COVID-19 from Extensive Pneumonia and Acute Massive Pulmonary Embolism to Death: A Case Report
Yasser Mohammed Hassanain Elsayed*
Critical Care Unit, Fraskour Central Hospital, Egyptian Ministry of Health (MOH), Egypt
Received Date: 05/06/2020; Published Date: 25/06/2020
*Corresponding author: Yasser Mohammed Hassanain Elsayed, Critical Care Unit, Fraskour Central Hospital, Damietta Health Affairs, Egyptian Ministry of Health (MOH), Damietta, Egypt
Cite this article: Yasser Mohammed Hassanain Elsayed, COVID-19 from Extensive Pneumonia and Acute Massive Pulmonary Embolism to Death: A Case Report. Op Acc J Bio Sci & Res 2(1)-2020.
Rationale: Coronavirus disease is one of the most serious infections today. The link between COVID-19 infection and thromboembolization is suggested. COVID-19 infection is known to induce severe inflammation and activation of the coagulation system, resulting in a prothrombotic state. Up till now, there is no effective treatment against COVID-19.
Patient concerns: A middle-aged female COVID-19 patient admitted to the critical care unit with extensive pneumonia and massive pulmonary embolism.
Diagnosis: COVID-19 patient admitted to the critical care unit with extensive pneumonia and massive pulmonary embolism.
Interventions: Electrocardiography, central venous catheterization, arterial blood gas test, chest CT scan, and intravenous streptokinase infusion.
Outcomes: Despite transient dramatic clinical improvement had happened, but death due to extensive pneumonia was the end.
Lessons: The association between COVID-19 infection and thromboembolization is proposed. It denotes the significance of thrombolytics in associated massive pulmonary embolism with COVID-19. Co-exist of both extensive pneumonia and massive pulmonary embolism may be a serious risk factor for sudden death.
Keywords: COVID-19; Coronavirus; Extensive pneumonia; Massive pulmonary embolism; Death
Abbreviations: ABG - Arterial Blood Gas; COVID-19 - Coronavirus Disease 2019; ECG - Electrocardiography; ICU - Intensive Care Unit; IV - Intravenous; IVB - Intravenous Bolus; VR - Ventricular Rate
Coronaviruses were initially detected in the 1930s when an acute respiratory infection of domestic chickens was seemed to be produced by the infectious bronchitis virus (IBV) . In December 2019, case series of acute respiratory illness, now named as a novel strain of coronavirus–infected pneumonia (NCIP) or atypical viral pneumonia first reported in Wuhan, Hubei Province, China [2-4]. It was defined as a coronavirus disease-2019 (COVID-19) . Indeed, up to 40% of admitted cases of COVID-19 had preexisting cardiovascular disease. High cardiac troponin is a hallmark for virus load-induced myocardial injury. About 7.2% of recognized ischemic heart disease and heart failure patients of elevated cardiac troponin are at higher risk than others. Higher mortality is expected when the cases are complicated by acute myocarditis, acute myocardial infarction, and acute heart failure .
However, autopsy in postmortem studies in the dead patients of respiratory failure had evidence of exudative diffuse alveolar damage, tremendous capillary congestion, and often associated with microthrombi. Nearly 40% of the patients revealed overlapped bronchopneumonia. The acute pulmonary embolisms, alveolar hemorrhage, and vasculitis are considered serious associations. Patients may have signs of thrombotic microangiopathy [5,6]. Thrombotic pulmonary embolism was reported at both the macroscopic and microscopic levels . COVID-19 infection is a strong trigger for inflammation and coagulation system yielding in a prothrombotic state . Post-COVID-19 exposure; there are several mechanisms implicated in the activation of coagulation pathways, such as the immune system, and platelet stimulation, and infection of the host cells. These mechanisms will be resulting in cellular damage, apoptosis, and further activation of inflammation and coagulation. The co-existing of diabetes, obesity, autoimmune disorders, and cancer will be increasing the risk of both inflammatory and coagulation. Individuals with these pre-existing conditions, along with cardiopulmonary disease, appear to be at the highest risk for the evolution of severe COVID-19 disease and mortality rate [8-12].
Acute coronary syndrome (ACS) is a condition characterized by symptoms and clinical manifestations associated with acute myocardial ischemia. According to 2012 data of the World Health Organization (WHO), the top three causes of death in the world are Ischemic Heart Disease with 7.4 million people, Stroke with 6.7 million people and Chronic Obstructive Pulmonary Disease (COPD with 3.1 people) ). AKS is the most common one among Ischemic Heart Diseases . Acute Coronary Syndrome occurs as a result of impaired integrity of the atherosclerotic plaque in the coronary vessel . The clot formed on the plaque disrupts coronary blood flow to various degrees. In addition to the clot, different degrees of coronary spasm may accompany the picture . As a result of these changes, acute elevation myocardial infarction (STEMI), ST elevation acute myocardial infarction (NSTEMI) or unstable angina pectoris (Unstable Angina Pectoris, UAP) may occur in the clinic . Patients with ischemic complaints may or may not have ST segment elevation in Electrocardiography (ECG). STEMI may be in patients with ST segment elevation and UAP or NSTEMI in patients without ST segment elevation. The distinction between these two conditions can only be made with cardiac enzymes. If there is an increase in cardiac enzymes, NSTEMI is UAP if there is no increase .
