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Vasculitides

GIANT CELL ARTERITIS

Giant cell (temporal) arteritis (GCA; see Chapter 43) is a medium-vessel chronic inflammatory vasculitis that affects the aorta and its branch vessels. It most commonly occurs in patients older than 55 years of age and is twice as common in women as men. rysms, most commonly in the thoracic aorta. patients with GCA-related TAAs, 16 developed aortic dissection, 15 had valvular annular expansion causing symptomatic aortic valve insufficiency, and 18 required surgery. patients with GCA, 18% developed aortic aneurysm or dissection, and these occurrences were inversely associated with development of intracranial disease manifestations. aortic aneurysm itself was not associated with increased mortality; however, the nine individuals who developed aortic dissection had significantly increased mortality. aneurysm formation seems to be similar to patients without GCA, with increases in MMP-2- and MMP-9-associated destruction of the vessel wall.

TAKAYASU'S ARTERITIS

Named for a Japanese professor of ophthalmology, Takayasu's arteritis (TA; see Chapter 42) is a large-vessel vasculitis that typically has its onset between the age of 10 and 30 years. The most common vascular presentation is occlusive disease, found in 80% to 94% of patients; however, aortic aneurysms may be found in up to one fourth of patients with TA. disease has been associated with worse outcome in a series of 120 Japanese patients followed for 13 years. and MMP-9 are elevated in TA, but the mechanism of aneurysm formation remains unknown.

BEHÇET'S DISEASE

Behçet's disease (see Chapter 41) is a small-vessel vasculitis originally characterized by a set of three symptoms: aphthous stomatitis, genital ulcers, and uveitis. sized and large arteries, as well as veins, arises not from direct vascular inflammation but rather due to vasculitis of the small arteries of the vasa vasorum that supply the vessel wall. Vascular involvement, including aneurysms, can be found in 7% to 38% of patients. in Behçet's disease depends in large part on the location of the abnormality and clinical circumstances. First-line therapy includes an antiinflammatory regimen with corticosteroids. As with other vasculitides, risk of intervention is greatest during the state of active inflammation, and there is an increased risk of rupture, dissection, and/or future aneurysmal dilation at the site of revascularization.

SERONEGATIVE SPONDYLOARTHROPATHIES

The spondyloarthropathies (see Chapter 41) are characterized by inflammation of the spine and sacroiliac joints, association with HLA-B27, and absence of rheumatoid factor (RF). These disorders are known to be associated with an increased risk of aortic aneurysm formation. Specific spondyloarthropathies include ankylosing spondylitis, Reiter's syndrome, and relapsing polychondritis.

presence of four of the five following features: onset younger than 40 years of age, back pain for more than 3 months, insidious onset of symptoms, morning stiffness, and improvement with exercise. Aortic root and valve disease is present in up to 80% of patients. valve disease were found in 82%; thickening of the aortic valve was noted in 41% of patients, and aortic dilation in 25%.

233

Between 1% and 20% of GCA patients develop aneu-

237,238

239,240

Development of aneurysmal

242

243

243,245

Management of aneurysmal disease

234

In a series of 41

235

In a series of 168

234

Presence of an

236

The mechanism of

241

Blood levels of MMP-2

Involvement of medium-

244

Ankylosing spondylitis is an HLA-B27 disease that requires the

242

In a series of 44 outpatients, aortic root disease and

246

Aortic

valve thickening manifested as nodularities of the aortic cusps, forming a characteristic subaortic bump.

242

Valve regurgitation was seen in almost half of patients, and 40% had moderate lesions.

Reiter's syndrome is a reactive arthritis that affects the lower limbs, causing an asymmetrical oligoarthritis. To make the diagnosis, patients must have evidence of a preceding infection, diarrhea, or urethritis 4 weeks preceding the syndrome.

247

Less than 1% of Reiter's syndrome patients develop cardiovascular complications. Among this group, aortic insufficiency is a late finding.

