Tuberculous aortitis

Last revised by Daniel J Bell on 2 Aug 2021

Tuberculous aortitis is a rare cause of aortitis in the context of disseminated tuberculosis. It usually is a result of direct seeding from a contiguous lymph node or via hematogenous or lymphatic spread of distant infection. Fatal outcomes of tuberculous aortitis are commonly reported despite aggressive medical and/or surgical management. Nowadays, however, this condition is rarely seen with the ubiquity of antituberculous chemotherapy.

A rare complication of disseminated tuberculosis, it occurs in less than 1% of patients with latent TB 1.

The aorta is usually not susceptible to infection, however, any underlying abnormality may predispose it to infectious aortitis 2.

Most patients present with systemic symptoms relating to active tuberculosis, rather than to the aortitis itself. Usually, these are constitutional: cough, fever, sweating, weight loss and general malaise.

Whilst tuberculous aortitis can affect any portion of the aorta, the most common segments are the distal aortic arch and descending aorta.

Granulomatous lesions with or without necrosis.

There are no pathognomonic imaging features for aortitis secondary to tuberculosis. It does share features of other aortitides highlighting the importance of marrying the imaging with clinical features. Differentiating between infectious aortitis (including tuberculous) and non-infectious is not always possible on imaging alone, but features such as distribution may prove helpful.

  • mural thickening of the aorta (>2-3 mm)
  • periaortic fluid or soft-tissue accumulation
  • mycotic aneurysm
  • gas in the aortic wall 4

Less coverage of the aorta but is still invaluable in settings where CT is not as readily accessible.

May demonstrate thickening of aortic and branch vessel walls, an echolucent “halo” due to mural edema, and aortic aneurysm.

Contrast-enhanced computed tomography and CT angiography are usually the preferred initial modality for any form of aortitis; they allow characterization of the aortic wall as well as luminal anatomy.

  • concentric wall thickening with or without stenotic regions
  • hypoattenuating wall which enhances post-contrast
  • periaortic fat stranding
  • mycotic aneurysm, if present

Immediate treatment is dictated by whether an associated aneurysm is present or not.

If no concerning aneurysm is present then a course of intravenous broad spectrum antibiotic coverage is advised followed by complete surgical excision. If there is an aneurysm with worrying features then a complete surgical excision of the infected region is performed. Antimicrobial therapy is usually continued many months after surgical intervention to ensure continued coverage for prophylactic stent purposes.

Despite aggressive therapy, mortality associated with tuberculous aortitis remains as high as 60%, this is usually attributed to the high risk of aortic rupture 5.

The most associated complication is of mycotic aneurysm formation which occurs in about half of the cases and is highly prone to rupture 3.

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