"IMH constitutes approximately 5–27% of acute syndrome cases, and is typically seen in elderly, hypertensive patients, with a predilection for the descending aorta. Patients with a Stanford type A IMH are more likely to have a known aortic aneurysm. The mortality rate in both groups is similar to that of aortic dissection."
"Emerging evidence — intimomedial tears: The vasa vasorum hypothesis is increasingly questioned on haemodynamic grounds: the vasa vasorum are low-pressure vessels, and this pressure differential relative to the high-pressure aortic lumen would be expected to limit haemorrhage, making it implausible that vasa vasorum rupture alone could account for significant haemorrhagic thickening of the aortic wall. Multidetector CT and surgical series have identified small intimomedial tears in a variable proportion of IMH cases (58–73% in type A series) 9,20, lending support to the view that a high-pressure communication with the aortic lumen — even a small one — may be the primary driver in many cases. This has led to significant debate about whether these represent true IMH or thrombosed/noncommunicating aortic dissections. Pathological studies suggest vasa vasorum dysfunction is the common denominator, with vasa vasorum rupture and intimomedial tears representing secondary phenomena 9."
"• type A IMH: maximum ascending aortic diameter >48–55 mm"
"• type B IMH: maximum aortic diameter >40–41 mm"
"Greater haematoma thickness decreases the likelihood of complete resorption and increases risk of progression, dissection, need for surgery, and death. Suggested threshold: >10–11 mm (measured on axial images perpendicular to the aortic lumen long axis). Mean IMH thickness >10 mm is associated with significantly increased risk."
"iatrogenic injury, e.g. post-catheterisation, post-cardiac surgery"
"iatrogenic injury, e.g. post-catheterisation, post-cardiac surgery"
"Traditional hypothesis: IMH was historically attributed to spontaneous rupture (rhexis) of the vasa vasorum — small vessels that penetrate the outer half of the aortic media from the adventitia to supply the aortic wall 9. Chronic hypertension causes smooth muscle hypertrophy, vasa vasorum constriction and occlusion, and ischaemic stiffening of the outer media. The resulting elasticity differential creates increased shear stress at the inner/outer medial interface, predisposing to medial haemorrhage 9."
"Emerging evidence — intimomedial tears: The vasa vasorum hypothesis is increasingly questioned on haemodynamic grounds: the vasa vasorum are low-pressure vessels, and this pressure differential relative to the high-pressure aortic lumen would be expected to limit haemorrhage, making it implausible that vasa vasorum rupture alone could account for significant haemorrhagic thickening of the aortic wall. Multidetector CT and surgical series have identified small intimomedial tears in a variable proportion of IMH cases (58–73% in type A series) 9,20, lending support to the view that a high-pressure communication with the aortic lumen — even a small one — may be the primary driver in many cases. This has led to significant debate about whether these represent true IMH or thrombosed/noncommunicating aortic dissections. Pathological studies suggest vasa vasorum dysfunction is the common denominator, with vasa vasorum rupture and intimomedial tears representing secondary phenomena 9."
"Key distinguishing concept: Unlike classic aortic dissection — which typically has both an entry tear and a reentry tear — IMH with an intimomedial defect often has only an entry tear. The medial dissection in IMH is located closer to the adventitial side, which may explain why IMH lacks a reentry tear and carries a higher risk of outward rupture 9."
"Traditional hypothesis: IMH was historically attributed to spontaneous rupture (rhexis) of the vasa vasorum — small vessels that penetrate the outer half of the aortic media from the adventitia to supply the aortic wall 9. Chronic hypertension causes smooth muscle hypertrophy, vasa vasorum constriction and occlusion, and ischaemic stiffening of the outer media. The resulting elasticity differential creates increased shear stress at the inner/outer medial interface, predisposing to medial haemorrhage 9."
