Stenotic-occlusive disease

Stenotic pathology of visceral arteries results in reduced blood flow and may lead to organ ischemia or secondary hypertension.

Atherosclerosis

Atherosclerosis is the most common cause of stenosis, characterized by progressive development of atherosclerotic intimal plaques, leading to luminal narrowing [24].

CTA shows focal and proximal stenosis, usually within the first 2 cm of the vessel course [24]. Stenoses are generally considered significant when involving > 50% of the vessel lumen, although it must be taken into account that CTA may overestimate the degree of stenosis in the presence of calcifications. Calcified plaques are easily identified, while non-calcified plaques require optimized arterial phase imaging. The condition predominantly affects patients with cardiovascular risk factors.

Fibromuscular dysplasia

Fibromuscular dysplasia represents a non-inflammatory, non-atherosclerotic vasculopathy affecting small and medium-sized arteries, usually in young women.

Unlike atherosclerosis, fibromuscular dysplasia typically presents with vascular stenosis involving the mid or distal segments of vessels, most commonly renal arteries, often manifesting as renovascular hypertension [25]. On imaging, there are no intraluminal filling defects as seen with atherosclerotic plaque; instead, it shows luminal narrowing without associated wall thickening, reflecting a fibrotic remodeling process (Fig. 1).

Fig. 1

A Virtual rendered reconstruction (VRT) showing severe stenosis of the celiac trunk and SMA (arrows) in a 72-year-old male patient with advanced atherosclerosis. B MIP reconstruction showing stent placement in the SMA (arrowhead). C: MIP reconstruction depicting right renal artery stenosis in a 35-year-old female patient without cardiovascular risk factors, consistent with fibromuscular dysplasia. Note the different underlying mechanisms, with atherosclerotic plaque-related luminal narrowing versus non-atherosclerotic dysplastic stenosis

Compressive syndromesMedian arcuate ligament syndrome

Median arcuate ligament syndrome results from compression of the celiac trunk by the arcuate ligament, a fibrous structure connecting both diaphragmatic crura which forms the anterior component of the aortic hiatus [26, 27]. A high origin of the celiac trunk or a low insertion of the ligament may contribute to its development.

Compression is more pronounced during expiration, when the celiac trunk moves cranially while the ligament remains fixed, resulting in more severe stenosis.

It predominantly affects young, thin women (20–40 years of age) and typically presents with postprandial epigastric pain, nausea, and weight loss, occasionally associated with an epigastric bruit. Symptoms often improve in the knee-chest position due to reduced ligament tension [26,27,28].

CTA shows a focal indentation of the celiac trunk with a characteristic “hooked” appearance. CTA protocols usually include an expiratory early arterial phase to assess maximal compression, followed by an inspiratory late arterial phase to demonstrate its reversibility. At our institution, we perform an expiratory early arterial phase followed by an inspiratory portal phase instead of the recommended late arterial phase, to better evaluate solid organ abnormalities [26,27,28].

Management is individualized, although surgical decompression is commonly performed in symptomatic cases, given the limited mid-term durability of endovascular stenting under persistent external compression, which may lead to stent fracture or migration [26,27,28] (Fig. 2).

Fig. 2

A 40-year-old patient with periumbilical pain, weight loss, and bowel habit changes. CTA MIP reconstructions demonstrate celiac trunk stenosis that worsened during the expiratory phase (A, B) consistent with median arcuate ligament syndrome. Patient was treated with stent placement. Months later, a knee radiograph C revealed stent migration to the left popliteal artery (arrowhead)

Superior mesenteric artery syndrome (Wilkie syndrome)

Wilkie syndrome is caused by compression of the third portion of the duodenum between the abdominal aorta and the SMA, resulting in high intestinal obstruction and diffuse abdominal pain [3]. Retroperitoneal fat reduction due to eating disorders, malignancy, surgery, severe burns, or malabsorption leads to narrowing of the aortomesenteric angle (normal value between 30–65º) [26, 29]. Severe spinal scoliosis or hyperlordosis may also contribute to narrowing this angle by altering the normal anatomical position of abdominal structures.

