Intramural collection caused by contrast extravasation into the ascending aortic wall

Abstract

Cardiac catheterization is a procedure routinely performed worldwide, with an estimated amount of 61 000 coronary angioplasties performed in the UK annually. Associated mortality—in the region of 0.1–0.2%—is minimal and complication rate approximately 1.5%. The most serious complications described are embolic stroke, cardiac chamber perforation, aortic dissection, coronary occlusions or dissection, and major peripheral vascular complications, including retroperitoneal haematoma and life-threatening haemorrhage. We report the case of a 75-year old patient who had inadvertent contrast agent injection into the aortic wall, leading to a localized contrast collection within the tunica media. This complication has been described before but only in association with coronary artery dissection. It is important to diagnose and manage such a situation, as most iodinated intravascular contrast agents exert a high osmotic load and thereby lead to tissue oedema and necrosis on extravasation. We describe the management of the case and discuss relevant therapeutic strategies.

INTRODUCTION

Cardiac catheterization is routinely performed in hospitals worldwide, with an overall associated mortality rate of 0.1–0.2% and a complication rate of 0.8–1.8% [1]. Inadvertent injection of contrast agent into the peripheral vessel’s entry site is a rare complication of angiogram that usually subsides spontaneously. Other serious complications include stroke, cardiac chamber perforation, dissection or occlusion of coronary artery and dissection or haematoma of peripheral vessels used in cannulation [1].

In this case, we present acute aortic syndrome that developed as a result of cardiac catheterization. Inadvertent injection of contrast directly into the aortic wall, as a complication of cardiac catheterization, is a rare event. Acute aortic syndrome is defined as a spectrum of aortic pathologies, ranging from penetrating aortic ulcers and intramural haematoma (IMH) to aortic dissection. Intramural aortic haematoma is defined as haemorrhagic collection within the aortic media, without a visible intimal tear, thought to be due to rupture of the vaso vasorum [2]. It is, however, possible for an intimal entry tear to occur, which leaks slowly into the media but cannot be visualized using the static imaging techniques that are routinely employed in the clinical diagnosis of acute aortic syndrome (i.e. computed tomography). Similarly, in this case an intramural contrast collection in the tunica media of the ascending aortic wall might resemble IMH pathologically.

CASE REPORT

A 75-year old female patient presented to the cardiology department at a local hospital for an elective angiogram to investigate anginal symptoms. Past medical history included diabetes mellitus, hypertension, chronic renal failure and osteoporosis.

During the coronary angiogram, contrast agent was inadvertently injected into the aorta during right coronary cannulation, leading to a localized contrast collection in the aortic wall (Supplementary Video 1). The patient complained of immediate ‘tearing’ chest pain, radiating through to her back, and the procedure was abandoned. Computed tomography (CT) showed a dense contrast in the anterior wall of the ascending aorta, from aortic valve to mid-portion of the ascending aorta (Figure 1). The patient was transferred to a specialist centre for management of the iatrogenic acute aortic syndrome.

Supplementary Video 1: Right coronary angiogram demonstrating the aortic wall intramural contrast collection.

Figure 1:

(a and b) Coronal and sagittal contrast CT scan demonstrating the ‘contrast cap’ in the ascending aorta.

The pain subsided within six hours and blood pressure was well controlled with oral beta-blockers. The patient was observed in hospital for five days, when a cardiac magnetic resonance imaging (MRI) scan demonstrated no significant change in aortic diameter, with improvement of the contrast collection. The patient was discharged and remains well at three-month follow-up.

DISCUSSION

This case demonstrates a rare complication of coronary angiography, where inadvertent contrast injection into the ascending root may mimic IMH, causing acute aortic syndrome. However, the situation was further complicated in this case as ULTRAVIST^® 300 (iopromide) (Bayer, Germany), the intravenous iodinated contrast agent used, exerts a high osmotic load. In cases of extravasation into tissue, the contrast agent draws water into the region, leading to local tissue oedema and consequent weakening of the aortic wall. Tissue extravasation of contrast agent has been well known to cause necrosis and/or compartment syndrome, particularly in patients with severe arterial or venous disease. It has a main elimination phase of 2 hours (97% elimination) and a terminal elimination phase with a half-life of 6.2 hours for the remaining 3%. The majority is excreted renally and only 3% in faecal matter. The consequences of inadvertent contrast injections into the ascending aortic wall have not previously been established.

Guidance on management of this case was difficult and we treated the patient as if she had a type A IMH. The clinical course of IMH is variable and it has been estimated that approximately 33% will progress to classical aortic dissection [2]. In addition, mortality associated with proximal IMH is higher than that of distal lesions. The management of IMH can be conservative, with aggressive pharmacological control of blood pressure and close surveillance or surgical replacement of the affected aortic segment. In some cases, spontaneous resolution of IMH has been reported: however, in 57% of cases during the surveillance period, ‘ulcer-like projections’ develop on the intima and these can progress to aortic dissection [3, 4]. It is also hypothesized that IMH could lead to weakening of the aortic wall and a consequent predisposition to aortic aneurysm [5].

IMH accounts for 17% of all dissections, while this condition is found in 4–13% of autopsy studies [3, 7]. The 30-day mortality of IMH is 24% (36% with type A and 12% with type B IMH; P <0.05) [3, 5]. The 30-day mortality of type A IMH is 14% for patients treated surgically and 36% for patients treated medically (P = 0.02) [3, 5]. Survival at 1, 2, 3, 5 and 10 years was, respectively, 81 ± 21%, 87 ± 8%, 83 ± 6%, 65 ± 22% and 44 ± 14%. However, type B IMH had favourable outcomes with medical treatment, with 8% mortality [3, 5]. It is believed that symptomatic patients and those with rapid progression on imaging or overt dissection during follow-up need emergency surgery. An ascending aortic diameter of >50 mm or sub-adventitial haematoma thickness of >12 mm should be considered as candidates for early surgery [5]. Although IMH has an improved prognosis over aortic dissection, survivors of IMH are at significant risk of progressive aortic pathological abnormalities. These include aortic rupture, aneurysm and ulceration.

Broadly applying the available literature to this complication, we conclude that patients who remain symptomatic, have evidence of aortic dilatation, wall thinning, development of an ulcer or suggestion of Herald dissection should undergo surgical treatment involving open distal replacement of the ascending aorta. This might results in lower mortality and longer survival, compared to conservative management. However, IMH/contrast collection without the above-mentioned features in the ascending aorta—or if affecting the descending aorta—could be managed with medical treatment, or with endovascular grafting in cases of visceral branch vessel occlusion. In either case, serial imaging of the aorta is recommended, as aneurysm formation is not uncommon and imaging informs the clinician of rapidly changing, underlying disease pathology.

Supplementary material

Supplementary material (Video 1) is available at ICVTS online.

Conflicts of interest: none declared.