Carotid and Vertebral Artery Dissection

Spontaneous dissection of the carotid or vertebral arteries in the absence of trauma is rare. It usually occurs in patients with underlying history of hypertension, fibromuscular dysplasia, or an underlying collagen disorder such as Marfan or Ehlers-Danlos syndrome. It can occur at any age, and clinical manifestations are variable, including neck pain or ipsilateral headache, Horner syndrome (ptosis, myosis, and unilateral anhydrosis), and acute or chronic focal neurologic events either in the form of transient ischemic attack or as a permanent neurological deficit. All imaging modalities including ultrasound, CT, and MRI can be used to demonstrate the intimal flap, a compressed true lumen, slow flow in the false lumen, or even thrombus formation. Catheter angiography is generally indicated to better assess flow patterns or the absence of flow (see Fig. 11-2). The majority of patients are successfully treated with anticoagulation, but stent placement in the true lumen may be necessary to maintain or restore cerebral perfusion.

Aortic Emergencies

Acute aortic syndromes encompass a spectrum of aortic emergencies that include traumatic aortic injury (TAI), aortic dissection, penetrating atherosclerotic ulcer of the aorta, intramural hematoma, and aortic aneurysm rupture. Chapter 2 covers the topics of aortic dissection, intramural hematoma, and penetrating ulcer. This section focuses on traumatic aortic injuries.

TAI is a novel term that encompasses a spectrum of injuries characterized by a variable degree of aortic wall laceration and that include intimal tear, intramural hematoma, traumatic dissection, traumatic pseudoaneurysm, and, in the most severe form, aortic transection. TAI may result from rapid decelerations, crush injuries, penetrating wounds, and surgical or angiographic instrumentation. Blunt trauma is the most frequent cause of TAI, usually as the result of shearing, hydrostatic forces, and/or torsion forces applied along the aortic arch during a motor vehicle accident and falls from heights. Less common causes include displaced clavicular and thoracic vertebral fractures with entrapment of the aorta between the anterior chest wall and the spine. The overall mortality at the scene of the accident has been reported to be as high as 80% in autopsy series, with only 10% to 20% of the victims surviving the initial trauma. Bleeding from a laceration or rupture can be controlled by the aortic adventia or the periaortic tissues, which can help the patient survive the initial injury; however, the end result is pseudoaneurysm formation, which, due to its instability, requires prompt diagnosis and treatment (Fig. 11-3). The region of the aorta most susceptible to blunt injury is the isthmus, where the relatively mobile proximal thoracic aorta and arch join the fixed distal arch at the insertion of the ligamentum arteriosum, just distal to the left subclavian artery origin (Fig. 11-4). This area is involved in as many as 90% to 95% of the cases. Other common areas of injury are the aortic root and the diaphragmatic hiatus. Injuries to the ascending aorta are uncommon (5% to 9%) and usually lethal due to the lack of surrounding connective tissue, resulting in rapid death due to exsanguination or cardiac tamponade. Clinical suspicion as well as a prompt diagnosis and treatment remain of crucial importance in TAI, given that 30% of the victims will die within 6 hours and 40% to 50% will die within 24 hours.

Figure 11-3 TAI in the mid-descending aorta following blunt trauma. Axial (A) and coronal reformat (B) images demonstrate a localized complete rupture of the aortic wall that led to mediastinal periaortic hematoma leaking into both pleural spaces (asterisks). A pseudoaneurysm (arrows) has developed at the rupture site. C, Thin maximal intensity projection showing complete pseudoaneurysm occlusion after repair with stent graft.

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

Figure 11-4 Axial CTA (A) and sagittal reformat (B) demonstrating a TAI with intimal tear (arrows) distal to the left subclavian artery origin and surrounding hematoma consistent with a contained aortic rupture. There are also partially visualized left rib fractures, subcutaneous emphysema, and atelectatic left lung (arrowhead).

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

The initial imaging screening of trauma patients is obtained with plain radiographs due to the availability and capacity to quickly assess injuries such as pneumothorax, hemothorax, mediastinal hematoma (Fig. 11-5), and fractures. Clinical signs and symptoms found in patients with TAI include chest pain, back pain, dyspnea, cough, hoarseness, hypotension, pulse discrepancy, shock, and coma; as many as 30% to 50% of these patients may not show external signs of trauma.

Figure 11-5 Portable radiograph demonstrating multiple signs of TAI including a widened mediastinum, slight tracheal shift, widening of the right paratracheal stripe, left apical cap, obliteration of the aortopulmonary window with poorly defined aortic arch, and a left hemothorax with chest tube in place and rib fractures.

A normal upright chest x-ray (CXR) has a negative predictive value of 98% when evaluating patients for aortic injury; however, these can rarely be obtained in the setting of severe multitrauma patients, who tend to get a frontal poorly inspired film in which mediastinal abnormalities frequently cannot be adequately assessed. Indirect signs for possible TAI in CXR include widening of the mediastinum, tracheal shift, deviation of the nasogastric tube or endotracheal tube to the right of the T3-T4 spinous processes, widening of the left or right paraspinal lines, apical cap, opacification of the aortopulmonary window, hemothorax, depression of the left main stem bronchus, and an ill-defined aortic arch. Mediastinal widening has reported sensitivities ranging between 81% and 100% with specificity of 60%; however, there is significant inter-reader variability when using this sign to predict aortic injury.

Catheter aortogram has long been considered the gold standard for the diagnosis of TAI with reported sensitivities and specificities approaching 100%. However, MD-CTA has become the preferred method for screening major traumatic and nontraumatic aortic emergencies, thanks to its improved spatial and contrast resolution and supplemental postprocessing techniques (thin sections, multiplanar reconstructions [MPRs], three-dimensional volume-rendered images), with a performance that rivals that of catheter angiography. MD-CTA has helped to better characterize the location and extent of TAI and other vascular injuries, allowing for faster diagnosis and treatment planning. In addition, MD-CTA can also recognize a greater number of normal variants of the vascular anatomy and subtle vascular injuries, which were less likely to be seen with conventional CT scans (Fig. 11-6). Furthermore, the need to perform an aortography to confirm the diagnosis of TAI is eliminated when direct signs of injury are present on CTA. Direct signs of TAI in CT include active extravasation of contrast, pseudoaneurysm formation, irregularity of the aortic wall, abrupt change in caliber of the aorta, aortic dissection, intimal flaps, and filling defects. Indirect signs of possible aortic injury include periaortic hematoma and mediastinal hematoma (Fig. 11-7).

Figure 11-6 A and B, CTA images in the axial and coronal plane obtained after blunt chest trauma demonstrate an intimal tear (arrows) in the mid-descending aorta without extravasation or surrounding hematoma.

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

Figure 11-7 Contrast CT image obtained in a patient who sustained a motor vehicle accident demonstrating a concentric para-aortic hematoma without active extravasation or obvious wall defects that was managed medically and followed until resolution.

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

Catheter angiography can accurately demonstrate abnormalities affecting the aortic lumen; however, it is an invasive procedure that may require higher doses of contrast material, it is time-consuming, and it is limited to diagnosing concurrent injuries in multitrauma patients, risking a delay in management of other potentially lethal injuries. A minority of patients may still require catheter angiography when MD-CTA examinations are nondiagnostic or have equivocal or indirect signs of TAI. The decision to perform a catheter angiogram on patients with indirect findings depends on the experience of the interpreter, the quality of the scan, and the clinical condition of the patient. Angiographic diagnosis of intimal injury is demonstrated by the presence of intimal irregularity, linear defects, or filling defects caused by an intimal flap. The presence of contrast material outside the lumen is consistent with active extravasation. It can be contained or free; both are consistent with a transmural laceration and require immediate attention. The current complication rate for angiography is less than 1%, and complications include aortic rupture, acute renal failure, anaphylaxis, and entry site hematoma.

