COVID-19 as we know, can be
critical in 5% of all patients.
Such patients, typically
demonstrate progression to,
acute respiratory distress
syndrome, hypotensive shock
and multi-organ dysfunction.
The risk for these individuals largely
is seen in those who are older age.
So, median age of the
critically ill COVID-19 patients
at least 60 years of age.
They also many times have co-morbidities such as,
insulin dependent diabetes,
pre-existing cardiovascular disease,
hypertension, immunodeficiency, et cetera.
Refractory cases, meaning those patients,
who wind up in intensive care unit
for even longer than is typical,
are most often seen in those who are men,
who are older, who present
with pre-existing anorexia
and or don't have the typical fever.
So, it may be their immune response
is largely to blame for their
acute severity of illness.
Especially predictive, is an individual
presenting to medical attention,
with a peripheral oxygenation
factor of less than 90%
and even less than 93%in some studies.
Median time of onset,
so, after initial presentation of
the classic mild respiratory illness,
which we know, most people
suffer from with COVID-19.
After 9 to 10 days, these
individuals have progressed to,
shortness of breath, respiratory failure,
which requires them to be transferred
to the intensive care unit.
Their critical care needs of course are extensive,
so respiratory support,
basically, anything needed to
support, multi-organ failure,
septic shock and acute
respiratory distress syndrome.
When looking at immediate causes of death,
in critically ill COVID-19 patients.
It is most often septic
shock and multi-organ failure
and the secondary complications of those,
that are the immediate causes of death.
Death due to acute respiratory distress syndrome,
is less common, only because there
are more modalities available,
to try and support one's respiratory status.
So, what is to blame for these complications?
What is to blame for the
severity of critical COVID-19?
It's typically going to be a
combination of direct organ damage
from infection by SARS Coronavirus II,
as we we've talked about in
the pathogenesis session,
but also, the triggering of local
inflammation and then cytokine storm,
by indirect pathogenic mechanisms.
So, as the immune system
organizes and reacts against,
the SARS-Coronavirus II infection.
Widespread endothelial damage can occur,
Typically, an endothelialitis
which involves, the vascular
beds of multiple organ systems,
especially lungs, but also heart,
kidneys, liver and intestines.
this is if not unique to a,
COVID-19 and SARS-Coronavirus II infection,
it is certainly different than
that which is seen in influenza,
in that SARS-Coronavirus II
produces pulmonary angiogenesis,
during its infection or infectivity
of the alveolar epithelium,
causing then new blood vessels,
which of course then be can become leaky
and flood the alveoli due to the cytokine storm.
Disseminated intravascular coagulation (DIC),
Again, is a secondary phenomenon
from the endothelialitis,
the inflammation and microangiopathy,
which triggers in effect, multiple microinfarcts,
of the endothelial cells themselves,
triggering then a consumptive
coagulopathy or (DIC),
along with that,
hypercoagulability and thrombosis,
because again of the cytokines storm,
one is both consuming and providing abnormalities,
of the clotting factors leading
to strokes to thrombosis,
to pulmonary emboli and all the other
complications, you could imagine.
And then atypical inflammatory
response and autoimmune phenomena,
also, can be driven,
so, Guillain-Barré syndrome,
certainly, a variety of gait
disturbances and muscle weaknesses,
as well as, an entity known as
multi-system inflammatory syndrome,
in children or MISC, which, is
due to an autoimmune phenomena,
triggered by SARS-Coronavirus II infection.
So, what if you look at the at the organs,
what are the list of
complications by organ system.
So, within the brain any
anywhere from simple headache,
although I would argue, a
headache is never simple,
but a headache all the
abnormalities, with a sense of smell
and therefore, sense of taste to anosmia dysgeusia
and then nausea and vomiting and certainly,
impaired consciousness and cognitive disarray,
all are complications seen with the brain.
Within the lung where the type II pneumocyte,
is the preferred target of SARS-Coronavirus II,
followed by inflammatory response,
one can get direct alveolar damage,
but then also lymphocytes
and macrophage infiltration
in cytokine storm,
which basically, floods the lungs.
The kidneys, patients can present
with or develop acute renal failure,
along with tubular necrosis and as
well lymphocyte and immune system
infiltration followed by glomerular injury.
The heart, absolutely can develop myocarditis.
So active inflammation of
various myocardial tissues,
along with leukocyte infiltration.
Spleen and lymph nodes this largely
is due to accumulation of macrophages,
but also, secondary lymphocytes
in the spleen and lymph nodes,
so, enlarged lymph nodes and
enlarged splenic sequestration,
followed by tissue disruption.
And then the liver of course, is a target,
both a primary and a secondary target,
for the inflammatory burst or cytokine storm,
followed, potentially routine
SARS-Coronavirus II infection,
and those patients who have liver
injury of course can develop steatosis.
So, what are then the actual
illnesses that one can see,
in a critical COVID-19.
So, a primary viral pneumonia as well
as a secondary bacterial pneumonia,
acute kidney injury, pulmonary
thromboembolism, sepsis and septic shock,
respiratory failure and acute respiratory
syndrome and then cardiomyopathy.
So, as you could see the
complications of critical COVID-19,
are robust unfortunately they are quite severe
and you can understand why an
individual with critical COVID-19,
will be at risk for such a high mortality rate,
as has been seen so far in this pandemic.