10 Aorta and Outgoing Branches

One of the first successful applications of abdominal sonography¹ was the detection of abdominal aortic aneurysms (AAAs). Due to the wide availability, screening is considered advisable. A meta-analysis by Eckstein et al showed a significant reduction in AAA-associated mortality among 65- to 80-year-old men by 44% after 3 to 5 years and by 53% after 7 to 15 years.² The number of ruptures had decreased.⁷ A screening program in Sweden showed a prevalence of screening-detected AAA of 1.5% with a mortality reduction of 39%.⁸ Procedures for elective AAA treatment increased and the number of emergency procedures decreased significantly. In addition to the diagnosis of aneurysms, sonography enables the identification of the most important morphologic findings such as diameter, distance from the visceral or iliac arteries, calcifications, stenoses and occlusions, dissections, and aortic wall changes, namely, vasculitis and perivasculitis.

Endovascular aortic repair (EVAR) as a minimal-invasive treatment option for percutaneous treatment has given rise to new pathophysiologic insights and indications.^{9 – 14}

New developments and improved modular stent design now enable treatment of more elongated aneurysms extending to juxtarenal, suprarenal, or distal to the aortic bifurcation into the iliac arteries.^{15 – 17}

Important factors for planning the intervention are

•Longitudinal and transverse diameter

•Proximal neck, i.e., distance from the renal arteries to the AAA

•Angulation of the proximal neck and iliac arteries

First prospective studies comparing interventional and surgical AAA therapy showed a similar mortality of 2 to 3% for both methods. Survival rates were between 65%-72%. This is confirmed in recent studies showing a mortality rate of 1.2% for EVAR in standard situation, while emergency procedures had a mortality rate of 7.3%.^{20 , 87} The advantages of EVAR are a significantly reduced blood loss and a lower rate of cardiopulmonary complications. A drawback of EVAR is the occurrence of endoleaks in 18% to 24% of cases. Therefore, early detection of retrograde perfusion or leakage with imaging procedures is required.

10.1.1 Color Duplex Sonography (CDS)

Although aortic wall pulsation is visible in B-mode, providing initial information on the blood flow, precise perfusion assessment of the abdominal aorta and its branches has only become possible with additional flow detection by CCDS. New methods, especially for planning and follow-up of interventional procedures, are used in complementary procedures such as

•Power mode (power Doppler)

•B-flow technology

•Contrast-enhanced ultrasound (CEUS)

In the following, the standard and advanced examination techniques, normal findings, and typical diseases of the abdominal aorta are presented. The diseases of the renal vessels and visceral arteries are addressed in Chapter 14 and Chapter 11, respectively.

10.2 Aortic Anatomy and Variants

The descending aorta along with the thoracic duct passes through the diaphragm at the level of vertebral bodies Th 12 and L 1. It runs directly in front of or to the left of the spinal column and divides at the level of the 4th lumbar vertebrae into the common iliac arteries (Fig. 10.1). The mean diameter below the diaphragm is about 21 mm in women and 24 mm in men. At the level of the bifurcation the diameters are 17 and 19 mm, respectively, due to tapering.

If the diameter of the aorta is up to 30 mm, it is called ectasia. There are many definitions of an arterial aneurysm.^{21 – 23} A general definition is an increase in diameter of at least 50% compared to the normal diameter of that artery. According to the guidelines of the European Society for Vascular Surgery,²³ the diagnosis of an AAA is based on a diameter of 3 cm or more; an iliac artery aneurysm is defined by a diameter of more than 2 cm (or twice the normal diameter).

10.2.1 Vascular Branches

Except the celiac trunk, and superior and inferior mesenteric arteries (Chapter 11), most branches of the abdominal aorta are paired. The phrenic arteries originate directly below the diaphragm, closely followed by the suprarenal arteries and the first pair of the lumbar arteries. The testicular or ovarian arteries usually originate ventral or ventrolateral from the aorta, caudal to the renal arteries. However, sonographic detection is only partly possible. The renal arteries are discussed in Chapter 14.

10.2.2 Anatomical Variants

Anatomical variants of the abdominal aorta are rare. They are found primarily in the “situs inversus” and secondarily as variants due to spinal kyphosis, retro-aortic hematomas, and tumors. A small aortic diameter is common in asthenic patients, although this could be the consequence of aortitis, periaortitis, or coarctation of the thoracic aorta. Hypoplasia or atresia and duplication of the aorta are rare.

