Abdominal Aorta

Abstract

The abdominal aorta is the extension of the thoracic aorta, running into the retroperitoneal space through an aortic hiatus, near to the inferior vena cava and in front of the spine. The abdominal aorta ends at the aortic bifurcation, where it divides into two common iliac arteries, right and left (Fig. 10.1, Table 10.1). No relevant anatomic variants are described.

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10.1 10.1 Anatomy

The abdominal aorta is the extension of the thoracic aorta, running into the retroperitoneal space through an aortic hiatus, near to the inferior vena cava and in front of the spine. The abdominal aorta ends at the aortic bifurcation, where it divides into two common iliac arteries, right and left (Fig. 10.1, Table 10.1). No relevant anatomic variants are described.

Fig. 10.1

Abdominal aorta anatomy

Table 10.1 Abdominal aorta anatomy

Table 10.2 Technical parameters using different scanners

Table 10.3 Contrast media administration with different scanners

10.2 10.2 CTA Technique

Patient Preparation

Patients should be placed in a supine position on the CT scanner, with the arms behind the head (to reduce beam hardening artifacts).

Image Acquisition

Peripheral venous access should be made in one arm, preferably in the elbow, and must be not less than 20 G. No metal objects should be visible within the field of view.

• 1) Topogram acquisition must be on the coronal plane, from the diaphragmatic dome to the proximal portion of the thigh.

• 2) The region of interest (ROI) must be placed on the infra-renal abdominal aorta, avoiding intimal calcifications as much as possible (if using bolus tracking), which could alter the diagram of density variation and thus affect the examination.

• 3) Image acquisition in the caudocranial direction.

Fundamental points for an optimal angiographic study of the abdominal aorta are:

• High contrast media delivery rate (at least 4mL/sec);

• High iodine concentration contrast media (350-400 mgl/mL);

• Fast image acquisition time

Image acquisition should start right after the threshold value is achieved (120-180 HU); distal vascular segments cannot be opacified by early acquisition. On the other hand, a delayed phase can cause venous and soft tissue contamination.

In older-generation scanners (8-16 detectors), the contrast injection length should be equivalent to the image acquisition time (Tables 10.2-10.3)

10.3 10.3 MRA Technique

This section will examine steady-state free precession sequences (SSFP), Gradientecho T1 3D sequences (GRE), and time-resolved sequences.

Patient Preparation

Patients should be placed in a supine position on the CT scanner, with the arms behind the head; peripheral venous access should be made in one arm, preferably in the elbow, and must be not less than 20 G. No metal objects should be visible within the field of view. Phased array coils for the abdomen and pelvis are necessary.

Table 10.4 Technical parameters

Steady-State Free Precession sequences (SSFP) are non-contrast bright blood sequences (2D or 3D) (Table 10.4) used in MR imaging in patients with a contraindication or intolerance to paramagnetic contrast media. SSFP uses a low repetition time (RT) and a high flip angle and is used in vascular imaging and for MR enterography.

Arterial and venous systems have the same intensity in SSFP imaging; several applications are used to distinguish one from the other.

• Acquisition of a localizer;

• FOV placed on the axial or coronal sequence;

• FAT and venous saturation.

All sequences are acquired in exhaled breath.

The main limitation is the difficulty in distinguishing between veins and arteries and the strong sensitivity to magnetic susceptible artifacts.

GRE T1 3D

GRE T1 3D are sequences that combine high spatial resolution (high matrix values), low slice thickness (1 mm) and short acquisition times (Fig. 10.2, Table 10.5). As for other bodily applications, it is also necessary for aortic imaging to acquire a pre-contrastographic mask for digital subtraction imaging:

• Localizer acquisition;

• Pre-contrastographic mask acquisition (GRE) on the coronal plane (Fig. 10.2a);

• Real-time contrast media visualization with multiple low-resolution coronal images used as a visual trigger to synchronize image acquisition for optimal timing (Fig. 10.2b-d, Table 10.6);

• Post-processing application with digital subtraction imaging (Fig. 10.2). All sequences are acquired in exhaled breath.

Time-Resolved Sequences

Time-resolved imaging is based on the examination of a vascular segment (in this case the abdominal aorta) repeated several times in single time lapse, with real-time visualization of the contrast media (Table 10.7).