Relapsing polychondritis is a paroxysmal and progressive inflammatory disease of the cartilaginous structures, affecting the ear, nose, and hyaline cartilage of the tracheobronchial tree. Cardiovascular disease, including aortic aneurysms, is found in 25% to 50% of patients.

248

Infectious Aortic Aneurysms

MYCOTIC ANEURYSMS

Also known as infective endarteritis aneurysms are rare phenomena. Two large necropsy studies including 22,000 and 20,000 patients, respectively, revealed a combined incidence of 0.03% in the United States. average age of patients with mycotic aneurysms is 65, and men are threefold more likely to develop mycotic aneurysms than women.

251,252

Hematogenous seeding, such as occurs in patients with endocarditis, affects a vessel that may be “at risk” because of preexisting atherosclerosis or previous damage and represents the most common cause of mycotic aneurysms. Indeed, as many as 15% of patients with endocarditis developed mycotic aneurysm before the antibiotic era. include septic microemboli, contiguous extension, and trauma with direct contamination. In contrast to the typical degenerative or vasculitic fusiform expansion, mycotic aneurysms are more likely to be saccular (see range in size from 1 mm to 10 cm and include components of acute and chronic inflammation, hemorrhage, abscess formation, and necrosis.

Clinical manifestations of mycotic aneurysm most commonly include pain and fever and, if related to a new aneurysm, should prompt directed investigation. The organisms that most commonly cause mycotic aneurysms include Staphylococcus and Salmonella species, which cause 40% and 20% of mycotic aneurysms, respec-

255,256

tively. to 80%.

Surgery should be prompt, since rupture occurs in up

257,258

Prognosis for cerebral vascular infection is dire, with 1-year mortality for patients who have cerebrovascular mycotic aneurysms reaching as high as 90%.

TUBERCULOUS ANEURYSMS

Aortic aneurysm due to tuberculosis is quite rare. In a series of more than 22,000 autopsies performed at one urban medical center in the first half of the 20th century, only 1 of 308 aortic aneurysms had tuberculous aneurysms, no tuberculous aneurysms among 20,000 autopsies performed in a rural setting.

250

Three mechanisms have been postulated to facilitate tuberculous adhesion and endarteritis. It is thought that direct extension from a contiguous source, such as the spine or lung, may cause 75% of tuberculous aneurysms. ties include adhesion to a vessel damaged by atherosclerosis or infiltration of the inner layers of the aorta via the vasa vasorum. The abdominal and thoracic portions of the aorta are affected similarly. The presentation of the patient with a tuberculous aneurysm varies significantly. The patient may be asymptomatic, have a palpable or radiologically visible paraaortic mass, complain of chest or abdominal pain, or present with aortic rupture and hypovolemic shock. Tuberculous aneurysms that are symptomatic or rapidly expanding and pseudoaneurysms typically require surgical repair.

(see Chapter 59), mycotic

254

Other etiologies

Fig. 37-4). The outpouching may

258

249

whereas there were

259

Other possibili-

249,250

The

253

259

465

CH 37

PATHOPHYSIOLOGY, EPIDEMIOLOGY, AND PROGNOSIS OF AORTIC ANEURYSMS

466

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

SYPHILITIC ANEURYSMS

Although syphilis may once have been a common cause of aortic disease, antibiotics have greatly diminished the incidence of syphilitic aortic aneurysm (luetic aneurysm), such that fewer than 50 cases have been reported in the antibiotic era.

vous system (CNS) and cardiovascular complications denote the

tertiary stage of syphilis. Classically, this arises after a latent phase

260

of roughly 10 to 30 years from initial spirochete infection. Syphilitic aortitis may occur in up to 10% of patients with tertiary syphilis (

Fig. 37-6). Destruction of the elastic lamina occurs as a conse-

quence of lymphoplasmacytic infiltrate around the vasa vasorum, owing to direct spirochete infection of the aortic media. This ultimately leads to expansion but also fibrosis and calcification, producing the classic “tree bark” radiographic pattern. Luetic aortic aneurysms commonly involve the ascending aorta and are saccular. Involvement of the coronary ostia may result in coronary stenosis and resultant anginal symptoms. Survival with syphilitic aortic aneurysm is worse than the general population.