Vascular deviations of the symmetric branches are seen in up to 40% of cases, mostly in the renal arteries (see Chapter 14). Multiple renal arteries occur unilaterally in approximately 30% of cases and bilaterally in up to 12%. Approximately 10% are accessory, while 20% are aberrant vessels. The phrenic arteries supply the upper and lower parts of the diaphragm. As a variant they may originate from the celiac trunk or from the left hepatic artery. However, there are also vascular branches from the abdominal aorta or the renal arteries.

Variations of the pelvic arteries are mainly found in the internal iliac artery. Normally it branches into two main (anterior and posterior) trunks, although in 10% of the cases only one is mature. In its subsequent course, three parietal and a total of seven visceral branches arise. In rare cases there are also complex variants, such as hypoplasia of the external iliac artery, with the leg being supplied via the internal iliac artery and the obturator artery, with a dorsal course of the main supplying artery to the thigh (persistent sciatic artery) (Fig. 10.2) which is detectable by ultrasound.

Aortic ultrasound is first performed in supine position. The proximal aorta is visualized in B-mode during inspiration using the liver as an acoustic window for the celiac trunk and the superior mesenteric artery (Fig. 10.3). Then the transducer is moved from cephalad to caudal, imaging transversely from the celiac axis to the aortic bifurcation. At least two diameter measurements of the aorta should be documented at multiple levels: anteroposterior and lateral. The lateral measurements are usually less accurate due to the lower lateral resolution of B-mode.²⁴ Maximum inspiration and a cranially directed transducer moving in caudal direction allow good visualization of the entire abdominal aorta even in obesity and meteorism. Finally, CCDS is activated at an inconspicuous location and adjusted as described in Chapter 2 (Fig. 10.4). For the pelvic arteries, oblique scan planes and a full urinary bladder are advantageous.

10.3.3 Color Duplex Sonography of the Aortic Branching Vessels

The iliac arteries are either approached from the cranial to the caudal side in the longitudinal section or in the opposite direction from the groin starting at the common femoral artery via the iliac arteries. The contralateral common iliac artery and external iliac artery can be assessed more easily with a filled urinary bladder. However, a full urinary bladder may be stressful to the patient during examination. Lumbar arteries can also be visualized by inclined plane from lateral. Each lumbar artery splits off into anterior and posterior branches that supply the spinal cord, cauda equina, meninges, and the deep back muscles. They can develop pronounced collaterals to subcostal and iliolumbar arteries, as well as to the inferior epigastric artery and circumflex femoral artery. This collateralization enables spontaneous retrograde endoleak perfusion after EVAR.

10.3.4 Contrast-Enhanced Ultrasound (CEUS)

The basis of CEUS (sonography) is the injection of gas-filled microbubbles into the bloodstream, which results in a large number of small interfaces providing high echogenicity (Chapter 4). In Europe, SonoVue^® (Bracco, Milan, Italy), recently approved as Lumason^® in America, is available as an ultrasound contrast agent. These microbubbles contain sulfur-fluorid (SF6) gas, which is surrounded by a shell of phospholipids for the purpose of stabilization.^{25 ,​ 26}

The gas components of the contrast medium are eliminated after bubble disintegration via the respiratory tract. These microbubbles have a diameter of 2 to 10 pm and are therefore in the order of magnitude of a red blood corpuscle. Due to their small size, they are freely able to access the capillary, but in contrast to standard computed tomography (CT) and magnetic resonance imaging (MRI) contrast media, they are not transferred into the interstitial fluid, but remain completely in the vascular system functioning as a blood pool contrast medium.

Contrast medium-specific techniques use low mechanical index in order to generate images which are based on the nonlinear acoustic interaction between ultrasound and stabilized microbubbles (Chapter 4). The microbubbles oscillate and resonate and therefore produce a continuous improvement in the contrast on the gray scale.^{27 ,​ 28}

The recommended dose for a single injection is between 1.0 and 2.4 mL, depending on the sonography device used.^{29 – 21} However, too high dosage should be avoided due to the risk of saturation (see Chapter 2), attenuation, and glare artifacts.³² After the injection of the contrast agent, 10 mL of a 0.9% saline solution should be injected additionally.²⁸

10.4 Normal Findings

10.4.1 Abdominal Aorta

Cranial Sections

During systole, the normal abdominal aorta shows a completely color-filled lumen in the CCDS or in power Doppler mode (Fig. 10.4). Spectral analysis normally indicates a high early systolic forward flow with a steep upstroke and a rapid downstroke. In the diastole, however, the flow pattern depends on the measurement location: proximal to the origin of the celiac trunk and renal arteries, there is—in younger patients in particular—a continuous, caudally directed residual flow which can still be detected over the entire vessel cross section, or at least in the middle of the vessel (Fig. 10.4a). The reason for this is the proximal, low, total vascular resistance due to the arteries of the parenchymatous organs such as the kidney, spleen, and liver (Chapter 3).

