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South Med J. 2010;103(2):172-174. © 2010 Lippincott Williams & Wilkins
Abstract and Introduction
Abstract
Arterial and venous thromboembolisms have long been associated with inflammatory bowel disease (IBD) and can cause significant morbidity and mortality. We present a patient with aortic arch thrombosis embolizing to the left lower extremity during hospitalization for active ulcerative colitis (UC). The limb was preserved following emergent embolectomy. Thrombophilia was attributed to UC, as hypercoagulable testing was negative. IBD is certainly a hypercoagulable state, and aggressive thromboembolism prevention should be considered for hospitalized patients with active disease.
Introduction
Inflammatory bowel disease-related thromboembolic complications were initially reported by Bargen in 1936.[1] The incidence of these events has been quoted in clinical studies to range from 0.7 to 7.5% of inflammatory bowel disease (IBD) patients.[2–5] Only about 7.6% of thromboembolic incidents were reported to involve peripheral arterial complications (including aortic mural thrombi), whereas the remaining arterial thromboses, such as coronary and mesenteric artery thrombosis, accounted for close to 27% of cases.[3] We report a case of acute limb ischemia secondary to unprecedented thoracic aortic thromboembolism during an active episode of ulcerative colitis (UC).
Case Report
A 63-year-old white male with UC was hospitalized for intravenous steroids following 4–6 weeks of abdominal cramps and bloody diarrhea (12–20 bowel movements/day). Initial exam on admission revealed a normotensive, afebrile, nondistressed patient with normal physical exam, including a soft, nontender abdomen and good (2+) distal extremity pulses bilaterally. Laboratory data showed mild anemia (Hemoglobin 13.2 g/dL) but normal electrolytes, creatinine, liver enzymes, cholesterol (138 mg/dL), and partial thromboplastin time/international normalized ratio (PTT/INR) values (26.9 sec, 1.0). The patient was placed on intravenous methylprednisolone (30 mg every 8 hours) along with enoxaparin (40 mg daily) for deep venous thrombosis prophylaxis. Six days of intravenous steroids did not produce major changes in bowel movements, at which time mesalamine suppositories (1000 mg twice daily) were added but without significant change. Later that day, the patient experienced the sudden onset of left calf and foot pain. Physical examination revealed a pale, cool, and dusky foot with weak femoral pulse. There were no palpable/dopperable popliteal, posterior tibial, or dorsalis pedis pulses. A diagnosis of acute left lower extremity ischemia was made prompting immediate diagnostic angiography which revealed acute thrombus in the common femoral, profunda, superficial femoral, popliteal, anterior tibial, and posterior tibial arteries. Iliofemoral, profunda, popliteal, and tibial thromboembolectomy was performed successfully, resulting in palpable dorsalis pedis and posterior tibial pulses. Heparin infusion was initiated without worsening of gastrointestinal bleeding.
Evaluation of the thromboembolic source included hypercoagulable testing, which was predominantly negative. In ruling out a cardiac embolic source, auscultation revealed a regular rhythm without any murmurs, and electrocardiogram showed normal sinus rhythm. Telemetry did not detect any episodes of arrhythmias and transthoracic echocardiography was normal. However, transesophageal echocardiography and computed tomography (CT) angiography of the chest did reveal an echodensity in the distal transverse aortic arch (1.9 × 0.9 cm) consistent with thrombus (Figs. 1 and 2).
The UC symptoms did not improve throughout the hospitalization. Two weeks following embolectomy, the patient chose to undergo total abdominal colectomy with end ileostomy versus medical therapy with infliximab. Heparin infusion was resumed twelve hours post surgery followed by warfarin therapy. The patient was discharged to home ten days later on six months of warfarin therapy. He was seen again at that time for followup, where repeat CT chest/abdomen showed resolution of the aortic thrombus (Fig. 3) and substantial improvement of rectosigmoid inflammation. Warfarin was discontinued and aspirin (81 mg/day) was started.