• Localizer acquisition;

• Pre-contrastographic mask acquisition on the coronal plane;

• Concurrent contrast media administration and imaging acquisition (Table 10.7);

Fig. 10.2

a GRE T1 non-Contrast mask. b-d Real-time visualization of constract media (arrow). e GRE T1 post-contrastographic sequence with digital mask subtraction

Table 10.5 Technical parameters

Table 10.6 Contrast media

Table 10.7 Technical parameters

10.4 10.4 Abdominal Aortic Aneurysm

Clinical Picture and Diagnosis

The abdominal aorta is considered aneurysmatic if the transverse diameter is > 3-3.5 cm; its prevalence in the population aged > 50 years is between 1 and 4% (gradually increasing with age).

Imaging and Reporting

The pre-contrastographic phase can provide additional information, which is necessary for adequate pre-surgical planning, such as thrombus calcification or the crescent sign (a hyperdense crescent image in the aneurysmal sac, which is predictive of an upcoming rupture).

With a standard examination technique, the flow turbulence in the aneurysmatic sac can produce irregular opacification of the vascular lumen (Fig. 10.3); this problem can be resolved by applying a small delay in the acquisition threshold or positioning the ROI directly in the aneurysmatic sac.

Localization

Abdominal aortic aneurysms can be classified as (Fig. 10.4):

• 1) Supra-renal: evaluating whether the dilatation involves the aortic thoracic tract;

• 2) Juxta-renal: the aneurysm originates at the same level as the renal arteries; it is necessary to evaluate potential renal involvement, by analyzing vascular segments and parenchymal perfusion (pay attention to the supernumerary arteries);

• 3) Infra-renal: these are the most common aneurysms, which originate > 1cm below the renal artery.

Fig. 10.3

Abdominal aortic aneurysm with internal blood flow turbulence

Fig. 10.4

a,b Infra-renal aortic aneurysm not involving iliac arteries. c MR coronal MIP of an aneurysm originating in the renal arteries; renal arteries (white arrow) and polar arteries (yellow arrows)

Fig. 10.5

a, b Segmental kindly infarction due to covering of the polar arteries

Fig. 10.6

a Aneurysm (red line) and residual lumen (yellow) transverse diameters. b Longitudinal and anterior-posterior diameter

Measurements

The diameters necessary for adequate pre-surgical planning are:

• 1) Distance between dilated aorta and renal arteries:

  • a. Longitudinal and transverse diameters;

  • b. Point out the presence of supernumerary renal arteries to avoid polar infarct due to the endoprosthesis (Fig. 10.5);

  • c. Vascular wall characterization, reporting evidence of thrombus or ulcerations.

• 2) Aneurysmal sac:

  • a. Longitudinal, anteroposterior and transverse diameters (Fig. 10.6);

  • b. Vascular wall characterization, demonstrating evidence of thrombi or ulcerations;

  • c. Residual lumen dimensions;

  • d. Coaxial study of diameters, adapting measurements to the shape of the aneurysm which is necessary to avoid serious bias in pre-surgical planning (Fig. 10.7).

• 3) Distance between dilated aorta and common iliac arteries:

  • a. Longitudinal and transverse diameters;

  • b. Vascular wall characterization, demonstrating evidence of thrombi or ulcerations;

  • c. Iliac arteries diameters, pointing to possible morphological alterations (Fig. 10.8, Tables 10.8 and 10.9).

Rupture of Abdominal Aneurysms

The most common (10%) complication in subjects with true abdominal aneurysms with a diameter of > 6 cm is rupture (Figs. 10.9 and 10.10). A retroperitoneal hematoma adjacent to an abdominal aortic aneurysm is the most common imaging finding of abdominal aortic aneurysm rupture; retroperitoneal extension can be an acute or delayed finding. Computed tomography (CT) is the method of choice for the evaluation of acute aortic syndrome, because of the speed of the examination and its widespread availability. Unenhanced CT scans make it possible to visualize periaortic blood and the extension into the perirenal space, pararenal space, or into the psoas muscles. Contained rupture of an abdominal aortic aneurysm is seen as a draped aorta sign, when the posterior wall of the aorta either is not identifiable as distinct from adjacent structures or when it closely follows the contour of adjacent vertebral bodies.

Fig. 10.7

a Abdominal aorta VR. b Incorrect transverse diameter measured on axial image (DT = 37 mm). c Co-axial diameter on coronal plane (DT = 28 mm)

Fig. 10.8

Essential diameters of the abdominal aorta. See also Tables 10.8 and 10.9

Table 10.8 10.8

Table 10.9 10.9

Fig. 10.9

a Draped aorta sign: no identifiable limit between aneurysm and psoas muscle (white arrow). b The posterior wall of the aneurysm is irregular (yellow arrow), with focal discontinuity on parietal calcification (sign of instability, not rupture)

Fig. 10.10

a,b Non-contrast phase with retroperitoneal hematoma. c,d Active bleeding after CM administration

On contrast-enhanced CT images, active extravasation of contrast material is frequently demonstrated.

