COVID-19 Like Findings in a Fatal Case of Idiopathic Desquamative Interstitial Pneumonia Associated With IgA Glomerulonephritis in a 13-Month-Old Child

Abstract

In the COVID-19 era, patients with severe acute respiratory syndrome (SARS) are suspected to be associated with SARS-CoV-2 infection. The aim of this paper is to present a case with COVID-like pneumonia, with fatal evolution. The clinical aspects were correlated with the autopsy findings and discussed on the background of the most recent data from the medical literature. A 13-month-old girl was admitted to the emergency room with acute severe shortness of breath and pulmonary bilateral ground-glass opacities and an almost complete opacified left lung. The patient suddenly deteriorated, and death was confirmed 3 h after admission. At autopsy, severe desquamative interstitial pneumonia was diagnosed and was associated with an unusual IgA glomerulonephritis. No SARS-CoV-2 infection was detected in the lung parenchyma by RT- PCR. This is a very unusual case of rapid deterioration of an infant with idiopathic desquamative interstitial pneumonia (IDP) and multiorgan involvement. Based on immunohistochemical stains, we hypothesize that, in IDP, the hyaline membranes arise from necrotizing desquamated pneumocytes. In the COVID-19 era, such cases are extremely difficult to diagnose; they can mimic SARS-CoV-2-induced lung injuries. This pattern of hyaline membrane formation might explain the poor response to oxygen therapy. The present case highlights the importance of autopsy in such challenging cases.

Clinical significance of cellular immunity function and inflammatory factors assays in alveolar lavage fluid for severe COVID‐19 pneumonia

“…SARS‐CoV‐2 infection mainly affects the respiratory system with typical clinical symptoms of fever, dry cough, fatigue, dyspnea, hypoxemia, acute respiratory distress syndrome (ARDS), and multiple organ insufficiency 16 . Recent reports have suggested that SARS‐CoV‐2 infection can also affect the cardiovascular system, causing acute myocardial injury with rapid progression and poor prognosis in severe cases 2,8,9 .…”

“…Moreover, Li et al 29 have reported that cytokine storm may be an important mechanism of viral sepsis and MODS in patients with COVID‐19, including acute kidney injury. Furthermore, some autopsy findings have revealed that extensive endothelial cell damage in the heart, kidney, small intestine and liver in COVID‐19, 30 triggering excessive thrombin production, inhibiting fibrinolysis, and activating the complement pathway, causing a thrombotic inflammatory response, ultimately leading to microthrombus deposition and microvascular dysfunction, which may promote further evolution of acute tubular necrosis into cortical necrosis, resulting in irreversible renal failure 16,31 …”

“…5 The SARS-CoV outbreak in 2003 can not only infect lung tissue but also other tissues and organs that express ACE2 protein, unfortunately, the SARS-CoV-2 in 2019 has also been confirmed to have such characteristics. [13][14][15] Gurzu et al 16 have reported that lung injury caused by SARS-CoV-like infection leads to pathological changes in multiple organs throughout the body, such as liver centrilobular fatty change, splenomegaly, proliferative glomerulonephritis, which may cause multiple organ dysfunction syndrome (MODS) eventually. SARS-CoV-2 infection mainly affects the respiratory system with typical clinical symptoms of fever, dry cough, fatigue, dyspnea, hypoxemia, acute respiratory distress syndrome (ARDS), and multiple organ insufficiency.…”

“…SARS-CoV-2 infection mainly affects the respiratory system with typical clinical symptoms of fever, dry cough, fatigue, dyspnea, hypoxemia, acute respiratory distress syndrome (ARDS), and multiple organ insufficiency. 16 Recent reports have suggested that SARS-CoV-2 infection can also affect the cardiovascular system, causing acute myocardial injury with rapid progression and poor prognosis in severe cases. 2,8,9 Based on previous studies related to SARS-CoV and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV), it is currently hypothesized that acute myocardial injury in patients with COVID-19 is associated with direct viral invasion of myocardial cells, severe hypoxemia-related myocardial oxygen supply-demand imbalance, and excessive inflammatory response-mediated myocardial injury.…”

“…Furthermore, some autopsy findings have revealed that extensive endothelial cell damage in the heart, kidney, small intestine and liver in COVID-19, 30 triggering excessive thrombin production, inhibiting fibrinolysis, and activating the complement pathway, causing a thrombotic inflammatory response, ultimately leading to microthrombus deposition and microvascular dysfunction, which may promote further evolution of acute tubular necrosis into cortical necrosis, resulting in irreversible renal failure. 16,31 Obviously, SARS-CoV-2 can affect the cellular immunity of patients. T lymphocytes are involved in the cellular immune function of the body and can be divided into two subgroups, CD4 + and CD8 + T lymphocytes, which have killing and auxiliary killing functions, respectively.…”