Discussion
Twelve previous cases have demonstrated that aortic mural thrombi can embolize peripherally to the lower extremities and can lead to amputation or even death.[3,6–12] Unlike our case, which involved thoracic aortic thrombosis, all these cases involved the abdominal aorta. Despite the relatively low frequency of arterial thrombotic events, they rank third as cause of mortality (9%) in chronic IBD patients.[3] The majority of thromboembolic events occurred in active disease (thought to be triggered by endotoxins), but up to one third of cases developed while in remission.[3,13] Certain acquired conditions associated with IBD promote thrombosis. These include inflammation, thrombocytosis, immobility, surgical procedures, steroid use, and placement of central venous catheters. As mentioned earlier, the majority of thromboembolic events, especially arterial thrombosis, occurred in active disease or during complications (abscesses or fistulas), and therefore, these states can be considered risk factors.[3,14] As seen in our patient, inflammation of the colon has been a suggested risk factor since a previous observation revealed thromboembolism occurred mostly in Crohn disease patients with colonic disease, or in patients with extensive disease of ulcerative colitis.[15]
It is important to note that in addition to hypercoagulable testing, patients with lower extremity arterial thrombosis should be evaluated for a cardiac embolic source with transthoracic and transesophageal echocardiography. CT scan of the aorta should then be considered if cardiac work up does not reveal an obvious etiology, particularly since the occurrence of aortic mural thrombosis is a well-documented complication of IBD and carries a significant mortality risk. Treatment of thromboembolic events often begins with anticoagulation using systemic heparin followed by warfarin. As in our case, arterial thrombosis is often urgently managed with surgical thrombectomy, although it has been reported that transcatheter fibrinolysis may be a viable alternative.[16]
Since the best treatment is prevention, minimizing acquired thrombotic risk factors should be incorporated whenever possible. This can begin with anticoagulation prophylaxis in hospitalized patients presenting with active disease (except those with profuse bleeding or other contraindications), along with controlling disease activity. The latter is true since many of the anti-inflammatory agents used in treating active disease also have some antithrombotic properties. Awareness for increased risk of thromboembolic events in IBD patients should be raised as complications can have detrimental and even fatal outcomes.
Abstract and Introduction
Abstract
Arterial and venous thromboembolisms have long been associated with inflammatory bowel disease (IBD) and can cause significant morbidity and mortality. We present a patient with aortic arch thrombosis embolizing to the left lower extremity during hospitalization for active ulcerative colitis (UC). The limb was preserved following emergent embolectomy. Thrombophilia was attributed to UC, as hypercoagulable testing was negative. IBD is certainly a hypercoagulable state, and aggressive thromboembolism prevention should be considered for hospitalized patients with active disease.
Introduction
Inflammatory bowel disease-related thromboembolic complications were initially reported by Bargen in 1936.[1] The incidence of these events has been quoted in clinical studies to range from 0.7 to 7.5% of inflammatory bowel disease (IBD) patients.[2–5] Only about 7.6% of thromboembolic incidents were reported to involve peripheral arterial complications (including aortic mural thrombi), whereas the remaining arterial thromboses, such as coronary and mesenteric artery thrombosis, accounted for close to 27% of cases.[3] We report a case of acute limb ischemia secondary to unprecedented thoracic aortic thromboembolism during an active episode of ulcerative colitis (UC).
Case Report
A 63-year-old white male with UC was hospitalized for intravenous steroids following 4–6 weeks of abdominal cramps and bloody diarrhea (12–20 bowel movements/day). Initial exam on admission revealed a normotensive, afebrile, nondistressed patient with normal physical exam, including a soft, nontender abdomen and good (2+) distal extremity pulses bilaterally. Laboratory data showed mild anemia (Hemoglobin 13.2 g/dL) but normal electrolytes, creatinine, liver enzymes, cholesterol (138 mg/dL), and partial thromboplastin time/international normalized ratio (PTT/INR) values (26.9 sec, 1.0). The patient was placed on intravenous methylprednisolone (30 mg every 8 hours) along with enoxaparin (40 mg daily) for deep venous thrombosis prophylaxis. Six days of intravenous steroids did not produce major changes in bowel movements, at which time mesalamine suppositories (1000 mg twice daily) were added but without significant change. Later that day, the patient experienced the sudden onset of left calf and foot pain. Physical examination revealed a pale, cool, and dusky foot with weak femoral pulse. There were no palpable/dopperable popliteal, posterior tibial, or dorsalis pedis pulses. A diagnosis of acute left lower extremity ischemia was made prompting immediate diagnostic angiography which revealed acute thrombus in the common femoral, profunda, superficial femoral, popliteal, anterior tibial, and posterior tibial arteries. Iliofemoral, profunda, popliteal, and tibial thromboembolectomy was performed successfully, resulting in palpable dorsalis pedis and posterior tibial pulses. Heparin infusion was initiated without worsening of gastrointestinal bleeding.
