British Journal of Radiology (2007) 80, e75-e77
© 2007 British Institute of Radiology
doi: 10.1259/bjr/26948582
Acute ventricular and aortic thrombosis post chemotherapy
J F Morlese, FRCR
T Jeswani, FRCR, MRCS
I Beal, FRCR
P Wylie, MRCS
and
J Bell, FRCR
Royal Free Hospital, Pond Street, London, UK
Correspondence: Dr James Bell, Royal Free Hospital, 10 Pond Street, London NW3 2QG, UK. E-mail: james.bell{at}royalfree.nhs.uk
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Abstract
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We present a rare case of spontaneous arterial thrombosis in a 42-year-old male with an acute history of bilateral lower limb pain and weakness. The previous day he had received the first cycle of cisplatin-based chemotherapy for oesophageal adenocarcinoma (T2/3N0/M0). Computed tomography (CT) and angiography showed extensive abdominal aortic thrombus in a native non-aneurysmal or grossly atheromatous aorta with separate thrombus in the left ventricle. We suggest that poor left ventricular function, a hypercoaguable state secondary to malignancy and cisplatin based chemotherapy may have induced severe arterial and intra-cardiac thrombosis.
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Case report
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A 42-year-old man presented to the Accident and Emergency Department with a 12 h history of bilateral lower limb pain and weakness. The previous day he had received the first cycle of intravenous cisplatin and 5-fluorouracil as part of a pre-operative chemotherapy regimen for oesophageal adenocarcinoma (T2/3N0/M0). 3 weeks previously he had been diagnosed with adenocarcinoma of the distal oesophagus after an oesophago-gastro-duodenoscopy (OGD) revealed a malignant stricture 40 cm from the incisors. There had been a 3 month history of progressive dysphagia with 20 kg weight loss. The staging CT chest and abdomen was unremarkable apart from showing distal oesophageal wall thickening with a few subcentimetre lymph nodes in the subcarinal region and adjacent to the lesser curve of the stomach. A staging fluorodeoxyglucose positron emission tomography (FDG-PET) scan demonstrated the primary lesion and also an area of possible increased uptake in the left lung apex and cervical chain. Cervical node biopsies were negative for tumour. A review of the CT chest did not reveal a left apical lesion suggesting that the FDG-PET abnormality was a false positive.
On examination, he was afebrile and had a pulse rate of 80 beats min–1 and a blood pressure of 120/80 mmHg. Both lower limbs were pale, cold and pulseless. The femoral, popliteal and foot pulses were impalpable. There was bilateral paraesthesia from the mid-calves distally. His abdominal examination was unremarkable. An expansile mass was not palpated.
Initial investigations revealed a haemoglobin level of 12 g dl–1, white blood cell count of 10.0x109 cells l–1. The chest radiograph was unremarkable. The electrocardiogram excluded acute cardiac disease. A clinical diagnosis of acute aortic thromboembolism was made. Emergency CT (Toshiba Asteion multislice CT scanner; Toshiba, Tokyo, Japan) imaging of his chest, abdomen and pelvis was performed using the following parameters: 120 kVp, 200 mA, scan time of 0.75 s, 3 mm/1.5 mm section collimation and 100 ml of Omnipaque 300 (Amersham Health, Little Chalfont, UK) injected at a rate of 5 ml s–1. A large thrombus was identified in the abdominal aorta, beginning in the mid-aorta, just superior to the origin of the renal arteries, and continuing distally into both common iliac vessels and involving the ostia of the inferior mesenteric artery. A small thrombus was also seen in the left ventricle. There was no evidence of atherosclerotic disease or aneurysmal dilatation of the aorta or common iliac arteries. The original pre-chemotherapy staging scan showed a normal aorta at the origin of the renal arteries. Figure 1
, obtained during the acute admission post chemotherapy, shows thrombus within the mid-abdominal aorta with multiple bilateral renal infarcts. The superior mesenteric and splenic arteries were seen to be patent. A therapeutic dose intravenous infusion of heparin was commenced.
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Figure 1. (a) Post-chemotherapy CT at the level of the mid-abdominal aorta demonstrating intraluminal aortic thrombus and multiple bilateral renal infarcts. (b) Post-chemotherapy CT at the level of the common iliac arteries showing the extent of thrombosis.
