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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 9  |  Issue : 4  |  Page : 256-258

Hepatic vein thrombosis secondary to COVID-19


Department of Medicine, MVJMC and RH, Bengaluru, Karnataka, India

Date of Submission02-Mar-2021
Date of Decision27-Mar-2021
Date of Acceptance06-Apr-2021
Date of Web Publication20-Oct-2021

Correspondence Address:
Dr. Kushal Markanday
Department of Medicine, MVJMC and RH, Hoskote, Bengaluru - 562 114, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ajim.ajim_27_21

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  Abstract 


COVID-19 is known to cause both arterial and venous thromboembolism. Although a lot of attention is being given to those presenting with myocardial infarction and stroke, splanchnic vein thrombosis which includes portal, mesenteric, splenic, and hepatic vein thrombosis is often underreported. A 21-year-old female presented with progressive abdominal distension and obstipation for the past 2 weeks. The patient was diagnosed as a case of moderate COVID-19 illness 2 weeks before the onset of these symptoms and recovered on receiving treatment according to the COVID protocol. Physical examination revealed pallor and bilateral pitting pedal edema up to ankles. Systemic examination revealed uniformly distended abdomen with signs of free fluid and tenderness in the right hypochondrium. Hematological investigations showed moderate-grade microcytic hypochromic anemia. Biochemically, indirect hyperbilirubinemia and transaminitis with moderately elevated D-dimers and Lactate dehydrogenase (LDH) was noted. Radiological imaging of the abdomen (including USG with doppler and CT contrast Scans) revealed gross ascites, nutmeg appearance of liver with completely obscured hepatic veins indicating no flow of blood, multiple intrahepatic portosystemic collaterals and a partially thrombosed inferior vena cava with no evidence of portal hypertension. All other workup to rule out other causes of hepatic vein thrombosis was inconclusive. The patient was treated with low-molecular-weight heparin and then continued with oral warfarin at discharge. On a 4-week follow-up, the patient showed marked clinical improvement with partial resolution of presenting symptoms.

Keywords: Anemia, COVID-19, thrombosed inferior vena cava


How to cite this article:
Markanday K, Bhardwaj N, Radhakrishnan B, Kumar P G. Hepatic vein thrombosis secondary to COVID-19. APIK J Int Med 2021;9:256-8

How to cite this URL:
Markanday K, Bhardwaj N, Radhakrishnan B, Kumar P G. Hepatic vein thrombosis secondary to COVID-19. APIK J Int Med [serial online] 2021 [cited 2021 Nov 29];9:256-8. Available from: https://www.ajim.in/text.asp?2021/9/4/256/328671




  Introduction Top


Hypothesized to be originated in Wuhan province of China toward the end of year 2019, over last 1 year, COVID-19 pandemic has been studied extensively worldwide by numerous researchers, right from its modes of transmission, manifestations, and complications associated with it even after recovery. With an ever-increasing incidence of thromboembolism among cases of acute and post-acute COVID 19 disease, the cumulative incidence of venous and arterial thrombo-embolism is estimated to be 28% and 3% respectively amounting to an overall specific mortality rate of 6%.[1]


  Case Report Top


A 21-year-old female, student, not a known case of any comorbidity, presented to the outpatient clinic of MVJ Medical College and Research Hospital, Bangalore, India, on October 17, 2020, with acute-onset pain abdomen for 2 weeks associated with gradually progressive abdominal distention and swelling of the bilateral lower limbs. The patient was admitted with the impression of acute abdomen for further evaluation. Three days prior to the onset of the above mentioned symptoms patient also had complaints of intermittent high grade fever associated with chills, bodyache and generalized weakness, pertaining to which she underwent COVID 19 RTPCR test and was found COVID positive. Patient received treatment for the same in district COVID Care Centre, where she recovered of her initial complaints and was recently discharged. There was no history of jaundice, vomiting, breathlessness, cough, or any bleeding manifestation. There was no history of loss of weight and reduced urine output.

The initial vital signs included a temperature of 99.6°F, a high-volume regular pulse of rate 106 beats per minute, blood pressure of 106/66 mmHg, and a respiratory rate of 24 cycles per minute. Pallor was present with no evidence of icterus, clubbing, or lymphadenopathy. Bilateral pitting pedal edema was present up to the ankles. On systemic examination, the abdomen was distended, with a horizontally stretched umbilicus but with no dilated veins or pulsations. Tenderness was noted in the right hypochondrial region without any evidence of palpable organomegaly, and free fluid was elicited by shifting dullness. Other systems were within normal limits.

