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Year : 2022  |  Volume : 9  |  Issue : 4  |  Page : 316-318

Subclavian artery thrombosis post modified radical mastectomy surgery - A rare case report

Department of Cardiovascular and Thoracic Surgery, JNMCH, AMU, Aligarh, Uttar Pradesh, India

Date of Submission30-Dec-2021
Date of Acceptance03-Mar-2022
Date of Web Publication8-Nov-2022

Correspondence Address:
Sheikh Saif Alim
Department of Cardiovascular and Thoracic Surgery, JNMCH, AMU, Aligarh, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijves.ijves_135_21

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Subclavian artery thrombosis is a relatively rare and unheard complication postmodified radical mastectomy (MRM) surgery and it is still not reported in the literature. We report a case of a 55-year-old female who underwent MRM for Stage II left ductal carcinoma of breast with level 2 lymph node involvement in a private hospital. She developed ischemic pain in the left upper limb on postoperative day 3. She came to JNMCH and was referred to us and initial imaging with computed tomography angiography revealed occlusion from the origin of the subclavian to axillary artery. We discuss the management of the aforementioned condition in our setup and would also discuss the steps needed to avoid the same in the future.

Keywords: Axillary dissection, modified radical mastectomy surgery, subclavian artery, thrombosis

How to cite this article:
Alim SS, Ammar A, Yadav M, Rabbani SS, Chawla S, Shama A, Haseen MA. Subclavian artery thrombosis post modified radical mastectomy surgery - A rare case report. Indian J Vasc Endovasc Surg 2022;9:316-8

How to cite this URL:
Alim SS, Ammar A, Yadav M, Rabbani SS, Chawla S, Shama A, Haseen MA. Subclavian artery thrombosis post modified radical mastectomy surgery - A rare case report. Indian J Vasc Endovasc Surg [serial online] 2022 [cited 2022 Nov 28];9:316-8. Available from:

  Introduction Top

Arterial occlusive diseases are uncommon delayed complications of surgery for underlying malignancies. We report a woman who presented with intermittent left upper limb discomfort, weakness, paresthesia, and acrocyanosis due to rare intraoperative vessel wall injury leading to thrombus formation from the origin of subclavian artery up to axillary artery which required a bypass grafting from proximal subclavian to brachial artery.

  Case Report Top

A 55-year-old woman presented in our emergency with a history of left upper limb discomfort, weakness, paresthesia, and acrocyanosis of fingers. She was a case of Stage 3 infiltrating ductal carcinoma of the left breast with regional level 2 lymph node extension, and she underwent a left modified radical mastectomy (MRM) with axillary lymph node dissection. On postoperative day 3, symptoms were present at rest and with activity. She noted intermittent paresthesia of her entire hand with sensory loss, slowly progressive arm weakness, and intermittent bluish discoloration of the fingertips of left hand.

Physical examination demonstrated a prominent right supraclavicular systolic bruit. Blood pressure was 136/90 mmHg in her right arm and 88/56 mmHg in her left arm. Left radial, ulnar, brachial, and subclavian pulses were greatly reduced compared to the right. All other pulses, including the carotid, femoral, popliteal, and dorsalis pedis, were normal and without bruits. Acrocyanosis of the fingertips of all fingers and thumb of her right hand was noted. Findings on a cranial nerve examination were normal with no Horner syndrome. Motor examination showed mild weakness of her right external rotators, pronator teres, triceps, and wrist extensors. Mild atrophy of her right supraspinous muscle was evident. Her right brachioradialis and biceps reflexes were reduced. Findings on a sensory examination were revealed loss of sensation over the dorsum of hand, along the wrist and lateral border of forearm up to elbow.

Routine laboratory studies demonstrated an elevated total cholesterol level of 256 mg/dL and a low-density lipoprotein level of 128 mg/dL. Noninvasive vascular tests indicated vascular compromise to the left upper extremity. Systolic blood pressure indexes were decreased, and continuous-wave Doppler ultrasonographic signals were abnormal, indicating obstructive arterial disease at the level of the subclavian artery. Upper arm exercise produced a further decrease in her right arm systolic pressure and was associated with symptoms of arm fatigue. Thoracic outlet maneuvres were mildly abnormal, suggesting additional dynamic arterial compression at the thoracic outlet level. Cervical spine X-ray films showed no evidence of an anomalous cervical rib. A chest X-ray film revealed no significant abnormality. Echocardiography revealed no significant cardiac abnormality. Computed tomography arteriography of the aortic arch and the left upper extremity revealed irregular stenosis at the origin of the right subclavian artery, with a thrombus at the subclavian-axillary junction and irregular luminal narrowing throughout the axillary artery [Figure 1].
Figure 1: Cutoff at subclavian-axillary junction

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The clinical findings and supporting investigations indicated subclavian artery thrombosis involving the left subclavian and axillary arteries with no evidence of tumor infiltration or recurrence. Her intermittent acrocyanosis was believed to be the result of recurrent microemboli from the ulcerated plaque. Emergency surgical revascularization was planned, and initially, left brachial embolectomy was done but we were unable to negotiate the Fogarty catheter beyond axillary artery. The arterial flow was not adequate through brachial, so later, a subclavian to brachial bypass was done.

We exposed the proximal subclavian artery just below the mid part of clavicle [Figure 2].
Figure 2: Exposed proximal subclavian artery

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We then took a ringed polytetrafluoroethylene graft and anastomosed the proximal left subclavian artery with mid part of left brachial artery. The arterial flow was adequate through the bypassed segment, and good Doppler signals were achieved in distal brachial, radial, and ulnar arteries. Postoperative recovery was uneventful, and the patient was discharged on postoperative 4 days.

