Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 8  |  Issue : 3  |  Page : 297-300

Endovascular management of post COVID-19 arterial thrombosis


Department of Vascular and Endovascular Surgery, Institute of Vascular and Endovascular Sciences, Sir Ganga Ram Hospital, New Delhi, India

Date of Submission10-Aug-2020
Date of Decision11-Aug-2020
Date of Acceptance01-Sep-2020
Date of Web Publication6-Jul-2021

Correspondence Address:
Ganesh Kumar Marada
Department of Vascular and Endovascular Surgery, Institute of Vascular and Endovascular Sciences, Sir Ganga Ram Hospital, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijves.ijves_116_20

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  Abstract 


Thrombotic complications have been reported widely in patients with severe coronavirus disease 2019 (COVID-19) infection. There has been an increasing trend of arterial thrombosis leading to significant morbidity and mortality. We report a case of a patient with COVID-19 related pneumonia who presented with acute limb ischemia.

Keywords: Arterial thrombosis, corona virus disease 2019, endovascular, hypercoagulable, inflammatory, penumbra


How to cite this article:
Marada GK, Bedi VS, Agarwal S, Yadav A, Satwik A, Srivastava A. Endovascular management of post COVID-19 arterial thrombosis. Indian J Vasc Endovasc Surg 2021;8:297-300

How to cite this URL:
Marada GK, Bedi VS, Agarwal S, Yadav A, Satwik A, Srivastava A. Endovascular management of post COVID-19 arterial thrombosis. Indian J Vasc Endovasc Surg [serial online] 2021 [cited 2021 Jul 26];8:297-300. Available from: https://www.indjvascsurg.org/text.asp?2021/8/3/297/320613




  Introduction Top


Severe coronavirus disease 2019 (COVID-19) infection is known to be associated with thrombotic complications due to inflammatory and hypercoagulable states.[1] Cardiovascular system has been greatly affected in this disease with many publications related to venous thromboembolism.[2],[3] Arterial complications are being reported recently, we report a case of arterial thrombotic event in a patient with severe COVID-19 infection.


  Case Report Top


Our patient, a 52-year-old male, known diabetic on oral medication and nonsmoker had severe COVID-19 infection, for which he was admitted and was on ventilatory support for a week to intensive care unit (ICU). The patient recovered from symptoms and was discharged from the hospital after 1 week on Aspirin 75 mg and Atorvastatin 20 mg with two subsequent negative reverse-transcriptase polymerase chain reaction (RT PCR) reports. The patient developed numbness and pain associated with cyanotic changes on the left great toe 3 weeks after diagnosis of COVID-19 during his recovery period at home, which gradually progressed to involve rest of the toes and foot. On examination, the left popliteal and distal pulses were not palpable and the left foot was cool up to ankle with gangrenous and cyanotic changes in the medial aspect of forefoot with gangrene of great toe, 2nd and 4th toes extending on the plantar aspect as shown in [Figure 1]. Sensations over the forefoot were partially decreased and calf tenderness was absent (Rutherford category IIb). Arterial duplex showed thrombotic occlusion of P2 and P3 segment of popliteal artery with no flows distally in tibial arteries. Computer tomography angiography revealed acute cutoff at P2 segment of popliteal artery with nonopacification of trifurcation with reformation of anterior tibial artery (ATA), and occluded posterior tibial artery and peroneal artery in the leg as shown in [Figure 2]. Blood investigations showed hemoglobin of 11 g/dl, total leukocyte count of 16000/ul, platelet count of 7,52,000/ul, and serum creatinine of 0.53 mg/dl. He had elevated inflammatory markers, i.e., serum ferritin, D-dimer, and lactate dehydrogenase (LDH) levels were 1570 ng/mL, 1.57 mcg/mL, and 325 IU/L, respectively, with negative RT-PCR report at present.
Figure 1: Gangrenous and cyanotic changes in the left foot

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Figure 2: Computer tomography angiography: Acute cut off in the left popliteal artery