Trauma

Aneurysms related to trauma are discussed in Chapter 61.

FIGURE 376 Volume-rendered (VR) maximum intensity projections (MIPs) from computed tomographic angiography (CTA) of chest of patient with tertiary syphilis, showing extensively calcified thoracic aortic aneurysm (TAA) measuring 11.5 cm × 11.4 cm in short axis and 18 cm in length. (From Tomey MI, Murthy VL, Beckman JA: Giant syphilitic aortic

aneurysm: a case report and review of the literature. Vasc Med 16:360–364, 2011.)

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255. Jarrett F, Darling RC, Mundth ED, et al: The management of infected arterial aneurysms,

J Cardiovasc Surg (Torino) 18(4):361–366, 1977.

256. Vogelzang RL, Sohaey R: Infected aortic aneurysms: CT appearance, J Comput Assist Tomogr 12(1):109–112, 1988.

257. Taylor LM Jr, Deitz DM, McConnell DB, et al: Treatment of infected abdominal aneurysms by extraanatomic bypass, aneurysm excision, and drainage, Am J Surg 155(5):655–658,

1988.

258. Johansen K, Devin J: Mycotic aortic aneurysms. A reappraisal, Arch Surg 118(5):583–588,

1983.

259. Long R, Guzman R, Greenberg H, et al: Tuberculous mycotic aneurysm of the aorta: review of published medical and surgical experience, Chest 115(2):522–531, 1999.

260. Pugh PJ, Grech ED: Syphilitic aortitis, N Engl J Med 346(9):676, 2002.

CHAPTER

38 Clinical Evaluation of Aortic

Aneurysms

Joshua A. Beckman, Mark A. Creager

The vast majority of aortic aneurysms are asymptomatic, accounting for a much higher disease prevalence than hospitalization and mortality statistics would suggest (see Chapter 37). These data underscore the central challenge in aortic aneurysmal disease: a common clinical problem that is silent until rupture and death. Aortic aneurysms typically increase in size slowly over years or decades, with few warning signs. The management of aortic aneurysmal disease, therefore, requires suspicion and diligence to avoid adverse outcomes. This chapter will focus on the history, physical examination, and diagnostic tests important to clinical evaluation of aortic aneurysms.

Clinical History

Thoracic Aortic Aneurysms

Aneurysms of the thoracic aorta typically produce no symptoms, but a variety of symptom complexes may arise related to aneurysm size and location within the thorax.

Patients with aneurysmal dilation of the ascending thoracic aorta may develop clinical manifestations of congestive heart failure (CHF) as a consequence of aortic valvular regurgitation. Enlargement of the sinuses of Valsalva may cause myocardial ischemia or infarction due to direct compression of the coronary arteries or coronary arterial thromboembolism. Right ventricular (RV) outflow tract obstruction and tricuspid regurgitation may result from aneurysmal deformation of the noncoronary sinus. Aneurysms of the sinuses of Valsalva may rupture directly into the RV cavity, right atrium, or pulmonary artery, causing heart failure associated with a continuous murmur. Chest pain may occur when the aneurysm compresses surrounding structures or erodes into adjacent bone such as the ribs or sternum. Compression of the superior vena cava may produce venous congestion of the head, neck, and upper extremities. Symptoms are frequently a harbinger of rupture or death. Rupture may occur into the left pleural space, pericardium, pulmonary artery, or superior vena cava.

