Immunology · Year 2 · from Immunology
Case 2: COVID-19-Associated Pulmonary Embolism
Clinical Image
Source: Wikipedia - Pulmonary embolism - CC BY-SA 4.0
Case Presentation
A 47-year-old female nurse presents to the emergency department on day 10 of symptomatic COVID-19 with sudden-onset pleuritic chest pain, hemoptysis, and worsening dyspnea. She had been managing mild-to-moderate symptoms at home and was not on prophylactic anticoagulation. She has no prior history of VTE, is on combined oral contraceptive pills, and has a BMI of 29. Vital signs reveal HR 124 bpm, BP 98/62 mmHg, RR 28/min, SpO2 88% on room air, and temperature 37.8C. Examination reveals a right ventricular heave, distended jugular veins, and an accentuated P2. ECG shows sinus tachycardia, right axis deviation, S1Q3T3 pattern, and T-wave inversions in V1-V4. Laboratory studies demonstrate D-dimer >20 mcg/mL FEU, troponin I 0.52 ng/mL, BNP 680 pg/mL, and lactate 3.8 mmol/L. CT pulmonary angiography reveals bilateral saddle pulmonary emboli with right ventricular dilation (RV/LV ratio 1.4). Bedside echocardiography confirms right ventricular dysfunction with McConnell sign. Given the submassive PE with hemodynamic compromise, she receives unfractionated heparin bolus 80 units/kg followed by 18 units/kg/hr infusion. Interventional radiology performs catheter-directed thrombolysis with alteplase 1 mg/hr over 12 hours per catheter, with subsequent hemodynamic improvement.
Key Learning Points
- SARS-CoV-2 triggers immunothrombosis through multiple mechanisms: direct endothelial infection via ACE2 receptors causes endotheliitis, complement activation (C5a, MAC) damages the vascular endothelium, and activated neutrophils release neutrophil extracellular traps (NETs) that serve as scaffolding for thrombus formation
- COVID-19 produces a prothrombotic state with elevated factor VIII, von Willebrand factor, and fibrinogen, alongside suppressed fibrinolysis due to elevated plasminogen activator inhibitor-1 (PAI-1), creating a net procoagulant milieu distinct from classic DIC
- The incidence of VTE in hospitalized COVID-19 patients ranges from 20-30% even with standard prophylactic anticoagulation, justifying intermediate- or therapeutic-dose thromboprophylaxis in critically ill patients
- Markedly elevated D-dimer (>4x upper limit of normal) in COVID-19 is an independent predictor of mortality and should prompt aggressive evaluation for thromboembolic complications