MR imaging is not recommended in emergencies because of the long acquisition time and the need for high-performance scanners.

Basic findings:

• 1) Impending rupture signs

  • a. Crescent sign;

  • b. Volumetric augmentation of the aneurysmatic sac;

  • c. Discontinuity of aortic wall calcifications in abdominal aortic aneurysm is a sign of instability.

• 2) Acute rupture

  • a. Retroperitoneal hematoma.

Left Renal Retro-Aortic Vein

A left renal vein with a retro-aortic or circum-aortic course is the most common venous abnormality of renal vessels (8.7% retro-aortic course and 2.1% circum-aortic course); findings must be pointed out for optimal surgical planning (mainly to avoid surgical lesions) (Fig. 10.11).

Treatment

An endovascular procedure is the treatment of choice for aortic abdominal aneurysm.

Endovascular Aortic Repair

The most common endovascular grafts are the aorto-biiliac prosthesis; self-expanding, bifurcated grafts composed of two single units (one for the body and iliac branch, the other for the opposite iliac branch). Endoprostheses are covered grafts, with an external steel or nitinol unit and an internal graft of Dacron.

• 1) Proximal connection: covered or not covered if localized cranially or caudally to the origin of the renal arteries;

• 2) Metallic body;

• 3) Secondary (or iliac) unit;

• 4) Distal connection: localized in the common or external iliac arteries.

An extra-unit can be added at the proximal connection if the grafts are not fully expanded, to avoid a type I endoleak.

Fig. 10.11

Retroaortic left renal vein (arrow)

The CT protocol involves a pre-contrastographic phase, followed by an angiographic phase and a delayed phase (120 sec); the pre-contrastographic phase is necessary to distinguish calcification from the CM, and the delayed phase serves to identify low-flow endoleak (Fig. 10.12).

MR imaging uses an angiographic protocol similar to CT (with the delayed phase); it is also possible to use time-resolved sequences to visualize contrast media flow in real time (yielding more information for endoleak classification).

In an MR study the possibility of susceptible artifacts due to the graft metallic body must be borne in mind.

For a comparison of CT and MR imaging techniques, see Fig. 10.13.

A more frequent complication after endovascular prosthesis positioning is the endoleak, defined as a blood flow external to the stent-graft and inside the aneurysmal sac (Figs. 10.14-10.16).

Endoleak classification is divided into four types; expansion of the aneurysmal sac without the presence of visible endoleak is commonly referred to as endotension or a type V endoleak.

Fig. 10.12

Hyperdense mass (a) is identified as calcification thanks to non-contrast phase (b)

Fig. 10.13

a-c CT imaging. d-f MR imaging. g Abdominal aorta VR

Fig. 10.14

a Endoleak type I: blood flow into the aneurysmal sac due to incomplete seal or ineffective seal at the end of the graft. b Endoleak type II: blood flow into the aneurysmal sac due to opposing blood flow from collateral vessels. c Endoleak type III: blood flow into the aneurysmal sac due to inadequate or ineffective sealing of overlapping graft joints or rupture of the graft fabric. d Endoleak type IV: blood flow into the aneurysmal sac due to the porosity of the graft fabric, causing blood to pass from the graft and into the aneurysmal sac

Fig. 10.15

a, d Non-contrast MR and CT acquisition. b,e Arterial phase MR an CT acquisition. c,f Delayed-phase MR an CT acquisition. The yellow arrow points to an endoleak, probably type II due to the hypertrophic lumbar arteries

Fig. 10.16

Time-resolved sequences make it possible to visualize CM leakage into the aneurysm in real time

Fig. 10.17

Inadequate sealing of overlapping graft joints. VR (a) and MIP (b)

Aneurysmal sac dimensions are an indirect index of graft validity, and are essential for follow-up planning or possible repeat surgery (Fig. 10.17).

Other complications are endoprosthesis rupture, graft migration, aneurysmal sac infection, and retroperitoneal bleeding (Figs. 10.18 and 10.19).

Fig. 10.18

a Patient with endovascular graft. b After 6 months of follow-up, the aneurysm is slightly enlarged

Surgical prosthesis

Surgical prosthesis (or bypass) is the treatment of choice for aneurysms > 5 cm and Surgical Prosthesis for aortic rupture (Fig. 10.20); the surgical procedure consists of opening the aneurys- mal sac with internal positioning of a surgical device (generally Dacron) and terminal anastomosis of the aorta and iliac arteries.