  Discussion Top

MRM is one of the main surgical treatments for breast cancers, in which the purpose to thoroughly eliminating breast cancer is achieved by removing the lesions and adjacent tissues of breast cancer. MRM is usually applied to patients with Stage I and II breast cancers, especially in patients with lesions distributed in the lateral breast and patients with axillary lymph node metastases.[1] However, in MRM, the entire breast tissues are removed, the wound is relatively large, the shape of the patient is seriously damaged because of which some of the patients cannot accept such change, the psychological state of the patient is affected leading to the deterioration in postoperative quality of life.[2],[3],[4]

Axillary artery injury sometimes rarely occurs during axillary dissection in MRM. Platelets accumulate at the site of vascular injury and are involved in many physiological and pathophysiological processes, including hemostasis and thrombosis.[5],[6] Binding of adenosine diphosphate and thromboxane A2 to their receptors (P2Y1 and P2Y12 and thromboxane receptor, respectively) induce aggregation of platelets.[7],[8] The (von Willebrand factor [vWF]) also plays a crucial role in hemostasis through adhesion and spreading of platelets.[9],[10],[11],[12],[13],[14] vWF binds to platelet glycoproteins Ibα and αIIbβ3, and subendothelial collagens, which induces platelet aggregation. Platelets interact with collagen through glycoprotein VI and α2 β1, leading to platelet activation, spreading, and secretion, which in turn leads to thrombus formation.[6]

  Conclusion Top

Axillary artery injury during axillary dissection is a very rare complication during MRM. It has serious outcomes leading to ischemic changes in the involved limb. Careful dissection is usually advised during nodal dissection in the axilla. Hence, it is usually advised to start prompt antiplatelet therapy if any vascular injury occurs during the course of surgery.

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

Franceschini G, Sanchez AM, Di Leone A, Magno S, Moschella F, Accetta C, et al. Update on the surgical management of breast cancer. Ann Ital Chir 2015;86:89-99.  Back to cited text no. 1
Stoyanov GS, Tsocheva D, Marinova K, Dobrev E, Nenkov R. Drainage after modified radical mastectomy – A methodological mini-review. Cureus 2017;9:e1454.  Back to cited text no. 2
Khan MA. Effect of preoperative intravenous steroids on seroma formation after modified radical mastectomy. J Ayub Med Coll Abbottabad 2017;29:207-10.  Back to cited text no. 3
Huang NS, Liu MY, Chen JJ, Yang BL, Xue JY, Quan CL, et al. Surgical management of breast cancer in China: A 15-year single-center retrospective study of 18,502 patients. Medicine (Baltimore) 2016;95:e4201.  Back to cited text no. 4
Kattula S, Byrnes JR, Wolberg AS. Fibrinogen and fibrin in hemostasis and thrombosis. Arterioscler Thromb Vasc Biol 2017;37:e13-21.  Back to cited text no. 5
Laurent PA, Hechler B, Solinhac R, Ragab A, Cabou C, Anquetil T, et al. Impact of PI3Kα (Phosphoinositide 3-Kinase Alpha) inhibition on hemostasis and thrombosis. Arterioscler Thromb Vasc Biol 2018;38:2041-53.  Back to cited text no. 6
Chen X, Qian S, Hoggatt A, Tang H, Hacker TA, Obukhov AG, et al. Endothelial cell-specific deletion of P2Y2 receptor promotes plaque stability in atherosclerosis-susceptible ApoE-null mice. Arterioscler Thromb Vasc Biol 2017;37:75-83.  Back to cited text no. 7
Niu X, Pi SL, Baral S, Xia YP, He QW, Li YN, et al. P2Y12 promotes migration of vascular smooth muscle cells through cofilin dephosphorylation during atherogenesis. Arterioscler Thromb Vasc Biol 2017;37:515-24.  Back to cited text no. 8
Smeets MW, Mourik MJ, Niessen HW, Hordijk PL. Stasis promotes erythrocyte adhesion to von willebrand factor. Arterioscler Thromb Vasc Biol 2017;37:1618-27.  Back to cited text no. 9
Biswas I, Panicker SR, Cai X, Mehta-D'souza P, Rezaie AR. Inorganic polyphosphate amplifies high mobility group box 1-mediated von willebrand factor release and platelet string formation on endothelial cells. Arterioscler Thromb Vasc Biol 2018;38:1868-77.  Back to cited text no. 10
Schillemans M, Karampini E, van den Eshof BL, Gangaev A, Hofman M, van Breevoort D, et al. Weibel-palade body localized syntaxin-3 modulates von willebrand factor secretion from endothelial cells. Arterioscler Thromb Vasc Biol 2018;38:1549-61.  Back to cited text no. 11
Doddapattar P, Dhanesha N, Chorawala MR, Tinsman C, Jain M, Nayak MK, et al. Endothelial cell-derived von willebrand factor, but not platelet-derived, promotes atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 2018;38:520-8.  Back to cited text no. 12
Chen W, Druzak SA, Wang Y, Josephson CD, Hoffmeister KM, Ware J, et al. Refrigeration-induced binding of von willebrand factor facilitates fast clearance of refrigerated platelets. Arterioscler Thromb Vasc Biol 2017;37:2271-9.  Back to cited text no. 13
Drakeford C, O'Donnell JS. Targeting von willebrand factor-mediated inflammation. Arterioscler Thromb Vasc Biol 2017;37:1590-1.  Back to cited text no. 14


  [Figure 1], [Figure 2]


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