New Mexico’s COVID-19 Experience

Abstract

The 2019 novel coronavirus disease (COVID-19) has spread worldwide, infiltrating, infecting, and devastating communities in all locations of varying demographics. An overwhelming majority of published literature on the pathologic findings associated with COVID-19 is either from living clinical cohorts or from autopsy findings of those who died in a medical care setting, which can confound pure disease pathology. A relatively low initial infection rate paired with a high biosafety level enabled the New Mexico Office of the Medical Investigator to conduct full autopsy examinations on suspected COVID-19–related deaths. Full autopsy examination on the first 20 severe acute respiratory syndrome coronavirus 2–positive decedents revealed that some extent of diffuse alveolar damage in every death due to COVID-19 played some role. The average decedent was middle-aged, male, American Indian, and overweight with comorbidities that included diabetes, ethanolism, and atherosclerotic and/or hypertensive cardiovascular disease. Macroscopic thrombotic events were seen in 35% of cases consisting of pulmonary thromboemboli and coronary artery thrombi. In 2 cases, severe bacterial coinfections were seen in the lungs. Those determined to die with but not of severe acute respiratory syndrome coronavirus 2 infection had unremarkable lung findings.

Findings and inferences from full autopsies, minimally invasive autopsies and biopsy studies in patients who died as a result of COVID19 — A systematic review

“…In one study, severe secondary bacterial infections were seen in the diabetic patients and also severe illness in preexisting disease conditions [ 89 ]. The treatment of COVID19 patients should also aim at the secondary acute bronchopneumonia and aspiration pneumonia developed during the course [ 21 , 46 ].…”

“…Thrombi and neutrophilic extracellular traps (NETs) [ 33 , 95 ] Heart Gross changes observed Ventricular dilatations [ 6 ] Thromboemboli [ 88 , 89 , 92 ] Ischemic changes [ 23 ]. Microscopic/Histopathological changes noted Myocyte enlargement, nuclear polymorphism [ 56 , 89 ]. Extensive inflammatory response [ 95 , 102 ].…”

“…Extensive inflammatory response [ 95 , 102 ]. Thromboemboli [ 88 , 89 , 92 ]. Intracellular oedema, sarcomere ruptures, viral transcription in cardiomyocytes [ 13 ].…”

“…Intracellular oedema, sarcomere ruptures, viral transcription in cardiomyocytes [ 13 ]. Myocarditis [ 25 , 36 , 56 , 59 , 68 , 89 , 91 ]. Ischemic changes [ 23 ].…”

Evaluation of postmortem pathological changes in the lung in SARS-CoV-2 RT-PCR positive cases

“…It was thought that SARS-CoV-2 could drastically modify the human coagulation system as well as trigger fibrin thrombus formation in the distal pulmonary arteries by increasing megakaryocytes [33]. Interstitial megakaryocytes are common, especially in patients with macroscopic pulmonary embolism [26,34]. These findings show us that COVID-19 infection, together with severe acute lung damage, affects the coagulation system, causing it to turn into a fatal infection by promoting coagulation.…”