The blood tests of the patient revealed a hemoglobin of 6.2 with microcytic hypochromic red blood cells alongside a reticulocyte count of 1.6 and a platelet count of 1.3 lacs/cumm and hyperbilirubinemia with total bilirubin of 3.38 mg/dL (0.79 direct and 2.59 indirect) with marginally elevated liver enzymes. The serum albumin, Albumin-Globulin Ratio (AG ratio), urine routine analysis, and renal profile were within normal limits. Serology for HCV, HBsAg, HIV, dengue, malaria, leptospirosis, rickettsiae, and brucellosis was negative.

Coomb's test was negative for hemolysis, but serum LDH was 605 U/L (normal – 140–280 U/L). Erythrocyte Sedimentation Rate (ESR) was 3 mm/h, and C-Reactive Protein (CRP) and D-dimers were moderately elevated.

The ascitic fluid analysis revealed a lymphocytic predominant transudative fluid with normal glucose (81.8 mg/dL), proteins (2.1 g/dL), and Serum Albumin Ascites Gradient (SAAG) of 1.3 with a total cell count of 1185 cells with the presence of reactive mesothelial cells. The adenosine deaminase levels were within normal limits (4.8 U/L), and microbial analysis of the ascitic fluid was negative for any bacterial, fungal, or tubercular organisms (Cartridge Based Nucleic Acid Amplification Test (CBNAAT) negative).

Ultrasonography of patient's abdomen showed gross ascites with increased hepatic parenchymal echogenicity and on conducting a venous doppler ultrasound of the liver - a partially thrombosed inferior vena cava with complete absence of blood flow via the hepatic veins was found. However, collaterals were patent and there was no evidence of portal hypertension. The contrast-enhanced abdominopelvic computed tomographic (CT) imaging [Figure 1] confirmed the ultrasound findings with features, suggesting nutmeg appearance of the liver with completely obscured hepatic veins and multiple intrahepatic portosystemic collaterals. A two-dimensional echocardiography showed normal cardiac function with ejection fraction of 60%. High-resolution CT chest revealed a score of COrona viral Disease Reporting And Data System (CORADS) 2 on evaluation.
Figure 1: Cect imaging with features of hepatic vein thrombosis. The encircled areas of the CECT-Scan depict completely obscured hepatic veins and multiple intrahepatic portosystemic collaterals in both transverse (b&c) and longitudinal (a&d) planes

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ANA screening, protein C, protein S, antiphospholipid antibody (APLA), antithrombin, sickling test, and Hb electrophoresis screenings were also negative.

Repeat nasopharyngeal and oral swabs tested positive for COVID-19.

Flowcytometry for Paroxysmal Nocturnal Haemoglobinuria (PNH) was planned but could not be done in view of infrastructural restraints. The patient was started on initial treatment with dexamethasone (4 mg IV 8th hourly) and low-molecular-weight heparin (LMWH, 40 U subcutaneous 12 h hourly) which was eventually bridged and continued with oral warfarin.

Trans-jugular Intrahepatic Porto-systemic Shunt (TIPS) was also planned. The patient was discharged on warfarin for continued use. On a 4-week follow-up, the patient had significantly improved with partial resolution of presenting symptoms.


  Discussion Top


We report a case of acute hepatic vein thrombosis as a complication of COVID-19. With time, newer studies are coming with patients presenting with extrapulmonary manifestations of COVID 19. It has been frequently found that about one-third of the patients with COVID-19 demonstrate thromboembolism and coagulopathy involving both arterial and venous events.[2],[3]

Splanchnic vein thrombosis (SVT), including portal, mesenteric, splenic vein thrombosis and Budd-Chiari syndrome, usually occurs in association with cirrhosis or liver malignancy or in patients with inherited or acquired thrombophilia.[4] Systemic and splanchnic venous thrombosis have been widely reported in COVID-19 illness such as pulmonary emboli, deep venous thrombosis, and visceral infarction, e.g., cerebral, hepatic, or pulmonary, especially in geriatric age group with pre-existing comorbidities such as diabetes and hypertension.[5] However, this patient belonging to a younger age group made us look for other prothrombotic states.

