Fig. 1. Maximum intensity projection (MIP) (a) and volume rendered display (b) of a 64-detector-row CT angiography of a saccular infrarenal aortic aneurysms, probably caused by a penetrating ulcer. Note the location of an acute extravasation (arrow), the retroperi-toneal hematoma (arrowheads) and another penetrating ulcer in the right common iliac artery (black arrow)

Fig. 1. Maximum intensity projection (MIP) (a) and volume rendered display (b) of a 64-detector-row CT angiography of a saccular infrarenal aortic aneurysms, probably caused by a penetrating ulcer. Note the location of an acute extravasation (arrow), the retroperi-toneal hematoma (arrowheads) and another penetrating ulcer in the right common iliac artery (black arrow)

Inflammatory aneurysms are characterized by peri-aneurysmal inflammatory tissue and fibrosis, similar to retroperitoneal fibrosis [3]. No infectious organism is found. Possible secondary effects are ureteral obstruction or the involvement of intestinal loops. Characteristically, three distinct layers surround the perfused lumen: mural thrombus, aortic wall with calcifications, and peri-aneurysmal soft tissue. The soft-tissue rim surrounding the aorta shows contrast enhancement that increases on late scans (> 90 s) after contrast injection.

Fistulation into adjacent organs is a rare but severe complication. Aorto-enteric fistula may cause hyperattenuating clots in the bowel lumen, as well as direct contrast extravasation into the affected bowel segment, which is often the horizontal portion of the duodenum. If there is mural thrombus, fistulation may cause air bubbles in the wall.

Concomitant vascular disease is quite frequent. Concomitant aneurysms are found in the visceral and renal arteries, and the iliac arteries. AAA are associated with stenoses of various side branches. Therefore it is important to evaluate the main branching vessels for the presence of stenoses or aneurysms. In patients with stenosis of the superior mesenteric artery and collateralization via the inferior mesenteric artery, left colonic ischemia may develop as a complication of surgery, if no reimplantation of this artery is performed. Involvement of the iliac arteries (aneurysms, stenoses) is an important factor in deciding whether to implant a tubular or Y-shaped prosthesis. Accessory renal arteries are present in 25% of the population. They may only be sacrificed during implantation of stent grafts if they are small.

Aortic Rupture

The most important complication of aortic aneurysms is rupture, which is defined as seepage of blood through clefts in the aortic wall. The larger the diameter of the aneurysm, the greater is the likelihood of eventual rupture. In the abdomen, the life-time risk for rupture grows from 10% in aneurysms smaller than 4 cm to 60% in aneurysms larger than 10 cm. Elective surgical or endo-luminal repair is usually indicated if the aneurysmal diameter exceeds 5 cm in the descending and abdominal aorta. Saccular aneurysms have a higher risk of rupture, and there is no absolute size limit that governs the decision to intervene. Surgical mortality rises substantially in patients with ruptured aneurysms.

CT is indicated for suspected aortic rupture, provided the patient is not referred for immediate surgery based on ultrasound findings. Non-contrast CT is no longer indicated. CTA is the present technique of choice. CTA is able to define whether insertion of a bifurcated prosthesis or reimplantation of the renal arteries is required. Scan delay has to be determined individually, because the circulation time may be substantially prolonged (to beyond 60 s) in patients with shock. The patient can be taken off the CT table as soon as it is clear that contrast enhancement of CTA is sufficient. To speed up evaluation, it may be advisable to reconstruct fewer images first with larger spacing to determine the major findings. Later an overlapping data set can be reconstructed, from which 3D representations for fine-tuning of the surgical procedure can be derived.

Impending rupture may be indicated by freshly clotted blood within the aortic wall or a mural thrombus. Hyperdense portions within a pre-existing hypodense mural thrombus on CT are an indicator of fresh thrombus formation and thus recent growth of an aneurysm. Furthermore, nose-like protrusions of perfused lumen into a clotted region suggest a higher risk for rupture. Small amounts of stranding around an aneurysm indicate minor hemorrhage and can be the precursor to aortic rupture.

Contained rupture occurs mainly in the abdominal aorta in a posterior-lateral location and is characterized by local hemorrhage or acute pseudoaneurysm formation. Sometimes interruption of a wall calcification may be detected at the site of the pseudoaneurysm.

AAA commonly rupture into the retroperitoneum, which contains the hemorrhage to a certain degree. If the peritoneum itself ruptures, the blood may freely flow into the peritoneal cavity, leading to a high risk of sudden death. Rarely, an aneurysm can rupture into the gastrointestinal tract, causing massive gastrointestinal hemorrhage (aortoduodenal fistula), or into the inferior vena cava, leading to rapid cardiac decompensation. Acute rupture leads to stranding of the retroperitoneal fat surrounding the aorta. Free intraperitoneal fluid is rare, but its presence signals a very unstable situation in which the rupture is no longer confined by the peritoneum. Acute hemorrhage need not be hyperattenuating, but may be isoattenuating relative to muscle because of a lack of clotting or separation between blood cells and serum. It may even be hypoattenuating if the hematocrit is low because of plasma expanders. Active bleeding is present if contrast extravasation can be observed.