Transesophageal echocardiography (TEE) is another imaging modality that can provide detailed real-time images of the aorta, heart, and pericardium and can be done at the patient’s bedside. Studies have shown sensitivity between 63% and 100% and specificity between 84% and 100% for detecting aortic rupture. The wide range of these results is explained by the fact that TEE is operator dependent. Direct signs of aortic injury include the detection of an intimal flap, evidence of intraluminal thick stripes, detection of pseudoaneurysm, aortic occlusion, and aortic wall hematoma. The main TEE limitation is its “blind spot,” which represents the lack of visualization of a 3- to 5-cm segment in the distal ascending aorta and proximal arch that can be the site for TAI in 10% to 20% of patients. TEE is an alternative in the evaluation of unstable patients. However, a negative TEE in the setting of suspicious clinical or radiological findings warrants further investigation.

MRA is not currently considered the imaging technique of choice for the evaluation of TAI due to the relatively long acquisition times, the limited access to manage and control hemodynamically unstable patients, and the difficulties in scanning patients with metallic fragments or devices that may preclude the exam.

Treatment

Immediate surgical intervention is the treatment of choice in patients with TAI who are hemodynamically unstable, have persistent bleeding, or have evidence of expanding hematoma. Surgical repair is usually a major intervention requiring thoracotomy, aortic cross-clamping, partial cardiopulmonary bypass, suturing or prosthetic grafting of the aorta, and treatment of concomitant injuries such as the evacuation of pericardial tamponade or large hemothorax. The operative mortality of open thoracotomy ranges between 9% and 28%, with a high rate of major morbidities including paraplegia (up to 20%) due to spinal cord ischemia and stroke. Patient triage and selection are essential to perform a successful thoracotomy since open thoracotomy can worsen the clinical condition of severely injured patients who may not be able to tolerate this procedure.

Alternative management of TAI consists of delayed operative intervention or no operation while the patient is kept under close monitoring and blood pressure (BP) control to reduce the risk of free rupture. The mainstay of treatment is to maintain systolic BP below 120 mm Hg (mean BP below 80 mm Hg) and allow patients who have suffered associated severe trauma to stabilize before surgical repair. This approach is indicated in hemodynamically stable patients with small aortic tears or those with associated injuries such as significant head, cardiac, or pulmonary trauma, large body surface burns, contaminated wounds, large retroperitoneal hematomas, or other high-risk medical comorbidities. Some of these aortic injuries might develop into a chronic pseudoaneurysm (Fig. 11-8), and others might even resolve during the period of observation. Close clinical and imaging follow-up is imperative to detect injury progression or aortic rupture.

Figure 11-8 A and B, 68-year-old patient who sustained blunt trauma during motor vehicle accident 1 year before presentation. Axial and sagittal CTA images demonstrate a pseudoaneurysm (arrows) in the characteristic proximal descending aorta. The patient refused invasive repair at the time of injury; 1 year follow-up showed stable appearance without interval rupture or growth.

More recently, endovascular treatment of TAI using stent grafts has been introduced as an alternative in the management of hemodynamically stable patients and patients with contraindications to cardiopulmonary bypass, such as severe coagulopathy, extensive additional injuries, and severe underlying cardiac or pulmonary disease. Mortality and morbidity appear to be lower than those of surgery, most likely because of the less invasive nature of the procedure, shorter operation time, and lack of the surgery-related comorbidities. The stent grafts are delivered via a common femoral artery cut-down access and positioned under angiographic and fluoroscopic guidance. The left subclavian artery origin often has to be covered with the endograft to provide adequate proximal support without significant clinical consequence in many patients. A significant number of patients with TAI are young, and therefore their aortic size is small; most stent grafts available today are made for the treatment of larger aortas with degenerative aortic aneurysms. Even though it is usually recommended to oversize the stent graft by 10% to 20% to ensure an adequate seal, excessive oversizing has been associated with type I endoleaks (Table 11-1) and stent graft collapse. Complications related to the endovascular repair include groin hematoma, iliofemoral dissection, endoleak, graft migration, and arterial rupture. Overall morbidity rates have been found to be around 12% with mortality rates of 4%. Clinical and imaging follow-up in both surgical and endovascular treatment modalities is required for early identification of post-treatment complications.

Table 11-1 Endoleak Classification

Endoleak type I	Inadequate seal around the proximal or distal end of the stent graft
Endoleak type II	Retrograde flow from branch vessels (intercostal, lumbar, inferior mesenteric, gonadal arteries) resulting in persistent filling of aneurysm
Endoleak type III	Stent graft laceration or fabric tears, dislodgment of modular graft devices
Endoleak type IV	Porosity of the graft fabric, diffuse leakage through interstices
Endotension	Excluded sac continues to enlarge without apparent endoleak formation

Penetrating Aortic Injury

Penetrating injuries to the intrathoracic great vessels are uncommon, with an incidence of 1%, and a high mortality rate that ranges between 50% and 85% despite advances in trauma care and prehospital resuscitation. These types of injuries can be caused by gunshot wounds (GSWs) or stab wounds (SWs) that traverse the chest or the base of the neck (Fig. 11-9). Overall, GSWs are more common and more lethal than SWs. Penetrating injuries to the thoracic aorta are more common along the ascending aorta and the arch branches, with a documented low incidence of descending thoracic injuries. These types of lesions are commonly associated with coexisting lethal intrathoracic injuries, which worsen the patient’s prognosis. Although the aorta is protected by osseous structures, a laceration in this large-caliber vessel with high intraluminal pressure can cause rapid exsanguination. Thoracic aortic injuries have a worse prognosis than injuries to the abdominal aorta, probably due to the retroperitoneal location of the abdominal aorta, which can slow down exsanguination. They usually manifest as hemorrhage into the mediastinum or pleural cavity presenting as a hemothorax, cardiac tamponade, or mediastinal hematoma.

Figure 11-9 A, Arch angiogram obtained after a stab wound to the neck. There is a large pseudoaneurysm at the level of the distal brachiocephalic trunk (white arrowhead) and a second pseudoaneurysm involving the arch and possibly the left subclavian artery origin (black arrowhead). Neither one of the subclavian arteries is visualized. B, After treatment with a covered stent (white arrowhead) the large brachiocephalic aneurysm has been occluded preserving the right carotid and reestablishing flow in the right subclavian. The aortic pseudoaneurysm was surgically repaired.

(Courtesy of Dr. W. Escobar, Cali, Colombia.)

A portable supine chest radiograph continues to be the best initial imaging modality to screen for chest trauma. Radiopaque markers should be placed in the entry and exit sites of the wounds in order to give a guide toward the possible wound trajectory and the organs that might have been injured. Penetrating vascular lesions are suggested by a large hemothorax, widened mediastinum, foreign bodies in the proximity of the great vessels, or a bullet in a position different from its predicted course, suggesting bullet embolism, also known as “missing missile.”

MDCT/CTA has become an integral part of the assessment of aortic injury due to blunt trauma, and its role in penetrating injuries to the aorta is currently growing due to its availability, short acquisition time, and ability to identify vascular lesions. It is also able to locate bullets and fragments, document the wound tract and bullet path, visualize associated fractures, and evaluate internal organ injuries. Its major role continues to be in hemodynamically stable patients with GSWs suspected to transverse the mediastinum, since it can define the wound tract and its relationship with vascular and aerodigestive structures, helping to plan further treatment.

Aortic angiography remains the gold standard for the diagnosis of vascular lesions due to its ability to show pseudoaneurysm formation, active extravasation, and arteriovenous fistulas. However, fewer catheter aortograms are being performed as a consequence of the already mentioned benefits of noninvasive imaging with MD-CTA. In the case of a penetrating injury to the major vessels, lesions in the major venous structures such as the innominate veins can be present in up to one fourth of the patients, and they account for nearly 22% of fatalities in penetrating chest trauma. When performing catheter angiography, a venous phase should be carried out in all arteriograms, and, if venous injury is suspected, conventional venograms should be considered.