Acute thrombosis in a case with existing or previous history of COVID-19 can be fatal with many cases reporting progression to sepsis-induced coagulopathy (SIC)/disseminated intravascular coagulation, hemophagocytic syndromes/hemophagocytic lymphohistiocytosis, APLA syndrome, and thrombotic thrombocytopenic purpura/hemolytic–uremic syndrome.

The exact pathophysiology of SVT occurring in COVID-19 is yet to be well understood and is probably multifactorial. Possible explanations include viral infection of the endothelial cell, leading to diffuse endothelial inflammation, or increased procoagulant factors such as factor VIII, von Willebrand factor, fibrinogen, or virus-induced cytokine storm leading to coagulation and fibrinolysis activation.[6] A cytokine profile characterized by increased IL-2, IL-7, granulocyte-colony stimulating factor, interferon-γ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and tumor necrosis factor-α has been noted in severe COVID-19 disease.[7]

LMWH appears to be associated with better prognosis in severe COVID-19 patients meeting SIC criteria or with markedly elevated D-dimer. The American Society of Hematology recommends that all hospitalized patients with COVID-19 should receive pharmacologic thromboprophylaxis with LMWH or fondaparinux, unless bleeding risk exists (abnormal PT or APTT is not a contraindication), and full therapeutic-intensity anticoagulation in the appropriate clinical scenario.[8]

Although surgical interventions such as shunting and transplantation are being propagated for cases of SVT,[9] an early detection and initiation of appropriate conservative treatment in the form of parentral and oral anticoagulants can also be helpful in prevention of long-term morbidity and mortality like in this case. However, monitoring and long-term follow-up are deemed mandatory for better outcomes.

Due to multifactorial occurrence of thromboembolic disease in a setting of COVID-19, further research is necessary for better outcomes. We intend to raise awareness for occurrence of such cases and urge for prompt reporting.

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 initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Boonyawat K, Chantrathammachart P, Numthavaj P, Nanthatanti N, Phusanti S, Phuphuakrat A, et al. Incidence of thromboembolism in patients with COVID-19: A systematic review and. Thromb J 2020;18:34:1-2.  Back to cited text no. 1
    
2.
Helms J, Tacquard C, Severac F, Leonard-Lorant I, Ohana M, Delabranche X, et al. High risk of thrombosis in patients with severe SARS-CoV-2 infection: A multi-centre prospective cohort study. Intensive Care Med 2020;46:1089-98.  Back to cited text no. 2
    
3.
Oxley TJ, Mocco J, Majidi S, Kellner CP, Shoirah H, Singh IP, et al. Large-vessel stroke as a presenting feature of COVID-19 in the young. N Engl J Med 2020;382:e60.  Back to cited text no. 3
    
4.
Singh B, Kaur P, Maroules M. Splanchnic vein thrombosis in COVID-19: A review of literature. Dig Liver Dis 2020;52:1407-9.  Back to cited text no. 4
    
5.
Ahmed S, Zimba O, Gasparyan AY. Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow's triad. Clin Rheumatol 2020;39:2529-43.  Back to cited text no. 5
    
6.
Abou-Ismail MY, Diamond A, Kapoor S, Arafah Y, Nayak L. The hypercoagulable state in COVID-19: Incidence, pathophysiology, and management. Thromb Res 2020;194:101-15.  Back to cited text no. 6
    
7.
Costela-Ruiz VJ, Illescas-Montes R, Puerta-Puerta JM, Ruiz C, Melguizo-Rodríguez L. SARS-CoV-2 infection: The role of cytokines in COVID-19 disease. Cytokine Growth Factor Rev 2020;54:62-75.  Back to cited text no. 7
    
8.
Barnes GD, Burnett A, Allen A, Blumenstein M, Clark NP, Cuker A, et al. Thromboembolism and anticoagulant therapy during the COVID-19 pandemic: Interim clinical guidance from the anticoagulation forum. J Thromb Thrombolysis 2020;50:72-81.  Back to cited text no. 8
    
9.
Valeriani E, Riva N, Di Nisio M, Ageno W. Splanchnic vein thrombosis: Current perspectives. Vasc Health Risk Manag 2019;15:449-61.  Back to cited text no. 9
    


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