Fig. 10.19

a Aneurysm infection with left-side psoas involvement (arrows). b After 2 months of follow-up, enlargement of the aneurysm is evident, with an infected fistula on the skin surface

Fig. 10.20

a Aorto-aortic bypass: arrows point to the two anastomoses. b Surrounding calcification (arrow) is part of the aneurysmal wall, which closes over the aortic device. c MR of an aorto-aortic bypass: arrows point to the two anastomoses

The study protocol consists of an angiographic phase possibly preceded by a non- contrast phase (Dacron is slightly hyperdense in CT imaging).

• 1) Evaluate the patency and integrity of the surgical device, pointing out occlusion or severe stenosis (Fig. 10.21); rupture is quite rare (generally iatrogenic);

• 2) Device morphology and positioning: surgical devices can be deformed, for example, by pre-anastomotic aneurysms (Fig. 10.22)

• 3) Pre- or post-anastomotic dilatation (Fig. 10.23);

• 4) Device infection (Fig. 10.24).

Fig. 10.21

Aortobifemoral by-pass with left iliac branch occlusion; MIP (a) and VR (b)

Fig. 10.22

Aortic by-pass distortion (a) with right iliac branch occlusion (b) (arrows), probably due to inadequate pre-surgical planning or to an alteration of the pre-anastomotic aorta (for example an aneurysm)

Fig. 10.23

Pre-anastomotic aneurysm. a Yellow arrow, points to the proximal anastomosis. b Left renal artery runs into the aneurysmal thrombus

Fig. 10.24

a, b Infected aorto-aortic bypass; the aneurysmal wall (white arrow) is thickened and hyperdense. A large infected collection is also present (yellow arrow)

10.5 10.5 Aortitis and Inflammatory Aneurysm

Clinical Picture and Diagnosis

Aortitis and inflammatory aneurysm (or mycotic aneurysm) are uncommon conditions (0.7-1%) defined as an infectious break in the wall of an artery with the formation of a blind, saccular outpouching that is contiguous with the arterial lumen (Figs. 10.25-10.27).

Staphylococcus and Streptococcus species are the most common causes; infectious arteritis causes destruction of the arterial wall with a subsequent contained rupture

Fig. 10.25

Infected aneurysm with perivascular inflammatory tissue

Fig. 10.26

a b Infected aortitis with surrounding inflammatory tissue; c,d arrows point to maximum stenosis

Fig. 10.27

a Inflammatory tissue can be slightly hyperintense on T2 weighted sequences (arrow); b axial T1 weighted post-contrastographic administration

and formation of a pseudoaneurysm. An infected aneurysm can rapidly develop or enlarge pathologically, the wall of an infected aneurysm consisting of compressed perivascular tissue, hematoma, and fibroinflammatory tissue.

Imaging and Reporting

Either in MR and CT imaging a portal phase is necessary to demonstrate perivascular tissue enhancement. Retroperitoneal tissue edema is slightly hypodense in CT imaging and slightly hyperintense in T2 FS sequences.

Is necessary to pay attention to the involvement of perivascular structures such as ureter and the duodenum.

Treatment

• Surgery

• Stenting

• Pharmacological therapy

10.6 10.6 Retroperitoneal Fibrosis

Clinical Picture and Diagnosis

Retroperitoneal fibrosis is characterized by a proliferation of fibrous tissue around the aorta. Retroperitoneal fibrosis is typically localized in the distal abdominal (infrarenal) aorta and the common iliac arteries; involvement of the pelvis is uncommon. About two-thirds of cases are idiopathic; otherwise it can be a manifestation of a systemic disease, caused by different drugs (such as beta blockers or antibiotics) and radiation therapy. There is a 3:1 male-to-female ratio among those affected by the disease. Perirenal involvement and significant compression on the ureters may be secondary to the extension of retroperitoneal fibrosis.

Imaging and Reporting

The area affected by active inflammation demonstrates high T2 signal intensity and early contrast enhancement, and areas of fibrosis show low T2 signal intensity and delayed contrast enhancement. The main differential diagnosis is with lymphoma (Fig. 10.28).

Treatment

Double J catheter to treat stasis nephropathy.

Fig. 10.28

Fibrous peri-aortic tissue extends over the retroperitoneum, (a) surrounding the iliac arteries and ureters, with consequent stasis nephropathy, treated with double “j” catheters (arrows) (b,c)

10.7 10.7 Penetrating Ulcer

Clinical Picture and Diagnosis

A penetrating atherosclerotic ulcer is defined as an atherosclerotic lesion with ulceration that penetrates the internal elastic lamina; this penetration facilitates hematoma formation within the medium of the aortic wall (Fig. 10.29).