Penetrating injuries to the thoracic aorta are usually treated with urgent surgical repair via an anterolateral thoracotomy. Endovascular repair with stent grafts may be possible for penetrating injuries in selected patients (see TAI section).

Thoracic Aortic Aneurysms

Thoracic aortic aneurysms (TAAs) are often the result of atherosclerotic disease or cystic medial degeneration with subsequent weakening and dilatation of the aortic wall. It is usually a silent process, less commonly seen than abdominal aortic aneurysm, and generally occurs in older men in their sixth and seventh decades. Based on their morphology, aneurysms are classified as either fusiform aneurysms, which involve the full circumference of the vessel wall, or saccular aneurysms involving only a focal portion. Thoracic aneurysms occur in the ascending aorta in 40% to 60% of the cases, descending aorta in 30% to 40% of the cases, and aortic arch and thoracoabdominal aorta in 10% of the cases. The incidence and prevalence of thoracic aortic disease including TAA are steadily increasing due to the aging population and improved diagnostic techniques. The reported incidence of TAA ranges from 6 to 10 cases per 100,000 patients per year. The natural history of untreated TAA is progressive expansion of the aneurysm and ultimately rupture (Fig. 11-10).

Figure 11-10 A and B, A patient with a large thoracic aortic aneurysm (arrows). This patient had a right arch and aberrant left subclavian atrery origin. Following treatment with endograft, an endoleak developed where the endograft overlapped the celiac trunk (arrowheads).

Given that most patients are asymptomatic, TAAs are commonly diagnosed as an incidental finding on imaging studies. However, they can also present with signs and symptoms related to compression of adjacent structures. Ascending aortic aneurysms can compress the coronary arteries or the origin of the great vessels causing myocardial or cerebral ischemia; together with arch aneurysms, they can erode into the mediastinum and compress the left recurrent laryngeal nerve causing hoarseness, or the phrenic nerve and lead to hemidiaphragmatic paralysis. They can also press on the tracheobronchial tree causing wheezing, dyspnea, cough, hemoptysis, and pneumonitis; on the esophagus and cause dysphagia; and on the superior vena cava (SVC) causing SVC syndrome. Mural thrombus from the aneurysms can be the source of emboli and cause strokes, as well as renal, mesenteric, or limb ischemia. Heart failure can result from aortic root aneurysms leading to aortic regurgitation, or from the rupture of a sinus of Valsalva aneurysm into the right side of the heart. Chest and back pain are rare symptoms associated with compression of intrathoracic structures or erosion into adjacent bones (Fig. 11-11).

Figure 11-11 A 40-year-old patient with back pain and history of gunshot wound 15 years prior. A, Lateral radiograph demonstrates the projectile overlying the spine and an anterior wedge-shaped lytic defect involving T11-T12 (arrow). B, CTA shows a large chronic saccular pseudoaneurysm with peripheral calcifications (arrow) and the patent inner lumen (arrowhead). C, Catheter angiography showing the thoracoabdominal aneurysm with preserved upper abdominal branches. D and E, Following repair with endograft there is complete exclusion of the aneurysm.

(Courtesy of Dr. W. Escobar, Cali, Colombia.)

The most feared complications of TAA are aneurysm dissection and rupture. Dissection can lead to arterial occlusion and end-organ ischemia, while rupture can cause massive hemorrhage that usually cannot be contained by adjacent structures and therefore is considered a surgical emergency. Patients present with hypotension and acute onset of chest pain, abdominal pain, back pain, or neck pain. Rupture occurs more commonly into the left pleural space, but it can also occur into the pericardium causing pericardial tamponade (Fig. 11-12), and into the esophagus resulting in aortoesophageal fistula and dramatic upper gastrointestinal bleeding.

Figure 11-12 A, Aortic dissection type A with hemopericardium. Dissection flap is identified along the descending and ascending aorta all the way to the aortic root (top arrow) and rupture into the pericardium (asterisk) and the mediastinum (arrowhead). B, There is compression of the left atrium by the hemopericardium consistent with impending tamponade.

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

The risk of rupture and dissection of TAA increases with aneurysm size. The mean rate of rupture or dissection for small aneurysms is around 2%; it increases to 3% for aneurysms measuring 5.0 to 5.9 cm, and to 7% in patients with aneurysms 6 cm in diameter or larger. The mean aortic growth rate has been estimated to be 0.1 cm per year. Greater growth rates are seen in patients with Marfan syndrome, aneurysms of the descending aorta, and dissecting aneurysms. Although men are more prone to develop thoracic aneurysms, women have a higher likelihood of rupture and dissection.

Multiple etiologies have been associated with thoracic aortic aneurysms, and they differ depending on their location within the thoracic aorta. Aneurysms of the ascending aorta and aortic arch are more commonly seen in elderly patients secondary to atherosclerosis or aortic valve stenosis leading to poststenotic dilatation. The younger patient population presenting with thoracic aneurysms in the ascending aorta and aortic arch (Tables 11-2 and 11-3) usually have a connective tissue disorder such as Marfan syndrome (mutation of fibrillin-1 gene), Ehlers-Danlos syndrome (defect in type III collagen), Loeys-Dietz syndrome, or Turner syndrome (associated to bicuspid aortic valves). Other infrequent etiologies include mycotic and syphilitic aneurysms. Aneurysms of the sinus of Valsalva can be congenital, infectious, or postsurgical in origin, and they are seen as dilatations in connection with the aortic root. Vasculitis can affect all portions of the thoracic aorta. Takayasu arteritis is one of the most striking entities, characterized by a chronic inflammatory process of unknown etiology that affects the aorta, its major branches, and the pulmonary arteries. It affects the vessel wall causing obliterative luminal changes, occlusion, or dilatation. Aneurysm formation can be a fatal complication of this disease since it may lead to heart failure secondary to aortic valve regurgitation or aortic rupture.

Table 11-2 Ascending Thoracic Aortic Aneurysms

Table 11-3 Aortic Arch Aneurysms

Thoracic aneurysms of the descending aorta are also most commonly degenerative in origin caused by atherosclerosis and usually associated with hypertension, hypercholesterolemia, and smoking. These aneurysms are generally fusiform with significant intimal calcifications and demonstrate associated tortuous aorta and mural thrombus. Other causes include chronic aortic dissection (Stanford type A or B), which can dilate over time as the wall of the false lumen weakens, creating a dissecting aneurysm with a high risk of rupture. Injuries to the descending thoracic aorta associated with blunt trauma can result in pseudoaneurysm formation, characteristically located near the aortic isthmus distal to the subclavian artery, and with a high risk of rupture (these are discussed in the TAI section). As with ascending thoracic aneurysms, younger patients with descending thoracic aortic aneurysms usually have an underlying connective tissue disorder (Table 11-4) or vasculitis. Mycotic aneurysms can also affect this segment.

Table 11-4 Descending Thoracic Aortic Aneurysm

Aneurysms located in the thoracoabdominal aorta are less frequent than abdominal or thoracic aneurysms, which is fortunate because these are difficult-to-treat lesions due to the numerous visceral branches that arise along this segment. They are divided into four types according to the Crawford classification (Table 11-5). Types II and III are the more complex ones, with type II having the highest risk of treatment-induced spinal cord infarction and renal failure.

Table 11-5 Crawford Classification of Thoracoabdominal Aneurysms

Diagnosis

Thoracic aortic aneurysms are usually seen on a routine chest radiograph as an incidental finding. Common findings include a widened mediastinum, enlarged aortic knob, tracheal deviation, aortic kinking, and blunted aortopulmonary window. However, CXR is limited in the diagnosis of thoracic aneurysms as it cannot accurately differentiate a tortuous aorta from an aortic aneurysm and can easily miss small aortic aneurysms.

