CT Techniques

With recent advances in MDCT technology, routine acquisition of a high resolution isotropic volumetric dataset at the peak of contrast enhancement is easily achieved. There are several advantages to MDCT, but perhaps the greatest is the ability to analyze and display the aorta and branch vessels in any plane and to perform three-dimensional volume rendering for improved visualization and vascular diagnosis.

Using MDCT, a helical volume is acquired with a detector collimation of between 0.5 and 1.5 mm, and reconstructed with a similar thickness using a matrix size of 512 × 512 or greater. The use of tube current modulation techniques (e.g., automated exposure control) reduces radiation exposure compared to fixed-tube current techniques. For MDCT angiography, increased vascular enhancement can be achieved by reducing the kVp to 100 keV (or 80 keV in smaller patients) because this increases photon attenuation by iodinated contrast and moves the mean energy closer to the k-edge of iodine (33.2).¹

Prior to acquisition of the arterial phase images, a noncontrast CT image set can be obtained. This is particularly useful where significant vascular calcification is expected, or in instances in which intramural hematoma is a differential consideration. Proper timing of the CTA volume acquisition with peak arterial contrast enhancement is critical for optimal arterial illustrations. For detection of associated parenchymal abnormalities, scar tissue, and endoleaks, the addition of delayed phase images can also be helpful. If multiple phases are used routinely, acquisition of those additional phases using lower radiation dose techniques should be considered to minimize patient radiation exposure doses.

After the patient is scanned, the dataset can be sent to a postprocessing workstation for both two-dimensional and three-dimensional image reconstruction, and for evaluation of the aorta and branch vessels in a double-oblique true axial plane.

MRI Techniques

Coils and Patient Position

Patients are imaged supine, ideally in a 1.5T or 3.0T MR scanner. Arms should be placed above the patient’s head, or folded across the chest to prevent wrap artifact (also known as image aliasing artifact).

Coil Choice

Signal-to-noise ratio (SNR) can be maximized with a surface phased array torso coil, positioned to cover the region from the suprarenal abdominal aorta to the iliac vessels. More than one coil may be used in series to maximize range in the z-axis.

The extra SNR, greater signal uniformity, and number of coil elements provided by phased array torso coils enable the use of parallel imaging techniques, higher spatial resolution, more rapid signal processing (if there are enough receiver channels), and lower doses of intravenous contrast. In obese or especially tall patients, a body coil can be employed, although this will result in lower SNR.

MR Pulse Sequences

Precontrast Techniques

Localizers: During a breath-hold, localizers are initially obtained in the sagittal, coronal, and axial planes. Performing localizers during breath-hold ensures that the intra-abdominal organs will be located in a similar place to the post-gadolinium sequences which are typically acquired using breath-holding. Localizers can be performed using a variety of sequences, but nongated two-dimensional steady-state free precession sequences (SSFP) provide good tissue contrast and bright-blood images of vessels. Alternatively, HASTE (half-Fourier acquisition single shot turbo spin echo) or SSFSE (single shot fast spin echo) sequences can be performed, which provide a single breath-hold overview of the abdominal organs, with rapidly flowing blood appearing black.

Precontrast Sequences

Axial T1 Weighted Sequences: To survey the intra-abdominal structures, axial T1 weighted images are useful. These can be performed as breath-hold in and out of phase sequences, or using a double inversion fast spin echo technique to eliminate signal from slowly flowing blood. Precontrast T1-weighted images are particularly important for evaluation of the aortic wall for possible pathologies, such as intramural hematoma, which may have high T1 signal related to the presence of hemorrhage. Axial T2 fast spin echo sequences (usually with fat suppression) can also be performed from the diaphragm to the iliac crests to evaluate mass lesions and fluid collections around grafts.

Steady-State Free Precession: Steady-state free precession sequences (also termed balanced-FFE, true-FISP, and FIESTA) are rapid, have high intrinsic contrast resolution, and have been shown to be accurate in evaluating renal artery stenosis,² aneurysm sac contents (Figure 102-1),³ thoracic aortic dissection, and aneurysm.⁴ These sequences can be performed with breath-hold techniques or free breathing with navigator gating, and they provide an overview of the aneurysm sac and surrounding contents.

Figure 102-1 Coronal (A) and axial (B) steady-state free precession sequence. A rapid breath-hold sequence without intravenous gadolinium, providing an overview of the aneurysm (arrows) location, relationship to major branch vessels, size, and internal contents.

Velocity Encoded Cine MR Techniques: Unlike the thoracic aorta, velocity encoded cine MR techniques (also known as cine phase contrast MR) are not widely used in the abdominal aorta. However, in cases of abdominal aortic coarctation or stenosis, these techniques may assist in quantifying the hemodynamic severity of the obstruction.

Postcontrast MRA: Following contrast injection, the abdominal aorta is scanned using a 3D spoiled gradient echo pulse sequence. The sequence should be optimized to acquire a near isotropic voxel size of 1 to 1.5 mm, in approximately 10 to 15 seconds.