Symptoms include weight loss, postprandial abdominal pain, and vomiting, which improve in the left lateral decubitus or knee-chest position.

Diagnosis requires both compatible symptoms and imaging findings, including an aortomesenteric angle < 25º, an aortomesenteric distance <8 mm measured at the duodenal crossing, and proximal duodenal and gastric dilation [26, 29]. Up to one-third of patients may also exhibit concurrent compression of the left renal vein between the aorta and the SMA, sometimes causing gonadal vein dilation and pelvic congestion syndrome, a condition known as Nutcracker syndrome (Fig. 3).

Fig. 3

A 37-year-old woman with postprandial abdominal pain, vomiting, hyporexia, and weight loss. CTA MIP and MPR reconstructions reveal a reduced aortomesenteric angle A and distance B, with upstream duodenal dilation (*). Both clinical history and imaging features are consistent with Wilkie syndrome. Concomitant Nutcracker syndrome is also present, with compression of the left renal vein and dilation of the left gonadal vein (arrow)

Aneurysms and pseudoaneurysms of visceral arteriesTrue aneurysms

An aneurysm is a focal and permanent dilation of a vessel involving all layers of the arterial wall (intima, media, and adventitia), often related to medial degeneration due to atherosclerosis, fibromuscular dysplasia, vasculitis, infection, or prior surgery [19, 24, 30]. Morphologically, aneurysms are typically fusiform (most common) or saccular.

Most visceral aneurysms are asymptomatic. However, they may present with abdominal pain, a palpable pulsatile mass, or rupture, leading to life-threatening hemorrhage [4].

Different considerations regarding aneurysms should be taken into account depending on their anatomical origin (Table 1).

Table 1 Practical overview of visceral artery aneurysms and pseudoaneurysms

CTA allows precise characterization of aneurysm size, morphology, and relationship with adjacent vessels and organs [3, 4]. Spectral CT technology, through iodine maps and virtual non-contrast images, enables differentiation between aneurysmal lumen enhancement, vascular calcifications, and perivascular hematomas [17].

Intervention, usually by endovascular procedures, is generally indicated when the aneurysm is bigger than 3 cm (except for the pancreatoduodenal arcade, with a limit of 15 mm), becomes symptomatic, during pregnancy, or demonstrates growth greater than 5 mm/year [4, 5, 29] (Fig. 4).

Fig. 4

VRT reconstruction showing incidental findings of aneurysms of the splenic and left renal arteries (arrowheads) in a CT staging study of a 64-year-old patient diagnosed with colon cancer

Pseudoaneurysms

Pseudoaneurysms result from disruption of the arterial wall, leading to a blood collection contained only by the adventitia or surrounding perivascular tissues [20]. Their main causes include inflammatory conditions (acute pancreatitis affecting the splenic, SMA, or gastroduodenal arteries), infections (mycotic pseudoaneurysms secondary to endocarditis), and iatrogenic or penetrating trauma [28, 29, 30].

Differentiating pseudoaneurysms from true aneurysms is critical, as pseudoaneurysms carry a significantly higher risk of rupture. CTA findings suggestive of pseudoaneurysm include poorly defined margins with the native vessel, associated perivascular hematoma, inflammatory fat stranding, and signs of recent bleeding or active contrast extravasation [19, 29].

The etiology and management of pseudoaneurysms also vary considerably depending on the affected vascular territory (Table 1).

Given their high risk of rupture, pseudoaneurysms are usually managed with endovascular or surgical treatment, although management should be tailored to clinical context and patient status [29] (Fig. 5).

Fig. 5

A 61-year-old patient with infective endocarditis presented with acute abdominal pain. CTA reveals a vascular lesion (arrows) with poorly defined margins, signs of perivascular hematoma, recent bleeding, and adjacent fat stranding, consistent with a mycotic pseudoaneurysm of the SMA. The pseudoaneurysm was successfully treated with endovascular stent placement

Acute mesenteric ischemia

Acute mesenteric ischemia is a life-threatening vascular emergency caused by gastrointestinal blood flow disruption [31].