CTA provides sufficient information to diagnose and follow up progression of TAA; angiographic sequences allow for precise delineation of the extension of the aneurysm, involvement of the great vessels, and other associated thoracic pathology (see Fig. 11-11). Unenhanced CT is used to identify areas of aortic calcification, mural thrombus, acute wall hematoma (circumferential or crescentic), and recent hemorrhage. Contrast administration helps to differentiate the patent lumen from mural thrombus and to demonstrate an intimal flap and a false lumen in areas of aortic dissection. CT also shows the relationship of the aneurysm to the adjacent structures and helps correlate associated patient symptomatology with imaging findings. Mycotic aneurysms can affect any portion of the aorta and are seen as saccular dilatations with multilobulated contour (Fig. 11-13). Cross-sectional CT imaging features include a perianeurysmal soft tissue mass, fluid collection, and occasionally gas-forming inflammation. Syphilitic aortic aneurysms are rarely seen nowadays, but if encountered they usually demonstrate extensive aortic calcification or linear calcifications with longitudinal wrinkling of the wall causing a “shaggy tree-bark” pattern; approximately 75% of the cases exhibit a saccular morphology.

Figure 11-13 A, Contrast-enhanced CT showing an avidly enhancing posterior aortic wall saccular aneurysm at the level of the celiac trunk; note the absence of atherosclerotic plaque. B, Conventional angiogram shows the size of the aneurysm and the proximity to the celiac trunk and renal arteries. These findings are typical for mycotic aneurysms. Salmonella was found on the specimen.

(Courtesy of Dr. Javier Casillas, University of Miami.)

Both CTA and MRA can be used successfully as preprocedural imaging techniques in order to plan surgical or endovascular repair, as they are both able to measure the dimensions of the aneurysm and detect the involved vessels. Accurate measurements are crucial when selecting the appropriate stent graft diameter for endovascular procedures in order to minimize stent-related complications such as endoleak, stent migration, and branch occlusion. CTA with multiplanar reconstruction and digital subtraction angiography (DSA) are considered to be the most useful techniques to depict morphologic characteristics of the aneurysm, as well as to detect graft complications.

Contrast-enhanced MRA (CE-MRA) can provide exquisite detail of the aneurysm and associated dissection or branch involvement; sometimes it can also visualize small vascular structures in greater detail, such as the Adamkiewicz artery, providing valuable information in the planning of surgical repair and helping avoid postoperative neurologic deficits. CE-MRA, however, cannot visualize aortic calcification, which can be important during treatment planning. These two modalities continue to complement each other as one may show certain characteristics that the other cannot.

In either case, serial imaging studies are usually required in this patient population in order to monitor aneurysm size. A repeat study can be obtained 6 months after the initial diagnosis, and if the aneurysm is stable, imaging follow-up can be obtained annually.

Abdominal Aortic Aneurysms

Abdominal aortic aneurysms (AAAs) are fusiform or saccular dilatations of the abdominal aorta, which form more frequently as a consequence of degeneration of the media from atherosclerotic disease, which causes weakening of the wall and widening of the luminal diameter. In the elderly population, degenerative aneurysms are more frequent, while in younger patients abdominal aneurysms are usually secondary to inheritable diseases such as Marfan syndrome and Ehlers-Danlos syndrome. Predisposing factors that have been associated with AAA include advanced age, family history, male gender, tobacco use, and white race with a lower incidence found in patients of Asian descent. Patients with AAA have a higher incidence of hypertension, atherosclerosis, myocardial infarction, heart failure, and peripheral vascular disease than matched controls for age and gender. Other types of AAA include inflammatory and infectious aneurysms. Inflammatory aneurysms, as their name indicates, show an increased inflammatory reaction in the aneurysm wall and surrounding tissues, and present with a triad of chronic abdominal pain, weight loss, and elevated erythrocyte sedimentation rate. Infectious or mycotic aneurysms are more frequently associated with transient bacteremia with Staphylococcus or Salmonella, which leads to infection of the vessel wall or an atherosclerotic, plaque by hematogenous spread. There are also rare reports of aneurysms caused by tuberculosis infection.

Patients with AAA are usually asymptomatic, and aneurysms are often detected as an incidental find, on radiologic studies. Sometimes clinical exam can detect AAA if a pulsatile abdominal mass or an abdominal bruit is present; unfortunately, physical exam sensitivity among studies varies widely and confirmatory imaging is usually required. Symptomatic patients usually complain of lower back pain or abdominal pain that can be nonspecific and easily confused with other disease processes. Patients with acute rupture present with abrupt onset pain in the lower back or abdomen, that can be associated with a pulsatile abdominal mass and hypotension. The natural history of abdominal aortic aneurysms is usually characterized by gradual expansion of the aneurysm sac with mural thrombus formation lining the inner surface. The aneurysm may then cause compression of adjacent structures, thromboembolic events, erosion into neighboring structures (e.g., duodenum or iliac vein), and, ultimately, rupture.

AAA rupture is a catastrophic complication with a reported mortality of up to 90%. It usually occurs in the posterolateral aspect of the aorta causing retroperitoneal hemorrhage. Less commonly, it ruptures in the anterolateral aspect causing intraperitoneal bleeding and quick exsanguination. Contained ruptures in the form of retroperitoneal hematomas might be associated with ecchymosis of the flanks, otherwise known as Grey-Turner syndrome. In general, the larger the aneurysm, the higher the risk for spontaneous rupture and the faster it tends to expand. The average expansion rate for aortic aneurysms 4.0 cm in diameter is 1 to 4 mm per year, followed by 4 to 5 mm per year for aneurysms measuring 4.0 to 6.0 cm, and 7 to 8 mm per year in larger aneurysms. The lifetime risk of rupture of abdominal aneurysms larger than 5.0 cm in diameter is 20%; it then increases to 40% for aneurysms that measure more than 6.0 cm, and to more than 50% for aneurysms that exceed 7.0 cm. The corresponding estimated annual rupture rates are 4%, 7%, and 20%, respectively.

Other AAA complications that may require immediate treatment are those related to compression or erosion of adjacent structures, as seen in large degenerative AAA, or inflammatory or mycotic aneurysms. Some examples include gastric outlet syndrome secondary to compression of the duodenum, aortoenteric fistula formation causing massive upper gastrointestinal bleed, and venous fistula formation into the inferior vena cava, the left renal vein, or the common iliac vein. These fistulae can have high flow rates and result in acute congestive heart failure or in hematuria and flank pain.

Diagnosis

Early AAA detection is imperative in order to reduce patient morbidity and mortality of this silent disease. The most common site of arterial aneurysms is the abdominal aorta, especially along its infrarenal segment. Abdominal aneurysms are diagnosed when the aorta is 1.5 times greater that the diameter of the normal aorta or when the minimum anteroposterior diameter is greater than 3.0 cm irrespective of age and gender.

Imaging techniques are currently relied on for the diagnosis and follow-up of aortic aneurysms. Real-time ultrasonography is a noninvasive and cost-effective modality useful to screen for AAA, with an accuracy that approaches 100% in the diagnosis of infrarenal aortic aneurysms. Its accuracy in measuring the aortic diameter below the level of the renal arteries has been shown to correlate well with direct intraoperative measurements. The size of the aneurysms is calculated by measuring the maximum anteroposterior aortic diameter or the largest transverse diameter measured in a plane perpendicular to the luminal arterial axis to avoid overestimation of the aneurysm size. AAAs are seen as dilated vessels with irregular lumen and eccentric echogenic thrombus material. Although convenient, ultrasound is limited by the patient’s body habitus and the interposition of bowel gas that obscures visualization of the deeper structures. Likewise it is not as reliable as CTA for detecting complications such as rupture, aneurysm extension into the suprarenal aorta, and detection of post-therapeutic complications such as endoleaks.