Figure 1: Serial ECG tracings.
A. Tracing was the initial ECG on ICU admission showing sinus tachycardia with VR of 104.
B. Tracing was the initial ECG on ICU admission showing normal sinus rhythm with VR of 90.
Plasma sodium was normal (136mmol/L) and serum potassium showed mild hypokalemia (3.1 mmol/L). Plain Chest X-Ray showed bilateral ground-glass extensive consolidation in the right upper lobe and left lower lobe (Figure 2). Also, there are regular widen mediastinum indicating enlarged pulmonary trunk and both pulmonary arteries. A chest CT scan showed bilateral ground-glass extensive consolidation in the right upper lobe and left lower lobe. Also, there is regular widen mediastinum (Figure 3). Suspected acute massive pulmonary embolism with bilateral pneumonia was the most probable diagnosis. The death was due to extensive pneumonia in the end.
Figure 2: Chest imaging showing bilateral ground-glass extensive consolidation in right upper lobe (red arrow) and left lower lobe (lime arrows). Also, there are regular widen mediastinum indicating enlarged pulmonary trunk and both pulmonary arteries (purple arrows).
Figure 3: Chest CT scan showing bilateral ground-glass extensive consolidation in right upper lobe (red arrow) and left lower lobe (lime arrows). Also, there are regular widen mediastinum (purple arrows).
A middle-aged female COVID-19 patient admitted to the ICU with extensive pneumonia and massive pulmonary embolism.
The objective primary for my case study was the presence of extensive pneumonia and massive pulmonary embolism within few days post-contact to confirmed COVID-19 patient.
The secondary objective for my case study was the question of; How did you manage the case?
a. Positive history of direct contact to confirmed COVID-19 case with the presence of ground-glass extensive consolidation and lymphocytopenia will be supporting the COVID-19 diagnosis.
b. The unknown shock, hypoxia, high d-dimer, and radiological evidence of enlarged pulmonary trunk and both pulmonary arteries is highly suggestive of massive pulmonary embolism.
c. Hypothermia on the case presentation may be interpreted by either shock or indicating the presence of severe infection (pneumonia).
d. The conversion sinus tachycardia normal sinus rhythm in ECG after intravenous streptokinase infusion is supporting the tachycardia was due to pulmonary embolism.
e. A transient dramatic clinical improvement had happened and continued for a few hours after IV streptokinase infusion.
f. It signifying the role of thrombolytics in associated massive pulmonary embolism with COVID-19.
g. A clinical deterioration had happened within 6 hours of transient dramatic clinical improvement after giving streptokinase may be interpreted by the presence of severe pneumonia.
h. I can’t compare the current case with similar conditions. There are no similar or known cases with the same management for near comparison.
Limitations of the Study
There are no known limitations to the study.
Conclusion and Recommendations
i. Despite transient dramatic clinical improvement had happened, but the death was due to extensive pneumonia.
ii. It denotes the significance of thrombolytics in associated massive pulmonary embolism with COVID-19.
iii. The association between COVID-19 infection and thromboembolization is proposed.
iv. Co-exist of both extensive pneumonia and massive pulmonary embolism may be a serious risk factor for sudden death.
Conflicts of Interest
There are no conflicts of interest.
I wish to thank Dr. Tarek Salem; MD for his medical support, Dr. Yasser Rizk; MD for his radiological consultation, and also the critical care unit nurses who make extra-ECG copies for helping me.
1. Estola T (1970). Coronaviruses, a New Group of Animal RNA Viruses. Avian Diseases 14 (2): 330-336.
3. Rajan R, Jarallah MAI, Dashti R (2020) Cardiovascular complications of novel Wuhan Coronavirus (COVID-19) - A 2020 update. J Cardiol Curr Res 13(1):28.
4. Wang D, Hu B, Hu C (2020) Clinical Characteristics of 138 Hospitalized Patients with 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA 323(11): 1061-1069.
5. Menter T, Haslbauer JD, Nienhold R (2020) Post-mortem examination of COVID19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings of lungs and other organs suggesting vascular dysfunction. Histopathology.
6. Schaller T, Hirschbühl K, Burkhardt K (2020) Postmortem examination of patients with COVID-19.
7. Lax SF, Skok K, Zechner P (2020) Pulmonary arterial thrombosis in COVID-19 with fatal outcome: results from a prospective, single-center , clinicopathologic case series. Ann Intern Med.
9. Zhou F, Yu T, Du R, Fan G, Liu Y, et al. (2020) Clinical course and risk factors for mortality of adult patients with COVID-19 in Wuhan, China: a retrospective cohort study. The Lancet. 395: 1054-1062.
11. Leung JM, Yang CX, Tam A, Shaipanich T, Hackett TL, et al. (2020) ACE-2 expression in the small airway epithelia of smokers and COPD patients: implications for COVID-19. Eur Respir J 55(5):2000688.
12. Zhao Q, Meng M, Kumar R, Wu Y, Huang J, et al. (2020) The impact of COPD and smoking history on the severity of Covid-19: A systematic review and meta-analysis. J Med Virol.