The complications that are known in critical patients with COVID-19 infection
are as mentioned before, acute respiratory distress syndrome.
This ARDS as we know from prior lectures accidentally presented by Lecturio.
This is a syndrome characterized by acute onset of hypoxemic respiratory failure, typically bilateral infiltrates
and it is due as a final kind of pathway to diffuse alveolar damage.
That damage then precipitates the hypoxic respiratory failure
which is associated with VQ mismatch and pulmonary shunting.
So after a certain point, as the immunologic mediators, the cytokine cascade
causes a diffused alveolar damage, then the patients are unable to be successfully ventilated.
They develop pulmonary shunting and they develop hypoxemic failure.
Along the same lines then. Septic shock, also a known complication with patients with critical COVID-19.
Again, this is likely due to an immunologic mechanism
in which cytokine cascade is precipitating not necessary cardiogenic shock, but perhaps peripheral shock.
So causing vasodilation, warm shock if you will, and an inability to profuse in organs
that therefore means patients with septic shock likely will also develop multi-organ dysfunction.
And in COVID-19 patients, the kidney appears to be preferentially targeted.
So, patients not only will have respiratory failure,
but they may have renal insufficiency or renal failure requiring advanced support.
Patients who meet these criteria -- who develop these complications with COVID-19 disease
have a much higher mortality than even the general estimates presented earlier in this talk.
From -- anywhere from 22 to 62% of patients who enter a critical care unit or critical care setting
with SARS coronavirus 2 infection or COVID-19 disease have a likelihood of death.
And these are patients who also meet the same criteria for the refractory COVID-19 disease we mentioned before.
E.g. male, somewhat older, presenting with low fever or lack of fever and potentially anorexia.
A major question emerging of course is how do we differentiate COVID-19
versus all the other respiratory diseases which are occurring in the world even at this time.
One of those are the diseases -- well, how -- we are still in the middle of influenza season,
there also are parainfluenza cases, rhinovirus cases, other coronaviruses
which aren't necessarily causing lower respiratory tract disease
but are presenting with upper respiratory tract disease with potential to progress.
And then some bacteria, for example;
Bordetella pertussis, whooping cough or atypical pneumonia is caused by mycoplasma chlamydia.
All of these are present in the world right now as we experience COVID-19 as a worldwide pandemic.
And they all have extensive overlap with COVID-19 presentations.
Certainly, initial presentation clinically is very similar: fevers, tactile or proven, a cough, typically dry
but sometimes productive, anorexia, fatigue, malaise, myalgias.
All these are very much flulike illnesses which are very typical.
And even physical examination fails to differentiate between COVID-19 disease and other respiratory infections,
so too with typical laboratory evaluation including the peripheral white blood cell count.
In fact, many patients with COVID-19 and other respiratory infections
which are non-bacterial are presented with a normal peripheral white blood cell count,
perhaps with a slight lymphopenia or a slightly lower number of circulating lymphocytes
only because those particular white blood cells are being consumed or marginated if you will by the underlying viral infection.
All these patients have signs and symptoms suggesting of a pneumonia which may be difficult to differentiate.
All have the potential to progress to severe disease with some risk factors.
And again, those of older age, those of immunodeficiency or immunosuppression,
those with comorbidities as mentioned before are all going to have risk of a progression
to severe to critical COVID-19 and severe to critical other viral respiratory disease.
So, how then can we make the distinction?
Well, first and foremost, maybe the exposure.
In the early days of the pandemic, patients who had traveled to or exposure to areas
with prevalent with COVID-19 were of course considered a patient under investigation; PUI.
So too those on cruise ships, so too those who had a known exposure to a known patient with COVID-19 disease.
However today, and this is end of March 2020,
the potential for local or community spread is quite extensive around the world.
And so, travel history no longer has the same significance in differentiating COVID-19 versus other diseases as it did before.
Initial presentation. Again, very difficult to differentiate the two.
However, there is the potential for those with refractory disease.
So, male, older, hypoxemia, especially with a peripheral oxygenation percentage of less than 90%
and those who have lack of fever. And then unilateral versus bilateral disease.
One feature of COVID-19 disease is that its pneumonia is bilateral and it is diffuse.
This can be differentiated in some cases from other respiratory infections such as influenza or other coronaviruses
which are more likely to have unilateral or single lobe; patchy densities.
So, chest CT scan is one way to differentiate COVID-19 infection versus other respiratory disease
in that it demonstrates in a significant majority of patients; bilateral,
ground-glass opacities in patients with COVID-19 disease versus more typically;
patchy shadows or densities in single lobes which are seen in other respiratory infections
such as influenza, parainfluenza and even other coronaviruses.
Emerging however, this has just been in the last week, is the potential to distinguish COVID-19 cases
from other respiratory infections via the presence of liver function abnormalities.
Specifically, patients with COVID-19 are presenting with
or developing increased numbers of aspartate-aminotransferase, AST, alanine aminotransferase,
ALT, gamma-glutamyl transferase, GGT, lactate dehydrogenase, LDH, and a-Hydroxybutyrate dehydrogenase.
Patients who present certainly with elevated liver enzymes
such as these, the transaminases along with the respiratory symptoms and signs we've discussed before
might then be considered to be more likely than not to have COVID-19 disease versus all the other possibilities.
Putting all these together then. Whom can we consider to be at risk for a severe or critical COVID-19 disease?
First and foremost, again are those who have older age.
Remember again, the median age of patients presenting with COVID-19
who then ultimately developed critical disease requiring intensive care unit support had a median age of 60 years of age.
Those with comorbidities: hypertension, coronary artery disease, cerebrovascular disease
and unfortunately, diabetes mellitus, both types I and II,
and certainly those who have a peripheral oxygenation presented of less than 90%.
And finally, those who develop or are found to have diffuse ground-glass opacities on chest CT scan.
This is beginning to become a case definition of patients with COVID-19 disease at risk for severe or critical progression.
So, as more is discovered, as more becomes available, certainly this case definition may become further fine-tuned.
But at this point, given the immunologic pathogenesis of the virus itself,
how it targets specific patient populations, those who have higher expression of ACE2 enzyme --
receptors or enzyme antigens at the cell surface of epithelial cells,
these are patients that we can consider at risk for disease versus other types of viral illnesses,
and certainly at risk for severe or critical progression. Until then, stay tuned to get more information.