MD-CTA has emerged as the new gold standard for the diagnosis of aortic abdominal aneurysms, replacing catheter arteriography. MD-CTA offers high-resolution imaging and shorter scan times, allowing the detection and characterization of aneurysms and related complications including impending rupture and contained or complete rupture. Several signs of impending rupture have been identified (see Box 11-3) on CT including increased aneurysm size, a low thrombus-to-lumen ratio, and mural thrombus hemorrhage that is usually identified as high-attenuation crescents in the wall of the aortic aneurysm in unenhanced CT images (Fig. 11-14). There are various signs that suggest a contained AAA rupture, including loss of definition of the posterior aortic wall; presence of an organized hematoma with contour abnormalities of the vessel wall; interruption of a continuous ring of aortic wall calcification; and a posterior wall of the aorta following the contour of the vertebra with or without associated vertebral erosion (sign known as a “draped” aorta). A ruptured AAA is determined by the presence of hemorrhage contiguous to the aorta, almost always involving the retroperitoneal space and rarely the iliopsoas compartment. Periaortic blood might be seen in the pararenal space, perirenal space, or both; a hematocrit sign (cellular-fluid level) and rectus sheath bleeds are more rare but helpful if present, and tend to be associated with coagulopathic hemorrhage (Fig. 11-15).

Figure 11-14 A and B, Noncontrast CT images obtained 1 year apart. The first image (A) shows an AAA with peripheral plaque and mural thrombus (arrow); 1 year later (B) the aneurysm (arrow) has increased in size and intramural crescents have developed (arrowhead), raising concern for impending aneurysm rupture.

Figure 11-15 A and B, CTA images demonstrating a large infrarenal aortic aneurysm (arrowheads) with rupture (arrows).

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

CT is also useful in differentiating between different types of aortic aneurysms. Mycotic aneurysms are usually seen as saccular-shaped collections with a lobulated contour; other features may include a periaortic soft tissue mass with stranding, retroperitoneal para-aortic fluid collection, vertebral erosion, gas-forming inflammation around the aneurysm, intra-aortic air pockets, and thrombus formation within a false lumen after aneurysmal rupture (see Fig. 11-13). In inflammatory aneurysms, CT and MRI can detect the cuff of soft tissue inflammation surrounding the aneurysm, thickening of the aneurysm wall, perianeurysmal and retroperitoneal fibrosis, and adherence of the anterior aneurysm wall to adjacent structures (Fig. 11-16). On precontrast CT images the thickened aortic wall has soft tissue attenuation that enhances after intravenous contrast administration. The arterial wall may become undistinguishable from periaortic fibrosis. Periaortic fibrotic tissue can adhere to the ureters, small bowel, duodenum, and inferior vena cava causing entrapment of these structures and further complicating surgical repair. Preoperative imaging is of great importance in the planning of surgical and endovascular treatment of patients with AAA. Important preoperative features and measurements done on CTA include the maximum transverse aneurysm diameter, relation of the aneurysm to the renal arteries, presence of a proximal neck (renals to aneurysm distance), presence of a distal neck (aneurysm to aortic bifurcation distance), extension of the aneurysm into the iliac arteries, identification of concomitant aneurysms, and appearance of the access pathway including femoral and iliac arteries. Some conditions that limit the delivery of an endograft include very large AAA, markedly tortuous aorta, pelvic arteries with abrupt angles, and extensive calcification causing luminal narrowing. Any of those factors can represent an exclusion criterion depending on the specific anatomy, and the degrees of angulation and stenosis. They determine the suitability or unsuitability for endovascular treatment, and cautious analysis of the images in conjunction with the surgical/interventional team is crucial to decrease the risk of endoleaks, attachment failures, graft migration, and conversion to open repairs. MRA has shown similar properties as CTA for the diagnosis of and for preoperative planning for AAA, providing precise information about the location and extent of the aneurysm. Conventional arteriography is currently used as an adjunct imaging modality for evaluating patients with complex vascular anatomy, for aneurysms that could not be fully characterized with CTA and MRA, and for intraprocedural graft positioning.

Figure 11-16 CTA demonstrating an aortic aneurysm with enhancing aortic wall, ill-defined margins, and mild stranding of the adjacent fat compatible with inflammatory aortic aneurysm.

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

Treatment

Treatment is usually recommended for AAAs measuring 5.5 cm or larger to eliminate the risk of rupture, and for symptomatic AAAs regardless of their diameter size. Ruptured aneurysms with hemodynamic compromise require immediate surgical repair. In selected cases, endovascular intervention might be indicated for the management of ruptured aneurysms that remain hemodynamically stable. Patients with aneurysms 4.0 to 5.4 cm in diameter should have imaging follow-up every 6 to 12 months for early detection of expansion. Currently, it is not recommended that patients with asymptomatic aneurysms less than 5.0 cm in men, or less than 4.5 cm in women, undergo elective repair. Higher mortality rates are seen in patients who have emergent repair rather than elective surgery, and it is for this reason that early detection and surveillance of high-risk populations remain crucial in the treatment of abdominal aortic aneurysms.

Open surgical treatment is usually offered to hemodynamically unstable patients and to patients who want an elective surgical repair. It involves a midline transabdominal incision or a left retroperitoneal flank access with subsequent clamping of the aorta, excision of the aneurysm, and placement of a synthetic graft. Aortic clamping can be linked to the development of significant morbidities such as ischemia of the lower extremities or bowel, or paraplegia.

Postoperative complications related to an elective open surgical approach vary between 0.4% and 10% and include pseudoaneurysm formation, graft infection, enteric fistulas, and graft limb occlusion.

Treatment of pararenal and suprarenal aortic aneurysms is more complex, since it requires cross-clamping of the aorta above the visceral arteries and sometimes branch vessel reimplantation, increasing operative morbidity and mortality, with up to 15% of the patients requiring temporary dialysis and 5% going into permanent renal failure. The overall 5-year survival rate among these patients is 40% to 50%.

Endovascular aortic aneurysm repair (EVR) offers a less invasive approach to reduce the operative morbidity and mortality. Blood losses are significantly reduced since the graft is placed intravascularly via femoral access, and, likewise, the risk for lower limb and visceral ischemia is lower since aortic clamping is not performed. EVR is offered to patients who are undergoing repair for asymptomatic AAA or symptomatic nonruptured AAA or those who are at high risk surgically and have significant comorbidities. The role of the endograft is to exclude the aneurysmal sac from the arterial circulation and decrease the mechanical stress over the vessel wall (Fig. 11-17). Studies have shown benefits in the perioperative mortality and a 30-day morbidity and mortality rate of less than 3% with EVR. Despite its short-term advantages, long-term survival and quality-adjusted life expectancy do not seem to vary significantly when compared with open surgery repair.

Figure 11-17 A, Conventional catheter angiography with bilateral marked catheters in place demonstrating a large lobulated infrarenal aortic aneurysm with 4-cm proximal neck suitable for endovascular repair. B, Post endovascular repair image demonstrates complete exclusion of the aneurysm with no endoleak and preservation of the renal and hypogastric arteries.

A common complication related to stent graft placement is the development of endoleaks (Fig. 11-18). An endoleak is defined as an incomplete exclusion of the aneurysmal sac. The estimated incidence oscillates in the 10% to 45% range, and currently lifelong imaging follow-up is recommended in order to detect endoleaks and other graft-related complications. Delayed rupture is rare (0.1% to 1% per year) and has been associated with type I and type III endo-leaks, graft migration, and endograft kinking. When type I or type III endoleaks are recognized, immediate treatment is indicated through graft extension, reintervention, or conversion to open repair. Other serious complications include graft infection and occlusion (Fig. 11-19). Occlusion is usually due to distortion of one of the graft limbs and can cause lower extremity ischemia if not promptly treated. Continuous aortic expansion at the “neck” can cause endograft migration and delayed type I endoleak, but this is rare since endografts are oversized at the time of placement by up to 20% to ensure adequate seal.

