Autopsy Comparison of COVID 19 vs. Flu vs. Normal Lungs

Autopsy Comparison of COVID 19 vs. Flu vs. Normal Lungs

Both COVID 19 and the flu can cause pneumonia and ARDS (acute respiratory distress syndrome). Both of these can cause respiratory failure and death. We know that COVID 19 is more likely to cause severe disease than influenza and has a higher case fatality rate. We also know that COVID 19 is much more likely to cause blood clots than influenza. In this recent study published in the NEJM, they compared lung autopsy findings from deceased COVID 19 patients and Influenza and compared those findings to people who died of other causes, who had normal lungs. This group, with the normal lungs, served as the control group. Pneumonia is a broad medical term that refers to an inflammation within parts of a lung or both lungs. This entails the tiny air sacs of the lungs, called alveoli, to fill up with inflammatory fluid, impairs oxygen flow from the air to the bloodstream.

The consequences of pneumonia, whether caused by COVID 19 or influenza, can result in dangerously low oxygen levels in the bloodstream and, if not treated, can result in death. Sometimes if pneumonia is severe enough, it can cause ARDS, which refers to severe inflammation within both lungs, which causes extreme difficulty with getting oxygen into the blood. This is a well-known syndrome that can occur with either COVID 19 or influenza pneumonia. COVID 19 inflicts a particular type of damage in human lungs that is somewhat different from the picture we see with influenza. To understand the differences, researchers looked at the lungs of seven patients who died of respiratory failure from COVID 19 and then compared them to the lungs of seven patients who died of pneumonia caused by influenza A.

They also compared them to the lungs of ten uninfected lungs, which came from people whose organs had been donated for transplant but were not used, so these were normal lungs. The researchers were careful to match and could the gender and age, so their comparisons among the groups of patients would be meaningful. All of the lungs came from older patients and whose average age in the covid 19 group ranged from 68 years old for the females and 80 for the males. The influenza group's average age ranged from 62 years for the females and 55 for the males. Perhaps the most interesting and important finding of this research revealed damage to the lungs' small blood vessels, meaning lung capillaries. The lining of these capillaries is called the endothelium, and the cells that make up the endothelium have ACE2 receptors. The cells were, in fact, infected with covid 19. In this study, the researchers found severe microscopic injuries to the endothelium here, with actual disruptions of the cell membranes.

They also found widespread clotting in these lung capillaries surrounding the alveoli, which included actual blockage of the capillaries, and microangiopathy, which involves thickening and weakening the small blood vessel walls leak blood and protein, further slowing the flow of blood. Although fibrin clots in the alveoli's capillaries were present in the lungs from both the COVID 19 and influenza patients, micro-clots in the capillaries surrounding the alveoli were nine times as prevalent in the lungs of COVID 19 patients as compared with the lung tissue of the influenza patients. What’s more, COVID 19 patients showed actual new blood vessel growth, primarily through a process known as intussusceptive angiogenesis. The word “angiogenesis” means the formation of new blood vessels. The term “intussusceptive” refers to something telescoping inside itself. In this context, it's referring to new blood vessels being formed by a pillar of tissue within another blood vessel, effectively splitting the vessel into two. The researchers believe this process contributes to more problems with clotting and inflammation of the lining of the blood vessels than is seen in the lungs of patients with influenza. Angiogenesis was seen much less frequently in patients' lungs with influenza and normal lung control. The researchers also looked at the ACE2 receptor, which allows the COVID 19 virus to gain entry into cells. Compared to the control group's lungs, there were more ACE2-positive cells in the lungs of both COVID 19 and influenza patients. The study speculates that the reason for more angiogenesis in the COVID 19 group is because of the evidence of viral invasion of these endothelial cells.

Doctor Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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Видео Autopsy Comparison of COVID 19 vs. Flu vs. Normal Lungs канала Doctor Mike Hansen