Contrast Media Dose

For abdominal aortic CTA, doses of up to 150 mL of nonionic contrast delivered at 3 to 6 mL per second have been routinely used in the past. However, with rapid acquisition techniques, doses as low as 50 mLs have been used, especially in smaller patients.⁵ For MRA, a typical gadolinium-chelate contrast agent dose is 0.2 mmol/kg injected at 2 mL/sec.

Prevalence and Epidemiology

Abdominal aortic aneurysms are nearly five times more common in men than in women and almost twice as common in people of European descent than African Americans. The prevalence of aneurysm is also increased in those with a family history of AAA, and is strongly related to a history of smoking.⁸ Other risk factors include age, coronary artery disease or another manifestation of atherosclerosis, high cholesterol, and hypertension. In a large ultrasound screening study,⁹ an abdominal aortic aneurysm was detected in approximately 5% of males older than 65 years. Ruptured AAA occurs in 1% to 3% of men per year aged 65 years or more, and mortality is 70% to 95%. Left untreated, AAA leads to death in about one third of patients.⁸

Etiology and Pathophysiology

Although the exact etiology of AAA remains unclear, it appears that degradation of elastin, collagen, and other structural proteins in the aortic wall is a major factor.¹⁰ Atherosclerosis is considered to play an important role in the etiology, likely via chronic inflammation in the aortic wall. An imbalance of T-helper and T-suppressor lymphocytes leads to a proliferation of B-lymphocytes. Elastin-derived peptides (EDPs), which are breakdown products of medial elastin, are thought to be the initiating and propagating antigen in this process. Chronic inflammation leads to excess matrix metalloproteinases and degradation of medial elastin and collagen.¹¹ However, the etiology is unquestionably multifactorial. Current research suggests that genetic, environmental, hemodynamic, and immunologic factors all contribute to the development of aneurysms.

Clinical Manifestations of Disease

Most AAAs are asymptomatic and are discovered incidentally on routine physical examination or during other imaging studies. Patients with ruptured AAAs often present with an abrupt onset of back pain as well as abdominal pain and tenderness. Patients may present critically ill. Most will have a pulsatile abdominal mass. Rupture has a high mortality rate, with 25% mortality prior to arriving at the hospital and an overall 30-day survival rate of approximately 10%.¹²

The rate of aneurysm growth increases with increasing diameter in concordance with Laplace law. Aneurysms smaller than 4 cm grow at 2 to 4 mm/year, those measuring 4 to 5 cm grow at 2 to 5 mm per year, and aneurysms >5 cm grow at 3 to 7 mm per year.¹³ The risk of rupture increases with aneurysm size and rate of aneurysm expansion. In the U.K. Small Aneurysm Trial,¹⁴ aneurysms with a cross-sectional diameter of 5 to 5.9 cm in size had an annual risk of rupture of 6.5%. Elective AAA repair carries a 4% to 6% mortality. Recommendations¹⁰ suggest elective repair of aneurysms greater than 5.5 cm in males, and greater than 4.5 to 5 cm in women. Aneurysm length is not thought to be associated with rupture risk.¹⁵

Imaging Indications and Algorithm

The U.S. Preventive Services Task Force (USPSTF)¹⁶ recommends screening for AAA in men aged 65 to 75 years of age who have ever smoked. It can also be considered in patients with a strong family history of AAA. Ultrasound is the modality of choice for screening in most patients. Its advantages include the absence of intravenous contrast, absence of ionizing radiation, and relatively low cost.

For asymptomatic and smaller aneurysms, ultrasound surveillance is recommended (Table 102-1). For aneurysms >4.5 cm, CT or MRI offer the advantages of greater measurement accuracy, better depiction of the suprarenal aorta and branch vessels, and superior reproducibility versus ultrasonography.

TABLE 102-1 Rescreening Intervals for Asymptomatic AAAs

* Also consider referral to a vascular surgeon.

Derived from Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation 2005; 111(6):816-828.

Imaging Techniques and Findings

Radiography

The presence of calcification in the abdominal aortic wall, although commonly present, is not invariable. Moreover, a tortuous and calcified aorta may mimic an AAA. A lateral radiograph (Fig. 102-2) may depict aortic calcification more clearly. However, radiographs are unreliable for diameter measurements of the aortic wall and are not recommended for diagnosis or surveillance.¹⁷

Figure 102-2 Lateral radiograph of an abdominal aortic aneurysm. Fusiform dilation of the infrarenal aorta with calcification of the intima (arrows). The superior and inferior extent of the aneurysm sac are not visible.

Ultrasonography

Examination of the abdominal aorta is an essential component of a complete abdominal ultrasound study, and should be examined in all patients presenting with acute abdominal pain. Abdominal aortic aneurysms should be detectable by sonography in up to 100% of patients.¹⁸

The aorta appears on ultrasound as a hypoechoic tubular structure with echogenic walls (Fig. 102-3A). The anterior and posterior walls of the aneurysm are usually better seen than are the lateral walls. Mural thrombus (see Fig. 102-3B) has low to medium echogenicity and is attached to the margins of the aortic wall. At times, mural thrombus will have a lamellated appearance. Thrombus that appears to “flutter” during the cardiac cycle may be at risk of embolization.

