Volume 26, Number 8—August 2020
Pulmonary Embolism and Increased Levels of d-Dimer in Patients with Coronavirus Disease
We report 3 patients with coronavirus disease who had a decline in respiratory status during their hospital course that responded well to intravenous steroids and interleukin-6 receptor antagonist therapy. These patients later showed development of persistent hypoxia with increased levels of
Coronavirus disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2, has been extensively reported since the outbreak in Wuhan, China, and can progress to involve major respiratory complications (1). Patients commonly have fever, cough, abdominal pain, and diarrhea.
During the second week of illness, decompensation occurs in some patients, possibly driven by the cytokine storm associated with increased levels of interleukin-6. We report 3 case-patients with COVID-19 who were improving after successful treatment during the critical period but showed development of pulmonary emboli (PEs) despite deep vein thrombosis (DVT) prophylaxis.
Three patients admitted to Northwell Plainview Hospital (Plainview, NY, USA) showed positive results for COVID-19 and had acute hypoxic respiratory failure secondary to COVID-19. All 3 patients received azithromycin and hydroxychloroquine, but their conditions continued to progress to more severe respiratory failure. During what was assumed to be the cytokine storm phase, on the basis of laboratory parameters and an increasing requirement for oxygen, the patients received intravenous steroids (solumedrol, 1–2 mg/kg/d for 5–8 d) and the interleukin-6 receptor antagonist tocilizumab (400 mg intravenously). Patients showed improvement and did not require intubation but later showed development of persistent hypoxemia with increases in levels of
Case-patient 1, a 52-year-old male former smoker with a history of asthma, came to our hospital 12 days after symptom onset. At admission, he reported chest tightness, difficulty breathing, and was afebrile. His respiratory rate was 34 breaths/min, heart rate 87 beats/min, and blood pressure 117/67 mm Hg. The
Case-patient 2, a 60-year-old female nonsmoker with a history of chronic bronchitis, ovarian cancer postoophorectomy, and provoked DVT 18 years earlier, was admitted on day 8 of symptoms. At admission, she reported worsening cough, nausea, and loss of sense of smell. She was afebrile; her respiratory rate was 20 breaths/min, heart rate 106 beats/min, and blood pressure 145/68 mm Hg. The
Case-patient 3, a 68-year-old male nonsmoker with a history of hypertension, and type 2 diabetes mellitus, was admitted on day 14 of symptoms. At admission, he reported cough, difficulty breathing, and progressive weakness. He was afebrile; his respiratory rate was 22 breaths/min, heart rate 107 beats/min, and blood pressure 144/92 mm/Hg, and he showed hypotoxicity. The
PEs can occur after the cytokine storm in COVID-19 patients, despite DVT prophylaxis. After initial improvements, patients might continue to have high or increasing oxygen requirements because of development of thromboembolic disease. Previous studies showed that low levels of platelets, increased levels of
Autopsy reports from COVID-19 patients have shown microthrombi in lungs and in other organs with associated foci of hemorrhage (3,4). These findings suggest that severe endothelial dysfunction, driven by the cytokine storm and associated hypoxemia, leads to disseminated intravascular coagulation, causing thromboembolic complications. In these patients, other parameters, such as the neutrophil–lymphocyte ratio, and inflammatory markers, including ferritin, C-reactive protein, and lactate dehydrogenase, were returning to reference levels despite increased
Although certain underlying conditions might have influenced the coagulation process in these patients, the hypothesis that hypercoagulability is driven by endothelial dysfunction is plausible. These case studies support the earlier observation that anticoagulation is associated with a decrease in mortality rates for COVID-19 patients (5). Monitoring disseminated intravascular coagulation and measurement of platelet counts,
Dr. Griffin is an instructor in clinical medicine and associate research scientist at Columbia University Medical Center, New York, NY. His primary research interests are HIV, stem cells, and malignancies.
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Original Publication Date: April 29, 2020