The caudal sections of the aorta—like the peripheral arteries—are characterized by an additional early diastolic reverse flow component followed by a brief forward flow (Fig. 10.4b). Probable explanations for this are reflections from high resistance level in the downstream bloodstream area and the ping-pong effect on the aortic valve.³³ This complex flow pattern is physiologic and should not be confused with turbulence.

A change in this curve shape is found in hyperemia (e.g., after stress), in aortic isthmus stenosis (see Chapter 9), as well as in severe aortic valve insufficiency and arteriovenous (AV) shunts of the large arteries.

Symmetrical Branches

At the origins of the symmetric aortic branches, only the renal arteries are generally detectable. The lumbar arteries can now also be displayed in the power Doppler (Fig. 10.5) and, if necessary, after administration of contrast medium. They are clinically relevant in EVAR. The origins of the phrenic, ovarian, and testicular artery can be rarely seen. However, it is often possible to depict branches in the ovary or testicle.

10.5 Pathologic Findings in the CCDS

The most common cause of pathologic changes in the aorta and pelvic arteries is arteriosclerosis. The term arteriosclerosis was first introduced by Marchand, describing the association of fatty degeneration and vessel stiffening.^{34 ,​ 35} Mechanical factors, deposits, and degeneration, as well as numerous endogenous and exogenous noxious agents, are the triggers of the complex reaction causing lipid deposits and the proliferation of smooth muscle cells in the intima. The precursors are the—initially reversible—stripe-shaped vascular wall lesions, which can be detected from the first year of life. These so-called fatty streaks consist of lipid-laden foam cells containing cholesteryl esters and a variable amount of extracellular lipid.³⁶ They are mainly found in the area of the ductus arteriosus, at the outlets of the supra-aortal branches, the celiac trunk, the superior mesenteric artery, and the renal arteries.

In the course of the disease, bleeding into the wall as well as ulcerations of the intima and thrombus deposits after the fibro-necrotic reconstruction of the plaques can occur. This can then lead to stenosis and vascular occlusions, which manifest clinically in different forms depending on the affected vessel. Changes in the aorta may remain asymptomatic for a long time. The symptoms depend on the following factors:

•Extent of the flow obstruction

•Rapidity of the occlusion

•Collateralization

10.5.1 Wall Thickenings, Plaques, Stenoses, and Occlusions

▶ Fibrous plaques. These are of low to moderate echogenicity. Calcifications cause brilliant reflexes with dorsal shadowing. If longer, low echogenic, circular wall thickenings are detected, consideration should be given to arteritis as the cause.³⁷ Simultaneous presence of homogeneous wall changes of the leg arteries or of the carotid, subclavian, and axillary arteries help to confirm the diagnosis (Chapter 8).

Depending on the extent of the wall changes such as plaques, gaps appear in the color-coded lumen. However, the prerequisite for this is an artifact-free depiction of the colors without blooming of the color. In cases of high-grade stenosis with confetti or vibration artifacts, it may be helpful to use new sonographic techniques, such as B-flow imaging or CEUS, which offer precise morphologic assessment options.

The form of the plaques may be prognostically relevant³⁸ because they can

•Tear off and embolize

•Dissect

•Induce local thrombosis

•Occlude a vascular outlet

The detection of homogeneous, echo-poor foci and fresh thrombotic deposits is only possible through the additional use of CCDS: these appear as a gap in the lumen, which in many cases would not be visible in the B-mode sonography alone. The advantage of CCDS is that it makes it possible to assess the obstruction and therefore the hemodynamic relevance.

