Grading ourselves against reality

One of the really enlightening parts of this crisis, from a medical perspective, is the emerging sense of how COVID-19 proves to be so deadly for specific patient groups. There were endless discussions during ward rounds as we sought to anchor the patterns of problems faced by our patients into presentations that we at least partially recognised and hence were able to have some rationale for our treatments.

We are now starting to get answers to some of the questions and a real sense of where we went right and where we went wrong. The lung problems were the most obvious. In the early stages we saw patients with quite ludicrously low levels of oxygen in their blood. Many of these patients were breath quickly but did not otherwise seem affected by having an oxygen level lower than someone on the top of Everest. We were all surprised by how many spoke in full sentences and did not seem the slightest confused.

Later, once the patients were on the ventilators we found COVID-19 lung a completely different beast. Lungs were filled with secretions and could be much harder to ventilate – often requiring high pressures with high concentrations of oxygen to get even barely adequate oxygen levels in the blood. We tried everything including turning the patients prone and then back again like a giant rotisserie, but many of the results were mixed and what worked in one patient didn’t generalise to others or often did not reproducibly work in the same patients. Moreover, COVID gives very distinctive radiological changes. COVID patients were clearly behaving very differently to previous patients with non-COVID-19 acute respiratory distress syndromes.

So a recent paper in the New England Journal of Medicine has taken our attention. The study authors looked at the lungs of people who had died of Coronavirus and compared this to patients dying of influenza. Many of the findings were similar, including tiny blood clots blocking vessels and damage to the air sacs that make the lung. However, one finding in COVID was the generation of new blood vessels in response to the lung inflammation – a feature not seen in acute respiratory distress syndromes caused by non-COVID insults to the lungs.

The study is small and limited by the extremely chaotic nature of lung changes, however does give us important clues that we were going along the right lines in supposing that COVID19 was causing a completely different type of pathology.

Unfortunately it is still a bit early to change our treatments, although there are already trials of drugs that would dampen over-exuberant inflammation. For now, it is certainly satisfying to see our (in hindsight quite naive) clinical suspicions prove to be founded on something real. The rapid reductions in COVID-19 make it difficult to know if there will be many future opportunities to study this disease – will it simply vanish like the flying Dutchman.