Both Coronavirus aka COVID-19 and the flu (influenza) can cause pneumonia, and ARDS, acute respiratory distress syndrome. Both of these can cause respiratory failure and death. We know that COVID is more likely to cause severe disease compared to influenza, and has a higher case fatality rate. We also know that COVID is much more likely to cause blood clots than influenza. In this recent study published in the NEJM, they actually compared lung autopsy findings from deceased patients of COVID 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 very broad medical term that refers to an inflammation within parts of a lung, or parts of both lungs. This entails the tiny air sacs of the lungs, called alveoli, to fill up with inflammatory fluid, which impairs the flow of oxygen from the air to the bloodstream.
The consequences of pneumonia, whether caused by Coronavirus 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 or influenza pneumonia. SARS-CoV-2 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 Coronavirus 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 as well as they could, the gender and age of the patients so their comparisons among the groups of patients would be meaningful. All of the lungs came from patients who were older and whose average age in the Coronavirus group ranged from 68 years old for the females and 80 for the males. The average age in the influenza group 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 small blood vessels of the lungs, 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 SARS-CoV-2. The researchers in this study found severe microscopic injuries to the endothelium here, with actual disruptions of the cell membranes.
The 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 of the small blood vessel walls, which begin to leak blood and protein, further slowing the flow of blood. Although fibrin clots in the capillaries of the alveoli were present in the lungs from both the Coronavirus and influenza patients, micro-clots in the capillaries surrounding the alveoli were nine times as prevalent in the lungs of patients with COVID-19 as compared with the lung tissue of the influenza patients. What’s more, is that 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 the lungs of patients with influenza as well as the control group of normal lungs. The researchers also looked at the ACE2 receptor, which is what allows the SARS-CoV-2 virus to gain entry into cells. Compared to the lungs of the control group, there were more ACE2-positive cells in the lungs of both COVID-19 and influenza patients. The researches in the study speculate that the reason for more angiogenesis in the COVID group is because of the evidence of viral invasion of these endothelial cells. Also, endothelial cells in the specimens in the COVID group showed cellular swelling and disruption of the junctions in-between cells.
Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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