COVID-19 cases have spiked in NSW, with the Delta strain of SARS-CoV-2 also leading to higher incidences of hospitalisation from severe symptoms. There are currently 357 COVID-19 cases admitted to hospital, with 60 people in the intensive care unit (ICU), 28 of whom require ventilation, and 29 deaths have occurred since 16 June.
While common symptoms of mild COVID-19 are well known – cough, fever, fatigue, loss of smell and shortness of breath – the symptoms for those admitted to hospital are much more serious.
So, what is it like to have severe or critical COVID-19?
Tissue damage in the lungs
As SARS-CoV-2 is a respiratory disease; it predominantly attacks lung tissue, specifically the cilia. These little hair-like structures exist on the outside of lung cells and form a protective layer to move fluid, mucous and debris.
However, as the cilia are eroded by coronavirus, the cells become infected and eventually die, exposing our microscopic air sacs. This disrupts breathing because oxygen and carbon dioxide exchange can’t function properly. The dead cells add to lung debris, and cells will continue to be damaged, leading to lung inflammation.
This inflammation triggers immune cells to come and clear out the virus. In mild cases, the immune cells may be successful, and symptoms may dissipate.
In severe cases, this can lead to lung damage.
Two common results of this in severe or critical cases are pneumonia and acute respiratory distress syndrome (ARDS). This is a life-threatening lung injury where fluid leaks into, and builds up, in the lungs so oxygen cannot be absorbed.
“The major complication that requires intensive care support is respiratory failure and low oxygen levels so people’s lungs, which should be filled full of air, predominantly their air sacs become filled with fluid and inflammatory material and it makes it difficult for them to breathe,” says Chris MacIssac, director of ICU at the Royal Melbourne Hospital.
When the inflamed tissue triggers an immune response, the immune cells aim to kill infected cells. However, sometimes the immune response is too strong and also kills healthy cells, so the lung tissue is eroded away, exposing the air sacs even further.
“A number of these patients require support through a breathing machine or what we call a ventilator.
“A proportion of patients – somewhere between 25% to 30% of patients who get hospitalised with COVID-19 – develop worsening respiratory failure.
“In our own hospital during 2020, for the 47 patients we cared for 60% of them required mechanical ventilation.”
People in this situation require emergency care as they are unable to breath on their own, and ventilators require constant supervision.
Another technique, called prone ventilation, aims to move the fluid around in the lungs so it doesn’t pool in the same place by lying patients on their front, instead of their back.
“If you’re lying in bed on your back [fluid] will predominantly fill up posterior, or back, parts of your lungs” says MacIssac. “And if you can shift that fluid around and improve what we call blood flow and airflow in the lungs and get that matching optimal, that can help.”
Regardless, ARDS is often fatal.
But the organ damage isn’t exclusive to the lungs – it can affect the brain, veins and heart, too.
A common complication seen in COVID-19 patients in critical conditions is encephalopathy, or diseases that change the brain’s structure and function.
These may affect around one third of patients and can manifest as stroke, movement and speech disorders or, in a few cases, seizures. A study in May 2021 showed that around 80% of people hospitalised with COVID-19 had some neurological condition. This may have been as mild as loss of smell, but 49% had acute encephalopathy, 17% had a coma, and 6% had a stroke, all of which increase the chance of death.
Blood conditions, clots and embolisms
Blood is responsible for delivering oxygen to cells and removing carbon dioxide, but blood conditions can also occur.
“[Patients] can have problems with their blood pressure, and require support of adrenaline like drugs to support their blood pressure,” says MacIssac.
Thrombosis has suddenly become a part of everyday vernacular, due to its association with the AstraZeneca vaccine, but it’s also a common symptom seen in people with severe and critical COVID-19.
A thrombosis is the formation of a blood clot – called a thrombus – that limits blood flow. An embolism occurs when a blood clot, or foreign object, gets stuck in a blood vessel and blocks most blood flow. They can move around in the veins and lodge in a different organ, such as the lung or leg.
Between 10% and 40% of COVID-19 patients in ICU experience an embolism in the lungs (pulmonary embolism) or legs (deep vein thrombosis), but there have also been reports of patients suffering strokes caused by an embolism.
When a blockage occurs in the veins, blood can’t get through and deliver oxygen to the organs beyond the blockade or make it back to the heart. That means blood backs up behind the clot and pools in the veins, pushing on muscles and other veins and arteries. Eventually, the tissue below the block, which isn’t receiving oxygen, will die. Depending on where in the body the embolism occurs, this can lead to gangrene or death if not removed.
Sometimes there may be no symptoms when somebody has a pulmonary embolism, but they often experience chest pain, loss of breath, rapid heartbeat and can be spitting blood. Most of these symptoms are also shared with heart complications.
Heart conditions and failure
Heart complications can manifest as faster heartbeat, chest pain, palpitations, heart failure and cardiac arrest. This may occur when SARS-COV-2 enters the heart and begins attacking heart tissue, causing inflammation that increases the likelihood of embolisms.
Some studies suggest that heart failure was present in around 50% of patients who died following critical COVID-19, but there isn’t yet substantial statistical evidence about the frequency of this occurrence.
When heart failure occurs, blood cannot be pumped around the body to provide oxygen to organs or remove carbon dioxide. Carbon dioxide is very acidic, and build up in cells and veins causes the pH of the cellular environment to drop. This can lead to hyperventilation and seizures.
According to a study from October 2020, patients who have a history of heart failure or heart conditions are at high risk of needing a mechanical ventilator or staying longer in ICU. The death rate among these people increases to about 40%, compared to 25% in people who have COVID-19-related heart failure without pre-existing heart conditions.
Some other symptoms that may occur during heart failure are dizziness, shortness of breath and fatigue.
The list goes on
While all these conditions may occur on their own, it is also common for patients to experience more than one, because of the flow-on effects of interrupted respiration when the lungs are weak.
When the immune system is so heavily compromised in these situations, the risk of other fungal, bacterial or viral infections and sepsis also increase.
Other types of complications can occur simply from being in bed for so long.
“People with the COVID-19, like all critically ill patients, are at risk of a range of complications that we try and guard against,” says MacIssac.
“Patients generally become weak. Your body is not designed to lie on a bed.
“Often, the lung problem takes several days if not weeks to resolve, so patients can develop weakness in their muscles and nerve function can deteriorate. And ultimately, when people are very sick their kidneys can require support.
“So, a range of organ systems can file and require additional support in severe overwhelming COVID-19.”
Each one is also exacerbated by pre-existing conditions, such as history of heart attack, asthma, obesity, cancer, diabetes, down syndrome, pregnancy or age.
Any one of these severe COVID-19 complications can land somebody in ICU, which provides intensive, consistent care during illness. However, when more people are admitted to ICU, resources run out and chance of death increases significantly.
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Deborah Devis is a science journalist at Cosmos. She has a Bachelor of Liberal Arts and Science (Honours) in biology and philosophy from the University of Sydney, and a PhD in plant molecular genetics from the University of Adelaide.
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