"Emerging evidence — intimomedial tears: The vasa vasorum hypothesis is increasingly questioned on haemodynamic grounds: the vasa vasorum are low-pressure vessels, and this pressure differential relative to the high-pressure aortic lumen would be expected to limit haemorrhage, making it implausible that vasa vasorum rupture alone could account for significant haemorrhagic thickening of the aortic wall. Multidetector CT and surgical series have identified small intimomedial tears in a variable proportion of IMH cases (58–73% in type A series) 9,20, lending support to the view that a high-pressure communication with the aortic lumen — even a small one — may be the primary driver in many cases. This has led to significant debate about whether these represent true IMH or thrombosed/noncommunicating aortic dissections. Pathological studies suggest vasa vasorum dysfunction is the common denominator, with vasa vasorum rupture and intimomedial tears representing secondary phenomena 9."
"Emerging evidence — intimomedial tears: The vasa vasorum hypothesis is increasingly questioned on haemodynamic grounds: the vasa vasorum are low-pressure vessels, and this pressure differential relative to the high-pressure aortic lumen would be expected to limit haemorrhage, making it implausible that vasa vasorum rupture alone could account for significant haemorrhagic thickening of the aortic wall. Multidetector CT and surgical series have identified small intimomedial tears in a variable proportion of IMH cases (58–73% in type A series) 9,20, lending support to the view that a high-pressure communication with the aortic lumen — even a small one — may be the primary driver in many cases. This has led to significant debate about whether these represent true IMH or thrombosed/noncommunicating aortic dissections. Pathological studies suggest vasa vasorum dysfunction is the common denominator, with vasa vasorum rupture and intimomedial tears representing secondary phenomena 9."
"Emerging evidence — intimomedial tears: The vasa vasorum hypothesis is increasingly questioned on haemodynamic grounds: the vasa vasorum are low-pressure vessels, and this pressure differential relative to the high-pressure aortic lumen would be expected to limit haemorrhage, making it implausible that vasa vasorum rupture alone could account for significant haemorrhagic thickening of the aortic wall. Multidetector CT and surgical series have identified small intimomedial tears in a variable proportion of IMH cases (58–73% in type A series) 9,20, lending support to the view that a high-pressure communication with the aortic lumen — even a small one — may be the primary driver in many cases. This has led to significant debate about whether these represent true IMH or thrombosed/noncommunicating aortic dissections. Pathological studies suggest vasa vasorum dysfunction is the common denominator, with vasa vasorum rupture and intimomedial tears representing secondary phenomena 9."
"Key distinguishing concept: Unlike classic aortic dissection — which typically has both an entry tear and a reentry tear — IMH with an intimomedial defect often has only an entry tear. The medial dissection in IMH is located closer to the adventitial side, which may explain why IMH lacks a reentry tear and carries a higher risk of outward rupture 9."
"Key distinguishing concept: Unlike classic aortic dissection — which typically has both an entry tear and a reentry tear — IMH with an intimomedial defect often has only an entry tear. The medial dissection in IMH is located closer to the adventitial side, which may explain why IMH lacks a reentry tear and carries a higher risk of outward rupture 9."
"Imaging Prognostic Factors — what to report 9"
"• ulcer-like projection: presence, neck diameter (>3 mm = ULP vs 10 mm) carry greatest risk"
"• pericardial effusion — associated with type A IMH and increased risk of progression"
"• pleural effusion — marker of severity"
"• periaortic haematoma — suggests contained rupture"
"Acute and early subacute phase intramural haematomas (approximately the first 2-4 weeks) are visible as crescentic wall-thickening, hyperattenuating (60-70 HU) to blood (35-45 HU) on non-contrast CT (high-attenuation crescent sign). Using a 5 mm slice thickness and a narrow window width e.g. level 40 HU and width 200 HU, will increase sensitivity 6. Attenuation decreases with time, becoming isoattenuating between 4 - 8 weeks and hypoattenuating later. Intimal calcification may be displaced inwards, and this is more conspicuous on the non-contrast CT."
"Traditional hypothesis: IMH was historically attributed to spontaneous rupture (rhexis) of the vasa vasorum — small vessels that penetrate the outer half of the aortic media from the adventitia to supply the aortic wall 9. Chronic hypertension causes smooth muscle hypertrophy, vasa vasorum constriction and occlusion, and ischaemic stiffening of the outer media. The resulting elasticity differential creates increased shear stress at the inner/outer medial interface, predisposing to medial haemorrhage 9."