Aneurysms of the aortic arch may produce symptoms by compression of contiguous structures, but most are asymptomatic. Dyspnea or cough may be caused by compression of the trachea or mainstem bronchi, dysphagia by compression of the esophagus, or hoarseness secondary to left vocal cord paralysis related to compression of the left recurrent laryngeal nerve. The superior vena cava syndrome and pulmonary artery stenosis result when these vessels are compressed. pression of adjacent structures or to erosion of ribs or vertebrae, is typically positional. Aneurysms of the aortic arch may rupture into the mediastinum, pleural space, tracheobronchial tree (causing hemoptysis), or esophagus (causing hematemesis). Arteriovenous fistulas (AVFs) may result from rupture into the superior vena cava or pulmonary artery. Tuberculous aneurysms, akin to other causes of thoracic aortic aneurysms (TAAs), may present with pain but are commonly asymptomatic or may present with hypovolemic shock as a consequence of rupture.

Symptoms of descending TAAs include chest pain from compression of surrounding soft tissues or erosion of vertebrae. Irritation of the recurrent laryngeal nerve may produce hoarseness. Dyspnea may result from bronchial compression, and hemoptysis from direct erosion into the lung parenchyma. Dysphagia and hematemesis are features of esophageal compression or erosion. Rupture may occur into the mediastinum or left pleural space.

1,2

Chest pain, related either to com-

Thoracoabdominal Aortic Aneurysms

Although most patients with thoracoabdominal aortic aneurysms (TAAA) are asymptomatic, discomfort occasionally develops in the epigastrium or left upper quadrant of the abdomen. Back or flank pain may occur when the patient lies in left lateral decubitus position. Erosion of the anterior surfaces of the vertebral bodies may occur, leading to radiculopathy. Visceral artery occlusion may occur, but frank ischemia and infarction are infrequent. Patients who complain of claudication also may have occlusive atherosclerotic disease of the aorta, iliac, or more distal arteries. Because mural thrombosis is so common in atherosclerotic aneurysms, they may be the source of peripheral atheroembolism, causing occlusion of distal vessels. Rupture of the thoracic component of these aneurysms generally occurs into the left pleural space, producing a hemothorax; the abdominal component may rupture into the retroperitoneum, inferior vena cava, or duodenum.

Abdominal Aortic Aneurysms

Most patients with abdominal aortic aneurysms (AAAs) are asymptomatic, yet symptoms may take the form of abdominal discomfort or back pain; some patients become aware of abdominal pulsation. Less frequently, pain may occur in the legs, chest, or groin; anorexia, nausea, vomiting, constipation, or dyspnea may develop. Compression of the left iliac vein may cause left leg swelling, just as compression of the left ureter may cause hydronephrosis, or compression of testicular veins may cause varicocele. As the aneurysm expands and compresses vertebrae and lumbar nerve roots, pain may develop in the lower back and radiate to the posterior aspects of the legs. Flank pain radiating to the anterior left thigh or scrotum may reflect compression of the left genitofemoral nerve. Nausea and vomiting may occur as the aneurysm compresses the duodenum. Bladder compression may cause urinary frequency or urgency.

Occasionally, nascent or frank rupture occurs and causes symptoms indicating a life-threatening emergency. The mortality of patients with AAA rupture is 60%; patients with symptoms suggestive of rupture require emergent surgical referral. The classical triad associated with AAA rupture includes hypotension, back pain, and a pulsatile abdominal mass; however, fewer than 50% of patients have all components of this triad. Diverticulitis, renal colic, and gastrointestinal hemorrhage represent common disorders in the differential diagnosis in these patients.

In the absence of patient complaints, physicians must intuit the presence of aneurysm based on the clinical characteristics of the patient. Risk factors for aortic aneurysm disease (see Chapter 37) can be used to guide directed physical examination and, if necessary, diagnostic testing.

Physical Examination

Physical examination is usually unhelpful in diagnosing TAAs because the rib cage precludes palpation of the aorta. Physical examination may demonstrate right sternoclavicular lift or tracheal deviation. Dilation of the aortic root may cause aortic valve regurgitation.