▶ Stenoses. Analogous to the changes to the peripheral arteries (Chapter 7), the stenoses of the aorta and pelvic arteries can be identified in the spectral analysis by spectral widening (loss of the systolic window) and—in the case of higher grade stenoses—by turbulences, flow acceleration with aliasing, and possibly vibration artifacts (Fig. 10.6).²⁴

In addition to the clinical picture, the frequency analysis of the inguinal arteries is of particular importance for the assessment of the hemodynamics. The typical changes in the CCDS are described in detail in Chapters 3 and 7. A combination of direct and indirect criteria with flow acceleration and/or a peripherally attenuated spectrum is observed in high-grade infrarenal aortic stenosis, as shown in Fig. 10.7.

▶ Occlusions. Aortic occlusion is a rare event. Leriche’s syndrome (infrarenal aortic occlusion which is usually located above the bifurcation) almost always develops on the basis of arteriosclerosis and usually includes the common iliac arteries. Isolated chronic occlusion is usually sufficiently compensated at rest through numerous connections between

•The celiac trunk, and the superior and inferior mesenteric artery and the pelvic arteries

•The collaterals via the internal iliac, epigastric, and external iliac arteries

This is often diagnosed as a chance finding or during the evaluation of potency disorders. Other causes include embolisms, trauma, sepsis, and primary idiopathic hyperlipidemia.

▶ Findings. In adults, an acute occlusion is generally diagnosed clinically. In B-mode, the occluding thrombotic material remains echo-poor for a long time. Although missing wall pulsations suggests an occlusion, proof is only provided by the absence of flow on CCDS (Fig. 10.8a). Location of the occlusion, the occlusion material, and the involvement of the renal arteries can be readily described with CCDS. The collaterals are usually easier to identify in the multislice CT (Fig. 10.8b) or angiography.

10.5.2 Aneurysms

▶ Etiology. An AAA is a circumscribed, concentric or eccentric lumen dilatation that can begin either infrarenal or suprarenal. The causes are degeneration, inflammation, trauma, or malformation of the supporting wall elements. Rarefication or fragmentation of the elastic membranes and atrophy of the media musculature lead to weakness of the wall. Another factor is the hemodynamic load: Increased reflections of the expanded bifurcation during elongation and the asymmetrical flow after one-sided amputation are suspected of promoting aneurysm formation via local wall loading.³⁹

▶ Risks. An AAA is a disorder that can be treated surgically or interventionally with a relatively low risk if diagnosed early enough. The mortality rate in the case of elective interventions is less than 5%, but it is up to 80% in case of ruptured aneurysms. Around 34% to 64% of these patients die before reaching the clinic. As a result, the overall mortality rate in the case of ruptured aortic aneurysms is up to 90%.

Current studies show that the prevalence in patients over 60 years of age is 2% to 6%. The risk indicators are dilatative arteriopathy associated with arterial hypertension and, above all, peripheral arterial occlusive disease. Smoking is another risk factor that persists even in the case of subsequent abstinence. In 20% of cases which are discovered by chance, the risk of rupture is already increased. This underlines the importance of a reliable ultrasound assessment.

▶ Aneurysm forms. A pathologic–anatomic distinction (see Fig. 7.52) is made between

•An aneurysm verum with bulging of all three wall layers

•A dissecting aneurysm

•The mostly traumatically caused aneurysm spurium (false aneurysm), which after tearing of the inner aortic wall layers perforates in concealed form into the surroundings

Further categories are mycotic and inflammatory aneurysms. A mycotic aneurysm is triggered by a bacterial infection (e.g., salmonella). In inflammatory aneurysms, however, no pathogen is found.

10.5.3 Aneurysm Verum

▶ Occurrence and clinical picture. Aneurysm verum is the most common form. This is mostly arteriosclerotic in origin, covers all wall layers, is usually fusiform, and is located infrarenally in 95% of cases. A vast majority of the patients are asymptomatic, and their aneurysms are diagnosed incidentally by sonography, CT, or MRI. A multicenter trial showed that there was no benefit in early surgical repair of small fusiform infrarenal aneurysms compared to surveillance with meticulous sequential US examinations.^{19 ,​ 40} Long-term studies showed that AAAs with a diameter of 3 to 3.9 cm expand slowly, and they are unlikely to require operation within 5 years. Many AAAs of 4 to 4.9 cm will reach a surgical size in the first 2 years of follow-up.⁴¹ For each 0.5-cm increase in AAA diameter, growth rates increased on average by 0.59 mm per year and rupture rates increased by a factor of 1.91.⁴² Aneurysms which are more than 5 cm in size or increasing by at least 5 mm a year require treatment due to higher risk of rupture in comparison to operation. This also applies to symptomatic aneurysms. Symptoms develop as a result of the compression effects as well as secondary complications such as arterio-arterial embolisms, spontaneous fistula formation, and perforation.