Imaging and Reporting

• CT: the ROI should be positioned in the true lumen, to avoid intramural hematoma. A pre-contrastographic phase can help to distinguish between hematoma and true vascular lumen;

• Point out the localization and extent of vascular lesions;

• Indicate the involvement of splanchnic vessels.

Treatment

Surgical or pharmacological treatment.

Fig. 10.29

a Penetrating ulcer with intimal lesion and intramural hematoma. b 6-month follow-up with significant hematoma reduction; intimal lesion is no longer noticeable

10.8 10.8 Dissection

Clinical Picture and Diagnosis

In the majority of cases this is an extension of thoracic dissection (see Chapter 7); primary involvement of the abdominal aorta is quite rare (Fig. 10.30).

• CT: The ROI should be positioned in the true lumen, to avoid a delay in the acquisition phase (a false lumen opacifies more slowly);

• It is necessary to point to splanchnic vessel origin, mentioning whether it from a false or true lumen; the main abdominal complications are due to ischemic events. Post-dissectional ischemia of abdominal organs is classified using two different pathogenetic mechanisms (Fig. 10.31):

• In static obstruction the dissection involves the abdominal vessel (red: true lumen, black; false lumen); concurrent formation of an atherosclerotic thrombus in the false lumen exacerbates vascular stenosis (Fig. 10.31 c,d);

• In dynamic obstruction the dissection does not involve the abdominal vessel but the intimal flap is pushed by internal false lumen pressure and covers the vascular ostium (Fig. 10.31 a,b);

• In mixed obstruction the dissection involves the abdominal vessel and the intimal flap covers the ostium (Figs. 10.31 d, e and 10.32).

Fig. 10.30

a ,b Abdominal aortic dissection with good evidence of the intimal tear. c T2 weighted imaging of the same dissection; displaced intimal wall is slightly hyperintense. d-g VR, MIP and axial images

Fig. 10.31

a, b Dynamic ischemia. c, d Static ischemia. e, f Mixed mechanism

Fig. 10.32

Aortic dissection with renal ischemia due to a mixed mechanism. Right renal artery (a, arrow) is involved in the intimal dissection; on the inferior wall of the vessel there is a small thrombus (b, yellow arrow)

Dynamic and static obstruction can lead to severe ischemic complications. Celiac obstruction can cause splenic or intestinal infarction.

Treatment

Surgical or pharmacological treatment.

10.9 10.9 Aortoenteric Fistula

Clinical Picture and Diagnosis

This is defined as a communication between the aortic and intestinal (in the majority of cases duodenal) lumen, and is classified in primary (if atherosclerotic) or secondary (if iatrogenic) (Fig. 10.33). Symptoms include abdominal pain, hematemesis, and melena.

Imaging and Reporting

Simply filling the duodenum with water can facilitate duodenal wall analysis. The pre- contrastographic phase can help to individualize air bubbles in the aortic lumen. A CT scan with the use of intravenous contrast media may show contrast material extravasation from the aorta into the involved portion of the bowel, if a patent fistula is present.

Treatment

Surgical treatment.

Fig. 10.33

Aortic aneurysm with endovascular graft. The air in the vascular lumen and the discontinuity in the vascular wall (arrows) are suggestive of an aortoentric fistula, in this case with the duodenum

10.10 10.10 Leriche Syndrome

Clinical Picture and Diagnosis

Complete obliteration of the aortic bifurcation (generally due to atherosclerotic disease) is called Leriche syndrome (Figs. 10.34 and 10.35). This term describes a complex of clinical symptoms (e.g., claudication, decreased femoral pulses) attributed to obstruction of the infrarenal aorta. A large network of parietal and visceral vessels may be recruited to bypass any segment of the aortoiliac arterial system by means of the formation of collateral channels.

Imaging and Reporting

Aortic occlusion can be classified as juxtarenal, or within 5 mm of the lower renal arterial origin; infrarenal, or cephalic at the origin of the inferior mesenteric artery; and inframesenteric, or caudal at the origin of the inferior mesenteric artery. It is also necessary to point out the concomitant occlusive disease affecting the visceral arteries.

Surgical treatment.

Treatment

Surgical treatment.

Fig. 10.34

a Coronal VR. b Infrarenal Leriche syndrome; iliac arteries are reperfused by the epigastric and lumbar vessels

Fig. 10.35

a Right common iliac artery occlusion. b Juxtarenal Leriche syndrome with distal reperfusion. c,d Juxtarenal Leriche syndrome treated with axillofemoral bypass and femoro-femoral crossover