ABSTRACT
The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected — asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki–Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. Сo-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome. © 2022 Saint Petersburg Pasteur Institute. All rights reserved.
ABSTRACT
The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected — asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki–Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. Сo-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome.
ABSTRACT
The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected - asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki-Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. So-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome. Copyright © 2022 Saint Petersburg Pasteur Institute. All rights reserved.
ABSTRACT
SESSION TITLE: COVID-19 Case Report Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Pneumomediastinum is the presence of air or other gas in the mediastinum which can be due to trauma related to mechanical ventilation or spontaneous in preexisting lung diseases. Here, we present the case of Covid-19 pneumonia, who developed pneumomediastinum without any trauma or other risk factors. CASE PRESENTATION: A 56-year-old male COVID unvaccinated with a history of essential hypertension presented to the ED with shortness of breath and worsening cough for one week. He was living with his father, who was admitted to the ICU and receiving treatment for COVID pneumonia. The patient appeared to be in respiratory distress. His initial vital signs were temperature of 99.6 F, respiratory rate of 26 breaths per minute, blood pressure 125/71 mm Hg, heart rate 109 beats per minute with a regular rhythm, and oxygen saturation of 50% while he was breathing ambient air. Pulmonary examination revealed use of respiratory accessory muscle and widespread bilateral coarse rhonchi on auscultation. The rest of the physical examination was within normal limits. RT- PCR COVID -19 test was positive. The blood gas analysis reported respiratory alkalosis. Inflammatory markers were elevated: erythrocyte sedimentation rate (35.2 mg/L), C-Reactive Protein (17.70 mg/dL), Ferritin (1108.1 ng/mL), Lactate Dehydrogenase (813 U/L), Lactate (2.4 mg/dL), D-Dimer (35.20 mg/L) and Troponin High Sensitivity-236.6 ng/L. His CBC, electrolytes, and kidney function were normal. Chest X-ray showed Pneumomediastinum with dense basilar predominant consolidation. CT Angio Chest with contrast reported Pneumomediastinum likely from the left central airway source and bilateral dense ground glass consolidation. An echocardiogram showed an ejection fraction of 60-65%, no valvular abnormalities. He was placed on vapotherm(Oxygen 40L/min) with 100% FiO2. He was given Dexamethasone 6mg for ten days, Remdesivir, Barcitinib, and a 7-day course of Azithromycin and Ceftriaxone for community-acquired pneumonia. He was advised to practice prone positioning for 12 hours or more per day. Pulmonology, Infectious Disease, and Cardiology were consulted. Gradually, his oxygen requirement was weaned down and Pneumomediastinum resolved on serial chest x rays. He was discharged on home oxygen in a clinically stable condition. DISCUSSION: Pneumomediastinum in viral pneumonia is rare. The exact mechanism is unknown. Covid-19 pneumonia causes diffuse alveolar wall damage, which might cause air leakage into the mediastinum. The development of pneumomediastinum is an ominous sign in these patients. Fortunately, our patient did not worsen and was weaned off high flow oxygenation requirement. CONCLUSIONS: Few isolated reported cases of pneumomediastinum in a COVID-19 patient have been associated with life-threatening complications. It should be used as a prognostic marker, and close monitoring of these patients is advisable. Reference #1: Damous, S.H.B., dos Santos Junior, J.P., Pezzano, Á.V.A. et al. Pneumomediastinum complicating COVID-19: a case series. Eur J Med Res 26, 114 (2021) DISCLOSURES: No relevant relationships by Saad Ansari No relevant relationships by Akshit Chitkara No relevant relationships by Sudeshna Ghosh No relevant relationships by Femina Patel
ABSTRACT