Figure 102-3 A and B, Abdominal aortic aneurysm on ultrasound. Transverse and sagittal ultrasound images of the aorta demonstrate a small aortic aneurysm, not appropriate for surgical repair. C, Abdominal aortic aneurysm containing mural thrombus. Measurements of the aneurysm are from outer wall to outer wall, not the caliber of the patent lumen.

Ultrasound measurements of abdominal aortic aneurysms are accurate and repeatable. The measurements are taken from the outer-to-outer wall of the aorta in a plane perpendicular to the long axis of the aorta.

In suspected aneurysm rupture, a bedside ultrasonogram may be helpful for those patients who are too unstable for CT, or if CT is not readily available. Ultrasound scanning may assist in determining the aneurysm size and the presence of retroperitoneal or intraperitoneal fluid (Fig. 102-4), although the role of ultrasonography in identifying impending rupture is limited.¹⁹

Figure 102-4 Bedside ultrasound (A) and subsequent CT (B and C) on a hypotensive patient with a pulsative abdominal mass. On ultrasound, a 9 cm aneurysm (asterisk) was diagnosed, but retroperitoneal blood was not suspected. On subsequent CT (B), a small periaortic hematoma was identified (arrow), in addition to a “draped aorta sign” of a deficient posterior wall. More inferiorly (C), a small fissure has formed within the posterior aspect of intramural thrombus (arrow). Ultrasound is not accurate in excluding small retroperitoneal ruptures.

CT and MRI

Compared to ultrasonography, CT and MRI (Fig. 102-5) provide superior depiction of the extent and shape of the aneurysm, involvement of the renal, mesenteric, and iliac arteries, and the suprarenal abdominal and thoracic aorta. On average, ultrasound underestimates aneurysm size by 3 to 9 mm compared to CT angiography.²⁰ Due to their excellent contrast resolution and multiplanar capabilities, CT and MR angiography are now the mainstay of aneurysm characterization prior to endovascular or surgical repair. CT is the modality of choice for the evaluation of suspected rupture of the abdominal aorta¹⁹; usually it can be performed within minutes, and has clear benefits in showing alternative causes of acute abdominal pain. Contrast-enhanced CT provides information about the lumen size, location, extent, relationship to branch vessels, presence of active contrast extravasation, and complications secondary to aneurysm rupture.

Figure 102-5 Infrarenal abdominal aortic aneurysm (arrow) demonstrated on maximum intensity projection (MIP) reconstruction of a gadolinium-enhanced MRA. The neck of the aneurysm and relationship to the renal arteries is clearly shown, as are the associated stenoses of the renal arteries and common iliac arteries.

Signs of Rupture, Impending Rupture, and Contained Rupture

Noncontrast CT is useful in demonstrating the presence of an abdominal aortic aneurysm, maximum aneurysm size, and the presence of retroperitoneal hemorrhage. A high attenuating crescent within the wall of aneurysm (Figs. 102-6 and 102-7) is a sign of impending or frank aneurysm rupture.²¹ A high attenuation crescent is denser than the psoas muscles (on enhanced CT) and the lumen (on nonenhanced CT scans).

Figure 102-6 Noncontrast CT of the abdomen demonstrates a high-density crescent in the periphery of the aneurysmal wall suggesting impending rupture (arrow).

Figure 102-7 In patients unable to receive intravenous contrast, noncontrast CT is useful in evaluating the presence of an aneurysm and retroperitoneal hematoma. A large left heterogeneous retroperitoneal hematoma is present on noncontrast abdominal CT. Crescentic hyperattenuating thrombus is also present within the posterior wall (arrows).

The most common finding in aneurysm rupture is a retroperitoneal hematoma adjacent to the abdominal aortic aneurysm (see Figs. 102-4, 102-7, and 102-8). This blood usually tracks into the pararenal and perirenal spaces (Fig. 102-9). Active extravasation (Figs. 102-9 and 102-10) is frequently visualized on contrast-enhanced CT images. The “draped aorta sign,” where the abdominal aorta is closely applied to the spine with lateral “draping” of the aneurysm around the vertebral body (see Fig. 102-4), has been described as a finding of a deficient posterior wall of the aorta and a contained leak.²² Other sites of rupture include the bowel (most commonly the duodenum), and inferior vena cava (Fig. 102-11).²³ Signs of AAA rupture, impending rupture, and contained rupture are (1) periaortic and retroperitoneal hemorrhage; (2) contrast extravasation; (3) high attenuating crescent sign; and (4) draped aorta sign.