Evaluation of the thromboembolic source included hypercoagulable testing, which was predominantly negative. In ruling out a cardiac embolic source, auscultation revealed a regular rhythm without any murmurs, and electrocardiogram showed normal sinus rhythm. Telemetry did not detect any episodes of arrhythmias and transthoracic echocardiography was normal. However, transesophageal echocardiography and computed tomography (CT) angiography of the chest did reveal an echodensity in the distal transverse aortic arch (1.9 × 0.9 cm) consistent with thrombus (Figs. 1 and 2).
The UC symptoms did not improve throughout the hospitalization. Two weeks following embolectomy, the patient chose to undergo total abdominal colectomy with end ileostomy versus medical therapy with infliximab. Heparin infusion was resumed twelve hours post surgery followed by warfarin therapy. The patient was discharged to home ten days later on six months of warfarin therapy. He was seen again at that time for followup, where repeat CT chest/abdomen showed resolution of the aortic thrombus (Fig. 3) and substantial improvement of rectosigmoid inflammation. Warfarin was discontinued and aspirin (81 mg/day) was started.
Discussion
Twelve previous cases have demonstrated that aortic mural thrombi can embolize peripherally to the lower extremities and can lead to amputation or even death.[3,6–12] Unlike our case, which involved thoracic aortic thrombosis, all these cases involved the abdominal aorta. Despite the relatively low frequency of arterial thrombotic events, they rank third as cause of mortality (9%) in chronic IBD patients.[3] The majority of thromboembolic events occurred in active disease (thought to be triggered by endotoxins), but up to one third of cases developed while in remission.[3,13] Certain acquired conditions associated with IBD promote thrombosis. These include inflammation, thrombocytosis, immobility, surgical procedures, steroid use, and placement of central venous catheters. As mentioned earlier, the majority of thromboembolic events, especially arterial thrombosis, occurred in active disease or during complications (abscesses or fistulas), and therefore, these states can be considered risk factors.[3,14] As seen in our patient, inflammation of the colon has been a suggested risk factor since a previous observation revealed thromboembolism occurred mostly in Crohn disease patients with colonic disease, or in patients with extensive disease of ulcerative colitis.[15]
It is important to note that in addition to hypercoagulable testing, patients with lower extremity arterial thrombosis should be evaluated for a cardiac embolic source with transthoracic and transesophageal echocardiography. CT scan of the aorta should then be considered if cardiac work up does not reveal an obvious etiology, particularly since the occurrence of aortic mural thrombosis is a well-documented complication of IBD and carries a significant mortality risk. Treatment of thromboembolic events often begins with anticoagulation using systemic heparin followed by warfarin. As in our case, arterial thrombosis is often urgently managed with surgical thrombectomy, although it has been reported that transcatheter fibrinolysis may be a viable alternative.[16]
Since the best treatment is prevention, minimizing acquired thrombotic risk factors should be incorporated whenever possible. This can begin with anticoagulation prophylaxis in hospitalized patients presenting with active disease (except those with profuse bleeding or other contraindications), along with controlling disease activity. The latter is true since many of the anti-inflammatory agents used in treating active disease also have some antithrombotic properties. Awareness for increased risk of thromboembolic events in IBD patients should be raised as complications can have detrimental and even fatal outcomes.
