Horrible as it may be to face the singular failure of the COVID-19 response in the United States and the ever-rising case count, the case fatality rate in the United States has been—slowly, slowly—falling. In the last week it finally edged below 5%, which is still awful, but it’s somewhat less awful than it has been since March. Some of that is because the age of those testing positive has been steadily moving younger, especially in the states like Texas, Florida, and California where cases have been increasing rapidly. Some of that is simply because cases are rising rapidly and death, sadly enough, is a trailing indicator.
But part of that improvement is simply improvement. It’s the result of six months of treating people in the United States and around the world, and learning what course of treatment works best for people who have serious cases of COVID-19. That doesn’t just mean things like treating patients with remdesivir and anti-inflammatory steroids; it means things as simple as rolling patients onto their sides when on respirators, and using more oxygen earlier. Patients who have survived COVID-19 have provided the best source of how that survival can be managed, as well as antibody-rich plasma, which itself is being used to treat other patients. However, at this point over 130,000 Americans have died from COVID-19—and as it turns out, they also have something to teach us.
As The Washington Post reports, autopsies of those who have died from COVID-19 are providing a wealth of information on, as might be expected, how COVID-19 damages bodies. The tendency of the virus to cause blood clots—a feature that is thought to be connected to how the virus binds to cells—means that what it does to the body can take many forms. Rather than the pneumonia typical of some related viruses, SARS-CoV-2 tends to damage the lungs by blocking and filling tiny blood vessels. The virus can cause strokes. It can cause heart attacks. It can damage the kidneys. It can even cause clots that block blood flow to limbs, which then require amputation.
Where some hemorrhagic diseases cause bleeding by destroying the cells that make blood clotting platelets, COVID-19 amplifies the effect of these cells, clotting the blood right in a patient’s veins.
These clots cause damage to the lungs specifically because the lungs are full of tiny vessels, vessels so small that blood cells pass through single file in order to promote the exchange of oxygen and carbon dioxide. It doesn’t take much to block these vessels. Or to turn sections of the lung into masses that look almost like stone in X-rays.
Understanding the way in which the disease operates has also provided some tools that can be used to determine just what percentage of the population might be expected to suffer critical effects from COVID-19. That number works out to around 4% — which matches well with the relationship between confirmed cases, the rate of hospitalization, and the number of serious or critical cases. If COVID-19 were to go unchecked, the number of Americans needing a hospital bed would exceed available beds by an order of magnitude.
One bit of relatively good news from the autopsies: Early reports out of China indicated that a large percentage of patients were being left with signs of myocarditis, a thickening of the heart that makes sudden heart attack more likely in the future. Autopsies in the U.S. have found that even in patients who died from heart attacks while suffering from COVID-19, there’s not much sign of the sections of dead tissue that would result from this condition. Instead, the heart attacks may also be coming from the same cause as so many other issues: those damn clots. Clotting cells that are normally very rare in the heart were much more common in COVID-19 patients.
The information that’s being found in the bodies of those who have died from COVID-19 offers the best window we have into the action of the virus and the way in which it attacks the human body. Unfortunately, so far at least, the drugs normally used to reduce clotting in patients with heart issues don’t seem to be effective in protecting patients with COVID-19. But understanding the mechanism of death is the first step in preventing it.