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Year : 2021  |  Volume : 8  |  Issue : 5  |  Page : 102-104

Intraoperative transesophageal echocardiographic detection of large mobile aortic thrombus in a patient with iron deficiency anemia presenting as acute limb ischemia

Division of Cardiac Anaesthesia, Meenakshi Multi-Speciality Hospital, Thanjavur, Tamil Nadu, India

Date of Submission19-Dec-2020
Date of Acceptance18-Jan-2021
Date of Web Publication30-Aug-2021

Correspondence Address:
G N Chennakeshavallu
Division of Cardiac Anaesthesia, Meenakshi Multi-Speciality Hospital, Thanjavur, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijves.ijves_171_20

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Quantitative and qualitative abnormalities in red blood cells are associated with arterial thrombosis. We report a case of a middle-aged female with iron deficiency anemia (IDA) presenting as bilateral acute limb ischemia (ALI) and on evaluation with transesophageal echocardiography (TEE) a large mobile thrombus was detected in the descending thoracic aorta. Her limbs were salvaged with successful bilateral surgical embolectomy and fasciotomies. The aortic thrombus was resolved with anticoagulation and correction of iron deficiency. We conclude that TEE evaluation of aorta is warranted in middle age females with IDA presenting as ALI.

Keywords: Acute limb ischemia, aortic thrombus, iron deficiency anemia, transesophageal echocardiography

How to cite this article:
Chennakeshavallu G N, Sankar S. Intraoperative transesophageal echocardiographic detection of large mobile aortic thrombus in a patient with iron deficiency anemia presenting as acute limb ischemia. Indian J Vasc Endovasc Surg 2021;8, Suppl S1:102-4

How to cite this URL:
Chennakeshavallu G N, Sankar S. Intraoperative transesophageal echocardiographic detection of large mobile aortic thrombus in a patient with iron deficiency anemia presenting as acute limb ischemia. Indian J Vasc Endovasc Surg [serial online] 2021 [cited 2022 Jan 26];8, Suppl S1:102-4. Available from:

  Introduction Top

Iron deficiency anemia (IDA) induces a hypercoagulable state and acts as a cofactor for thromboembolism in women of reproductive age.[1] The authors report a case of bilateral ALI in the middle-aged female with IDA, who had a thrombus visualized in descending thoracic aorta on evaluation with transesophageal echocardiography (TEE). The resolution of aortic thrombus was achieved with anticoagulation and correction of hyper-dynamic circulatory state with iron therapy without recurrence of further episodes of emboli. The report warrants TEE examination in patients with IDA presenting with embolic phenomena. Written informed consent was obtained from the patient for publication of this report.

  Case Report Top

A 32-year-old female presented to our emergency department with sudden onset and progressively worsening severe bilateral lower limb pain since 24 h (right > left). She had a history of menorrhagia and was intolerant to oral iron therapy due to gastritis. There was no history suggestive of gastrointestinal bleeding. There was no risk factor for cardiovascular disease and she was not on birth control pills. On examination, there was the absence of femoral, popliteal, dorsalis pedis, and posterior tibial arterial pulse on the right side, with feeble femoral and absent popliteal pulse on the left side. Transthoracic echocardiogram (TTE) and electrocardiogram were normal. Her laboratory studies were suggestive of severe IDA with thrombocytosis (hemoglobin: 5.6 g/dl, hematocrit: 19%, MCV: 55 μm3, MCHC: 24 g/dl, serum iron: 31.9 μg/dl, serum ferritin: 8.6 ng/ml, transferrin saturation :9.3%, total iron-binding capacity :343 μg/dl, hemoglobin electrophoresis: 100% hemoglobin A, normal thyroid profile and platelet count of 560,000/ml). Ultrasound abdomen and computed tomography (CT) abdomen were normal. CT angiogram of both lower limb arteries revealed filling defect in right common iliac, internal iliac, external iliac, and popliteal artery with absent contrast opacification of tibio-peroneal trunk. On the left side, filling defect was noted in the popliteal artery till its bifurcation and extending into the origin of the anterior tibial artery [Figure 1]. She was classified as grade 2b stage ALI according to Rutherford classification[2] and was posted for emergency bilateral femoral embolectomy. She received two units of packed red blood cells before shifting to the operation room (OR).
Figure 1: CTA showing filling defect in common iliac, internal/external iliac (white arrow) and popliteal artery (red arrow) on the right side. On the left side, filling defect noted in popliteal artery till its bifurcation (yellow arrow). CTA: Computed tomography angiography

