Penetrating Ulcer & Intramural Hematoma
- These two are the underappreciated cousins of aortic dissection — together they make up the "acute aortic syndrome" trio.
- Intramural hematoma (IMH): blood inside the aortic wall, but with no visible flap and no flow channel. A crescent of clotted blood baked into the wall.
- Penetrating atherosclerotic ulcer (PAU): an atherosclerotic plaque erodes through the inner lining, letting blood burrow into the wall — an ulcer crater that pokes beyond the normal lumen line.
- A PAU can cause an IMH, and either can progress to frank dissection or rupture — so location and the aortic diameter matter a lot.
- The same first move applies to all three: ECG-gated CT angiography of the chest, abdomen, and pelvis.
Everyone learns aortic dissection first, with its dramatic flap flapping in the lumen like a divider in a pool lane. Then one day a CT lands on your screen with chest pain, a clearly sick aorta, and no flap anywhere. Congratulations — you've met the other two members of acute aortic syndrome, the ones that show up to the party without the costume.
The wall is a sandwich
Quick refresher, because both of these diseases live inside the aortic wall. The aorta has three layers, like a sandwich: intima (the inner lining you can almost lick), media (the thick muscular-elastic meat in the middle), and adventitia (the outer crust holding it all together). Normal blood stays politely in the lumen, touching only the intima.
Acute aortic syndrome is the umbrella term for the three ways blood breaks that rule and gets into — or through — the wall. Classic dissection tears the intima and splits the media into a true and false lumen. The other two are subtler.
Intramural hematoma: a bruise in the wall
Imagine the tiny nutrient vessels that feed the aortic wall itself — the vasa vasorum, the wall's own little plumbing — springing a leak. Blood seeps into the media and clots there. No intimal tear you can find, no flowing false lumen, no flap. Just a crescent of blood entombed in the wall, like a bruise under your fingernail that has nowhere to go.
On CT, the giveaway is a smooth, crescent-shaped thickening of the aortic wall that does not enhance with contrast (it's clotted blood, not flowing blood). On a non-contrast scan it's often slightly bright — fresh hematoma is denser than the surrounding wall.
Don't mistake an IMH for plain old mural thrombus lining an aneurysm. Thrombus tends to sit on an irregular, calcified, atherosclerotic surface and the calcium stays at the inner edge. With IMH, the wall is smooth and any intimal calcium gets pushed inward, away from the outer wall — a useful tell that the blood is behind the lining, not in front of it.
Penetrating ulcer: a crater that digs in
A penetrating atherosclerotic ulcer is the opposite mechanism — it starts from the inside. Take a gnarly atherosclerotic plaque, the kind that's been quietly trashing the intima for decades. One day it ulcerates and erodes straight through the inner lining, and blood starts burrowing into the media.
The radiologic signature is a focal contrast-filled outpouching — a crater — that projects beyond the expected line of the aortic lumen, almost always surrounded by heavy, ratty atherosclerosis. Think of a pothole in the road: the surface should be smooth, but here's a crater where the asphalt eroded and water (contrast) has pooled into the hole.
These three diseases talk to each other. A penetrating ulcer can bleed into the wall and cause an intramural hematoma. An intramural hematoma can re-tear and become a classic dissection. Any of them can rupture. So when you find one, you describe all of it — and you say where it lives.
Why location is the whole ballgame
Just like dissection, where it sits drives everything. Disease involving the ascending aorta (think Stanford type A territory) is the scary one — close to the heart and coronaries, generally pushed toward surgery. Disease confined to the descending aorta (type B territory) is more often managed medically with aggressive blood-pressure control and close imaging follow-up, with intervention reserved for trouble. If that A-versus-B logic feels fuzzy, it's worth a detour through dissection classification, because the same map applies here.
The aorta you scan today is not the aorta you'll scan next week. Both IMH and PAU are dynamic — they can regress, stay put, or progress to dissection or rupture. That's why these patients get follow-up imaging rather than a one-and-done read. Note the maximal aortic diameter and the depth of any ulcer; growth is the thing everyone's watching for.
How you actually catch it
The workup is the same reflex as for any acute aortic syndrome: ECG-gated CT angiography of the chest, abdomen, and pelvis. The gating freezes the pulsing aortic root so a normal motion blur doesn't get over-called as a flap.
One detail that earns its keep: get a non-contrast series first. A fresh intramural hematoma is bright on non-contrast and can vanish into the opacified lumen once contrast goes in. Skip the pre-contrast images and a subtle IMH can hide in plain sight.
| Feature | Intramural hematoma | Penetrating ulcer | Classic dissection |
|---|---|---|---|
| Intimal flap | Absent | Absent (focal defect only) | Present |
| Flowing false lumen | Absent | Absent | Present |
| Hallmark | Crescent wall thickening, non-enhancing | Contrast-filled crater beyond lumen | True + false lumen separated by flap |
| Background | Variable | Heavy atherosclerosis | Variable |
So: no flap doesn't mean no emergency. If you see a smooth high-density crescent in the wall, think IMH. If you see a contrast crater clawing out past the lumen through nasty plaque, think PAU. Then look at the ascending aorta, measure the diameter, and pick up the phone — because these quiet cousins can turn into the loud one (dissection or rupture) without much warning.