Figure 11-18 CTA demonstrating the proximal end of the stent graft (arrow) and prompt enhancement of the surrounding aneurysm sac (arrowhead) consistent with type I endoleak.

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

Figure 11-19 CTA obtained after AAA repair with endografts. The patient presented with fever and elevated white blood cell count. Images demonstrate aortic wall enhancement and a small amount of periaortic fluid (arrowheads) consistent with infected aortic stent graft.

(Courtesy of Dr. Daniel J.A. Margolis, UCLA, David Geffen School of Medicine.)

Acute Mesenteric Ischemia

This is a critical condition, poorly tolerated, with high mortality rates even in the setting of early intervention. A delayed diagnosis further complicates the overall prognosis of the patient and is almost always lethal. More than 50% of the cases are embolic in origin; 20% are due to thrombosis of preexistent stenotic lesions, 20% are related to low flow states (nonocclusive mesenteric ischemia), and 10% are due to portomesenteric venous thrombosis. The classic presentation is generalized abdominal pain out of proportion to the physical findings. However, since this is a disease process identified predominantly in the elderly, the presentation can be more subtle, with minimal findings on physical exam and vague pain.

The classic plain film findings of gas in the wall of the affected bowel loops (pneumatosis intestinalis) and in the portal vein occur late in the process, once bowel infarction has already occurred. Early signs are nonspecific and include bowel thickening and dilatation. CT/CTA is the preferred initial imaging modality to evaluate for suspected bowel ischemia, as it allows visualization of the mesenteric arteries, veins, bowel luminal diameter, and wall thickness.

Catheter angiography remains an important diagnostic modality. Mesenteric embolic occlusion characteristically appears as convex filling defects outlined by contrast. Most of the emboli are identified in the proximal segment of the superior mesenteric artery (SMA), resulting in profound ischemia in the absence of collateral flow. The standard management is surgical embolectomy or bypass with resection of the nonviable bowel segment. If there are no signs of irreversible bowel ischemia, endovascular intervention may be indicated. Catheter embolectomy with or without thrombolysis can be attempted.

In the absence of an embolic source, arterial thrombosis secondary to an underlying stenotic lesion is the most frequent etiology. Usually patients have associated history of peripheral vascular disease. Catheter thrombolysis followed by treatment of the underlying stenosis with angioplasty and stenting is the preferred approach, provided that there are no signs of irreversible bowel ischemia.

Nonocclusive mesenteric ischemia is a syndrome characterized by low flow in the superior mesenteric artery without evidence of embolus, thrombus, or any other fixed lesion. It is more frequently encountered in hypotensive patients undergoing infusion of vasopressor agents.

Acute Gastrointestinal Bleeding

Acute gastrointestinal bleeding is classified into upper and lower causes based on its origin proximal or distal to the ligament of Trietz. Upper gastrointestinal (GI) bleeds are approximately five times more common than lower gastrointestinal causes, and lower gastrointestinal bleeding originates in the colon in approximately 80% of the cases. Localization of the bleed is critical to determine management. Upper bleeds occur secondary to gastritis and gastric or duodenal ulcers, while the most common cause of lower GI bleed is colonic diverticulosis followed by angiodysplasia. Depending on the site of origin (proximal or distal) and the severity of the hemorrhage, a GI bleed will manifest as hematemesis, melena, and/or hematochezia (Fig. 11-23). A positive nasogastric aspirate and lavage is an effective way to determine if there is an upper GI bleed. In these patients, the initial evaluation is performed with endoscopy, which not only confirms the diagnosis and identifies the source in more than 95% of the cases, but also can offer therapy with sclerotherapy, clipping, cauterization, or banding. With lower GI bleeds, identification of the bleeding site with colonoscopy is more difficult, with an overall reported success rate of 70%. More than 85% of lower GI bleeds resolve spontaneously with supportive therapy alone (Fig. 11-24). It is crucial that all GI-bleeding patients be stabilized, with large bore venous accesses placed for fluid resuscitation and transfusion as needed. If the source of bleeding is still unknown despite endoscopy and colonoscopy, there are various diagnostic imaging alternatives available. One option is to perform a tagged red-blood cell nuclear scan, which can detect bleeding rates as low as 0.1 mL/min; however, its ability to localize the bleeding to a particular segment of bowel is limited. Catheter angiography is another option, which detects a bleeding rate of approximately 0.5 to 1 mL/min. Given the often intermittent nature of GI bleed, and the time required to stabilize and transfer the patient, angiograms are positive in only about 50% of the cases. However, if performed immediately after a positive tagged red-blood cell scan, or when obtained during an episode of active bleed, the likelihood of finding the source increases. MD-CTA is a promising noninvasive first-line diagnostic modality that offers fast scanning times that vary between 6 and 20 seconds and allows for accurate diagnosis or exclusion of active gastrointestinal hemorrhage by comparing pre– and post–intravenous contrast images and identifying abnormal hyperattenuating areas of extravasated contrast material within the bowel lumen.

Figure 11-23 A and B, A 75-year-old patient with recurrent lower gastrointestinal hemorrhage. SMA catheter angiography shows a focal area of abnormal contrast pooling fed by one of the distal ileal branches most consistent with a small bowel hemangioma that caused recurrent bleeding episodes. Following coil embolization, the abnormal enhancement was no longer identified and the symptoms resolved.

Figure 11-24 A and B, A patient with hematochezia. Selective SMA angiography demonstrates contrast extravasation at the level of the cecum arising from a branch of the ileocecal artery compatible with a diverticular bleed (white arrow). Subselective embolization could not be performed, but the sheath was kept in place. Repeat angiography the next morning demonstrated spontaneous resolution of the bleed with supportive medical treatment (black arrow).

During catheter angiography, it is important to first study the vessel that has the highest likelihood of being the source of bleeding with selective angiograms. Visualization of both the arterial and venous phases is required, as some bleeds may be caused by varices related to portal hypertension or thrombosis. The presence of contrast extravasation into the bowel is diagnostic. Extravasation is usually seen during the arterial phase and persists after venous washout before slowly dissipating. Catheter-directed therapy options include embolization and vasopressin infusion. When supraselective catheterization of the bleeding branch is possible, it can be followed by embolization with Gelfoam, large particles (polyvinyl alcohol or spheres), and microcoils to stop the bleeding. When the bleeding is diverticular, postpolypectomy, or mucosal in origin, then intra-arterial vasopressin infusion is an effective alternative. Vasopressin is not effective for bleeding secondary to pseudoaneurysms or arteriovenous malformations, and is contraindicated in cases of bleeding secondary to ischemic bowel. After embolization, patients should be monitored closely, as approximately 20% of them may have recurrent bleed and some may develop bowel ischemia.

Aneurysms of the Visceral Arteries

Aneurysms of the visceral arteries are rare in comparison to aortoiliac and femoropopliteal aneurysms. The most commonly affected vessels are the splenic, hepatic, and superior mesenteric arteries. The most frequent etiologies for true aneurysms are atherosclerosis and vasculitis, and for pseudoaneurysms pancreatitis, trauma, and infection. The majority of these aneurysms are asymptomatic and discovered as an incidental finding, but some may present with rupture.