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The patient was transferred immediately to a nearby vascular centre where an emergency transbrachial angiogram was performed, which revealed a large saddle-like filling defect in the aorta and both common iliac arteries. Although this could have represented embolic material, it was subjectively judged to be thrombus due to its texture at angiography. There were also emboli in both renal, internal iliac and profunda arteries (Figure 2). Interestingly, the superior mesenteric and splenic arteries were not patent. This discrepancy with the findings on CT may possibly be related to the time delay between the two tests. A surgical embolectomy and bilateral lower limb fasciotomies were successfully performed. The patient was transferred to the intensive treatment unit (ITU) where he had an echocardiogram. This revealed a globally impaired systolic function with an estimated left ventricular ejection fraction of 35% but normal diastolic function. A sessile 1.6 cmx1.6 cm thrombus attached to the apex of the left ventricle was found. In addition, there was a small pedunculated mobile thrombus on the apical segment of the inferior wall of the left ventricle. The left atrium was not dilated but there was mild secondary mitral regurgitation noted. The valves and right heart were normal.
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Figure 2. Aortofemoral angiogram showing thrombus within the mid-abdominal aorta and both common iliac arteries.
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The patient's post-operative course was complicated by sepsis, severe rhabdomyolysis and acute renal failure requiring haemodialysis. He subsequently developed an acute abdomen and died 7 days after admission due to small bowel infarction.
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Discussion
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Chemotherapy agents have been documented as possible causes of acute arterial thrombosis [1, 2]. The majority of cases have been seen in patients with pre-existing peripheral vascular disease [3]. In addition to peripheral arterial thrombosis, cases have been reported of localized aortic thrombosis secondary to cisplatin therapy [1]. Many reasons for this have been postulated. Patients with cancer are considered to be hypercoagulable and therefore at an increased risk of thrombosis especially in the low flow venous system. Licciardello and colleagues have reported that cisplatin-induced increases in von Willebrand factor concentrations increase the risk of arterial occlusive complications [4].
<1?tlsb=-.02w?>Acute abdominal aortic thrombosis is very rare [5]. Strong risk factors include the presence of an abdominal aortic aneurysm (AAA), cardiac disease and atherosclerosis [6]. It can present with limb paralysis delaying the diagnosis whilst neurological causes are excluded [7]. There is a high mortality especially in patients with poor left ventricular function, as with our case [6]. Prompt diagnosis and treatment is a strong factor in determining recovery [7].
Our patient was unique. He was young and previously fit and well prior to the diagnosis of oesophageal adenocarcinoma. He had a native non-aneurysmal aorta and no history of cardiac disease, yet presented not only with extensive arterial thrombosis but also a separate concurrent left ventricle thrombus. We suggest that a number of factors may have combined to cause this. With a recent history of dysphagia, dehydration may have contributed to the hypercoagulable state induced by the underlying oesophageal adenocarcinoma. Cisplatin and 5-FU therapy 1 day prior may also have contributed to the thrombosis. Both cisplatin and 5-FU have been linked with cardiac and arterial thromboembolic disease and shown to reduce left ventricular function [8–10]. The degree of thrombosis is more extensive than previously documented in the literature. It is possible that the additive effects of 5-FU and cisplatin may have increased the risks of thromboembolism. Our patient was diagnosed and treated rapidly (within 7 h) giving the best chance of a favourable outcome. The importance of systematic investigation for arterial thrombosis is emphasised by the increasing number of reports describing this phenomenon post chemotherapy [11].
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Conclusion
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Aortic thrombosis is a rare cause of limb paralysis. The diagnosis must be considered especially in patients in a hypercoagulable state and post cisplatin or 5-FU based chemotherapy, even in previously fit and well young individuals. Chemotherapeutic agents have been implicated as risk factors for thromboembolic disease. The degree of thrombosis can be variable and we present a case of previously unreported extensive thrombosis within the left ventricle and abdominal aorta. All radiologists involved in the care of oncology patients should be aware of this rare but potentially fatal condition as prompt diagnosis and therapy increases the chances of a favourable outcome.
Received for publication February 8, 2005.
Revision received May 24, 2005.
Accepted for publication June 27, 2005.
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References
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Abstract
Case report