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In the OR, after induction of general anesthesia, TEE was done to look for the cardiac source of emboli considering her age and normal TTE findings. It revealed a 1 cm × 1 cm mobile thrombus in the descending thoracic aorta attached distal to the origin of the left subclavian artery [Figure 2]. There was no atherosclerotic thickening of the thoracic aorta. Intraoperatively, anticoagulation was achieved with 5000 IU of unfractionated heparin. She underwent bilateral embolectomy with fasciotomy, following which there was the restoration of palpable pulse and audible arterial Doppler signals in both limbs. The intraoperative course was stable and the trachea was extubated.
Figure 2: TEE image showing the presence of thrombus in mid-esophageal short-axis view (a) and long axis view (b) of descending thoracic aorta. TEE: Transesophageal echocardiography

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Based on the TEE morphology of aortic mass and absence of underlying atherosclerosis, we considered the lesion on the DTA to be thrombus and started anticoagulation therapy. Anticoagulation was maintained with heparin infusion (1000 IU/h) for the 1st postoperative day and overlapped with warfarin 3 mg OD thereafter to maintain the INR between 2 and 3. There was a negative workup for hyper-coagulable condition (prothrombin, anti-cardiolipin antibody IgG/IgM, lupus anticoagulant, homocysteine, protein C, and protein S activity) before starting warfarin and her serum Vitamin B12 and folate were within the normal limits. A screening TTE performed on day 7 showed resolution of the thrombus and was further confirmed with TEE [Figure 3]. She received a course of intravenous ferro-therapy to correct iron deficiency. The patient was discharged on aspirin and oral iron supplementation. She did not report any further embolic events in 4 months follow-up.
Figure 3: TEE of descending thoracic aorta showing resolved thrombus in mid-esophageal short-axis view (a) and long axis view (b) of descending thoracic aorta. TEE: Transesophageal echocardiography

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  Discussion Top

Mobile aortic thrombus with the underlying complex atherosclerotic lesion is often detected by TEE in patients presenting with embolic events. Usually, such patients have risk factors for cardiovascular diseases and substantially with a mean age of around 70 years.[3] However, aortic thrombus without bulky atheromatous disease has also been regarded as an unanticipated but possible cause of arterial thromboembolism. Laperche et al. published a case series of 23 young patients (mean age around 45 years) with recent arterial embolism due to mobile aortic arch thrombosis without diffuse aortic atherosclerotic debris.[4] Thus, aortic thrombus and thromboembolism in nonatherosclerotic aorta are likely to occur in relatively young patients.

Aortic thrombus in nonatherosclerotic aorta is frequently associated with hypercoagulable states.[5] In the present case, IDA might have acted as cofactor for thromboembolism by promoting hypercoagulability. Yakushiji et al. reported brain embolism caused by aortic thrombus with no apparent aortic atheroma in two female patients with severe IDA.[6] Our patient had IDA and descending aorta thrombus just distal to the origin of the left subclavian artery in absence of aortic atheroma. The association between IDA and arterial thrombosis can be explained by several factors. First, thrombocytosis and increased platelet adhesion occur secondary to iron deficiency.[1] Second, in anemia, there is increase in plasminogen activator inhibitor-1 concentration which may cause a decrease fibrinolytic activity.[7] Third, arterial bruit a sign of turbulent flow are common in patients with severe anemia and this increased sheer force can cause endothelial disruptions which can serve as nidus for thrombus.[8]

Anticoagulation, thrombolysis, surgery, and endovascular treatment are effective strategies in the treatment for aortic mural thrombus. However, the most appropriate strategy remains unclear. Anticoagulation therapy has been proven effective in the resolution of aortic thrombus.[9] Hence, it should be considered as primary treatment for patients without contraindications. Furthermore, the appropriate duration of anticoagulation is unclear. In our patient, anticoagulation with warfarin for 7 days leads to resolution of aortic thrombus which was confirmed with TEE. Simultaneously, iron deficiency was corrected with intravenous iron therapy. Considering her symptoms of menorrhagia and the risk of bleeding with warfarin, we decided to discontinue anticoagulation after the resolution of aortic thrombus was confirmed with TEE. As there is no consensus on how long anticoagulation should be continued, we must consider the duration on case-by-case basis.

