ABSTRACT
Introduction: Individuals with COVID-19 may have complex coagulation abnormalities in consistence with hypercoagulability. This manifests as high plasma level of certain coagulation factors, particularly fibrinogen. DIC, on the other hand, is characterized by consumption of these factors. We present a case of COVID-19 respiratory failure at which a DIC phase was followed by thromboinflammation and organ failure. Case Presentation: A 51-year-old male presented with 3-day duration of fever and dyspnea. He had laboratoryconfirmed COVID-19 infection a day prior to his presentation. He displayed significant hypoxia and respiratory distress which led to mechanical ventilation at 48 hours post presentation. His laboratory evaluation showed a platelet count of 45 x 1000/ mm3, International Normalized Ratio (INR) of 3.2, activated Partial Thromboplastin Time of 39 seconds, Fibrinogen of 30 mg/dl, D-Dimer of <4 mcg/ml and Fibrin Split Products of 320 unigram/ml. Peripheral blood smear showed schistocytes and ultrasound of the lower extremities showed bilateral deep venous thrombosis. Thrombotic thrombocytopenic purpura (TTP) and Disseminated Intravascular Coagulation (DIC) were considered. Serum Disintegrin And Metalloprotease with a ThromboSpondin type 1 motif, member 13 (ADAMTS-13) level was ordered, plasmapheresis trial initiated and IV argatroban drip started. Platelet count normalized with 48 hours. ADAMTS-13 level was inconsistent with TTP. On the sixth day of admission, serum fibrinogen level increased to 457 mg/dl which coexisted with worsening ventilatory requirements. A similar pattern of increasing serum D-Dimer level, ferritin and creatinine was observed together with the development of shock and multiorgan failure syndrome. Patient eventually succumbed to his critical illness on the 28th day of admission. Discussion: Endothelial injury [1] and hypercoagulable status [2] cause COVID Coagulopathy. DIC is predominately a consumptive disorder associated with bleeding, COVID- associated coagulopathy is associated with increasing thrombosis. In s series that reported on thromboembolic events, none of the patients developed overt DIC[3]. While thromboembolic events in COVID-19 are associated with increased mortality, the clinical significance of this compensated form of DIC is unknown. Conclusion:Critically ill patients with COVID-19 may display “compensated” DIC. Whether this is a separate entity or lies within a large spectrum of different coagulation abnormalities is unknown. The clinical significance of it is unknown wither. Randomized clinical trials are needed for further understanding.
ABSTRACT
SESSION TITLE: Fellows Critical Care Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: The Coronavirus Disease 2019 (COVID-19) pandemic has displayed heterogeneity in disease manifestations and complications;cardiac, renal, neurological complications and coagulopathy are reported. We present a case of COVID-19 with pneumomediastinum. CASE PRESENTATION: A 59-year-old male was admitted after a reverse transcriptase polymerase chain reaction (RT-PCR) test- confirmed COVID19. He was confused and was intubated for hypoxia. Laboratory investigation showed white blood cells of 2.8x1000/mm3 (normal: 3.4-9.4x1000/ mm3) [differential: 59%(normal: 47-67%) neutrophils and 39% ( normal: 25-45%) lymphocytes], aspartate aminotransferase 1174 IU/l(normal:13-39IU/l), alanine aminotransferase 598 IU/l(normal:7-52IU/l), ferritin > 7500 ng/ml (normal: 20-200 ng/ml), C reactive protein 306.1 mg/l (normal: 0-5 mg/l) and D-dimer 10 mcg/ml (normal: 0-0.50 mcg/ml). Arterial blood gases showed pH 7.14 (normal: 7.35-7.45), PCO2 59 mmHg (normal: 34-46 mmHg) and PO2 54 mmHg (normal: 80-97 mmHg) on 100% oxygen. Computed tomography of the chest (CT chest) showed diffuse groundglass opacities. Diagnosis of acute respiratory distress syndrome (ARDS) was made. On day 5, given low lung compliance (static compliance 13.5 ml/CmH2O), mode was switched to airway pressure release ventilation(APRV). On day 8, subcutaneous emphysema was noted with worsening hemodynamics. CT chest showed pneumomediastinum, pneumopericardium and subcutaneous air without pneumothorax. APRV was changed to conventional mode and infraclavicular incisions completed. Patient‘s status continued to decline;he died on the 13th day of admission. DISCUSSION: COVID-19 causes pulmonary involvement ranging from atypical pneumonia to ARDS. Few cases of COVID-19-associated pneumomediastinum are reported in the literature. Barotrauma from mechanical ventilation accounts for one third cases of pneumomediastinum. Although, large tidal volumes are thought to predispose to barotrauma, these associations are related to the severity of lung disease. ARDS is most associated and is the only independent risk factor for barotrauma[1]. APRV does not demonstrate any difference regarding the onset of barotrauma when compared to conventional modes used in ARDS[2]. Different pathological patterns ranging from interstitial lymphocytic infiltrates to organizing pneumonia to diffuse alveolar damage are reported in COVID-19[3]. These possibly define the spectrum of COVID-19 and hence the increasing rate of severe complications with worsening injury. CONCLUSIONS: COVID-19 patients display diverse complications;pneumomediastinum is an emerging one. Further research is needed to study COVID-19 and barotrauma within the clinical and pathological phenotypes of the disease. Reference #1: Airway pressures and early barotrauma in patients with acute lung injury and acute respiratory distress. Eisner MD, Thompson BT, Schoenfeld D, et al. Am J Respir Crit Care Med. 165:978-982 2002. Reference #2: Airway pressure release ventilation during acute hypoxemic respiratory failure: a systematic review and meta-analysis of randomized controlled trials. Carsetti et al. Ann. Intensive Care (2019) 9:44. Reference #3: Time to consider histologic pattern of lung injury to treat critically ill patients with COVID-19 infection. Marie-Christine Copin, Erika Parmentier, […], and The Lille COVID-19 ICU and Anatomopathology Group. Intensive Care Med. 2020 Apr 23 :1–3. DISCLOSURES: No relevant relationships by Moses Hayrabedian, source=Web Response No relevant relationships by Faraaz Nayeemuddin, source=Web Response No relevant relationships by Rajagopal Sreedhar, source=Admin input