▶ B-mode. Sonographically, the diameter, demarcation with respect to the surroundings, and the extent of the intraluminal thrombus material can be depicted in B-mode (Fig. 10.9). The thrombotic deposits may

•be layered,

•become detached from the wall, and/or

•liquefy again.

An eccentric position of the lumen through which the flow passes, diverticular bulges, a transverse diameter of more than 5 cm, growth of more than 5 mm/year,⁴³ or abdominal pain (symptomatic aneurysm) are signs of a high risk of rupture and are therefore regarded as indications for intervention.

▶ Color duplex sonography. It is possible to identify two different flow patterns:^{24 ,​ 33 ,​ 44}

•In uncomplicated cases the flow is laminar (Fig. 10.9b).

•With increasing flow velocity and size, turbulences occur, some with wall-directed flow peaks.

▶ Additional techniques. B-flow technology and CEUS allow an angle-independent and pinpoint representation of the lumen through which the flow passes. Postprocessing procedures of CT and MR technology with three-dimensional reconstructions allow clear and precise representation of the extent of the aneurysm.

Peattie et al demonstrated the presence of local pressure peaks with increased shear forces in a model test.³³ In contrast, local, parietal, concentric thrombus deposits appear to reduce the growth of the dilated vascular lumen. The interaction of these parameters and the extent of the arteriosclerotically induced wall damage result in the different growth risk of aneurysms, which can be estimated in the first approximation of CCDS. CCDS makes it possible to analyze origin and course of the aortic branches, as well as their relationship to the aneurysm.

10.5.4 Aortic Dissection

▶ Occurrence and clinical picture. Abdominal aortic dissections are mostly associated with thoracic aortic dissection, whereas isolated abdominal aortic dissections are rare.⁴⁵ Hypertension is one of the main risk factors. Iatrogenic aortic dissections due to intravascular catheterizations are often located in the abdominal or descending thoracic aorta and occur in up to 5% of cases.^{30 ,​ 46 ,​ 57} In former times mortality related to aortic dissection was up to 30%. Advances in surgical techniques have lowered mortality rates at about 20%.^{47 ,​ 48}

Typical symptoms of aortic dissection such as different blood pressures of the sides, chest or abdominal pain, signs of vascular occlusion (e.g., mesenteric ischemia or renal symptoms), and paraplegia or hemiplegia are not always present and may also resemble the symptoms of other diseases that lead to emergency admission of patients.⁴⁹ Up to 38% of aortic dissections are overlooked in the initial examination and up to 28% of aortic dissections remain undetected until autopsy.⁴⁹

An aortic dissection can be caused by bleeding around the area of the vasa vasorum causing tearing of the intima and separation of the wall layers. Dissection can primarily occur in an aneurysm or, after dissection, an aneurysmatic dilatation of the weakened vessel wall can also develop. However, aortic dissection alone without dilation is often referred to as a dissecting aneurysm, although this is not semantically correct. The triggers are trauma, arteriosclerosis, media-necrosis aortae cystica idiopathica, mesaortitis luetica, Marfan’s syndrome, and several other lately found genetic mutations.⁵⁰ The starting point is usually the ascending thoracic aorta.

Depending on its onset and extent, a dissecting aneurysm emanating from the thoracic aorta is classified according to Stanford A or B or De Bakey I–III. It can dissect, thrombose, or rupture even further caudally. Distal re-entry results in self-limitation if there is sufficient pressure equalization between a true and false lumen, and is characterized by a sudden decrease in pain symptoms. A rupture toward the outside leads to acute life-threatening hemorrhaging. If the dissection reaches into the abdominal aorta, the visceral arteries and the iliac arteries may be acutely affected. In up to 10% of cases, acute aortic dissection is accompanied by acral ischemia of the upper and lower extremities with necrosis formation.⁵¹

▶ B-mode. In the B-mode, a dissection membrane with typical undulating movement can be seen in the ideal case (Fig. 10.10). However, the membrane—which is initially less than 1 mm thick—cannot always be delineated and often can only be identified indirectly by the flow pattern in the CCDS or after the administration of contrast medium in ultrasound or CT (Fig. 10.11). Experience has shown that the thin membrane quickly turns into a thicker, stable tissue due to “scarring” and is readily visible in B-mode. Differential diagnostic problems may arise in individual cases due to an incorrect interpretation of the crus of the diaphragm (see Fig. 10.3) or the connective tissue bridge of a horseshoe kidney as a second lumen.