The key physical finding for an AAA is a pulsatile abdominal mass. The patient should be positioned supine with the knees flexed. A pulsatile epigastric or periumbilical mass may be visible as well as palpable. To distinguish an AAA from paraaortic masses

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FIGURE 381 Examination to detect lateral borders of an aortic aneurysm should be performed with fingertips of both hands. Aneurysm

should expand laterally with each heart beat. Aortic aneurysm transverse diameter may be estimated as distance between closest fingers.

requires that the examiner's hands address the lateral borders (

Fig. 38-1). An aneurysm expands laterally with each systole. This

technique also permits estimation of the transverse diameter of the aneurysm. Auscultation may reveal a bruit over the mass, but abdominal bruits are not specific for aneurysm formation, and

only about 40% of such aneurysms are associated with bruits. Proper physical examination of the abdomen may detect the presence of an AAA in 30% to 48% of patients with AAA. of 15 studies, sensitivity of abdominal examination for aneurysm detection was 49%

(Table 38-1).

3,4

In a review

Several factors limit the potential for AAA diagnosis. First, palpation for an aneurysm requires consideration of the diagnosis prior to examination. Routine physical examination decreases the sensitivity of the exam. Second, size matters; as the size of an aneurysm increases, so does the likelihood of making the diagnosis. Sensitivity of palpation increases to 75% in patients with aneurysms greater than 5 cm in diameter.4 Third, increasing abdominal girth decreases the likelihood of discovery. In one study of 201 patients, all six aneurysms present were diagnosed in patients with an abdominal girth less than 100 cm, but only 3 of 12 were detected when the abdominal girth exceeded 100 cm.5 So although the directed physical examination has moderate sensitivity and specificity for AAA diagnosis, routine examination misses the diagnosis more commonly than making it.

The finding of a pulsatile mass in the groin, suggesting an iliac artery aneurysm, or in the popliteal fossa, suggesting a popliteal artery aneurysm, should raise the index of suspicion that an AAA may be present, since multiple aneurysms often coexist. Physical signs such as carotid bruits or diminished arterial pulses in the lower extremities may reflect atherosclerosis of other vessels.

Rupture of an AAA usually produces the clinical picture of extreme distress as a result of abdominal catastrophe. Despite surgical advances, mortality is still the rule because of the abrupt nature of circulatory collapse, which prevents timely intervention in most cases. Patients frequently have severe abdominal or back pain, but the pattern of pain varies considerably and may be either persistent or intermittent, sharp or dull, constricting or burning. The aneurysm may rupture into the retroperitoneum or into the peritoneal or pleural cavities. Patients may develop hypotension, tachycardia, pallor, diaphoresis, or shock, depending on the extent of rupture and associated blood loss into the extravascular space. On occasion, rupture occurs directly into the duodenum, causing an aortoduodenal fistula and acute gastrointestinal bleeding. This possibility should be considered when gastrointestinal bleeding is evident along with signs of an aneurysm on physical examination.

TABLE 38-1 Sensitivity and Specificity of Physical Examination for Abdominal Aortic Aneurysm

SOURCE AGE RANGE NO. SCREENED ALL AAA SENSITIVITY 44.9 CM AAA SENSITIVITY ≥5 CM AAA SENSITIVITY

Cabellon

Ohman

Twomey

Allen

Allardice

Lederle

Collin

Shapira

Andersson

Spiridonov

MacSweeney

Karanjia

Molnar

al-Zahrani

Arnell

Fink

SUMMARY 3155 293 49%

AAA, abdominal aortic aneurysm; NA, not available. Adapted from Lederle FA, Simel DL: The rational clinical examination. Does this patient have abdominal aortic aneurysm? JAMA 281:77–82, 1999.