Figure 102-8 A, Early rupture of an abdominal aortic aneurysm. Contrast-enhanced axial CT of the abdomen shows a large abdominal aortic aneurysm with adjacent fat stranding (arrow) suggesting aortic leak or impending rupture. B, Contrast-enhanced coronal CT of the abdomen demonstrates a saccular aneurysm of the infrarenal aorta (black arrow) with adjacent fat stranding (white arrows) suggesting aortic leak or impending rupture.

Figure 102-9 A and B, Ruptured abdominal aortic aneurysm. Contrast-enhanced axial CT and VR images of the abdomen demonstrate a saccular infrarenal abdominal aortic aneurysm with frank rupture into the left retroperitoneum. Active contrast extravasation is also present (arrows). C, Contrast-enhanced coronal CT of the abdomen demonstrates a saccular infrarenal abdominal aortic aneurysm with a massive left retroperitoneal hemorrhage (thin arrows). Active contrast extravasation is again present (thick arrow). Sparing of the perinephric space excluded the kidney as the bleeding source.

Figure 102-10 Two ruptured abdominal aortic aneurysms. A, Intraperitoneal contrast extravasation (arrow) is uncommonly encountered. B, More commonly retroperitoneal extravasation is seen (arrow).

Figure 102-11 A, Abdominal aortic aneurysm with a fistula between the aorta and inferior vena cava. Axial images from arterial phase of a contrast-enhanced CTA demonstrates a large infrarenal abdominal aortic aneurysm; a crescentic structure just lateral to the aorta demonstrates enhancement during this arterial phase study (arrow). B, Sagittal reconstruction demonstrates a fistula connection between the abdominal aortic aneurysm and the inferior vena cava (arrow). C, Volume rendered AP image of the aorta demonstrates contrast filling the right iliac vein and the lower IVC (arrows).

FDG-PET

Recent evidence suggests that increased aortic wall metabolism, as measured by FDG-PET, may suggest increased rupture risk. Increased metabolism may represent increased activation of inflammatory cells in the aortic wall, which leads to increased degradation of elastin and collagen in the aneurysm wall.²⁴ Pilot studies examining the role of FDG-PET-CT in asymptomatic and symptomatic AAAs,²⁵ have demonstrated increased activity in those with symptomatic AAAs, and increased activity in focal areas of increased inflammation and collagen degradation.

Differential Diagnosis

Nonruptured AAAs are often asymptomatic. Pain associated with a ruptured aneurysm is nonspecific. Other diagnoses which could manifest similarly include biliary disease, renal colic, diverticulitis, pancreatitis, cardiac ischemia, and mesenteric ischemia.

The imaging findings of AAA are pathognomonic in the correct clinical situation. The differential diagnosis of atherosclerotic AAA includes mycotic aneurysms and traumatic pseudoaneurysms.

Treatment Options

Definition

Inflammatory abdominal aortic aneurysms are defined by the presence of a thickened aneurysm wall, marked peri-aneurysmal and retroperitoneal fibrosis, and dense adhesions of adjacent abdominal organs.¹¹

Prevalence and Epidemiology

IAAAs constitute approximately 3% to 10% of abdominal aortic aneurysms. Male sex and smoking are both strong risk factors, with a male-to-female ratio ranging from 6 : 1 to 30 : 1. From 77% to 100% of patients smoke.¹¹ Other risk factors include northern European descent and autoimmune disease.

Etiology and Pathophysiology

Like AAA, the etiology of IAAAs is multifactorial. Current understanding suggests a common immune-mediated inflammatory pathogenesis shared with degenerative AAA, but in IAAA, the inflammation is more pronounced. White blood cells in the aortic wall cause degradation of the extracellular matrix by releasing proteolytic enzymes and cytokines. Based on this knowledge, steroid and other anti-inflammatory agents have been found by some to inhibit aneurysm growth. Some have postulated a role of infection in the aortic wall. Suggested agents include herpes simplex virus, cytomegalovirus, and Chlamydia organisms.

CLINICAL MANIFESTATIONS OF DISEASE

Unlike degenerative AAAs, in which back or flank pain is present in a minority of patients, a great majority of patients with IAAAs have back pain. In patients with a known aneurysm, the classic triad of back pain, weight loss, and elevated erythrocyte sedimentation rate (ESR) is highly suggestive of an inflammatory aneurysm.

Imaging Techniques and Findings

CT and MRI

MDCT and MRI are the mainstays in the investigation of suspected inflammatory abdominal aortic aneurysms. CT accurately distinguishes IAAA from AAA in 93.7% of cases.³⁰ Signs include a thickened, calcified aortic wall surrounded by a low density soft tissue mass (Figs. 102-12 and 102-13). There is relative sparing of the posterior wall of the aorta. The inflammatory soft tissue surrounding the aorta undergoes contrast enhancement in both CT and MRI (Fig. 102-14). On CT, periaortic inflammatory soft tissue generally has lower density than acute blood, helping differentiation from acute AAA rupture. CT and MRI are useful to assess associated effects on adjacent structures, such as ureteric encasement, hydronephrosis, inferior vena cava narrowing, and bowel involvement. Ureteric involvement is present in approximately 25% of cases (see Fig. 102-13) at presentation.¹¹

Figure 102-12 A and B, Inflammatory abdominal aortic aneurysm. Axial images from arterial phase of contrast-enhanced CTA demonstrates a small saccular, infrarenal abdominal aortic aneurysm with an irregular soft tissue rim (arrows) which undergoes enhancement. There is relative sparing of its posterior margin consistent with an inflammatory abdominal aortic aneurysm. C, Coronal reformat demonstrates the saccular aneurysm (arrow) to better detail.

