It is now known that COVID-19 not only involves the lungs, but other organs as well including the gastrointestinal tract. Although clinic-pathological features are well-described in lungs, the histopathologic features of gastrointestinal involvement in resection specimens are not well characterized. Herein, we describe in detail the clinicopathologic features of intestinal resection specimens in four patients with COVID-19 infection. COVID-19 viral particles by in situ hybridization and immunofluorescence studies are also demonstrated. All four patients were males, aged 28–46 years, with comorbidities. They initially presented with a severe form of pulmonary COVID-19 and showed gastrointestinal symptoms, requiring surgical intervention. Histopathologic examination of resected GI specimens, mostly right colectomies, revealed a spectrum of disease, from superficial mucosal ischemic colitis to frank transmural ischemic colitis and associated changes consistent with pneumatosis cystoides intestinalis. Three patients were African American (75%), and one was Caucasian (25%); three patients died due to complications of their COVID-19 infection (75%), while one ultimately recovered from their GI complications (25%), but experienced prolonged sequela of COVID-19 infection including erectile dysfunction. In conclusion, COVID-19 infection, directly or indirectly, can cause ischemic gastrointestinal complications, with predilection for the right colon.
Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is commonly associated with myocardial injury and heart failure. The pathophysiology behind this phenomenon remains unclear, with many diverse and multifaceted hypotheses. To contribute to this understanding, we describe the underlying cardiac findings in fifty patients who died with coronavirus disease 2019 (COVID-19). Methods Included were autopsies performed on patients with a positive SARS-CoV-2 reverse-transcriptase-polymerase-chain reaction test from the index hospitalization. In the case of out-of-hospital death, patients were included if post-mortem testing was positive. Complete autopsies were performed according to a COVID-19 safety protocol, and all patients underwent both macroscopic and microscopic examination. If available, laboratory findings and echocardiograms were reported. Results The median age of the decedents was 63.5 years. The most common comorbidities included hypertension (90.0%), diabetes (56.0%) and obesity (50.0%). Lymphocytic inflammatory infiltrates in the heart were present in eight (16.0%) patients, with focal myocarditis present in two (4.0%) patients. Acute myocardial ischemia was observed in eight (16.0%) patients. The most common findings were myocardial fibrosis (80.0%), hypertrophy (72.0%), and microthrombi (66.0%). The most common causes of death were COVID-19 pneumonia in 18 (36.0%), COVID-19 pneumonia with bacterial superinfection in 12 (24.0%), and COVID-19 pneumonia with pulmonary embolism in 10 (20.0%) patients. Conclusions Cardiovascular comorbidities were prevalent, and pathologic changes associated with hypertensive and atherosclerotic cardiovascular disease were the most common findings. Despite markedly elevated inflammatory markers and cardiac enzymes, few patients exhibited inflammatory infiltrates or necrosis within cardiac myocytes. A unifying pathophysiologic mechanism behind myocardial injury in COVID-19 remains elusive, and additional autopsy studies are needed.
In order to elucidate the cause of acute respiratory distress syndrome of unknown etiology in a pre-pandemic patient, molecular techniques were used for detection of SARS-CoV-2. We used a SARS-CoV-2 nucleocapsid protein immunofluorescence stain to retrospectively identify an individual with diffuse alveolar damage on autopsy histology who had negative respiratory virus panel results in February, 2020, in Birmingham, Alabama. In situ hybridization for SARS-CoV-2 RNA revealed evidence of widespread multiorgan SARS-CoV-2 infection. This death antecedes the first reported death of a State of Alabama resident diagnosed with SARS-CoV-2 by 26 days.
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