Teaching Case

A 75-year-old male patient arrived complaining of breathlessness and chest pain. He was on medication and had a documented diagnosis of chronic obstructive pulmonary disease and CKD. Saturation in room air was 80%, and on oxygen, it was 98%. A contrast-enhanced CT thorax with angiography was performed.

Irregular atherosclerotic wall thickening of the descending thoracic aorta was noted.

Saccular aneurysmal dilatation was seen in the descending thoracic aorta below the level of the carina for a length of 6.5 cm. The aneurysm showed a mural crescentic thrombus of 4 cm thickness (Figure 1). An irregular contrast leak was seen extending from the lumen into the thrombus (thrombus fissuration sign), suggesting an impending rupture (Figures 2a and 2b).

A focal thinning of the wall of the arch of aorta with a contrast-filled outpouching was noted as suggestive of a focal penetrating atherosclerotic ulcer (Figure 3).

Panacinar emphysematous changes were seen in bilateral lung parenchyma (Figure 4).

Mild bronchiectasis changes with fibrotic bands were seen involving the left upper lobe, right middle lobe, and bilateral lower lobes.

Background

An aneurysm is defined as a permanent dilatation of the aorta exceeding the normal measurements by more than 2 SDs at a given anatomical level [1]. A diameter equalling or exceeding 1.5 times the expected normal diameter is considered an aneurysm.

Atherosclerosis is the most common cause of aneurysm [1], followed by chronic hypertension.

Male gender, increased age, hypertensive history, chronic obstructive pulmonary disease (COPD), coronary artery disease, smoking, and previous aortic dissection are risk factors for aneurysm [2]. The pooled incidence and prevalence of thoracic aortic aneurysms (TAAs) were 5.3 per 100,000 individuals per year and 1.6 per 100 individuals, respectively [3].

Aneurysm pathophysiology involves both biochemical and mechanical factors. Chronic diseases like hypertension lead to structural weakening of the arterial walls and are often exacerbated by genetic predispositions. The release of proteolytic and inflammatory mediators leads to further wall weakness and expansion. Endothelial dysfunction and matrix degradation with haemodynamic stress contribute to arterial remodelling. These cascades culminate in the progressive dilation of aneurysms [1,2].

Clinical Perspective

Most of the patients with TAA are asymptomatic. They may present with chest pain [4]. Sudden chest pain with hypotension should alarm the rupture of the aneurysm. Compression of adjacent structures leads to different symptoms, like SVC syndrome or hoarseness of voice [2].

Imaging Perspective

The CT angiogram is the investigation of choice for evaluating aneurysms because of its excellent multiplanar reformatting and non-invasiveness, which allow for a comprehensive evaluation [5]. Other modalities include MR angiography, transthoracic echocardiography, and transesophageal echocardiography. The size, shape, luminal diameter, and vessel diameters proximal and distal to the aneurysm and its relation to vessel branches should all be outlined in the description of the aneurysm. Wall characteristics like atheromatous changes or intramural thrombus should also be included. Involved complications should also be described [6].

Mild to moderate cases are managed conservatively, which includes control of hypertension. Cases with severe dilatation or impending rupture are treated with endovascular graft repair. In the event of a rupture, immediate surgery should be done [6,7]. CT/MRI plays a crucial role in deciding management.

Outcome

The patient was admitted to the ICU, and surgery was planned once the patient’s general condition improved. However, due to multiple comorbidities, the patient succumbed to death 2 hours after admission.

Take Home Message

TAA should be identified and managed at an early stage to minimise complications. Coordination among emergency medicine, cardiology, radiology, and cardiac surgery is vital to treat patients with a thoracic aortic aneurysm.

All patient data have been completely anonymised throughout the entire manuscript and related files.