43-79 73 9 22% NA NA NA NA

50-88 50 3 0% 1 0% 0 NA

>50 200 14 64% 3 100% 4 75%

>65 168 3 0% 0 NA 1 0%

39-90 100 15 33% 3 100% 2 100%

60-75 201 20 45% 5 20% 5 80%

65-74 426 23 35% NA NA NA NA

31-83 101 4 0% 0 NA 2 0%

38-86 288 14 29% NA NA NA NA

17-67 163 10 70% 4 100% 3 100%

NA 200 55 24% 16 44% 6 100%

55-82 89 9 100% 5 100% 2 100%

65-83 411 7 43% 3 33% 2 50%

60-80 392 7 57% 4 50% 2 100%

55-81 96 1 100% 0 NA 0 NA

51-88 200 99 68% 44 69% 14 82%

Rupture may also occur into the inferior vena cava or iliac veins, producing an arteriovenous fistula; this is suggested by rapid development of leg swelling or so-called high-output CHF in the presence of an AAA.

Screening and Surveillance of Aortic Aneurysms

Several trials have evaluated the possibility of reducing AAA event rates as a result of screening. In a study from Chichester, United Kingdom, 15,775 men and women aged 65 to 80 years were divided in two, and half were invited for an abdominal ultrasound screening. invitation, and aneurysm was detected in 4%. A 55% reduction in rate of aneurysm rupture (2.8 per 1000 vs. 6.2 per 1000 subjects) and a 42% reduction in AAA-related mortality in men only (3 per 1000 vs. 5.3 per 1000 male subjects) were noted in the screening group compared to controls. A similar study in Denmark offered 12,658 65- to 73-year-old males a screening invitation, of whom 9620 accepted and 3038 declined. tion in AAA-related death in the group that accepted the invitation compared with those who did not (.006% vs. .06%). Only one trial has assessed the impact of screening on total mortality. The Multicentre Aneurysm Screening Study (MASS) assessed the impact of AAA screening in 67,800 men aged 65 to 74 years.8 Half were invited for AAA screening, and the others were not. Long-term mortality was monitored in both groups. In the screened group, there was a 42% relative risk reduction in aneurysm-related mortality from 0.33% to 0.19%, representing 48 fewer deaths. Reduction in absolute mortality, however, was a statistically insignificant 0.27%.

Some clinical features exist to suggest which patients should definitely undergo screening for aortic aneurysm, and AAA in particular. These include patients with a family history for aneurysm and inherited disorders of connective tissue (e.g., Marfan's syndrome [MFS]) and those with arteritis (e.g., Takayasu and giant cell arteritis [GCA]). Siblings of patients with an AAA have a 25% chance of having an aneurysm.

On the basis of these data, the American College of Cardiology/ American Heart Association (ACC/AHA) Practice Guidelines for the Management of Peripheral Arterial Disease recommends that “Men 60 years of age or older who are either the siblings or offspring of patients with AAAs” and “men who are 65 to 75 years of age who have ever smoked should undergo a physical examination and one-time ultrasound screening for detection of AAAs.” The U.S. Preventive Services Task Force recommends one-time screening for AAA by ultrasonography in men aged 65 to 75 who have ever smoked, but does not recommend routine screening in women. ing the “Welcome to Medicare” preventive visit if the patient has a family history of AAA or is a man aged 65 to 75 who has smoked at least 100 cigarettes in his lifetime.

Nearly 70% of those offered screening accepted the

There was a tenfold reduc-

Medicare will pay for a one-time ultrasound screen dur-

Screening for TAAs is less well established. Recent data have shown that bicuspid aortic valve (BAV) disease is an autosomal dominant condition that may be associated with TAA formation. Interestingly, patients with this condition may manifest the valvular or aneurysmal findings alone or in tandem.

Thus, the ACC/AHA thoracic aortic disease guidelines recommend that all patients with a BAV should have both the aortic root and ascending thoracic aorta evaluated for evidence of aortic dilatation. In pedigree analysis of more than 500 patients with TAA, Albornoz et al. have shown that one in five non-MFS patients have an inherited pattern of disease.

