Penetrating aortic ulcer (PAU) is a focal lesion resulting from ulceration of an atherosclerotic plaque that penetrates the internal elastic lamina into the aortic media. It falls within the acute aortic syndrome (AAS) spectrum (along with classic dissection and intramural hematoma). Typically associated with age 70+, advanced atherosclerosis, and hypertension. Most common in descending thoracic aorta (90%), rarely in ascending or abdominal aorta. Frequently associated with intramural hematoma (IMH) and carries risk of progression to classic dissection, pseudoaneurysm, or rupture. CTA is the gold standard — focal crater-like outpouching with surrounding IMH is the typical appearance. Requires aggressive antihypertensive therapy and close follow-up; complicated cases need surgical/endovascular intervention.
Age Range
55-85
Peak Age
70
Gender
Male predominant
Prevalence
Uncommon
PAU pathogenesis begins with ulceration of an advanced atherosclerotic plaque. The atherosclerotic plaque grows in the intimal layer and ulceration occurs when the fibrous cap overlying the lipid core ruptures. This ulcer penetrates the internal elastic lamina reaching the medial layer — vasa vasorum damage and mechanical disruption in the media create local intramural hemorrhage (IMH). IMH weakens the lamellar structure of the media, predisposing to further destruction. Unlike classic dissection, PAU does not create a wide intimal flap — it remains as a focal, crater-shaped lesion. However, medial damage may propagate to progress into classic dissection. When it reaches the adventitia, pseudoaneurysm forms; when it extends beyond the adventitia, rupture occurs. PAU's predilection for the descending aorta is explained by the greater atherosclerotic burden and turbulent flow conditions in this region. On CT, the focal contrast-filled outpouching corresponds to the ulcer itself, while the surrounding hyperdense crescent thickening corresponds to IMH.
Focal crater-shaped contrast-filled outpouching extending from the aortic wall with surrounding intramural hematoma on CTA — diagnostic signature of PAU.
On arterial phase, a focal crater-shaped contrast-filled outpouching extending from the aortic wall is seen. The ulcer typically has a wide-based, shallow or deep crater morphology. Irregular contour and calcified atherosclerotic plaque in the surrounding aortic wall. PAU usually appears as a solitary lesion but multiple PAUs are possible. Size and depth determine progression risk — >20 mm width or >10 mm depth indicates high risk.
Report Sentence
Focal crater-shaped contrast-filled outpouching measuring ___ mm in width and ___ mm in depth in the descending thoracic aorta consistent with penetrating aortic ulcer.
Non-contrast CT shows crescent or circumferential hyperdense thickening in the aortic wall around the PAU — intramural hematoma. Acute IMH is hyperdense at ~60-70 HU (fresh blood), decreasing to ~40-50 HU in the subacute period. IMH extent may be local around the PAU or involve a long segment. IMH thickness >11 mm and aortic diameter >50 mm increase complication risk.
Report Sentence
Non-contrast CT demonstrates ___ mm thick crescent-shaped hyperdense intramural hematoma in the aortic wall surrounding the PAU.
When PAU penetrates to the adventitia, focal pseudoaneurysm forms — an enhancing saccular outpouching extending beyond the aortic contour with a narrow neck and wide body. Pseudoaneurysm differs from true aneurysm by not involving all wall layers — contained by adventitia or surrounding tissue. Rupture risk is high and strengthens treatment indication.
Report Sentence
Focal pseudoaneurysm measuring ___ mm arising from the PAU is noted; treatment indication should be evaluated due to rupture risk.
On delayed phase, contrast retention in the PAU crater and assessment of IMH extent are performed. Increasing contrast accumulation suggests active bleeding or ulcer deepening. On serial follow-up CTs, increase in ulcer size, IMH thickening, pseudoaneurysm development, or aortic diameter increase indicate progression and affect intervention decision.
