Author(s)

Savastano S, Dall’Acqua J, Beghetto M, Dal Borgo D, Giacomini D, Giorgi B

Department of Radiology, Ospedale S. Bortolo, Vicenza, Italy.

Patient

male, 69 year(s)

A 69-year-old man with long-lasting hypertension and sudden onset of upper back pain.

A 69-year-old man presented with sudden onset of upper back pain, referred to as “stabbing”. The patient had history of a long-lasting hypertension; ECG and laboratory tests excluded a myocardial infarction. Physical examination did not evidence pulse deficit. The multidetector computed tomography (MDCT) evidenced elongation and mild dilatation of descending thoracic aorta, whose wall showed a crescent thickening displacing intimal calcifications; the aortic wall thickening was hyperattenuating on non-enhanced scans and did not enhance after intravenous contrast medium administration (Fig. 1, 2). No intimal tear of the descending aorta was evident on thin-slice scans, retrospectively reconstructed; walls of the ascending aorta and the aortic arch were not thickened. A diagnosis of a type B- intramural haematoma (IMH) was then accomplished on the basis of CT findings. The patient was treated with medical therapy and symptoms relieved as arterial blood pressure normalised. A MR-angiography, performed after a few days, confirmed the absence of intimal tear (Fig. 3). The patient was discharged with medical therapy but, after one month, he complained of a new episode of upper back pain. A prompt contrast enhanced MDCT detected three intimal ruptures of the descending aorta, one distal to the origin of the left subclavian artery and two along the lateral wall of the middle third and the lower third of the descending aorta (Fig. 4, 5). An endovascular treatment was then undertaken and successfully accomplished.

Acute aortic syndrome (AAS) encompasses a spectrum of abnormalities of the thoracic aorta sharing clinical presentations, outcome and therapeutic strategies. It includes aortic dissection, IMH, subtle dissection as found in Marfan syndrome, penetrating ulcer, iatrogenic or traumatic lesion and, in some instances, symptomatic aortic aneurysms. IMH is responsible of 6-10% of AAS in Western countries, and up to 40 % of cases in Asian patients.
Diagnosis of IMH relies on typical CT or MRI findings: round or crescent thickening of the aortic wall, displacement of intimal calcifications; in early phases the IMH is hyperattenuating on non-enhanced CT scans and hyperintense on T2 weighted images on MRI.
As prognosis and treatment depend on the aortic segment involved, IMH of the thoracic aorta is divided into type A and Type B, according to the Stanford classification of dissection.
IMH can rarely spontaneously reabsorb, or can progress towards a dissection, an aneurysmal development or a contained rupture.
Persistent pain and presence of a penetrating ulcer are negative predictors; younger age, an aortic diameter less than 4 cm and an intramural haematoma thickness less than 1 cm are more favourable prognostic indexes.
If a conservative therapy is initially considered in patients with type B IMH, a close CT follow-up is mandatory for an early diagnosis and a prompt treatment of complications.