Figure 102-13 A, Inflammatory abdominal aortic aneurysm. Axial contrast-enhanced CT (A) demonstrates thick periaortic soft tissue thickening with relative sparing of the posterior aorta (arrow). There is obstruction of the left ureter, with left hydronephrosis (asterisk) and left renal hypoperfusion. Axial and coronal images from fused FDG-PET CT (B,C) demonstrate avid uptake within the periaortic soft-tissue thickening (arrows) consistent with inflammation.

Figure 102-14 MRI of inflammatory aortic aneurysm. Cuff of tissue surrounding the aorta (A) with relative sparing of the posterior wall (arrow). Following intravenous gadolinium (B), there is enhancement of the cuff and the surrounding soft tissues (arrows).

Differential Diagnosis

Treatment Options

Prevalence and Epidemiology

Mycotic AAAs are rare, representing 0.7% to 2.6% of all aortic aneurysms.³³ They are associated with immunosuppression and chronic comorbid conditions, such as diabetes or renal failure.³⁴

Etiology and Pathophysiology

Staphylocccus aureus and Salmonella are the most common organisms. Previously common organisms such as Streptococcus pyogenes, pneumococcus, and Enterococcus are less common with widespread antibiotic use. The organism may infect the vessel wall either via the vaso vasorum or by implantation in diseased vessel wall (e.g., intimal injury, ulcerated plaque, or mural thrombus).

Clinical Manifestations of Disease

Most patients have nonspecific symptoms including fever and pain. Diagnosis is challenging until late in the disease. Even with recent advances, a high rate of aneurysm rupture has been reported (50% to 85%).³⁴

Imaging Findings

The imaging findings of mycotic aneurysms are similar across all modalities including ultrasound, CT scan, MRI, and angiography.

CT and MRI

Approximately two thirds of infected aortic aneurysms involve the abdominal aorta, although most also involve the suprarenal or thoraco-abdominal aorta. Aneurysms are mostly saccular (95%) (Fig. 102-15) and may have an irregular contour. In the largest published series,³³ about 50% of patients had a periaortic soft tissue mass, soft tissue stranding, and/or fluid surrounding the aneurysm. One of the characteristic features of infected aortic aneurysm is rapid progression. Periaortic gas, adjacent vertebral body destruction, and psoas muscle abscesses are also signs of infection and additional clues of a mycotic AAA.

Figure 102-15 A, Large saccular aneurysm in a patient presenting with abdominal, back pain, and fever. Axial images from contrast-enhanced CT demonstrates a large saccular aneurysm (white arrows) projecting from the left aspect of the superior abdominal aorta. Mural wall thickening is also present. The left kidney is underperfused, implying involvement of the left renal artery (asterisk). B, Coronal images demonstrates the saccular aneurysm (arrows) in better detail.

Treatment Options

Prevalence and Epidemiology

Early endoleaks, according to the EUROSTAR registry, occur in 18% of patients. These are usually graft related, and seal spontaneously. A meta-analysis of endoleaks following EVAR revealed a total of 24% of patients experiencing endoleaks, with the majority (66%) present immediately after stent graft placement. These most commonly arose from the distal stent attachment site, and were persistent.⁴⁰

Etiology and Pathophysiology

Endoleaks are classified according to the site and cause of the leak (Table 102-2). Deficient sealing at the proximal or distal end of the stent graft causes type I endoleaks. Primary type I endoleaks are usually caused by difficult anatomy (e.g., angulated aneurysm neck), a noncircular landing zone, malpositioning, or underdilation of the stent graft. Secondary type I leaks may be caused by aneurysm remodeling, stent graft migration, or progressive dilation of the neck.⁴¹ Systemic blood pressure occurs within the aortic sac in type 1 endoleaks, and there is persistent tension on the aortic wall.

TABLE 102-2 Classification of Endoleaks

Radiography

Radiography plays a useful role in the evaluation for stent graft expansion; migration, kinking, dislocation, and hook or tent fracture can be identified.⁴⁵ Although multiplanar reformations on CT allow characterization of many of these complications, plain radiographs have the advantage because they are less susceptible to artifact from metallic prostheses.

Stent migration usually involves caudal migration of the proximal end, whereas the distal end of the stent is more likely to move cranially. Care should be taken to avoid parallax error when assessing for migration.⁴⁵ Kinking or deformity of the stent often accompanies migration.

