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Inflammatory Bowel Disease-Related Thoracic Aortic Thrombosis

Inflammatory Bowel Disease-Related Thoracic Aortic Thrombosis

Bargen was the first person to report inflammatory bowel disease-related thromboembolic complications In 1936. A case of acute limb ischemia secondary to unprecedented thoracic aortic thromboembolism during active episode of ulcerative colitis (UC) is reported in this article.

Clinical studies have quoted that the incidence of these events range from 0.7 to 7.5 % of inflammatory bowel disease (IBD) patients. While about 7.6 % of thromboembolic incidents were reported to involve peripheral arterial complications, which include aortic mural thrombi, coronary and mesenteric artery thrombosis accounted for about 27 % of the cases, which are some of the remaining arterial thromboses.


Case Report

After 4-6 weeks of abdominal cramps and bloody diarrhea, including 12-20 bowel movements/day, a white man who was 63 years old was hospitalized for intravenous steroids. When he was admitted, the initial exam showed that he was an afebrile, nondistressed and normotensive patient, and his physical exam was normal, with nontender abdomen and good (2+) distal extremity pulses bilaterally. The data that came from laboratory showed that he had normal electrolytes, creatinine, cholesterol (138 mg/dL), liver enzymes, and partial thromboplastin time/international normalized ratio (PTT/INR) values (26.9 sec, 1.0), however he had mild anemia, meaning that his Hemoglobin was 13.2 g/dL. He was placed on intravenous methylprednisolone (30 mg every 8 hours), in addition to enoxaparin (40 mg daily) for deep venous thrombosis prophylaxis. Bowel movements didn’t change significantly after six days of intravenous steroids; at that point, mesalamine suppositories (1000 mg twice daily) were included in the treatment, but there was no major change. In the course of that day, the patient’s left calf and foot started suddenly to be painful. A cool, pale, and dusky foot with weak femoral pulse was revealed in the physical examination, and there were no palpable/dopperable dorsalis pedis, posterior tibial, or popliteal pulses. Acute thrombus in the common femoral, profunda, superficial femoral, popliteal, anterior tibial, and posterior tibial arteries, were revealed by the immediate diagnostic angiography, which was needed after a diagnosis of acute left lower extremity ischemia. Palpable dorsalis pedis and posterior tibial pulses was the result of the successful performing of iliofemoral, profunda, popliteal, and tibial thromboembolectomy. Then heparin infusion was started, which didn't make gastrointestinal bleeding worse.


Hypercoagulable testing was included in evaluation of the thromboembolic source, and it was predominantly negative. In ruling out a cardiac embolic source, sinus rhythm was normal in the electrocardiogram, and the rhythm was regular without any murmurs in auscultation. Transthoracic echocardiography was normal and telemetry didn’t detect any episodes of arrhythmias. But there was an echodensity in the distal transverse aortic arch (1.9 × 0.9 cm) consistent with thrombus, which was revealed in the transesophageal echocardiography and computed tomography (CT) angiography of the chest. (Figures 1 and 2).


Figure 1.
Transesophageal echocardiogram (TEE) revealing aortic arch thrombus. There is a mobile echodensity measuring 1.9 × 0.9 cm attached to the posterior wall of the distal transverse arch consistent with thrombus.


Figure 2.
This is a CT of chest revealing thrombus. There’s an iregular mass in the aortic arch measuring 1.3 × 0.7 × 0.6 cm with a narrow base of attachment to the inferior aspect of the aortic arch. The underlying aortic wall seems unremarkable. Appearances are most consistent with thrombus.


During hospitalization, the UC symptoms didn’t improve. The patient chose to undergo total abdominal colectomy with end ileostomy versus medical therapy with infliximab, after two weeks of the embolectomy. Twelve hours after surgery, heparin infusion was resumed, and it was followed by warfarin therapy. After another ten days, the patient was discharged, and he had to undergo six months of warfarin therapy. Resolution of the aortic thrombus and substantial improvement of rectosigmoid inflammation were shown in the repeat CT chest/abdomen that were done in the follow up. Then, warfarin therapy was stopped and aspirin (81 mg/day) was started.


Figure 3.
This is a CT of the patient’s chest after 6 months. There has been interval resolution of the irregular mass in the aortic arch. The course is most consistent with a result thrombus.



Aortic mural thrombi can embolize peripherally to the lower extremities and can lead to amputation or even death, as was shown in twelve other cases, all of which involved the abdominal aorta, unlike the case reported in this article, which involves the thoracic aorta. Although the frequency of arterial thrombotic events is relatively low, but they are in the third position as cause of death, meaning that they account for about 9% in chronic IBD patients. Up to one third of the cases developed while in remission, even though the majority of thromboembolic events occurred in cases where the disease was active, and it's thought to be triggered by endotoxins. Thrombosis is promoted by certain acquired conditions associated with IBD. Steroid use, immobility, inflammation, surgical procedures, placement of central venous catheters, and thrombocytosis are among these conditions. Some states can be considered risk factors, such as active disease or during complications (abscesses or fistulas), because most of the thromboembolic events occurred in these states, particularly arterial thrombosis. In addition to that, since another observation showed that thromboembolism occurred mostly in Crohn disease patients with colonic disease or in patients with an extensive disease of ulcerative colitis, inflammation of the colon has also been a suggested as a risk factor, as demonstrated in this case.


It is worthwhile mentioning that patients with lower extremity arterial thrombosis should undergo an evaluation for a cardiac embolic source with transthoracic and transesophageal echocardiography, in addition to hypercoagulable testing. Since the occurrence of aortic mural thrombosis is a well-documented complication of IBD and carries a serious risk of death, if cardiac work up does not reveal an obvious etiology, a CT scan of the aorta should be considered. Systemic heparin followed by warfarin is used in anticoagulation that is often conducted in the beginning of the treatment of thromboembolic events. In spite of the fact that it has been reported that transcatheter fibrinolysis may be a viable alternative, but arterial thrombosis is often managed urgently with surgical thrombectomy.


Minimizing acquired thrombotic risk factors should be incorporated whenever possible, as the best treatment is prevention. In addition to controlling disease activity, minimizing the risk factors may start with anticoagulation prophylaxis in hospitalized patients presenting with active disease, except in the cases of patients with profuse bleeding or other contraindications, noting that many of the anti-inflammatory agents used in treating active disease have some antithrombotic properties as well. Complications may have harmful and even killing outcomes, so the awareness for increased risk of thromboembolic events in IBD patients should be raised.


Prepared By: Dr. Mehyar Al-khashroum
Edited By: Miss Araz Kahvedjian

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