Report Sentence
Delayed phase shows contrast retention in the PAU crater with contrast leak into surrounding IMH, suggesting active bleeding/progression; close follow-up or intervention is recommended.
MRI can age IMH based on T1 signal characteristics. Acute IMH (<7 days) is iso- to slightly hyperintense on T1 (deoxyhemoglobin). Subacute IMH (7-14 days) is markedly T1 hyperintense (methemoglobin) — this is the most diagnostic period as T1 hyperintensity clearly separates IMH from aortic wall and lumen. Chronic IMH is T1 hypointense (hemosiderin). PAU itself appears as a focal contrast-enhancing outpouching post-gadolinium.
Report Sentence
MRI demonstrates T1 hyperintense intramural hematoma in the aortic wall with focal post-gadolinium enhancing ulcer crater consistent with PAU + subacute IMH.
When rupture complicates PAU, active contrast extravasation beyond the aortic wall is seen in the arterial phase. Periaortic hematoma, mediastinal/pleural hemothorax, or retroperitoneal hematoma (abdominal PAU) are indirect rupture signs. Enhancing ulcer crater extending beyond the outer aortic contour suggests impending rupture. Rupture is an indication for emergent surgical/endovascular intervention.
Report Sentence
Active contrast extravasation from PAU with periaortic hematoma/hemothorax consistent with acute rupture; emergent intervention is required.
Criteria
Focal ulcer crater without surrounding IMH. Smaller, more stable lesions. Incidence ~30-40%.
Distinct Features
Usually manageable with medical therapy and follow-up. Lower progression risk. 3-6 month CT follow-up may suffice.
Criteria
PAU with surrounding IMH. Most common form (~60-70%). IMH thickness >11 mm or aortic diameter >50 mm high risk.
Distinct Features
More aggressive course: 20-40% progression risk to dissection, pseudoaneurysm, or rupture. Close follow-up (first week CT, then monthly) or proactive TEVAR considered.
Criteria
Pseudoaneurysm development or rupture from PAU. Emergent intervention indication. Untreated mortality 75%+.
Distinct Features
TEVAR (endovascular) preferred treatment — lower mortality than open surgery in elderly comorbid population. Ascending aorta PAU prefers surgery.
Distinguishing Feature
Classic dissection shows intimal flap and dual lumen; PAU shows no intimal flap but focal crater + IMH. Dissection involves longer segment; PAU is focal.
Distinguishing Feature
Isolated IMH has no ulcer crater — only hyperdense wall thickening. In PAU, focal contrast-filled crater accompanies IMH. IMH may be a PAU component or independent entity.
Distinguishing Feature
Traumatic or post-surgical pseudoaneurysm is related to prior history and specific location. PAU-related pseudoaneurysm develops in setting of advanced atherosclerosis and is accompanied by IMH.
Distinguishing Feature
Mycotic aneurysm develops in infective endocarditis/bacteremia setting with lobular morphology and periaortic inflammation/abscess. PAU results from atherosclerotic plaque ulceration without infectious signs.
Urgency
emergentManagement
interventionalBiopsy
Not NeededFollow-up
3-monthPAU is an acute aortic syndrome entity requiring emergent management. First-line is aggressive antihypertensive therapy (target SBP <120 mmHg, HR <60/min). Uncomplicated PAU is managed with medical therapy + serial CT follow-up (first week, 1, 3, 6, 12 months). TEVAR indications: progressive ulcer growth, IMH thickening, pseudoaneurysm development, aortic diameter increase, rupture signs, or refractory pain. TEVAR provides lower mortality (5-10% vs 20-30%) and morbidity than open surgery in elderly comorbid population. Ascending aorta PAU (rare) requires surgical treatment.
PAU is part of acute aortic syndromes and carries risk of progression to rupture, pseudoaneurysm, and aortic dissection. Large (>20 mm) or deepening ulcers and rapidly growing intramural hematomas are indications for TEVAR. Stable cases are managed with medical therapy and serial imaging.