Splenic artery aneurysms are the third most common intra-abdominal aneurysm, after aortic and iliac aneurysms, and account for 60% of the cases of visceral aneurysms (Fig. 11-25). Most are saccular, single, and less than 3 cm in diameter. As with other intra-abdominal aneurysms, common causes include pancreatitis, atherosclerosis, trauma, and fibrodysplastic disease. Interestingly, these aneurysms are four times more prevalent in females than males, with higher incidence among pregnant and multiparous women. The catastrophic complication of rupture in pregnancy results in high mortality rates in the order of 70% to 90% for both the mother and fetus. Treatment options include surgical resection and embolization. Endovascular stent graft placement can be another option in select cases.

Figure 11-25 A to D, A patient with chronic pancreatitis and enlarging splenic artery pseudoaneurysm. The patient did not want to undergo any invasive procedures, so he was followed with serial CTA every 6 months, where progressive enlargement of the aneurysm was demonstrated (arrows); in the last follow-up dense crescents worrisome for impending rupture were identified. Catheter angiography (D) showed the aneurysm (arrowheads) had increased further in size; the patient was then taken to surgery for aneurysm resection.

Hepatic artery aneurysms represent approximately 20% to 40% of all splanchnic artery aneurysms. They can be extrahepatic or intrahepatic, with the former representing about two thirds of cases. The etiologies of hepatic aneurysms include atherosclerosis and trauma. Less common causes include pancreatitis, vasculitis, hereditary telangiectasias, cystic medial necrosis, liver abscess, and tuberculosis.

The SMA is the third most common location for visceral artery aneurysms. The frequency of these aneurysms is estimated at 5.5% of all splanchnic aneurysms and less than 0.5% of all intra-abdominal aneurysms. In the past, it was believed that most of these were of infectious etiology; however, more recent reports have suggested that most cases are due to atherosclerosis. Collagen vascular disorders and polyarteritis nodosa have also been implicated. These aneurysms usually manifest with severe mid-epigastric pain.

Involvement of the celiac, ileocolic, and gastroduodenal arteries has also been described. Aneurysms of the gastroduodenal artery are often associated with pancreatic pathology and can cause bleeding in the peritoneal or retroperitoneal space and more rarely into the portal vein or into a pancreatic pseudocyst (Fig. 11-26). In general, elective repair is recommended for splachnic aneurysms when they reach a size greater than 2 to 2.5 cm. Pseudoaneurysms are always considered to carry a high risk of rupture, and so repair is recommended on detection regardless of their size.

Figure 11-26 A and B, Contrast-enhanced CT images through the level of the pancreas demonstrate a large heterogeneous mass with enhancement pattern similar to the aorta and located lateral to the head of the pancreas (arrows). The duodenum is not visualized. Findings correspond to a large pseudoaneurysm secondary to pancreatitis. Conventional angiography demonstrates an enlarged gastroduodenal artery feeding a very large aneurysm (arrow).

(Courtesy of Dr. Javier Casillas, University of Miami.)

Acute Renal Ischemia

Normal kidneys have no significant collateral blood supply, and acute occlusion will lead to rapid loss of kidney function if not effectively revascularized within 1 to 2 hours. The most common cause of acute occlusion in middle-aged and elderly patients is embolic disease of a cardiac source, while in the young patient population it is trauma. Other etiologies include aortic or renal artery dissection, thrombosis of a focal stenosis, thromboembolism from renal artery aneurysm, and procedural complications (Fig. 11-28). Patients with acute renal artery ischemia classically present with flank pain and hematuria. Occlusion in the setting of progressive renal artery stenosis is less likely to end in acute ischemia as collateral flow usually via capsular, adrenal, or gonadal arteries will have developed. Both CT and MRI are useful to demonstrate the areas of asymmetric renal perfusion with generalized lack of enhancement seen with complete arterial occlusion or areas of segmental infarction due to smaller emboli. CTA and MRA can demonstrate renal artery stenosis, arterial dissection, and other renal artery anomalies as well as accessory arteries or collateral flow. Revascularization of acute renal artery occlusion is difficult due to the narrow time window before irreversible changes develop. If an occlusive dissection develops during renal artery angioplasty, stenting is indicated; if the occlusion is secondary to thrombosis, then treatment is done with thrombolysis, and thrombectomy or surgical revascularization is indicated.

Figure 11-28 A and B, CTA of a complex aortic dissection. Part of the aortic false lumen in the posterior aspect of the aorta has thrombosed. The dissection flap is partially involving the origin of the right renal artery causing flow impairment (A, white arrowheads); compare to the preserved celiac trunk origin (B, white arrow).

Aneurysms of the Renal Artery

Aneurysms of the renal arteries are rare. Etiologies include degenerative aneurysms, which are usually asymptomatic, fibromuscular dysplasia, infection, trauma, idiopathic, and iatrogenic. Other etiologies such as polyarteritis nodosa tend to involve small peripheral intraparenchymal branches. The risk of rupture increases when the aneurysm diameter exceeds 2 cm, and this risk has been found to be higher in pregnant patients. These aneurysms may also be complicated with renal infarction, hypertension, and spontaneous fistula formation. The decision to treat depends on aneurysm size and clinical presentation. Minimally invasive angiographic alternatives such as coil embolization and stent graft placement are effective techniques; however, these cannot always be implemented, and surgical reconstruction or bypass may be required.

Renal Neoplasm–Related Vascular Emergencies

Some benign and malignant renal neoplasms can be the source of acute clinical symptoms including pain, hemorrhage, and gross hematuria. Angiomyolipomas are benign renal neoplasms that contain fat, smooth muscle, and blood vessels. They are well known for their association with tuberous sclerosis and their tendency to bleed, particularly when larger than 4 cm. Ultrasound or CT evaluation is usually performed in the emergency setting due to acute flank pain that may be associated with hemodynamic changes. Images will demonstrate the acute renal and perirenal hemorrhage with or without contrast extravasation. The mass itself as well as the characteristic intralesional fat can usually be identified, although it can be difficult in the setting of acute hemorrhage (Fig. 11-29). The presence of other angiomyolipomas can help the diagnosis. These lesions are usually treated with percutaneous embolization using a combination of particles, coils, and sometimes alcohol. Follow-up scans are performed to document resolution of the hematoma and shrinkage of the lesion.

Figure 11-29 A 35-year-old patient presented with sudden left flank pain. Contrast CT shows a fatty mass lesion in the lower pole of the left kidney in addition to perirenal fluid (arrows); findings are consistent with left renal angiomyolipoma complicated with acute hemorrhage.

Renal cell carcinomas are the most common malignant renal neoplasm in the adult. The so-called classic triad of flank pain, hematuria, and mass is present in only one third of the patients. Percutaneous embolization for tumor control is generally not indicated except in selected cases where the tumor size is too large for resection and embolization may help control operative bleed. Other indications for percutaneous embolization include severe gross or recurrent hematuria or perirenal hemorrhage.

Iliac Occlusive Disease

Atherosclerosis is the most common cause of iliac occlusive disease, and it frequently involves the distal aorta. Patients tend to present with unilateral or bilateral leg claudication or ischemia depending on the level of obstruction and the presence of collateral circulation; bilateral symptoms suggest aortic involvement. Aortoiliac occlusive disease is part of the lower extremity peripheral vascular disease spectrum (see section covering the lower extremities), and as such it can lead to loss of the extremity or even the loss of life when it becomes acute. Causes for acute presentation include embolism, thrombosis, dissection, trauma, low cardiac output states, and hypotension. Emboli are the most common cause of sudden lower extremity ischemia, with 80% originating in the heart due to atrial fibrillation, valvular disease, or recent myocardial infarction. Emboli can also originate in the peripheral circulation proximal to the occlusion as a consequence of irregular or ulcerated plaque, aneurysms, and previous interventions such as stent grafts. Emboli tend to get wedged at bifurcation points or in areas where vessels narrow abruptly. The iliac arteries are involved in 18% of the cases of acute ischemia of the lower extremity, the aorta in 15%. Emboli tend to have a more acute and severe presentation owing to the lack of collateral circulation. Occlusive thrombosis is caused by the disruption of an atheromatous plaque that leads to exposure of its core products with subsequent activation of the coagulation cascade (Fig. 11-33). In patients who present with acute ischemic symptoms, a history of thigh or buttock claudication is suggestive of underlying iliac atherosclerotic disease. Leriche syndrome is described as the combination of intermittent claudication, impotence, and significantly decreased or absent femoral pulses. This syndrome can be identified in approximately one third of male patients with aortoiliac occlusive disease and indicates chronic peripheral arterial insufficiency due to narrowing of the distal aorta. Iliac occlusive disease can also present as “blue toe” syndrome when it causes distal emboli.

