomes more intense and other gastrointestinal symptoms appear including nausea, vomiting, diarrhea, and abdominal distension. Although it is initially benign, the abdominal examination evolves into an acute abdomen with diffuse tenderness, guarding, rebound, and eventually peritonitis. A detailed history and physical exam should point to the diagnosis of AMI and allow the distinction from CMI. Most patients with AMI have associated dehydration and electrolyte imbalances that require intravenous fluid resuscitation. Other abnormal lab values such as leukocytosis, metabolic acidosis, and amylasemia usually occur in late presentations of AMI and reflect more advanced ischemia.
Patients with CMI typically give a history of postprandial abdominal pain, weight loss, and intermittent diarrhea. They complain of crampy abdominal pain that characteristically occurs 15–45 min after food ingestion. “Food fear” is the term used to describe the behavior of patients with CMI who do not eat in an attempt to avoid postprandial pain. Although “food fear” is pathognomonic for CMI, it is not a required symptom for the diagnosis. Some patients with proven CMI completely deny postprandial abdominal pain and “food fear.” Only with specific questioning does it become obvious that these patients restrict their diet to small amounts of specific food (e.g., toast and crackers) that allows them to avoid pain after eating. While CMI itself does not cause intestinal malabsorption, food avoidance and diet restrictions over the protracted course of CMI usually causes malnutrition and frailty in this elderly population. On physical exam, up to two-thirds of patients with CMI have an abdominal bruit on abdominal auscultation [21].
Plain abdominal X-rays for the evaluation of intestinal ischemia are usually nondiagnostic. Nonspecific plain film findings include air in the wall of the intestine or portal venous system in advanced cases of AMI and calcification of the aorta and the visceral arteries in patients with CMI. Duplex ultrasound has limited utility for diagnosing AMI because patients often have an ileus and the dilated, air-filled bowel loops prevent adequate sonographic visualization of the visceral arteries. In contrast, duplex ultrasound has greater than 80 % accuracy for the diagnosis of CMI [21]. Although its accuracy depends on the skill of the operator and requires external validation, the duplex ultrasound has emerged as a useful, noninvasive screening test for patients suspected of having CMI. Moreover, weight loss and the thin body habitus, prevalent among many patients with CMI, allows for technically straightforward ultrasound visualization and interrogation of the visceral vessels. Widely accepted velocity criteria for the diagnosis of stenosis include a peak systolic velocity greater than 275 cm/s for the SMA and greater than 200 cm/s for the celiac artery in a fasting state [21].
CT angiography has replaced catheter-directed DSA as the imaging modality of choice for diagnosing mesenteric ischemia. CTA can be used to confirm the diagnosis in patients suspected of having either acute or chronic mesenteric ischemia. Multidetector CT systems and 3-dimentional-reconstruction software also generate an indispensable guiding road map for planning a mesenteric revascularization [22, 23]. Patients with abnormal renal function may not be candidates for a standard CTA because of the risk of contrast nephropathy. Diagnostic imaging exams that lower the risk of nephrotoxicity include MR angiography (with gadolinium), highly selective diagnostic angiography, or CTA using intra-arterial (as opposed to intravenous) contrast administration.
Treatment
Acute mesenteric ischemia requires early diagnosis and prompt treatment to avoid ongoing bowel ischemia which will ultimately lead to necrosis, perforation, and peritonitis. After confirming the diagnosis treatment begins with systemic anticoagulation with intravenous heparin unless an absolute contraindication exists. The main goal of anticoagulation is to prevent thrombus propagation within the mesenteric vessels. Because AMI can occasionally present as a complication in patients suffering an acute myocardial infarction, an electrocardiogram and cardiac enzymes should be obtained prior to any intervention. Patients with an acute abdomen on physical exam require immediate transfer to the operating room for abdominal exploration.
Over the past several years, endovascular intervention has proven to be a viable treatment option for selected patients with AMI. Ideal patients for endovascular therapy include those who present early in the course of AMI (less than 8 h from the onset of symptoms) without an acute abdomen or evidence of bowel ischemia based on physical examination and laboratory evaluation. Patients with high surgical risk and severe comorbidities may also be considered for endovascular therapy [24]. A combination of catheter-directed mechanical thrombectomy and thrombolysis with or without ultrasound acceleration and balloon angioplasty and/or stenting may be required to restore SMA patency and treat the culprit lesions. Incorporating diagnostic laparoscopy into this minimally invasive approach allows for an evaluation of bowel viability.
Patients with AMI and advanced ischemia or peritonitis require an exploratory laparotomy for bowel resection and surgical revascularization. If a mesenteric embolism is suspected, the SMA is exposed and controlled at the root of the mesentery. Balloon embolectomy catheters are advanced proximally to remove the embolus. Distal arterial branches usually require manual milking of the mesentery to extrude the thrombus. Bowel resection and ostomies are then performed as required. A second-look exploration to assess bowel viability should be performed 24–48 h later regardless of the patient’s clinical improvement.
If mesenteric thrombosis or chronic ischemia is suspected or confirmed, the proximal SMA is exposed by mobilizing the fourth portion of the duodenum and incising the ligament of Treitz. A bypass procedure to the SMA is frequently required using antegrade or retrograde inflow. The supraceliac aorta, the infrarenal aorta, or common iliac arteries are the most frequent inflow vessels. Autologous vein graft is preferable in cases of acute thrombosis because of the risk of contamination if bowel viability is compromised. Bypass to both the SMA and the celiac or hepatic artery are frequently performed for chronic mesenteric ischemia using bifurcated prosthetic grafts [23, 24]. The supraceliac aorta is the preferred inflow vessel in these chronic cases as it is rarely affected by advanced atherosclerotic disease. Nonocclusive mesenteric ischemia, which is usually secondary to hypoperfusion in the setting of hypovolemia, vasopressors, or underresuscitation, requires treatment of the underlying condition and occasionally catheter-directed, intra-arterial papaverine infusion. Surgical exploration is indicated if bowel ischemia is suspected.
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