Dr. William Brown

Special to The Lake Report

With COVID-19 we had some idea of what to expect because of earlier encounters with the SARS and MERS viruses whose genomes resemble that of the latest virus.

So, it was no surprise to learn that the most common, severe and feared complication of infection with COVID-19, reported first from China, turned out to be Acute Respiratory Distress Syndrome (ARDS), which carries a mortality rate of roughly 50 per cent for those who end up on a ventilator, especially in older patients.

On a case-by-case basis, SARS in 2002 and MERS in 2012 were more lethal but far less transmissible than COVID-19. Within four months, the latter infected close to three million worldwide and killed many thousands – more than 20,000 – in New York City alone.

The reason COVID-19 spread so widely and quickly is related to evidence that patients infected with COVID-19 shed the virus beginning as early as day two or three and may continue to do so for up to two weeks before clinical symptoms develop, or perhaps no symptoms at all.

That’s a long period in which infected patients can covertly spread the virus by as little as breathing or talking – never mind the coughing and sneezing that are features of the later symptomatic period.

This means that without widespread community testing for the virus using nose swabs to detect its molecular fingerprint, epidemiological modellers and planners have no idea how widely the virus has spread within communities and especially among health care workers in hospitals, long-term care facilities and other vital services.

And without equivalently widespread testing using reliable tests for antibodies, we have no idea how many people have had the disease and are now resistant to the virus.

There are other oddities associated with COVID-19. For example, although early reports suggested the virus strikes hardest those with pre-existing chronic medical problems and those over 60 years of age or usually both, more recent evidence suggests that as many as one-third of healthy young people may develop COVID-19.

In the case of health care workers, repeated exposure to high viral loads and perhaps the associated fatigue and high stress levels characteristic of their work, may increase the risk of them developing the disease and – not a few – dying.

The clinical course of COVID-19 is more complicated compared to other coronavirus infections. COVID-19 symptoms often begin with fatigue, aching in muscles and joints, headache, fever, loss of smell and perhaps taste, tightness in the chest, and diarrhea, any one or more of which symptoms may be incapacitating enough to force some to stay home in bed.

In this phase acetaminophen for pain and fever and hydration may help alleviate the symptoms. From this stage, most go on to recover after a few days.

However, some – especially high-risk patients – may develop significant hypoxemia (low blood oxygen levels) paradoxically unaccompanied by shortness of breath – a sure sign of developing pneumonia.

This, often missed, intermediate stage is when patients need the close surveillance and support of intensive care units – should the hypoxemia worsen – which can happen quickly – and intubation and ventilator support become necessary.

COVID-19 may also seriously attack other systems, such as the heart, sometimes simulating a heart attack, but here caused by viral myocarditis, the bowel associated with diarrhea, or the kidneys, sometimes requiring dialysis. Any one or more of these may develop. Those extra-pulmonary targets of COVID-19 may be the result of the virus targeting ACE receptors in those tissues as well as the primary target – the lungs.

Given the sudden worsening in some patients, there’s a lively debate about what to do. Is the collapse the result of an overactive immune response and release of proteins called cytokines, some of which, like interleukin-6 (IL-6), may attack the body’s own cells such as those that line the walls of the tiny alveoli where gas exchange normally takes place?

And if so, would drugs such as tocilizumab – ordinarily used in rheumatoid arthritis block to block IL-6 – help patients? Or would corticosteroids, which blunt the immune system across the board, make sense? Those are critical questions and highlight dilemmas in treating this disease.

The trouble now, at the four-month mark in this pandemic, is that those who treat patients with COVID-19, especially the more severely affected patients, don’t have all the answers – which means some care decisions might turn out to be wrong and even make matters worse!

That’s what happens when a novel virus like COVID-19 crops up out of nowhere. It takes time to find out what works, what doesn’t work and even what makes matters worse, and share what’s been learned with others facing the same challenges elsewhere.

As the journal Science put it on April 16, “As people with COVID-19 flood hospitals worldwide, physicians are wading through streams of incomplete data and preprints that have not been peer-reviewed, struggling to find ways to help their patients and sharing their experiences on social media. … People are watching patients deteriorate before their eyes, and there’s a very strong motivation to reach for any therapy that you think could be effective said Kenneth Baillie, an intensive-care anesthetist at the University of Edinburgh.”

It must be very tough indeed to be on the front lines these days and all the more reason to be thankful that those who are there for us, trying their best at considerable risk to themselves.

So, thank those working in the front lines of this pandemic when you have the chance – they deserve it

* Check out this item on intensive care from BBC radio: https://medium.com/@mark.tan.zy/telephone-lament-for-coronavirus-5180d2984617

Dr. William Brown is a professor of neurology at McMaster University and co-founder of the Infohealth series held on the second Wednesday of each month at the Niagara-on-the-Lake Public Library.