Ultrasound

Techniques used for endoleak surveillance include color duplex ultrasound (CDU) and contrast enhanced ultrasound (CEUS) using a micro-bubble agent. Overall, studies have shown a greater sensitivity for endoleak detection when contrast-enhanced ultrasound is used. Reported sensitivities vary widely, ranging from 12% to 100%, likely because sonography for endoleaks is operator and experience dependent.⁴⁴

Computed Tomography

MDCT remains the widely accepted gold standard for endoleak detection. Advantages of CT include multiplanar reconstructions, reproducibility, and fast speed of acquisition. A multiphasic technique is recommended, comprising precontrast imaging, an arterial phase, and a “delayed phase” acquired 60 to 120 seconds following the beginning of contrast injection. Delayed phase imaging has been shown to detect endoleaks not seen on the arterial phase, especially smaller endoleaks and type II endoleaks. It has been suggested that noncontrast CT can be omitted from examinations after the baseline examination to reduce radiation dose.

MRI

MRI is particularly suitable for the surveillance of nitinol stents, which have fewer artifacts on MRI. Stainless steel stents and elgiloy stents can cause extensive artifacts on MRI such that they may preclude proper visualization of the abdominal aortic lumen.⁴² Studies have shown MRI to be at least as sensitive for endoleak detection as CT. MRI is typically performed using dynamic gadolinium-enhanced MRA (Fig. 102-17) using timing similar to CTA.

Figure 102-17 Type II endoleak demonstrated with MRA. Axial T2 weighted sequence (A) demonstrates the heterogeneous signal of blood products and flow artifacts within the native sac (arrows). Following gadolinium (B), the endoleak is visible adjacent to one of the iliac limbs (arrow).

Prevalence and Epidemiology

Abdominal aortic injuries are rare, and represent only 4% to 6% of aortic injuries. These injuries are commonly associated with high-speed motor vehicle accidents and have been linked to steering wheel injury to the lower abdomen and the use of lap-belt restraints.⁴⁸

Etiology and Pathogenesis

The mechanism of injury is thought to be due to direct compression of the aorta against the spine, although other theories implicate stretching of the aortic wall from increased intraluminal pressure and aortic distraction from hyperflexion.

Clinical Manifestations of Disease

Acute manifestations include symptoms of acute arterial insufficiency, an acute abdomen, or neurologic deficits. The lesion may be asymptomatic when there are no associated injuries to produce an acute abdomen or when there is a nonocclusive intimal flap.

Imaging Techniques and Findings

CT and MRI

On CT, the direct signs of abdominal aortic injuries include intimal flaps, irregular aortic morphology, focal enlargement of the aorta, and contrast extravasation.⁴⁹ Periaortic retroperitoneal hematoma may also be present. Abdominal aortic injuries are typically limited in length. The most commonly injured sites are at the level of the inferior mesenteric artery, renal arteries, and between the IMA and bifurcation (Fig. 102-18).⁵⁰ Given long acquisition times, MRI is not appropriate for imaging of aortic trauma in the acute setting.

Figure 102-18 A through E, Young male in a high-speed motor vehicle accident with a “stretch type” traumatic abdominal aortic injury. Intimomedial flaps at the level of the IMA and aortic bifurcation on axial and coronal CT are well demonstrated on catheter angiography (D). Owing to the presence of an associated bowel injury, endovascular repair (E) was performed.

Treatment Options

Treatment is necessary, except for those with minimal intimal disruptions. Surgical treatment is associated with an overall mortality of 27%. Because of the high incidence of associated bowel injury, surgical placement of a prosthetic graft at the time of initial laparotomy risks graft infection. Endoluminal treatment of aortic injuries using uncovered stents provides excellent results with inframesenteric aortic dissections.⁵⁰ For those cases of contained transection, both covered and uncovered stents have been employed successfully.

Etiology and Pathophysiology

Acute aortic occlusion may result from an aortic saddle embolus, thrombosis of preexisting atheromatous plaque, thrombosis of a small abdominal aortic aneurysm, or thrombosis related to aortic dissection. The high mortality likely results from the absence of collateral pathways at the time of presentation and common comorbid conditions such as cardiac disease (61%).⁵¹

Clinical Manifestations of Disease

The absence of both femoral pulses in a patient without significant atherosclerosis risk factors is highly suggestive of the diagnosis.⁴⁹ Patients may present with paralysis mimicking acute spinal cord compression, and a subsequent delay in diagnosis may increase mortality. Coexistent cardiac arrhythmias suggest a saddle embolus.

Imaging Indications and Algorithm

When acute aortic occlusion is suspected, CT is the most appropriate imaging modality given its wide availability and quick acquisition. If iodinated contrast is contraindicated (contrast allergy), MRI and ultrasound (Fig. 102-19) can also be used.

Figure 102-19 Color (A) and spectral Doppler of acute aortic occlusion. With high color gain settings, just noise is visible on color Doppler. No flow was present on spectral Doppler (B).