▶ Color duplex sonography and CEUS. With CCDS, it is possible to depict different directions of flow and flow velocities in the true and false lumen.⁵² The lower velocities in the false lumen are often easier to detect in power mode or with contrast medium. The exact delineation of the dissection membrane is possible in B-flow. Retrograde flow components promote thrombus formation.⁵² Depending on the examination conditions, it is possible to determine the re-entry of the blood (Fig. 10.12, Fig. 10.13) as well as the size of the re-entry opening and the flow dynamics.^{53 ,​ 54}

If the renal arteries are involved, perfusion failure or—in the case of embolized thrombotic material with or without complete occlusion—renal infarction can be seen. A complete examination should therefore include a complementary assessment of renal perfusion and the visceral arteries. In addition to the iliac arteries, the femoral arteries should also be examined, as it is not unusual for the dissection membrane to extend into iliac and femoral arteries.

With CEUS, it is possible to clearly identify the true and false lumen of the dissection (Fig. 10.13). The true lumen is characterized by the early influx of contrast medium, whereas in the case of the false lumen inflow of the contrast medium is late, unless it is not thrombosed.^{55 ,​ 56}

For the detection of abdominal aortic dissection, the sensitivity and specificity of conventional ultrasound, CEUS, and CT angiography are stated as 68%, 97%, and 100% and 88%, 100%, and 100%, respectively.⁵⁷ However, since a CT scan is required to decide and plan a possible endoprosthetic treatment, not too much time should be wasted from diagnosis to therapy.

10.5.5 Inflammatory Aneurysm

▶ Occurrence and pathogenesis. A distinction should be made between simple atherosclerotic aneurysms and an inflammatory aneurysm, which was initially considered rare as it made up only 3% to 5% of all aneurysms.⁵⁸ Inflammatory endarteritis may also affect the vasa vasorum and, in contrast to an infected aneurysm, it is always attributed to nonbacterial inflammation. Autoallergic reactions of the aortic wall to oxidized low-density lipoprotein (LDL) and lipoprotein polymers (ceroid) and the recruitment of T- and B-lymphocytes are assumed to be the beginning of a self-sustaining inflammation of the media and adventitia. General symptoms and associated autoimmune diseases indicate that these are systemic events.^{59 ,​ 60} The newly discovered entity of IgG4-related arterial lesions occurs mainly in the aorta and its main branches and is radiologically characterized by homogeneous arterial wall thickening corresponding to pathologic features of IgG4-related sclerosing inflammation in the adventitia. Based on immunologic studies on inflammation, a classification of inflammatory AAA as immunoglobulin IgG4 related and IgG4 unrelated has been proposed, emphasizing an immunologic role in the development of the disease.^{61 ,​ 62}

Typically, inflammatory wall changes predominantly occur ventrolaterally with retroperitoneal lymphomas.⁵⁸ It tends to spare the posterior wall. Adhesions and retroperitoneal fibrosis may also be present. Perianeurysmatic fibrosis often involves the duodenum.⁶³ If the inflammation extends to the inferior caval vein, this may result in thrombotic occlusion. Other complications are ruptures or fistulas, as well as the encasing of the ureters, which leads to hydronephrosis in up to 19% of cases.⁶⁴

Accompanying inflammatory reactions may also be seen after prosthesis implantation.⁶⁵ In addition to increasing intraluminal thrombolysis, this results in pre- and postprosthetic dilatation and the inflammation spreading to the pelvic vessels with lumen constriction.

Inflammation is a frequent trigger of severe isolated aortic sclerosis in middle-aged patients. Inflammatory AAA can also develop associated with large-vessel vasculitis (giant cell arteritis).

▶ Findings. A characteristic feature in B-mode is a solid aortic wall thickening or a secondary perianeurysmal retroperitoneal fibrosis ( Fig. 10.14). This presents itself as a homogeneous echo-poor fringe that surrounds the aortic wall like a cuff. Accordingly, the CT shows a solid structure which becomes denser after the administration of contrast. With modern high-resolution transducers and CEUS, it is possible to detect early and intensive enhancement of the contrast medium both in the broadened adventitia and in the perivascular tissue before the initiation of steroid therapy (Fig. 10.14b).

Stay updated, free articles. Join our Telegram channel

Join