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Postgrad Med J 88:729-730 doi:10.1136/postgradmedj-2012-131008
  • Images in medicine

An octogenarian with painless type A aortic dissection and cardiac tamponade

  1. Victor Chao3
  1. 1Department of Cardiovascular Medicine, National Heart Centre Singapore, Singapore
  2. 2Department of Pathology, Singapore General Hospital, Singapore
  3. 3Department of Cardiothoracic Surgery, National Heart Centre Singapore, Singapore
  1. Correspondence to Dr Calvin Woon-Loong Chin, Mistri Wing, 17 Third Hospital Avenue, Singapore 168752, Singapore; cchin03m{at}gmail.com
  1. Contributors All the authors contribute equally to the preparation of the manuscript. The histopathology slide was prepared by S-HL. CC and NK wrote the manuscript which was also reviewed by all the authors before submission.

Introduction

Painless aortic dissection (AD) has a reported prevalence of 6.4% and occur more commonly in older patients.1 They carry a worse prognosis compared with patients with painful AD. In patients with type A AD (TAAD), cardiac tamponade is the leading cause of death.

We describe an octogenarian with painless TAAD and cardiac tamponade. The pathophysiology contributing to the findings on CT and histology will be discussed.

Case presentation

An 80-year-old woman complained of abdominal colic, which worsened 2 days before admission. She had no chest pain and was haemodynamically stable during admission.

Initial investigations including an abdominal CT suggested biliary colic from cholelithiasis. Incidentally, a moderate-sized pericardial effusion was also seen. Subsequently, a contrast-enhanced CT thorax demonstrated an enhancing saccular outpouching at the aortic arch and intramural haematoma extending into the pericardium. No dissection flap or a false lumen was seen (figure 1).

Figure 1

Coronal (A) and axial (B) contrast-enhanced CT scans of the thorax show circumferential non-enhancement surrounding the aortic lumen and in the pericardium. The entry site (*) was identified at the aortic arch proximal to the subclavian artery.

Initially the patient was managed conservatively, but agreed to surgery after a transthoracic echocardiogram showed worsening haemopericardium 2 days later (9 days post-hospitalisation). An ascending aorta and arch replacement was performed successfully and the patient was discharged 2 weeks post-surgery.

Discussion

The diagnosis of a true TAAD was confirmed intra-operatively. The intimal tear was located at the aortic arch. The false lumen was thrombosed and pericardium contained stale blood. Microscopic examination revealed dissection along the outer third of the tunica media. There was no plaque ulceration, or any evidence of cystic medial degeneration (figure 2).

Figure 2

Montage of various stains performed on aortic wall fragments. The dissection occurred within the outer aspect of the tunica media. This is associated with secondary haematoma (arrow) from the dissection and adventitial fibrosis (*) that is walling the haematoma. There were mild atheromatous plaques on the intima but no ulceration was seen. No cystic medial degeneration or vasculitis was demonstrated (A, H&E; B, Elastic van Giesen; C, Martius Scarlet Blue; D, Masson's Trichrome).

The presence of an intimomedial flap is pathognomonic of an AD on a contrast-enhanced CT, and helical CT has an overall sensitivity of 100% and specificity of 98% in diagnosing an AD.2 However, as illustrated in the case, insufficient contrast flow in the false lumen precludes the detection of a dissection flap. In patients with suspected AD, a non-enhanced CT should be performed first. The thrombosed false lumen or a contained haematoma without intimal tear (intramural haematoma) will attenuate with a non-enhanced CT.

Emergency surgery in older patients with TAAD, especially if presented beyond 48 h, is controversial. The operative mortality risk exceeds 40% in these patients.3 Besides, the long-term survival whether surgically or medically managed is nearly identical after the initial post-dissection period.4 Therefore, initial medical stabilisation can be considered in stable patients who presented late but this must be guided by the evolution of complications and haemodynamic changes.

As illustrated, some patients with TAAD and haemopericardium are stable haemodynamically. The seal from the flap or thrombus in the false lumen slows bleeding. Furthermore, the tamponade reduces the pressure gradient between the false lumen and pericardium. However, pericardiocentesis disrupts this pressure gradient, leading to rapid haemodynamic deterioration.

Our patient had an unusual presentation of a complicated TAAD. There was clear evidence of an intimal tear although the contrast-enhanced CT did not reveal a dissection flap because of the thrombosed false lumen and the lack of a re-entrance tear. Importantly, a non-enhanced CT would be helpful and should be performed first in patients with suspected AD.

Footnotes

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

References