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Since the patient had recently recovered from major stress, he was planned for endovascular approach as a first option. Contralateral femoral artery was accessed under local anesthesia in the Hybrid Vascular Cathlab and a crossover 7 mm × 70 cm Rabbie Sheath (COOK, Bloomington, USA). Digital subtraction angiogram (DSA) showed thrombotic occlusion of popliteal and tibial vessels with faint reformation of the pedal arteries as shown in [Figure 3]. Thromboaspiration was done from popliteal artery and selectively from all the tibial arteries using Indigo Penumbra CAT 6 System (Pneumbra, Alameda, CA, USA) as shown in [Figure 4] and [Figure 5]. Post thrombus aspiration, DSA revealed good clearance of thrombus in popliteal and tibial arteries as shown in [Figure 6]. Access site was closed using Proglide 6Fr suture mediated closure device (Abbott Vascular, Santa Clara, CA, USA). Perfusion angiogram (I-Flow; Siemens) was done which showed significantly improvement in average peak time from 20 to 10 s as shown in [Figure 7]. Post procedure, the patient was monitored in recovery and started on heparin infusion and antiplatelet drug. In the postoperative period, the foot became warm with complete resolution of pain. The patient had palpable popliteal and ATA pulses. The patient was discharged on postoperative day 2 on therapeutic dose of low molecular weight heparin (LMWH) fondaparinux 7.5 mg once daily for 5 days along with rosuvastatin 20 mg once daily, aspirin 75 mg once daily and rivaroxaban 2.5 mg twice daily for 6 months.
Figure 3: Digital Subtraction angiography: Thrombotic occlusion of popliteal artery with faint reformation of pedal vessels

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Figure 4: Fluoroscopic-guided thrombosuction from popliteal and anterior tibial arteries by Penumbra CAT 6 catheter

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Figure 5: Fluoroscopic guided thrombosuction from peroneal and posterior tibial arteries by Penumbra CAT 6 catheter

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Figure 6: Digital subtraction angiography: Good clearance of thrombus in popliteal and tibial vessels

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Figure 7: Perfusion angiogram (I-Flow; Siemens): Improvement in peak time from 20 to 10 seconds

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  Discussion Top


Risk of thrombotic complications is high in patients with severe COVID-19 infection mainly due to hypercoagulability, stasis, and inflammatory state.[4] Recent data reported high risk of venous thromboembolism in patients suffering from COVID-19 infections.[5] More recently, arterial thrombosis has been reported in patients with severe COVID-19 infection. Giacomelli et al. reported a patient of severe COVID-19 infection presenting with acute limb irreversible ischemia due acute thrombosis of aortic graft.[6] They reported that the patient could not be revascularized due to poor general condition. Similarly, Kashi et al. reported a series in which the patients with the arterial complications of COVID-19 infection at various locations in aorta and peripheral arterial system leading to severe irreversible limb ischemia.[7] Majority of patients in their series presented with acute irreversible ischemia with couple of incidentally diagnosed cases. Our patient presented with acute reversible limb ischemia (Rutherford category IIb) with thrombotic occlusion of infra-geniculate arterial tree.

Various studies have hypothesized that virus acts directly on the vascular endothelium leading to cytotoxic injury, which leads to catastrophic release of cytokines. This causes a hypercoagulable state, causing arterial thrombosis.[8] Huertas et al.[9] illustrated the possible mechanisms of endothelial dysfunction and pulmonary vascular changes by COVID-19 as shown in [Figure 8]. These mechanisms can apply for peripheral vascular endothelium leading to arterial and venous thrombosis. Magro et al.[10] demonstrated that complement activation can cause vascular injury leading to microvascular thrombosis and prothrombotic state. Our patient had elevated levels of inflammatory markers such as serum ferritin, D-dimer and LDH levels correlating with etiology of the arterial thrombosis. Thrombophilia panel workup is usually not indicated in acute thrombotic state as it could give false positive results. Literature published by Zhang et al.[11] and Harzallah et al.[12] suggested that elevation of antiphospholipid antibodies (APLA) in patients with severe COVID-19 infection and role of early anticoagulation in these patients. However, Schouwers et al.[13] reported that lupus anticoagulant can be falsely elevated in the presence of inflammation due to high C-reactive protein levels and Galeano-Valle et al.[14] reported that antibodies are not elevated in patients with severe covid-19 infection associated with venous thromboembolism. Overall, the role of APLA in COVID-19-associated thrombosis is unclear and needs further research. Ponti et al.[15] hypothesized the possibility of homocysteine as a new specific biomarker for thromboembolism as high levels of plasma homocysteine can cause vascular injury and results are yet to be published. In this case, APLA and homocysteine levels were not done and it was observed that in spite thromboprophylaxis being used in the ICU, the patient developed thrombotic complication. This might lead to a conclusion that therapeutic dosage of LMWH would require to prevent thrombotic episodes.[1] Patients in ICU or with comorbidities such as diabetes as seen in our patient need therapeutic anticoagulation therapy to prevent thrombotic complications. Patients with acute arterial thrombosis need to be anticoagulated, thrombolysed or may require surgical revascularization, if the patient is stable. Our patient had a progressive gangrene so we opted for endovascular approach to mitigate the surgical stress. We did endovascular thrombus aspiration using Indigo Penumbra CAT6 system, which resulted in good thrombus clearance and post procedure patient had a palpable popliteal artery and ATA.
Figure 8: Schematic diagram of pathogenesis.[9] Copyright 2020 by European Respiratory Journal. Abbreviations: ACE: Angiotensin converting enzyme, Ang: Angiotensin, AT: Angiotensin receptor, MAS: Macrophage activation syndrome, NO: Nitric oxide, PAF: Platelet activating factor, PAI-1: Plasminogen activator inhibitor-1, PGI2: Prostaglandin I2, SARS-CoV-2: Severe Acute Respiratory Syndrome coronavirus 2, TF: Tissue factor, tPA: Tissue plasminogen activator