Because of the frequency of both known and unknown genetic conditions associated with TAA, the ACC/AHA thoracic aortic disease guidelines recommend that first-degree relatives of patients with a bicuspid aortic valve, premature onset of thoracic aortic disease with minimal risk factors, and/or a familial form of TAA and dissection should be evaluated for the presence of a BAV and asymptomatic thoracic aortic disease.

Diagnostic Testing

Major objectives of imaging studies include identifying the aorta and its branches, diagnosing and characterizing the type of aneurysm (fusiform or saccular), determining the transverse and longitudinal dimensions of the aneurysm, and detecting associated pathology that may affect treatment. Imaging studies are also indicated for longitudinal surveillance of known aneurysms, or for anatomical definition before endovascular or surgical repairs. An understanding of the benefits and limitations of the several imaging modalities will enable appropriate test selection (Table 38-2).

Chest roentgenography may provide the first indication of a TAA (

Fig. 38-2). Aneurysms of the ascending thoracic aorta are usually

evident on the right side of the mediastinum. Aneurysms of the aortic arch widen the mediastinal shadow and may project more toward the left. These aneurysms may displace or compress the trachea or left mainstem bronchus. Descending TAAs typically appear as mediastinal masses extending into the left hemithorax. Assessment of the aorta by chest roentgenography requires both posteroanterior and lateral projections. Failure to detect TAA roentgenographically, however, does not exclude the diagnosis, since aneurysms may not become apparent until considerable dilation has occurred.

Similarly, plain abdominal roentgenography frequently discloses an unsuspected AAA. of the abdomen may disclose a curvilinear rim of calcification in the wall of the aneurysm, and the diameter of the aneurysm may be estimated when such calcification is visible in two opposing walls. In 25% to 50% of suspected cases, however, the walls of the aneurysm are not sufficiently calcified to permit radiographic identification. Furthermore, it may underestimate anteroposterior aneurysm size by 15%.

Anteroposterior and lateral views

473

CH 38

CliniCAl EvAluATion of AoRTiC AnEuRysms

TABLE 38-2 Abdominal Aortic Aneurysm Imaging Modalities: Strengths and Weaknesses

MODALITY ADVANTAGES DISADVANTAGES OPTIMAL USE

Ultrasound Highly accurate sizing Unable to discern longitudinal extent Initial diagnosis

Inexpensive Cannot define branch artery anatomy Follow-up until repair

CT Highly accurate sizing Ionizing radiation Pre-repair assessment

Defines branch artery involvement well Contrast required Stent graft follow-up

MRA Highly accurate sizing Cannot image some stent grafts Pre-repair assessment

No ionizing radiation Defines branch artery involvement well

Contrast angiography Defines branch artery involvement well Cannot size aneurysm Stent graft implantation

Invasive Ionizing radiation Contrast required

NOTE: Sensitivity and specificity of each examination exceed 95% for diagnosis of abdominal aortic aneurysm (AAA). CT, computed tomography; MRA, magnetic resonance angiography.

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FIGURE 382 Posterior-anterior chest radiograph demonstrating widened mediastinum in patient with a 5-cm ascending thoracic aortic aneurysm (TAA).

Ultrasound

Ultrasonography is the most commonly used method for identification and characterization of AAA. It is the least expensive modality, does not expose the patient to ionizing radiation, and can accurately determine the anteroposterior, transverse, and longitudinal dimensions of an AAA ( 3 cm or larger approaches 100%.10 The examination is rapid and easily performed. The abdominal aorta is subject to anteroposterior, transverse, and longitudinal evaluation. Sonographic classification of AAA begins when the maximum diameter exceeds 3 cm in either anteroposterior or transverse dimensions. Care must be taken to image the aorta perpendicular to its longitudinal axis to avoid eccentricity, which may lead to overestimating its true diameter. Thrombus is frequently identified within the lumen, and echodense calcification may be present in or adjacent to the aortic wall. Beyond determining the size of an aneurysm, ultrasound imaging may help define the relation of major arterial branches and adjacent organs. Certain ultrasound characteristics have potential value in predicting rupture. Intramural hematoma, appearing as a hypoechoic soft-tissue mass surrounding the aorta that may silhouette the psoas muscle, appears to represent such a sign.15 This may be indistinguishable from periaortic fibrosis, which appears on ultrasound examination as a hypoechoic mantle surrounding the aortic wall in patients with inflammatory aortic aneurysms.

