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Case Report
 
COVID-19 Infection and Splenic Infarct
Keywords :
Joe Francis Mathew, G N Ramesh, Ismail Siyad, Geetha Mammayil, Jeffey George, Prashanth Menon, Nilesh Namdeo Toke
Department of Medical Gastroenterology, Aster Medcity, Kochi - 682027, Kerala, India.


Corresponding Author
:
Dr Joe Francis Mathew 
Email: joefm1987@gmail.com


DOI: http://dx.doi.org/10.7869/tg.658

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COVID -19 pandemic has proven to be a great challenge to the entire mankind and health care community. Majority of the patients present with respiratory symptoms such as shortness of breath, dry cough and sore throat. In a recent study conducted in Wuhan, it was found that there is a subset of patients who only had digestive symptoms of diarrhoea, nausea and vomiting1. Also with the available literature, it is evident that there is a strong correlation of thrombotic events in patients with COVID-192. Here we present a case of biliary pancreatitis, subsequently diagnosed with COVID-19 infection complicated with splenic infarct who presented with symptoms of abdominal pain.

Case Report

A 34 year healthy male patient presented with complaints of dull aching abdominal pain in the epigastrium and jaundice of 3 days duration. He was evaluated elsewhere and was found to have cholelithiasis. He was symptomatically treated but the intensity of pain increased and he developed jaundice. His serial blood investigations showed features of conjugated hyperbilirubinemia (Total Bilirubin -  9.1mg/dl; Direct – 6.3mg/dl), transaminitis (OT/PT-243/250 U/l) along with elevated amylase (2146 U/l) and lipase (12320 U/l). He was diagnosed clinically as biliary pancreatitis. As he came from a hotspot region, a  COVID -19 PCR ( Gene Expert ) test was done which turned out to be positive. In view of jaundice and pancreatitis - a CT scan Abdomen was taken which revealed features of  pancreatitis with common bile duct stone ( 8 mm ), splenomegaly (19 cm ) and early lung parenchymal infiltrates (Figure 1). He was managed  with intravenous antibiotics, IV fluids, HCQ and other supportive measures in view of respiratory findings on CT scan. However in view of the serial increase in bilirubin and persistent abdominal pain it was decided to proceed with ERCP with CBD clearance. On the 5th day after admission, he developed breathlessness along with high grade fever and Left sided upper abdominal dullaching pain with tenderness on palpation. He had  a drop in oxygen saturation to 92 percent. Chest X-ray showed new infiltrates and due to worsening clinical condition, subsequently was shifted to Intensive Care Unit. A repeat cross sectional imaging of the abdomen and chest imaging revealed worsening of pancreatitis and patchy peri bronchial consolidation classical of COVID pneumonia. Imaging also revealed splenomegaly (18 cm) multiple splenic infarcts which were new developments (Figure 2). His D-dimer levels ( 6160 ng/ml ) and ferritin (675ng/ml) were elevated and was initiated on steroids and Low Molecular Weight Heparin . He  showed clinical improvement over the next 5 days. Heparin and steroids were stopped after 5 days.







Discussion

COVID 19 infections usually present with flu like illness. Abdominal symptoms are well documented in COVID 19 infection. In our case the patient had left flank pain, which is not a common symptom of pancreatitis but of splenic infarcts which occurs as a complication of the COVID 19 virus infection. Splenic infarction is well documented in viral infections. Splenic infarction is an uncommon disorder that occurs when splenic artery branches become occluded, either by an embolus or thrombus. The causes of splenic infarction are cardiogenic emboli such as atrial fibrillation, autoimmune diseases such as antiphospholipid syndrome, hematological diseases, and infection. Various infectious diseases, such as varicella zoster virus, HIV, and malaria, were previously reported to cause splenic infarction. The hypercoagulable state caused by these diseases can induce thromboembolic complications. The pathophysiology of unusually high pathogenicity for SARS-CoVhas not been completely understood. Patients infected with 2019-nCoV also had high amounts of IL1B, IFN?, IP10, and MCP1, probably leading to activated T-helper-1 (Th1) cell responses3. The immune dysregulation characteristic of severe COVID-19 infection may be initiated by ‘pyroptosis’, a particularly pro-inflammatory form of apoptosis initially described in macrophages, with rapid viral replication leading to massive release of inflammatory mediators4. Even though there are reports of thrombotic events in many COVID – 19 cases, the real pathophysiology is still unknown and needs further studies. SARS-CoV-2 has been shown to gain entry to cells by binding to angiotensin-converting enzyme 2 receptors, and the spike protein plays a vital role.5 The interaction of SARS-CoV-2 with angiotensin-converting enzyme 2 receptor may cause endothelial damage as a fivefold rise of von Willebrand factor levels has been reported in COVID-19 patients. 

Reference
  1. Pan L, Mu M, Yang P, et al. Clinical Characteristics of COVID-19 Patients With Digestive Symptoms in Hubei, China: A Descriptive, Cross-Sectional, Multicenter Study. Am J Gastroenterol. 2020 May;115(5):766-773.
  2. Cui S, Chen S, Li X, et al. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J Thromb Haemost 2020 Apr 9. 
  3. Wong CK, Lam CWK, Wu AKL, et al. Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome.Clin Exp Immunol 2004; 136: 95–103
  4. Léonard-Lorant I, Delabranche X, Séverac F, et al. Acute Pulmonary Embolism in Patients with COVID-19 at CT Angiography and Relationship to d-Dimer Levels. Radiology. 2020 Sep;296(3):E189-E191. 
  5. Khan IH, Zahra SA, Zaim S, Harky A. At the heart of COVID-19. J Card Surg. 2020 Jun;35(6):1287-1294.