key: cord-0987987-rr7262vz
authors: Atıcı, Semra Demirli; Akpınar, Göksever
title: Splenic infarct in a COVID-19 patient under anticoagulant therapy with normal D-dimer levels
date: 2022-02-18
journal: Int J Surg Case Rep
DOI: 10.1016/j.ijscr.2022.106847
sha: a8ae007b1dea039ef866fe67f998dacdcadf95bb
doc_id: 987987
cord_uid: rr7262vz

BACKGROUND: Many studies have shown that COVID-19 can progress with coagulopathy and multisystemic thrombotic events. We report a patient who presented with abdominal pain after COVID-19 and was found to have splenic infarction (SI) concomitant with acute myocardial infarctus (MI) under anticoagulant treatment. CASE PRESENTATION: A 45-year-old man was admitted to the emergency department with left-sided abdominal pain radiating through to his back persisting for one day. He had COVID-19 PCR positivity nine days ago. After seven days of hospitalization due to COVID-19 pneumonia, he had been discharged with low-molecular-weight heparin (LMWH). Abdominal computerized tomography (CT) showed SI. His ECG and laboratory parameters were normal except for 17.2 × 10∧3/μL leukocytosis. The anticoagulant drug dose that he was taking was increased to 2 × 0.6 mL during hospitalization. He described new-onset chest pain during follow-up. Acute anterior MI was detected on ECG. Successful percutaneous coronary angiography was performed by cardiologists. No problems were observed in the follow-up. The patient was discharged on the fifth day of conservative treatment due to splenic infarction. CONCLUSION: Thrombosis prophylaxis with prophylactic doses of LMWH in hospitalized COVID-19 patients may not be sufficient to prevent the development of coagulopathy in patients. Abdominal-visceral thromboembolism should be suspected in a COVID-19-positive patient presenting with abdominal pain despite receiving anticoagulant therapy and normal d-dimer levels.

Coronavirus 2019 disease (COVID-19) is a viral multisystemic disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1] . A predisposition to arterial and venous thromboembolism associated with impaired coagulopathy has been demonstrated in COVID-19 [1, 2] . Thromboembolic events are multisystemic and can be seen most frequently in the lungs but also in the heart, brain, kidney, intestine and spleen [2] . Increased D-dimer levels and low antithrombin levels are among the factors blamed in these situations, but the data obtained could not clearly explain the cause of this coagulation disorder.

Herein, we present a case of SI with acute MI secondary to COVID-19. This highlights the need for diagnostic alertness and high suspicion for significant thromboembolic disease in patients with COVID-19 despite receiving anticoagulant therapy with low d-dimer levels.

A 45-year-old male patient was admitted to the emergency department nine days ago with complaints of cough and sore throat. Initial observations showed oxygen saturation of 88% on room air, heart rate of 104 beats per minute, blood pressure of 105/75 mm Hg, and temperature 38.5°C. Naso-and oropharyngeal swabs using the real-time PCR method were positive for SARS-CoV-2 infection. and post-COVID emergency admission laboratory findings are summarized in Table 1 .

Abdominal CT showed an approximately 57x48 mm noncontrast hypodense area extending from the capsular region to the hilus in the middle of the spleen ( to him by the department of infectious diseases, and discussion with the department of radiology concluded that follow-up imaging was not indicated. The work has been reported in line with the SCARE 2020 criteria [3] .

Thromboembolic events are most common in the lungs and have been reported to be less common in the heart, brain, kidney, gastrointestinal system and spleen in COVID-19-positive patients [1] . These thromboembolic events can be seen simultaneously in COVID-19-positive patients, as in our case. SI is a rare condition in which many predisposing factors, such as obesity, malignancy, cardioembolic events, vasculitis, autoimmune disorders, atrial fibrillation, endocarditis history, red blood cell abnormalities, and hypercoagulopathy, are involved in its etiology [4] . Rarely, it can be seen in COVID-19-positive patients. Ninety-two percent of cases of SI coexisting with COVID are seen in men in the literature, and the average age has been reported to be sixth decade [4] .

Thromboembolic events are usually observed in these patients two weeks after the diagnosis of COVID-19. Hypertension has been reported as the most common comorbidity in patients.

However, it has been reported that it can also be seen in patients without comorbidities, as in J o u r n a l P r e -p r o o f Journal Pre-proof our case. Most patients diagnosed with SI present with pain in the left hypochondrium or left flank. SI can present with a wide perspective ranging from an asymptomatic clinic to acute abdomen or hypovolemic shock [5] . In the definitive diagnosis of the disease, imaging methods are most frequently utilized by CT.

Although our patient's result was normal, increased d-dimer levels were also remarkable in these patients [6] . D-dimer is an increased fibrin degradation product in many thrombotic events, and its increased levels in patients with COVID-19 pneumonia have been reported to be associated with a higher risk of venous thromboembolism (VTE), disease severity, and increased mortality rates [7, 8] . High D-dimer levels have low specificity for VTE since they can be seen as increased in many different conditions (pregnancy, sepsis, malignancy, etc.).

Although it has low specificity, normal D-dimer levels in a patient can rule out VTE [9] . The risk of thromboembolism is higher in patients with a chronic disease, obesity, high Ddimer level and positive COVID-19 [7] [8] [9] . One of the most important features that distinguish our case from other patients with SI is that our patient did not have any predisposing factors that would increase thromboembolism and d-dimer levels, and he was followed under anticoagulant therapy from discharge to the diagnosis of SI. Although LMWH dose was increased and treated, MI developed in the patient and was successfully treated with emergency coronary angiography. Therefore, prophylactic anticoagulant therapy has an important role in preventing the development of arterial and venous embolism in the postdischarge period even in the absence of high-risk factors, obesity, high D-dimer levels or inactivity in patients with COVID-19 pneumonia [8, 11] .

In conclusion, guidelines support the use of prophylactic doses of anticoagulants in all hospitalized COVID-19 patients, but thrombosis prophylaxis with LMWH may not be sufficient to prevent the development of coagulopathy in patients who have been hospitalized due to COVID-19 pneumonia. Prospective studies involving patients without risk factors for this condition will help guide the best prophylaxis and treatment after discharge. Financial Disclosure: The authors declare that this study has received no financial support.

Conflict of Interest: No conflict of interest was declared by any of the authors. 

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Unusual arterial thrombotic events in Covid-19 patients

Multisystemic Infarctions in COVID-19: Focus on the Spleen

The SCARE 2020

Guideline: Updating Consensus Surgical CAse REport (SCARE) Guidelines

Concomitant renal and splenic infarction as a complication of COVID-19: a case report and literature review

A case report of spontaneous hemoperitoneum in a COVID-19 patient

Splenic infarction as a complication of covid-19 in a patient without respiratory symptoms: A case report and literature review

Venous thromboembolism in COVID-19 patients

D-Dimer, Fibrinogen, and IL-6 in COVID-19 Patients with Suspected Venous Thromboembolism: A Narrative Review. Vasc Health Risk Manag

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