CASE: A 35-year-old female with history of pulmonary coccidiomycosis s/p treatment 15 years ago, ex-smoker who quit 8 years ago, unvaccinated for COVID-19 presented with two weeks of progressively worsening shortness of breath, fever, chills, generalized body aches, sore throat with hoarseness of voice, nonproductive cough, wheezing and midsternal chest pain. Denied sick contacts, recent travel, allergies or bird contact. On presentation, vitals were significant for hypoxia with SpO2 84% requiring 2L of nasal canula, sinus tachycardia to 109, tachypneic in 30s. Physical exam showed stridor and bilateral diffuse expiratory wheezing. Stridor improved with racemic epinephrine and dexamethasone 10mg IV. CBC, CMP, Procalcitonin, BNP, COVID-19 and Respiratory PCR were negative, while coccidioidomycosis antibody was positive. UDS was positive for methamphetamine. Chest X-ray showed features of atypical pneumonitis. CT Chest showed similar findings and was negative for pulmonary embolism. She was managed symptomatically with albuterol inhaler. Respiratory symptoms improved during hospitalization without any further interventions. IMPACT/DISCUSSION: Methamphetamine can cause toxic lung parenchyma injury irrespective of frequency of use. With recent increase in use of methamphetamine, paucity of literature and unclear mechanism in lung injury, it is important for physicians to be aware of methamphetamine associated lung injury as a differential diagnosis of acute/subacute respiratory distress with the risk factors of illicit drug use in the era of COVID pandemic. According to National Survey on Drug Use and Health (NSDUH) in 2018, 1.6 million people (age > 26 years) used methamphetamine in one year which is 0.5% more than 2016-2017. Crystalline methamphetamine is a widely used inhaled stimulant with few reported cases of acute respiratory distress syndrome, eosinophilic pneumonia, pneumonitis, and diffuse alveolar hemorrhage. Even though the mechanism of injury is unclear in human beings, toxicity was studied in animals. Chronic methamphetamine use causes thickened alveolar walls and reduced alveolar sacs by oxidative stress and by increased free radical formation. Patients often present with non-specific symptoms including cough, shortness of breath, sore throat or chest pain. The temporal relation of symptomatology with methamphetamine use and exclusion of infectious and other pulmonary etiology based on labs and radiological findings are crucial in establishing the diagnosis. Early diagnosis, symptomatic treatment and cessation of substance use are core management. CONCLUSION: We discussed a case of methamphetamine-induced pneumonitis, who presented with upper and lower respiratory symptoms that resolved dramatically with the early diagnosis and supportive care. We recommend considering methamphetamine-induced lung injury as a differential diagnosis in patients with risk factors of illicit drug use, especially in the era of the COVID-19 pandemic for early diagnosis and appropriate management.
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Introduction: Management of acute respiratory distress including COVID-19 pneumonia involves O2 supplementation, which is lifesaving, but causes severe hyperoxic acute lung injury (HALI). AT2 cells are the most affected cell type in hyperoxia (HO). NADPH oxidase (NOX) is a major source of reactive oxygen species (ROS) in HO. NOX4, the only functionally active NOX present in mitochondria, and primarily produces H2O2 as well as mtROS has been shown to be involved in several human pathologies. Not much is known about NOX4-induced mitochondrial injury in HALI. The current study aims to determine the role of AT2 epithelial cell NOX4 in HALI and the impact of HO on the modulation of mtROS and mitochondrial dynamics in HALI. Methods: Nox4-/-Spc-Cre animals were generated using tamoxifen induction and the knockdown was validated. The Nox4- /-Spc-Cre knockout (KO) and wild type (WT) mice were exposed to room air (NO) or 95% O2 (HO) for 66h to study the structural and functional changes in the lung. Transmission Electron Microscopy (TEM) was used to study the HO-induced changes in mitochondria. Isolated primary AT2 and/ mouse lung epithelial (MLE) cell line was investigated for mtROS, mt dynamics and apoptosis. Mitochondrial injury was assessed in Nox4 WT and Nox4 silenced cells. Results: C57BL/6J WT animals subjected to HO for 66h showed increased expression of NOX4, determining the role of NOX4 in HALI. The H&E staining demonstrated significant HALI in Nox4 WT animals exposed to HO compared to Nox4 KO as determined by increased infiltration of neutrophils, alveolar wall thickening and presence of proteinaceous debris in the alveolar space. Further, increased BAL cell count and protein levels, increased AT2 cell death and elevation of the proinflammatory cytokine IL- 6 and the chemokine KC was seen in WT animals compared to Nox4 KO. Analysis of lung tissues by TEM showed mitochondrial swelling, cristae damage and mitophagy in AT2 cells due to HO. Changes in mt injury markers were also observed. HO-induced NOX4 increase in primary AT2/ MLE-12 cells resulted in increased mtROS production and apoptosis, which was reduced with Nox4 siRNA silencing. Conclusion: This study suggests that the HO induced NOX4 expression in mouse lung, and deletion of Nox4 gene in AT2 cells reduced mtROS production and apoptosis and protected the lungs from severe hyperoxic lung injury. These results suggest NOX4 as a potential target for the treatment of HALI.