Its most frequent clinical feature is an abdominal pain out of proportion to physical examination [5]. Although a classic triad (severe pain, bowel emptying/vomiting, and embolic source) exists, it is only present in 40%-80% of cases. Serum lactate and D-dimer are late and non-specific markers, and should not be used as standalone diagnostic tools [5, 30, 31].

Multidetector CTA is the first-line imaging modality, reaching sensitivities of 96% and specificity up to 100% for occlusive disease, with 70–80% sensitivity for non-occlusive cases. Optimal protocol includes biphasic acquisition (arterial and portal venous phases), and avoiding oral contrast, as it may obscure bowel wall enhancement [7, 31].

Findings are best assessed using an “inside-out” approach [7, 30, 31]:

Bowel wall: Absent or reduced enhancement is highly specific for ischemia. Wall thinning (“paper-thin”) suggests irreversible arterial ischemia, while wall thickening and the “target sign” are more typical of venous or reperfused ischemia.

Intestinal signs: Dilated loops may be an early finding. Pneumatosis intestinalis and portomesenteric gas indicate advanced ischemia and transmural necrosis.

Vascular signs: Direct visualization of a filling defect or a “vessel cutoff sign”, better evaluated on MPR/MIP reconstructions.

Table 2 summarizes the four main subtypes of acute mesenteric ischemia, their pathophysiology, and imaging features (Figs. 6, 7 and 8).

Table 2 Comparative clinical, imaging, and therapeutic characteristics of acute mesenteric ischemia subtypesFig. 6

45-year-old patient with a history of gastric bypass surgery with Roux-en-Y reconstruction, presents with acute abdominal pain that improves in a knee-chest position, nausea and vomiting, without fever. A represents a CTA examination previous to this event showing normal anatomical distribution. B Axial CTA image showing morphological distortion of the mesenteric vascular pedicle, which is difficult to fully characterize on axial images alone. (C, D) VRT and MIP reconstructions provide a better depiction of the mesenteric vascular pedicle torsion (arrows), resulting in SMA occlusion. Exploratory laparotomy confirmed the imaging findings, and the twisted alimentary loop was resected

Fig. 7

59-year-old patient undergoing evaluation before renal transplantation presents with acute abdominal pain, after discontinuing anticoagulant medication. Ugrent CTA demonstrated SMA thrombosis (red dotted lines) with acute mesenteric ischemia signs: paper-thin like bowel wall without mural enhancement (arrows), pneumatosis intestinalis (*), and portal and mesenteric gas (arrowheads)

Fig. 8

51-year-old patient with known history of hepatocellular carcinoma and factor VII deficiency associated with lupus anticoagulant, presenting with acute abdominal pain. Signs of acute mesenteric ischemia with portal and superior mesenteric vein thrombosis (arrow), bowel wall thickening without serosal enhancement (*), free fluid (solid arrowheads), and mesenteric edema (open arrowheads) are identified

Vasculitis and segmental arterial mediolysisVasculitis

Vasculitis consists of inflammation of the vessel wall, which may be driven by immune cellular mechanisms, immune complexes, or antineutrophil cytoplasmic antibodies. These entities are typically classified according to vessel size (small, medium, or large). Abdominal visceral arteries are involved in up to 50% of cases, including Takayasu arteritis, giant cell arteritis, and polyarteritis nodosa [29].

The clinical profile usually combines systemic symptoms (fever, myalgias, arthralgias, and constitutional syndrome) with abdominal manifestations, including abdominal pain, nausea, diarrhea, or melena [29]. Additionally, it is associated with increased acute-phase reactants and specific antibodies.

The presence of mesenteric ischemia or unexplained vascular abnormalities in a young patient should raise suspicion for vasculitis.

CTA findings include circumferential wall thickening, luminal stenosis or beading, and microaneurysms, particularly in polyarteritis nodosa [29, 32]. Bowel involvement may also be present in acute phases (Fig. 9).