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  Conclusion Top


Hospitalized patients with severe COVID-19 infection are at a high risk of arterial thrombosis. The involvement of multiple arterial beds could be catastrophic leading to increased morbidity and mortality. Further large studies are required to outline the arterial events and to conceptualize the necessity of therapeutic anticoagulation in high risk patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Klok FA, Kruip MJ, van der Meer NJ, Arbous MS, Gommers DA, Kant KM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020;191:145-7.  Back to cited text no. 1
    
2.
Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G, et al. Cardiovascular considerations for patients, health care workers, and health systems during the COVID-19 pandemic. J Am Coll Cardiol 2020;75:2352-71.  Back to cited text no. 2
    
3.
Madjid M, Safavi-Naeini P, Solomon SD, Vardeny O. Potential effects of coronaviruses on the cardiovascular system: A review. JAMA Cardiol. 2020;5:831-40. doi:10.1001/jamacardio.2020.1286.  Back to cited text no. 3
    
4.
Spiezia L, Boscolo A, Poletto F, Cerruti L, Tiberio I, Campello E, et al. COVID-19-related severe hypercoagulability in patients admitted to intensive care unit for acute respiratory failure. Thromb Haemost 2020;120:998-1000.  Back to cited text no. 4
    
5.
Marone EM, Rinaldi LF. Upsurge of deep venous thrombosis in patients affected by COVID-19: Preliminary data and possible explanations. J Vasc Surg Venous Lymphat Disord 2020;8:694-5.  Back to cited text no. 5
    
6.
Giacomelli E, Dorigo W, Fargion A, Calugi G, Cianchi G, Pratesi C. Acute thrombosis of an aortic prosthetic graft in a patient with severe COVID-19-related pneumonia. Ann Vasc Surg 2020;66:8-10.  Back to cited text no. 6
    
7.
Kashi M, Jacquin A, Dakhil B, Zaimi R, Mahé E, Tella E, et al. Severe arterial thrombosis associated with Covid-19 infection. Thromb Res 2020;192:75-7.  Back to cited text no. 7
    
8.
Han H, Yang L, Liu R, Liu F, Wu KL, Li J, et al. Prominent changes in blood coagulation of patients with SARS-CoV-2 infection. Clin Chem Lab Med 2020;58:1116-20.  Back to cited text no. 8
    
9.
Huertas A, Montani D, Savale L, Pichon J, Tu L, Parent F, et al. Endothelial cell dysfunction: A major player in SARS-CoV-2 infection (COVID-19)? Eur Respir J 2020;56:2001634.  Back to cited text no. 9
    
10.
Magro C, Mulvey JJ, Berlin D, Nuovo G, Salvatore S, Harp J, et al. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: A report of five cases. Transl Res 2020;220:1-3.  Back to cited text no. 10
    
11.
Zhang Y, Xiao M, Zhang S, Xia P, Cao W, Jiang W, et al. Coagulopathy and antiphospholipid Antibodies in Patients with Covid-19. N Engl J Med 2020;382:e38.  Back to cited text no. 11
    
12.
Harzallah I, Debliquis A, Drénou B. Lupus anticoagulant is frequent in patients with Covid-19. J Thromb Haemost 2020;18:2064-5.  Back to cited text no. 12
    
13.
Schouwers SM, Delanghe JR, Devreese KM. Lupus Anticoagulant (LAC) testing in patients with inflammatory status: Does C-reactive protein interfere with LAC test results? Thromb Res 2010;125:102-4.  Back to cited text no. 13
    
14.
Galeano-Valle F, Oblitas CM, Ferreiro-Mazén MM, Alonso-Muñoz J, Del Toro-Cervera J, di Natale M, et al. Antiphospholipid antibodies are not elevated in patients with severe COVID-19 pneumonia and venous thromboembolism. Thromb Res 2020;192:113-5.  Back to cited text no. 14
    
15.
Ponti G, Ruini C, Tomasi A. Homocysteine as a potential predictor of cardiovascular risk in patients with COVID-19. Med Hypotheses 2020;143:109859.  Back to cited text no. 15
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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