A COVID–19 patológiája.
Authors: Schaff Zsuzsa , Danics Krisztina , Pesti Adrián , Lotz Gábor , Várkonyi Tibor , Dobi Deján , Vályi-Nagy István , Törő Klára , Glasz Tibor , Kiss András 
Published: October 2021

Összefoglaló. A SARS-CoV-2-pandémia óta a Semmelweis Egyetemen és
egyéb intézményekben rendszeresen végeznek boncolásokat, melyek feltárták a
COVID–19 jellegzetességeit. A legsúlyosabb kép a tüdőben mutatkozik, melynek
légtelensége változó kiterjedésű, oka összetett, így tüdővizenyő, fehérjében
gazdag izzadmány, az erek vérrög okozta elzáródása és gyulladás. A szív, a vese,
az agy és a máj változó mértékben érintett, érrögösödés, elhalás, degeneratív
elváltozások mutatkoznak. A SARS-CoV-2-vírus fehérjéi (tüske, nukleokapszid) és
a vírus genetikai anyaga (RNS) kimutatható az egyes szervekben, leginkább a
tüdőben. Klinikopatológiai elemzéssel megállapítható, hogy a halál a
SARS-CoV-2-fertőzés mint közvetlen kórok következménye, vagy egyéb krónikus
megbetegedés, melyet súlyosbított a SARS-CoV-2-fertőzés, vagy a halál a
vírusfertőzéstől függetlenül következett be.
Summary. Since the beginning of the Severe Acute Respiratory
Syndrome Coronavirus-2 (SARS-CoV-2) pandemic with substantial mortality, serial
autopsies at the Semmelweis University Budapest Hungary and other institutions
revealed the most characteristic pathological changes and cause of death of
patients in Coronavirus Disease-19 (COVID-19). The virus primarily affects the
respiratory system and the most severe alterations can be seen in the lungs. The
most characteristic changes, however, are non-specific, as the atelectasis of
various extents and severe congestion. The alveoli are filled with edema fluid,
protein-rich alveolar exudates, often forming hyalin membranes. Diffuse alveolar
damage (DAD) can be noted, which have exudative and fibroproliferative forms.
The desquamated alveolar epithelial and inflammatory cells which fill the
alveolar spaces further block the oxygen transportation, causing hypoxia and
induces ventilation problems. Vascular thrombosis and emboli coming from
thrombotic vessels from other organs, might involve the small and larger vessels
are common findings in COVID-19 sometimes associated with vasculitis. Extended
hemorrhages and giant cells are common findings too. Superimposed bacterial
infection might cause purulent bronchopneumonia. Aspiration pneumonia, in which
remnant of food and parts of filters etc might be present in the bronchi,
causing acute bronchopneumonia, occurs specially in intubated patients. Other
organs such as the heart, kidneys, the central nervous system and the liver are
similarly, though less severely involved by thrombosis, necrotic and
degenerative changes. Myocardial fibrosis is common, however usually associated
with previous chronic diseases similarly to the findings in the kidneys. Liver
steatosis is common, partly as the result of infection, however treatment and
previous liver diseases could be in the background too. Smaller and larger
cerebral bleedings, cerebral infarcts of various sizes are detected often. The
protein components (spike and nucleocapside) of the SARS-CoV-2 could be
demonstrated by immunohistochemical methods and the RNA genome of the SARS-CoV-2
by in situ hybridization in several organs, with highest amounts in the lungs.
Clinicopathological analyses effectively determine whether the cause of death in
SARS-CoV-2 infection had been the direct result of the infection, or any other
previously known chronic disease, which had been superposed by the viral
infection. However, in certain cases, the death might not be associated with the
SARS-CoV-2 infection. The correct determination of the cause of death of the
patients with COVID-19 is by consultation between clinicians and
pathologists.