Fig. 9

A 60-year-old patient with weight loss and rectal bleeding, without abdominal pain. CTA shows mural thickening of the mid-SMA, causing stenosis (arrows). The patient was studied for vasculitis, diagnosed with polyarteritis nodosa

Segmental arterial mediolysis

Segmental arterial mediolysis (SAM) is a rare, non-inflammatory, non-atherosclerotic vasculopathy of unknown etiology [24], usually involving the celiac axis and its branches (70–80%) [33]. Histopathologically, it is characterized by segmental lysis of the arterial media, leading to loss of wall integrity and predisposing to aneurysms and dissections [35].

Disease evolution can be divided into phases (Slavin classification) [35]:

Lytic phase: medial vacuolization and fibrin deposition, presenting as arterial dilations.

Aneurysmal phase: formation of gaps leading to saccular or fusiform aneurysms; multiple gaps produce a “string-of-beads” appearance.

Dissection phase: blood enters arterial gaps, resulting in intramural hematomas and dissection flaps.

Stenotic phase: reparative fibrosis leading to arterial stenosis and thrombosis.

Remodeling phase: complete repair with fibrous tissue and spontaneous resolution of imaging findings.

Differentiation from medium-vessel vasculitis remains challenging, as angiographic findings may be indistinguishable [35]. Both conditions can manifest with multifocal aneurysms, dissections, stenoses, and occlusions. However, SAM lacks the systemic inflammatory features typically associated with vasculitis, including constitutional symptoms, elevated inflammatory markers, positive serological testing, and extra-vascular organ involvement. Recent diagnostic criteria have highlighted the importance of combining the characteristic splanchnic arterial distribution of lesions with the absence of inflammatory findings and the dynamic evolution of vascular abnormalities over time. Consequently, diagnosis should integrate imaging, clinical presentation, and laboratory evaluation [25, 36].

Treatment depends on clinical severity. Symptomatic patients with hemorrhage require endovascular urgent intervention. Asymptomatic patients are managed conservatively with imaging follow-up (typically at 6-month intervals initially, and annually thereafter) to monitor lesion stability or spontaneous resolution [37] (Fig. 10).

Fig. 10

A A 50-year-old man initially evaluated for urolithiasis. CTA MPS reconstruction reveals a normal anatomical variant of the hepatic artery, arising from the aorta, with no associated abnormalities. B Three months later, the patient presented with intermittent epigastric pain. Imaging demonstrates marked stenosis, vessel tortuosity and inflammatory changes of the arterial wall (arrow). The patient was evaluated for suspected vasculitis: however, negative antibody and inflammatory marker tests supported the diagnosis of segmental arterial mediolysis. C Conservative management was adopted. CTA MPR reconstruction two years later shows morphological changes of the vessel (arrowhead) including increased tortuosity and a beaded appearance, with partial recanalization

Vascular malformations

Vascular malformations comprise a heterogeneous group of structural anomalies that are typically congenital, although they may become clinically apparent during adulthood. They are classified into high-flow and low-flow vascular malformations [4]. This article focuses on high-flow malformations, due to their greater clinical relevance in the abdominal territory (Fig. 11).

Fig. 11

A VRT reconstruction demonstrating an incidental right renal AVM (arrow) in a 30-year-old patient, showing a nidus and early contrast enhancement within the inferior vena cava. (B, C) A 73-year-old patient presenting with right lumbar pain and anemia following the removal of a nephrostomy catheter. Doppler ultrasound B demonstrates turbulent flow with aliasing at the access site. CTA MIP reconstruction C shows a right renal AVF (arrowhead) with communication to the urinary tract, likely of iatrogenic origin

Arteriovenous malformation

Arteriovenous malformations (AVM) are defined by the presence of multiple abnormal connections between an artery and a vein, allowing blood flow to bypass the capillary bed [17, 4].

The key diagnostic feature on CTA is the presence of an early draining vein or a dilated vein associated with a hyperenhancing vascular nidus in the arterial phase.

In the gastrointestinal tract, they often present with hematemesis, melena, or anemia of unknown origin. In the renal territory, they may present as sec