CT diagnosis and destiny of acute aortic intramural hematoma

Abstract

Acute aortic intramural hematoma (IMH) is a relatively uncommon but potentially life-threatening aortic disease that can occur primarily in hypertensive and atherosclerotic patients. The course of IMH varies widely, with the condition either regressing, remaining stable, or progressing until it leads to outward rupture or intimal layer disruption, eventually resulting in overt aortic dissection. Therefore, poor prognostic computed tomography (CT) features must be promptly recognized and reported by the radiologist. In emergency departments, readily accessible non-invasive CT angiography is crucial for achieving a rapid and accurate diagnosis essential for appropriate management. For Type A and B aortic dissection, surgery is typically recommended in Western countries for patients with Stanford Type A IMH and those experiencing irrepressible pain. For Stanford Type B IMH patients without complications or incessant pain, medical treatment is suggested but with imaging follow-up. In complicated Stanford Type B situations, thoracic endovascular aortic repair (TEVAR) is currently indicated. This review aims to present pathophysiology, CT diagnosis, and IMH fate and provide the reader CT image-based review of the CT diagnostic criteria, complications, and associated critical prognostic findings of this rather rare aortic disease.

Keywords: acute aortic syndrome (AAS); aortic dissection (AD); aortic intramural hematoma; computed tomography angiography (CTA); diagnosis; penetrating atherosclerotic ulcer (PAU).

Figure 1

Iatrogenic intramural hematoma (IMH). Computed tomography (CT) axial scans. (A) Right intercostal active bleeding after lung biopsy (thin arrow). (B) Axial CT performed for chest pain 1 day after the intercostal artery transcatheter embolization procedure shows the appearance of hyperattenuated aortic wall thickening from IMH with (C) displacement of intimal calcification and bronchial artery in the contest of the Type B IMH. (D) No more active bleeding in the site of embolization (thick arrow).

Figure 2

Infected endocarditis in a 65-year-old male patient with aortic bioprosthetic valved conduit. (A) A non-enhanced axial CT scan shows a hyperattenuating aortic prosthetic wall (arrowheads). (B) Thickening of prosthetic valvular leaflets with endocarditis vegetation (arrowhead) and (C) a 3D volume rendering reconstruction showing distal graft aortic anastomosis (arrow).

Figure 3

Non-contrast CT axial image in a 73-year-old female patient shows the diagnostic hallmark of IMH: displacement of intimal calcifications and hyperattenuating crescentic thickening of the aortic wall (arrowheads).

Figure 4

CT scan in a 62-year-old male patient with acute chest pain and Type B IMH. (A) Axial non-enhanced CT image shows hyperattenuating crescentic thickening of the aortic wall (arrow). (B) Axial contrast-enhanced CT scan shows a reduced diameter of the aortic lumen and the slick interface between the lumen and wall. (C) Contrast-enhanced sagittal multiplanar reformation CT image shows a reduced diameter of the aortic lumen and its constant circumferential relationship with the wall.

Figure 5

(A) Coronal multiplanar reformation CT in subacute Type B IMH (arrowheads). (B,C) One-month CT follow-up shows the appearance of an ulcer-like projection (ULP) treated (D) with thoracic endovascular aortic repair (TEVAR) (arrowheads).

Figure 6

Longitudinal CT imaging of IMH evolving patterns. IMH is a vulnerable dynamic condition, with unpredictable late fate (16, 18, 57, 61).

Figure 7

Maximal IMH thickness and pericardial effusion as poor prognostic factors in a 68-year-old male patient with acute back pain and dyspnea. (A) Axial contrast-enhanced CT scan shows a Stanford Type A IMH with hematoma thickness >10 mm (white arrow). (B) Axial contrast-enhanced CT image shows hemorrhagic pericardial effusion (asterisk) and mass effect (black arrow) on the right atrium suggesting impending cardiac tamponade.

Figure 8

Temporal evolution of unstable Type B IMH. Initial unenhanced scan (A) and contrast-enhanced axial (B) and sagittal (C) CT images showing a Type B IMH with tiny intimal erosion of the descending aorta (white arrows). Four-day follow-up unenhanced scan (D) and contrast-enhanced axial (E) and sagittal (F) CT images at the same level showing enlargement of the intimal defect and enhancing ULP with neck >3 mm from the aortic lumen into the hematoma (white arrows), indicative of overt intimal tear and impending dissection.

Figure 9

Unstable Type B IMH. (A) Sagittal contrast-enhanced baseline CT shows Type B IMH (arrowheads) in a 68-year-old male patient with hypertension peak and persistent thoracoabdominal pain; pleural effusion is present (asterisk). (B) Six-day follow-up contrast-enhanced CT sagittal multiplanar reformation shows the appearance of an ULP close to the aortic isthmus (arrow). (C) Sagittal oblique 3D volume rendering (VR) reconstruction confirms ULP (arrow). The patient undergoes TEVAR.

Figure 10

Intramural blood pool (IBP) in a 61-year-old patient with systemic hypertension and Type B thoracoabdominal IMH and acute back pain. (A) Axial CT maximum intensity projection (MIP) reconstruction image shows a T9 level intercostal artery pseudoaneurysm (arrow) in the contest of the Type B IMH with absent communication with the true aortic lumen. (B) Enhanced CT axial image obtained 3 months later shows a partial IBP and IMH regression (arrowheads).

Figure 11

PET/CT in aortitis. (A) Axial PET/CT fusion image in a 68-year-old male patient with diffuse aortitis showing an [18F]-fluorodeoxyglucose (FDG) uptake in the thoracoabdominal aortic wall (arrow). (B) Sagittal multiplanar reconstruction CT image acquired in the portal phase shows thickened aortic wall enhancement. In a different 70-year-old female patient with giant cell arteritis, arterial-phase CT scan (C) shows thickening of the descending aortic wall mimicking an IMH (arrow), and venous phase CT image (D) shows enhancement of thickened aortic wall (arrow). (E) Axial PET/CT fusion image in the same patient shows FDG uptake of the descending aorta wall (arrowheads).