Thrombolysis with the consequent risk of distal embolization is not considered as primary treatment for aortic thrombus. Surgical thrombectomy and segmental aortic resection is an invasive strategy with fewer recurrent embolic events when compared to anticoagulation.[10] However, considering the high peri-operative morbidity and mortality associated with surgical procedures on the aorta, anticoagulation tends to be favored as primary treatment in most of cases. Surgery retrieval of the thrombus for patients not responding to anticoagulation after 2 weeks of therapeutic anticoagulation has been suggested.[11] Successful endovascular treatment of aortic thrombus has been reported.[12]

  Conclusions Top

We conclude that ALI in the middle-aged female with IDA, aortic thrombus is the most likely source of emboli. Severe IDA is one of the factors implicated in aortic thrombus formation in the nonatherosclerotic aorta. Therefore, the TEE examination of the aorta is warranted in patients with IDA presenting with embolic phenomena.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Byrnes JR, Wolberg AS. Red blood cells in thrombosis. Blood 2017;130:1795-9.  Back to cited text no. 1
Rutherford RB, Baker JD, Ernst C, Johnston KW, Porter JM, Ahn S, et al. Recommendation standard for reports dealing with lower extremity ischemia revised version. J Vasc Surg 1997;26:517-38.  Back to cited text no. 2
Kronzon I, Tunick PA. Aortic atherosclerotic disease and stroke. Circulation 2006;114:63-75.  Back to cited text no. 3
Laperche T, Laurian C, Roudaut R, Steg PG. Mobile thromboses of the aortic arch without aortic debris. A transesophageal echocardiographic finding associated with unexplained arterial embolism. The Filiale Echocardiographie de la Société Française de Cardiologie. Circulation 1997;96:288-94.  Back to cited text no. 4
Tsilimparis N, Hanack U, Pisimisis G, Yousefi S, Wintzer C, Rückert RI. Thrombus in the non-aneurysmal, non-atherosclerotic descending thoracic aorta – An unusual source of arterial embolism. Eur J Vasc Endovasc Surg 2011;41:450-7.  Back to cited text no. 5
Yakushiji Y, Terasaki Y, Otsubo R, Yasaka M, Oe H, Yamada N, et al. Brain embolism caused by a mobile aortic thrombus with iron deficiency anemia. Cerebrovasc Dis 2005;20:475-8.  Back to cited text no. 6
Vaughan DE. PAI-1 and atherothrombosis. J Thromb Haemost 2005;3:1879-83.  Back to cited text no. 7
Akins PT, Glenn S, Nemeth PM, Derdeyn CP. Carotid artery thrombus associated with severe iron-deficiency anemia and thrombocytosis. Stroke 1996;27:1002-5.  Back to cited text no. 8
Stöllberger C, Kopsa W, Finsterer J. Resolution of an aortic thrombus under anticoagulant therapy. Eur J Cardiothorac Surg 2001;20:880-2.  Back to cited text no. 9
Fayad ZY, Semaan E, Fahoum B, Briggs M, Tortolani A, D'Ayala M. Aortic mural thrombus in the normal or minimally atherosclerotic aorta. Ann Vasc Surg 2013;27:282-90.  Back to cited text no. 10
Choukroun EM, Labrousse LM, Madonna FP, Deville C. Mobile thrombus of the thoracic aorta: Diagnosis and treatment in 9 cases. Ann Vasc Surg 2002;16:714-22.  Back to cited text no. 11
Luebke T, Aleksic M, Brunkwall J. Endovascular therapy of a symptomatic mobile thrombus of the thoracic aorta. Eur J Vasc Endovasc Surg 2008;36:550-2.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3]


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