Dissection of the Abdominal Aorta

Isolated dissection of the abdominal aorta is rare and is usually caused by a penetrating ulcer. Abdominal malperfusion as a consequence of a thoracic dissection of the aorta is not uncommon. Compression or occlusion of major aortic branches may lead to renal failure, mesenteric ischemia, or acute claudication. The false channel has a propensity to dilate and to compress the true lumen or the orifice of a side branch vessel.

CTA has almost completely substituted for angiography in the diagnosis and evaluation of abdominal complications in patients with suspected aortic dissection. MRA is a good alternative in patients with chronic dissection, but patient monitoring is problematic in the acute stage and makes MRA not very convenient for this patient group.

Imaging is used to evaluate whether there is compression of the true or false channel, thrombosis of one channel, or stenosis of a side branch. The risk of malperfusion becomes higher if there is no distal reentry but imbalance between blood velocities, inflow and outflow from the false channel, as well as compression of one channel or obstruction of the branch vessel by intimal flaps can all cause clinically relevant organ malperfusion. Some pat terns may look quite harmless because CT will display opacification of all vascular beds that are perfused, despite high-grade obstruction of the blood flow. Differences between left and right-sided enhancement of the kidneys or markedly reduced organ perfusion may be readily apparent on CT. Malperfusion of the bowel may occur with involvement of one or more splanchnic arteries, especially when combined with pre-existing stenoses.

The true lumen and false channel can be distinguished by tracing the true lumen from the beginning of the dissection in the ascending aorta (type A), or following the continuity of the normal aorta (type B), but this requires a combined for thoraco-abdominal evaluation, which is always suggested in an acute situation [4].

Aortic dissection at unusual locations should raise the suspicion of a penetrating aortic ulcer as the etiology. Initially, such dissections are localized, but can dissect in an antegrade or retrograde fashion and involve large portions of the aorta.

Aortic Stenosis and Aortic Occlusion

Aortic stenosis may occur in older patients as a consequence of severe atherosclerosis. In young patients it is caused by congenital hypoplasia or midaortic syndrome. The latter has an unknown etiology but is probably related to fibromuscular hyperplasia. In midaortic syndrome it is common to find involvement of the renal arteries and splanchnic vessels [5]. Extensive collateralization with a hypertrophic artery of Riolan is present if the splanchnic vessels are involved. The stenoses are most pronounced in the proximal vessel segments. Inflammatory para-aortic changes are not observed.

Leriche syndrome includes an acute occlusion of the aortic bifurcation, usually caused by acute thrombosis at a preexisting site of atherosclerotic stenosis. An embolic patho-genesis is less common. The terminal aortic occlusion in acute Leriche syndrome is usually located just above the bifurcation. In chronic cases the aorta becomes filled with clot to the level of the renal arteries. Concomitant renal artery stenosis has to be excluded. Thrombotic and embol-ic occlusions can be distinguished by detecting an intralu-minal embolus, which appears as a partially occlusive filling defect. Embolic occlusions are typically associated with a milder grade of aortic sclerosis.

CTA and MRA provide excellent information about the vascular lumen. In addition, CTA is able to detect large calcified plaques or other wall changes in atherosclerotic stenosis. CTA can diagnose Leriche syndrome, but only multislice scanning can exclude concomitant renal artery stenosis and assess the peripheral arteries. Gd-enhanced MRA requires modern equipment to assess multiple levels from the aorta to the peripheral arteries. Only under these conditions is MRA a diagnostic alternative.

Endovascular Aortic Repair

Endovascular aortic prostheses (stent grafts) are used for minimally invasive treatment of abdominal aortic aneurysms and penetrating aortic ulcers. CTA has an essential role in the preinterventional planning and postin-terventional follow-up of these procedures, but MRA is assuming an increasingly important role for follow-up because superior for the detection of endoleaks (Table 2).

After successful endovascular repair, associated abnormalities affecting the aneurysm wall or periaortic fat tissue (e.g., stranding in covered perforation) should disappear. Even the periaortic reaction in inflammatory aneurysms has been reported to decrease over time.

Fracture of stent material can best be appreciated on conventional plain radiographs of the stent area, but MIP or volume-rendered displays from multislice CT data may also demonstrate such events. Stenoses of the stent lumen may occur in aortoiliac grafts, especially at juncture sites between the various components of the graft. Dissection of the access vessel during graft placement is usually associated with excessive vascular tortuosity. Thrombosis of the stent lumen is most frequently caused by mechanical obstruction, either by the stent itself or by dislocated coating material. In very large aneurysms, the stent graft may migrate to the anterior portion of the aortic lumen, especially when the distal anchoring site is not stable. Such a migration may cause massive type I endoleaks and has an increased risk of aneurysm rupture.

The diameter of the aneurysm (lumen including thrombus) is measured at follow-up, and serial measurements should not show an increase in size. Successfully treated aneurysms or dissections should thrombose completely and shrink in size over a period of months to years. An

Table 2. Types of endoleaks after stent graft placement (from [6])

Type Description

Table 2. Types of endoleaks after stent graft placement (from [6])

Type Description

Type I

Attachment site leaks

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