Figure 11-33 The patient presented with sudden painful cold left foot. A, Catheter angiography shows a large thrombus developing from an occluded right iliac artery stent and extending into the left common iliac artery. B, Left lower extremity angiogram shows complete occlusion at the level of the popliteal artery due to an embolus (arrow). C, Following catheter-directed thrombolysis, patency of the popliteal, posterior tibial, and peroneal arteries was reestablished, and there is partial restoration of the anterior tibial artery flow.

Examination will reveal the absence of femoral pulses and a decreased ankle brachial index (ABI). Ultrasound evaluation with Doppler of the iliac arteries is difficult; however, the analysis of the duplex spectral waveforms demonstrating spectral broadening and the absence of a normal triphasic pattern can provide valuable information about proximal disease.

CE-MRA and CTA can both detect aortoiliac disease with great sensitivity and specificity and allow for adequate therapeutic planning. CT tends to overestimate the degree of stenosis, particularly in the presence of calcification. MRA offers limited evaluation of segments containing stents, due to the metal-induced susceptibility artifact.

In general, both CTA and MRA provide excellent characterization of the aortoiliac vasculature for diagnosis, follow-up, and therapeutic planning. Occasionally, both are used in cases of conflicting results or when assessment of the calcified wall is important for therapeutic planning.

Catheter angiography is usually reserved for cases where intervention is anticipated or to answer specific inquiries regarding pressure gradient measurements and information on flow dynamics. Definitive treatment of hemodynamically significant aortoiliac disease is usually done by aortobifemoral bypass, with a 5-year patency rate of approximately 90%. Patients in whom aortoiliac disease becomes symptomatic but who have comorbidities that increase the operative risk may benefit from a less invasive approach such as endovascular repair with angioplasty and stenting, axillary-femoral bypass, or femoro-femoral bypass. Focal concentric iliac artery stenosis usually responds well to angioplasty with more than 60% primary patency rate at 4 years; however, since stents are approved for iliac use, most iliac lesions are treated nowadays with primary stenting, with a 4-year patency rate of almost 80% for stenotic lesions and 60% for recanalized occlusions. Minimally invasive treatment of bilateral common iliac artery occlusive disease will require placement of bilateral stents, also known as “kissing” stents when they touch each other at the aortoiliac confluence. When dealing with patients complaining of acute or recent onset of symptoms and a fresh thrombus is suspected, thrombolysis is an excellent recanalization alternative (see Fig. 11-33).

Iliac Aneurysms

Degenerative aneurysms of the iliac arteries tend to involve the common iliac artery (CIA) and are frequently seen in association with abdominal aortic aneurysms or dissection (Fig. 11-34). External and internal iliac artery aneurysms are rare. As with AAA, the most feared complication is aneurysm rupture, which can be free, contained, or into a venous structure. Findings of rupture can be subtle with only mild perivascular stranding noticed, or dramatically florid with retroperitoneal and/or intraperitoneal hemorrhage. Rupture into venous structures causes high output congestive heart failure. Chronic ruptures usually contain thrombus associated with saccular dilatation and disruption of intimal calcification. Isolated CIA aneurysms warrant repair when they reach 2.5 to 3.0 cm in diameter, and they can be managed with stent graft placement provided there is an adequate access pathway and sufficient landing zones to allow appropriate attachment of the graft.

Figure 11-34 Coronal CTA reconstruction demonstrating a 3.5-cm aneurysmal dilatation of the left common iliac artery (arrow). There is also an abdominal aorta dissection flap (arrowheads) that extends into the iliac (not shown).

Iliac Artery Dissection

Dissection of the iliac arteries is usually an extension of thoracoabdominal aortic dissection. Primary iliac artery dissection is relatively rare and has been described in association with fibromuscular dysplasia and vigorous training in professional athletes. Both CTA and MRA are excellent for the evaluation of thoracoabdominal and iliac dissection (see Fig. 11-20).

Upper Extremity Aneurysms

Upper extremity artery aneurysms are rare; etiologies include atherosclerosis, acute or repetitive trauma, chronic dissection, connective tissue disorders, and, in cases of distal ulnar aneurysms, hypothenar hammer syndrome. Aneurysms of the intrathoracic subclavian artery are usually atherosclerotic in nature, while the ones in the extrathoracic segment are usually secondary to thoracic outlet syndrome. Atherosclerotic aneurysms can present with pain, hoarseness, distal embolization, stroke, and rupture. Occasionally, the dilated origin of an aberrant subclavian artery known as the diverticulum of Kommerell can evolve into a true aneurysm that can be associated with pain, dysphagia, and dissection. CTA and MRA can provide a complete aneurysm characterization that allows for a safer therapeutic planning.

Knee Dislocation

Knee dislocation can cause arterial injuries in approximately 40% of cases. Most patients are young and have limited collateral flow, which makes them highly vulnerable to popliteal occlusion, and a delay in diagnosis and treatment can lead to amputation due to irreversible ischemic changes. Physical exam with emphasis on the distal pulses and associated signs of vascular injury is crucial for a prompt diagnosis; however, an abnormal pedal pulse as an isolated finding on the initial examination of patients with knee dislocations is not sensitive enough to detect an injury that invariably requires vascular intervention. Patients with signs of ischemic limb should proceed directly to surgery, and, if required, intraoperative angiography can be performed for confirmation. Catheter angiography should include multiple projections in order to exclude intimal tears, spasm, and partial thrombosis. Small and nonocclusive lesions are managed conservatively. Patients who have been treated with prompt reduction and those with normal vascular exams can be further evaluated with CTA to determine the integrity of the popliteal artery.

Femoral Artery Pseudoaneurysm

Pseudoaneurysm of the femoral artery is more frequently the result of an arterial puncture to perform cardiac or peripheral angiography, occurring in 1% to 5% of the cases. Patients may present with a large inguinal hematoma or a pulsatile mass. Most pseudoaneurysms thrombose spontaneously, but up to 3% to 5% may persist, increase in size, or rupture. Because of their location these aneurysms are generally diagnosed with duplex ultrasound. Occasionally MRA or CTA is required when they cannot be adequately characterized with ultrasound due to their large size or multilobulated characteristics, ultrasound’s inability to visualize the pedicle, or when they persist despite an initial attempt to treat them. Most femoral pseudoaneurysms can be treated with ultrasound-guided compression of the pedicle (or neck) to interrupt the flow and induce thrombosis; when this fails, thrombin injection can be performed under direct ultrasound visualization to control the aneurysm flow as the thrombin is being administered (Fig. 11-38).

Figure 11-38 A, Contrast-enhanced MRA demonstrates a large pseudoaneurysm of the right common femoral artery that occurred as a complication of catheterization for coronary angiography. In addition. there is prompt enhancement of the common femoral vein, iliac vein, and IVC consistent with arteriovenous fistula. B, Under ultrasound guidance a 22G needle is advanced into the aneurysm lumen, and thrombin is slowly injected under constant monitoring until complete thrombosis of the sac is achieved. C, Post-thrombin therapy MRA demonstrates complete thrombosis of the pseudoaneurysm and persistent AV fistula.