Several groups have recently demonstrated the reliability of a “quick screen” in emergency departments. 125 emergency department patients, quick evaluations did not miss an AAA. Emergency department testing had 100% sensitivity

Fig. 38-3). Sensitivity for diagnosis of an AAA

16,17

In a prospective study of

and 98% specificity.18 Indeed, accuracy is maintained at 100% when the “quick screen” and classical examination approaches are compared within a noninvasive vascular laboratory.

Accuracy of ultrasonography should be considered in respect to other imaging modalities (see later discussion). In the Abdominal Aortic Aneurysm Detection and Management (ADAM) Veterans Administration Cooperative Study Group study, computed tomography (CT) and ultrasound were compared. Although both techniques demonstrated sizing variability between local and central reading sites,

in a third of subjects, the variation between ultrasound and CT was 0.5 cm or more. Ultrasonographic evaluation undersized the aneurysm by a mean of 0.27 cm compared with CT measurements. Similarly, in 334 patients participating in an aneurysm endograft study, CT reported a greater aneurysm diameter than ultrasound 95% of the time.21 The correlation between the two measurements was strong at 0.7, but in nearly half the patients, aortic diameter varied by a centimeter or more between the ultrasound and CT studies. Smaller studies confirm both the high sensitivity yet consistent undersizing by ultrasound.

Despite these observations, two large surgical trials have shown that ultrasonography is an appropriate method to evaluate and follow AAA. The U.K. Small Aneurysm Trial Detection and Management Trial

used ultrasonographic monitor-

and the Aneurysm

ing to determine the time of surgical repair in the group of patients randomized to surveillance. More recently, in the Comparison of Surveillance versus Aortic Endografting for Small Aneurysm Repair (CAESAR) trial, which compared early endovascular repair to watchful waiting, ultrasonographic monitoring was used similarly for monitoring.

In the absence of any clinical data suggesting the inadequacy of ultrasound, it remains the primary tool for diagnosis and follow-up.

Postoperatively, ultrasound can evaluate important ongoing clinical issues including perianeurysm aortic size and anastomotic aneurysm and pseudoaneurysm formation. Currently, duplex ultrasonography is not the ideal imaging test following endovascular aneurysm repair (EVAR). Its sensitivity and specificity are less than computed tomographic angiography (CTA) for a variety of problems encountered after endovascular aortic stent grafting (e.g., endoleaks, device migration, thrombosis), so it should not be used as the primary method of follow-up.25 Improvements in technique, including contrast agents and three-dimensional (3D) imaging, are currently in development and likely will improve ultrasound's accuracy to diagnose complications of endografts. Indeed, recent data suggest that ultrasonography may be approaching acceptability for EVAR follow-up.

In a prospective study, 108

26–28

patients underwent color Doppler ultrasound, contrast-enhanced ultrasonography, CTA, and magnetic resonance angiography (MRA) for follow-up after EVAR. Contrast-enhanced ultrasonography demonstrated accuracy similar to CTA and MRA, while all three were superior to color Doppler ultrasonography.

Ultrasound can also be employed to diagnose and monitor TAA. Transthoracic echocardiography (TTA) visualizes the aortic root and a portion of the ascending aorta. Transesophageal echocardiography (TEE) images much of the thoracic aorta well,

FIGURE 383 A, Transverse B-mode ultrasound image of widest portion of abdominal aorta. Electronic calipers have been applied and demonstrate a

5.6-cm transverse diameter and 5.2-cm anteroposterior diameter. B, Sagittal view of same vessel demonstrating transition from normal to aneurysmal aorta.

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