This is an excerpt from Second Opinion, a weekly roundup of eclectic and under-the-radar health and medical science news emailed to subscribers every Saturday morning. If you haven’t subscribed yet, you can do that by clicking here.
Understanding how COVID-19 attacks the human body is essential to developing an effective treatment or vaccine to stop the global pandemic — but there’s still so much we don’t know about how it can kill us.
As researchers around the world race to understand the illness, they are compiling and sharing their early observations of patients hit by a virus that has sickened more than two million people. The findings are preliminary, but they can help point researchers in the right directions.
They have seen that in severe cases, COVID-19 invades our respiratory cells and triggers an immune system response that targets those infected cells, destroys lung tissue and ultimately clogs our airways, cutting off our oxygen supply.
That’s when organ failure can also occur, causing severe damage to the kidneys, liver and heart, similar to other conditions like sepsis.
But they will look to determine whether the virus is targeting and shutting down organs in a new way or just behaving like other infections that cause such common complications.
Why COVID-19 can be so deadly
One key thing to understand about the deadliness of the coronavirus is how it infects the body and how our body responds to fight it.
Cytokines are small molecules released by the immune system that travel throughout the body to co-ordinate an immune response against an infection or injury — even with something as common as a mild fever.
But if the immune system overproduces them in response to the infection, they can cause “cytokine storms” that can rampage through the bloodstream and severely damage the body.
Dr. Douglas Fraser, an ICU doctor at London Health Sciences Centre and a researcher at Western University in London, Ont., has been studying that exaggerated immune response by collecting blood from critically ill COVID-19 patients in an effort to find new ways to treat the disease.
“The immune response to this particular disease is very different than what we’ve seen in other infected patients that end up in the ICU,” he said. “It’s a unique response and it’s going to require unique therapies.”
Fraser said his research shows there are different types of cytokines released in the body at unusual times and levels in response to COVID-19 compared with those that are typically found in critically ill patients from more common diseases.
“What we’re seeing seems to be occurring in all of the very sick patients: those who are requiring the ICU admissions, those who are requiring assistance with their breathing and those that are ultimately dying,” he said.
Kidneys tied to severe complications
Kidney damage was an “important complication” in a preliminary publication of a recent observational study of 287 COVID-19 patients in China, which found almost one in five had some stage of sudden or “acute” kidney injury, putting them at “substantially higher” risk of death.
While it’s not yet known what rate of Canadian COVID-19 patients have acute kidney damage, the majority occurs in severely ill patients, said Dr. Jeffrey Perl, a nephrologist at St Michael’s Hospital in Toronto and an assistant medical professor at the University of Toronto.
“As people’s blood pressure gets very low from a very massive, overwhelming inflammatory immune response, the kidneys are starved of blood,” he said, adding that it can often lead to the need for a dialysis machine to clean the patient’s blood.
To give an idea of how serious a complication it can be, Perl said the mortality rate for patients who had developed acute kidney injury from SARS in 2003 was 92 per cent, compared to just eight per cent in those who didn’t.
Chronic kidney patients are also at higher risk of death with COVID-19 compared to those without pre-existing conditions who are otherwise well, he added.
“We’re very worried about those patients getting a COVID-19 infection,” he said. “Similar to the elderly population that we’re very concerned about, I would consider these patients another high-risk group.”
Heart may be ‘directly’ targeted by virus
One essential organ that may be at direct risk from the virus is the heart.
A cohort study published in JAMA last month found almost 20 per cent of 416 hospitalized COVID-19 patients in China had heart damage during hospitalization, putting them at a higher risk for death.
Recent research from the American College of Cardiology found arrhythmia, or irregular heartbeat, in 16 per cent of patients and acute cardiac injury in 7.2 per cent.
“There’s the possibility and the likelihood that some of the virus might actually get taken directly up into the heart muscle cells and cause that heart injury,” said Dr. Patrick Lawler, a cardiologist and clinician scientist at the Peter Munk Cardiac Centre in Toronto.
“We hear anecdotes from other people that have had a little bit more experience, unfortunately, with this that really are consistent with the heart suddenly starting to become weak.”
An observational study of 187 patients hospitalized with COVID-19 published in the New England Journal of Medicine last month found high levels of troponin, which can indicate problems with the heart, in 28 per cent of hospitalized COVID-19 patients in Wuhan, China, which concluded they were at risk of “much higher mortality.”
Lawler said the outcomes for COVID-19 patients with cardiac issues are “dramatically worse,” and even though the virus enters through the respiratory system, it can take root in other areas of the body.
“The heart is really a critical, critical part of what determines whether or not patients are going to recover from this or not,” he said.
Can it help us find a cure?
Lawler is currently looking at the use of blood thinners as a possible treatment for COVID-19 patients, which may prevent the virus from binding to ACE2 receptors — enzymes found in cells throughout the human body that can act as an entryway for coronaviruses.
He said research suggests blood clots may play a role in organ failure in critically ill patients, so different doses of anticoagulants may prevent that from happening.
Fraser is also using his research on the “cytokine storm” immune response to COVID-19 to find “targets” to further efforts toward an effective treatment.
He said there could be multiple components to why different people are susceptible to the virus that range from genetics, to pre-existing conditions to age.
“Once we have an understanding of what’s going on, we can develop therapies, we can develop vaccines,” he said.
“Then we can get back to a normal life.”
To read the entire Second Opinion newsletter every Saturday morning, subscribe by clicking here.