CT and MRI

On CT, acute aortic occlusion is manifested by the absence of contrast enhancement of the aorta distal to the occlusive site (Figs. 102-20 and 102-21). Collateral vessels will be largely absent. Secondary ischemia in bowel or solid organs may also be present due to global decreased perfusion or to small cardiac emboli. Cardiac sources of emboli are sometimes seen (Fig. 102-20). When present, abdominal aortic aneurysms are well evaluated by CT.

Figure 102-20 A, Contrast-enhanced CTA in a 91-year-old woman with long-standing atrial fibrillation who presented with white, pale, and pulseless legs. Abrupt cutoff of contrast within the infrarenal abdominal aorta (white arrow) is accompanied by infarction of the right kidney (B, thin arrow). This suggests a more proximal embolic source. C and D, CT of the chest in the same patient demonstrates left atrial enlargement (asterisk) and thrombus in the left atrial appendage (white arrow).

Figure 102-21 Curved planar reformat of chronic aortic occlusion in an 81-year-old male. The rounded contour of the aortic occlusion and collateral filling of the left external iliac artery (arrow) is consistent with chronic occlusion.

Findings in MRI are similar to those seen on CT. Noncontrast bright blood or black blood sequences may be useful when contrast cannot be administered. When present, abdominal aortic aneurysms are well evaluated by MRI. Given its long acquisition time, MRI is often not appropriate in acute presentations.

Treatment Options

Acute aortic occlusion is a surgical emergency. Heparin should be started to prevent further propagation of clot. Surgical procedures include transfemoral embolectomy (most useful in cases of saddle embolus) and bypass procedures.

Etiology and Pathogenesis

The exact etiology of TA remains unclear, although infections, autoimmune and genetic factors may play a role. T cells and natural killer cells, which infiltrate the vessel wall, play a role in vascular injury; antiendothelial antibodies have also been reported.⁵² Moreover, certain human leukocyte antigen (HLA) alleles, such as HLA-B52, HLA-B39, and HLA-DRB1*1301 have been associated with the disease in certain ethnic groups and in certain clinical situations.⁵²

Histologically, TA is associated with a panarteritis in the acute phase. Mononuclear cell infiltrates occur in the adventitia with cuffing of the vasa vasorum, and the media is infiltrated by lymphocytes and the occasional giant cells. During the chronic phase of the disease, there is thickening of the vessel wall with fibrosis of the adventitia, destruction of the media, and intimal proliferation with secondary luminal narrowing. Medial destruction, without significant intimal fibrosis, can lead to aneurysm formation. Involvement is usually patchy, with intervening “skipped areas.”

Prevalence and Epidemiology

Takayasu disease predominantly affects young women, with a mean age of diagnosis of 35 years, although nearly 20% of cases present after the age of 40.⁵³ It has been most commonly reported in people of Asian descent.

Clinical Manifestations

Three clinical phases are described in TA: an early “prepulseless” systemic phase, a later occlusive phase, and a final “burned out” phase. The phases usually overlap. Most patients present during the occlusive phase of disease. During the “prepulseless” phase, diagnosis is difficult because patients have nonspecific signs including fever, weight loss, and arthralgias. In the occlusive phase, ischemic complications dominate: claudication, angina, visual impairment, and syncope. The American College of Rheumatology has developed classification criteria for Takayasu disease.⁵⁴

Differential Diagnosis

The differential diagnosis depends on patient symptoms and signs. Other vasculitides should be the main consideration if there is multisystemic inflammation.

Imaging Indications and Algorithm

CT and MRI

Both the vessel wall and lumen are well evaluated on CT and MRI. Therefore, these techniques have advantages for the detection of early disease. Concentric arterial wall thickening is seen early on. With continued inflammation, vascular stenoses, occlusions, and aneurysms develop (Fig. 102-22).

Figure 102-22 Takayasu arteritis. Irregular narrowing of the suprarenal abdominal aorta (A) is accompanied by right pulmonary artery stenosis (B). In addition, there is occlusion in C (dotted arrow), stenosis (small arrow), and focal aneurysm formation (large arrow) of the branches of the aortic arch.

Not only does MRI enable assessment of vessel wall involvement, it is ideal for serial follow-up in young patients. Patients can be comprehensively evaluated with MRI without the risks of ionizing radiation. The pulmonary arteries and extracranial arteries, as well as the aorta, can be evaluated. Findings described with MRI and MRA include increased T2 signal around inflamed vessels, aortic wall thickening, vascular dilation, multifocal stenoses, and collateral vessels.⁵⁶

Treatment Options

Prevalence and Epidemiology

The prevalence of giant cell arteritis in the United States is approximately 160,000 cases (approximately 0.06%), which is likely an underestimate given that many patients have subclinical disease.⁶⁰ Affected patients tend to be older than 50 years of age.