"Emerging evidence — intimomedial tears: The vasa vasorum hypothesis is increasingly questioned on haemodynamic grounds: the vasa vasorum are low-pressure vessels, and this pressure differential relative to the high-pressure aortic lumen would be expected to limit haemorrhage, making it implausible that vasa vasorum rupture alone could account for significant haemorrhagic thickening of the aortic wall. Multidetector CT and surgical series have identified small intimomedial tears in a variable proportion of IMH cases (58–73% in type A series) 9,20, lending support to the view that a high-pressure communication with the aortic lumen — even a small one — may be the primary driver in many cases. This has led to significant debate about whether these represent true IMH or thrombosed/noncommunicating aortic dissections. Pathological studies suggest vasa vasorum dysfunction is the common denominator, with vasa vasorum rupture and intimomedial tears representing secondary phenomena 9."
"Key distinguishing concept: Unlike classic aortic dissection — which typically has both an entry tear and a reentry tear — IMH with an intimomedial defect often has only an entry tear. The medial dissection in IMH is located closer to the adventitial side, which may explain why IMH lacks a reentry tear and carries a higher risk of outward rupture 9."
"Imaging Prognostic Factors — what to report 9"
"1. Stanford Classification"
"2. Maximum Aortic Diameter"
"3. Maximum IMH Thickness"
"4. Focal Contrast Enhancement"
"5. Effusions"
"6. Compression of True Lumen"
"Acute and early subacute phase intramural haematomas (approximately the first 2-4 weeks) are visible as crescentic wall-thickening, hyperattenuating (60-70 HU) to blood (35-45 HU) on non-contrast CT (high-attenuation crescent sign). Using a 5 mm slice thickness and a narrow window width e.g. level 40 HU and width 200 HU, will increase sensitivity 6. Attenuation decreases with time, becoming isoattenuating between 4 - 8 weeks and hypoattenuating later. Intimal calcification may be displaced inwards, and this is more conspicuous on the non-contrast CT."
"• ulcer-like projection: presence, neck diameter (>3 mm = ULP vs 10 mm) carry greatest risk"
"Conservative management is usually indicated for an intramural haematoma of the descending aorta (Stanford B). In high-risk type B cases, such as those with ulcer-like projections, significant haematoma thickness or large aortic diameters, TEVAR is the recommended treatment 16,27."
"aortitis: typically shows concentric uniform thickening of the aortic wall with or without peri-aortic inflammatory stranding, whereas an intramural haematoma is often eccentric in configuration"
Expected headings
"Associations"
"Classification"
"Echocardiography"
"Signal characteristics"
"The clinical features of IMH are those of acute aortic syndrome: acute severe chest pain (often tearing or ripping in character) radiating to the back, typically in the context of chronic hypertension 2,9. Type A IMH is associated with anterior chest pain; type B with interscapular or back pain."
"IMH is clinically indistinguishable from aortic dissection 9,18. Elevated plasma D-dimer may be seen but is non-specific; it may also indicate extension of existing IMH or evolution towards dissection 16,24."
"The natural history of IMH is highly variable; it may regress, resolve, enlarge, or progress to aneurysm, dissection, or rupture. Multiple imaging features predict adverse outcomes and should be included in every radiology report when IMH is diagnosed:"
"Acute and early subacute phase intramural haematomas (approximately the first 2-4 weeks) are visible as crescentic wall-thickening, hyperattenuating (60-70 HU) to blood (35-45 HU) on non-contrast CT (high-attenuation crescent sign). Using a 5 mm slice thickness and a narrow window width e.g. level 40 HU and width 200 HU, will increase sensitivity 6. Attenuation decreases with time, becoming isoattenuating between 4 - 8 weeks and hypoattenuating later. Intimal calcification may be displaced inwards, and this is more conspicuous on the non-contrast CT."