key: cord-0953542-ucrci4q0
authors: Alfaki, Musaab; Flemming, Nia; Sittol, Rani; Grant, Janeen; Lisung, Fausto
title: ACUTE PULMONARY EMBOLISM AND MYOCARDIAL INJURY IN COVID-19 PATIENT
date: 2020-10-31
journal: Chest
DOI: 10.1016/j.chest.2020.08.1839
sha: b93b3fb5a11e83b4501b835fd39b56dcc60af1b3
doc_id: 953542
cord_uid: ucrci4q0

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) main presenting feature is hypoxia which coincidentally is a feature of Pulmonary Embolism (PE) that can be life-threatening if not diagnosed early. COVID-19 causes excessive inflammation that can induce expression tissue factors, which is a major coagulation activator1,2. Therefore, PE should also be a consideration for those presenting with COVID-19 with worsening hypoxia.

CASE PRESENTATION: 79-year-old a man with non-ischemic cardiomyopathy with Ejection Fraction (EF) 45-50% presented with worsening shortness of breath, dry cough, and bilateral lower limb edema for 2 weeks. On presentation, he was afebrile normotensive with tachypnea, tachycardia, and hypoxia. On physical examination, he was in respiratory distress with faint bilateral crackles and bilateral lower limb edema. Lab Investigations showed elevated Brain Natriuretic Peptide to 1830 pg/ml (normal range 0-100 PG/ml), troponin level to 6.89 ng/ml (normal range 0.00-0.03 ng/ml) and the D-dimer level was >20.00 UG/ ml FEU (normal range 0.00-0.40 UG/ml FEU). Viral PCR confirmed COVID-19. No ischemic changes noted in EKG. Echocardiography (Echo) revealed EF (Ejection Fraction) at 10-15%, dilated right ventricle with reduced function, and left ventricular thrombus. In CT chest with contrast noted to have acute segmental right middle lobe pulmonary arterial embolus. He was therapeutically anti-coagulated with enoxaparin. He received antibiotics, systemic steroids, and diuresis On day 3 of admission, he had worsening hypoxia and dyspnea while on 100% oxygen therapy. The patient opted for no escalation in care with ventilation or resuscitation. As he had no clinical improvement, the family agreed on comfort care. He died on day 5 of admission.

We described a case of COVID-19 complicated by PE, which is found among 13% of COVID-19 patients in a study done in Netherland1. Studies showed that elevated D-dimer levels can correlate with risk for pulmonary embolism. In this case, D-dimer found to be elevated which is consistent with prior cases 3. The patient found to have cardiomyopathy with ejection fraction at 15% during presentation despite prior Echo done about 6 months earlier revealed an EF 45%. Evidence of myocardial injury was found in previous articles from China as found in 19.7% of patients (total 416) with evidence of cardiac injury including elevated troponin and reduced ejection fraction. It was noted to be independently associated with a higher risk of mortality 4.

CONCLUSIONS: Diagnosis of pulmonary embolism in COVID19 patients may represent a diagnostic challenge as hypoxia is arguably the feature of COVID19 that could be explained by a viral lung infection. Thus, it is necessary to have a lower index of suspicion and CT chest to be considered in patients with worsening hypoxia so as to evaluate for pulmonary embolism especially among patients with an elevated D-dimer level.

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