Etiology and Pathophysiology

Alhough both the humoral and cellular immune system are involved in the pathogenesis of giant cell arteritis, cell-mediated processes are paramount.⁶¹ The initial activating factor is unknown; autoantigens, infectious agents, and toxins have been implicated. Transmural inflammation of the arteries results in eventual luminal occlusion through intimal hyperplasia of branch vessels of the aorta. However, in the aorta, inflammation results in aneurysm formation, dissection, and rupture.

Differential Diagnosis

Other vasculitides should be the main consideration if there is multisystemic inflammation.

Clinical Manifestations of Disease

Almost all patients with giant cell arteritis demonstrate signs of systemic inflammation: anorexia, weight loss, fever, malaise, and night sweats. Abrupt visual disturbances and jaw claudication occur commonly. Approximately one third of patients will have polymyalgia rheumatica. Inflammatory markers are typically elevated. Diagnosis is typically achieved through temporal artery biopsy.

Imaging Indications and Algorithm

Abdominal aortic aneurysms and dissection associated with giant cell arteritis may be detected on CT, MRI, and angiography. Abnormal FDG-PET uptake may also be helpful in the setting of giant cell arteritis.

Imaging Techniques and Findings

CT and MRI

Abdominal aortic aneurysms, dissections, and rupture can be detected with CT or MRI. On CT, associated mural aortic thickening (Fig. 102-23) (possibly representing inflammatory tissue proliferation) may also be present.⁶² On MRI, high mural signal on fluid-sensitive sequences and mural wall enhancement within the aorta may represent active inflammation.⁶³

Figure 102-23 Vessel wall thickening in a 71-year-old woman with giant cell arteritis and a chronically elevated erythrocyte sedimentation rate. Axial contrast-enhanced CT demonstrates circumferential soft tissue thickening of the abdominal aortic wall (A, arrows) and branch vessel of the aortic arch (B, arrows).

Treatment Options

Prevalence and Epidemiology

Approximately 80% of aortoenteric fistulas arise in the duodenum, and about 60% of these arise in the third part.⁶⁶ Outside the duodenum, the jejunum, sigmoid colon, stomach, and ileum can be involved. Aorta-duodenal fistulas following surgical repair of a prior aortic aneurysm (secondary) are more common than de novo aorta-duodenal fistulas from an abdominal aortic aneurysm (primary). Aorta-duodenal fistulas occur approximately 0.4% to 2.4% of the time following aortic aneurysm surgery. They can manifest soon after surgery or years later.

Etiology and Pathogenesis

The propensity for fistula to the duodenum likely relates to the location of the third part of the duodenum, which is fixed in the retroperitoneum just anterior to the aorta. Aortic expansion and inflammation likely lead to duodenal inflammation, and eventual fistulization. Failure of separation of the bowel from the graft, accompanied by mechanical pulsations of the prosthetic graft, can lead to pressure necrosis of the bowel. Infection may also play a role. Primary aortoenteric fistulas arise from atherosclerotic aneurysms, mycotic aneurysms, and traumatic pseudoaneurysms, as well as many other inflammatory and neoplastic diseases of the aorta and gastrointestinal tract.

Clinical Manifestations of Disease

The classic clinical triad consists of gastrointestinal hemorrhage, abdominal pain, and a pulsatile abdominal mass, but this is found in a minority of patients. Patients may present with an initial small “herald” bleed (hematemesis or hematochezia), and later develop uncontrollable bleeding leading to exsanguination. Alternatively, there may be recurrent intermittent gastrointestinal bleeding. Associated constitutional symptoms occur—likely related to concomitant periaortic infection.

Imaging Indications and Algorithms

Because patients with aortoenteric fistulas can quickly exsanguinate, CT is used most commonly. Endoscopy is also performed. Ultrasound, nuclear medicine studies, and MRI do not reliably detect aortoenteric fistulas.

CT

There may be significant overlap in the CT appearance of periaortic infection and aortoenteric fistulas. In both cases, ectopic gas (Fig. 102-24), periaortic fluid, periaortic soft tissue thickening, bowel wall thickening, periaortic fat plane obliteration, and pseudoaneurysms may be present.⁶⁷ To definitively diagnose aortoenteric fistula, blood or contrast leaking into bowel must be visualized. The presence of a secondary aortoenteric fistula can also be inferred if the aortic graft is seen within bowel lumen.⁶⁸

Figure 102-24 Axial (A) and sagittal (B) contrast-enhanced CT angiogram in a 78-year-old man with an aortoduodenal fistula who presented with hematemesis. He had an open aneurysm repair ten years earlier. Gas is present within the aortic sac (white arrow). The proximal end of the aortic graft is surrounded by soft tissue and is inseparable from the third part of the duodenum (open arrow). On duodenoscopy, aortic graft material was seen eroding through the posterior wall of the duodenum.

Treatment Options

Surgical treatment and antibiotic treatment are paramount. In cases of secondary fistulas, the infected graft is removed and extra-anatomic bypass is placed. Infected graft removal and in situ graft replacement has also been proposed as an alternative. Primary fistulas can be treated similarly. Endovascular repair may be a temporizing step in patients too ill for immediate surgery.⁶⁹