COVID-19 Autopsy Pathology Findings
Summary
TLDRIn this detailed presentation, pathologist Dr. Andrea Gilbert shares autopsy findings of a patient who died from COVID-19. The patient, a young to middle-aged woman with obesity and possible asthma, presented with severe respiratory failure and was diagnosed with acute respiratory distress syndrome (ARDS) due to the virus. Autopsy revealed extensive lung damage with large areas of consolidation, pulmonary edema, and desquamation of pneumocytes. Notable was the presence of diffuse alveolar damage, perivascular lymphocytic infiltrates suggestive of vasculitis, and rare multinucleated giant cells. The heart showed signs of takotsubo cardiomyopathy and edema without evidence of viral myocarditis. Acute kidney injury was also observed. Dr. Gilbert emphasizes the importance of ventilator use in severe cases and cautions against the misuse of hydroxychloroquine. This comprehensive analysis provides valuable insights into the pathogenesis of COVID-19, highlighting the need for serious consideration of the disease, even among younger individuals.
Takeaways
- 🧬 The patient, a young to middle-aged woman with obesity and possible asthma, presented with COVID-19 and experienced severe respiratory failure, leading to acute respiratory distress syndrome (ARDS) and death.
- 🩺 Clinically, the patient showed signs of heart dysfunction with elevated cardiac markers, low oxygen levels, and a diagnosis of septic shock and cardiogenic shock, indicative of the multi-system impact of COVID-19.
- 🔍 Autopsy findings revealed extensive lung damage with large areas of consolidation, severe pulmonary edema, and desquamation, which are consistent with the patient's clinical hypoxia and respiratory distress.
- 🔬 Microscopic examination showed evidence of viral cytopathic effects, suggesting direct damage to lung cells by the virus, and the presence of multinucleated giant cells and hyaline membranes, characteristic of diffuse alveolar damage.
- 🫀 The heart showed no signs of ischemic injury, but there was evidence of a rare congenital condition affecting the right atrium, which may have contributed to cardiac abnormalities during the severe lung infection.
- 🩸 Peripheral blood smear showed atypical lymphocytes and a left shift, indicating the body's active response to infection, but no clear evidence of thrombosis.
- 💊 The patient had received hydroxychloroquine, a drug with a narrow therapeutic window, which requires close monitoring due to its potential toxicity.
- 🧠 The neuropathology findings were not discussed in the script, but the presenter mentioned presenting such findings in other episodes, highlighting the multi-organ impact of the virus.
- 📉 The kidneys showed no signs of primary infection or inflammatory disorder but had focal areas of acute tubular injury, potentially linked to severe hypoxia from the lung injury.
- ⚖️ The autopsy findings underscore the severe impact of COVID-19 on the respiratory system and the importance of understanding the pathogenesis of the disease for clinical management.
- ⚠️ The presenter emphasized the importance of not dismissing the use of ventilators in severe cases, as they are often necessary to prevent patients from drowning in their own fluids due to lung failure.
Q & A
What is the significance of sharing autopsy results for a patient who was positive for COVID-19?
-The significance lies in the limited pathology data available for COVID-19. Autopsy results can provide valuable insights into the disease's impact on the body, which is crucial for clinicians in ICUs and emergency departments to better understand and combat the virus.
What was the patient's clinical presentation before her death?
-The patient, a young to middle-aged woman, presented with a one-week history of fever, cough, and dyspnea (difficulty breathing). She had obesity and a possible history of asthma. In the emergency room, she experienced severe respiratory failure and hypotension.
What was observed in the patient's lung during the autopsy?
-The lungs were heavy, boggy, and consolidated, with a firm or rubbery consistency instead of the normal spongy feel due to air. There was significant pleural edema and areas of consolidation. Microscopically, there was diffuse consolidation, pulmonary edema, and desquamation of pneumocytes.
What is the 'viral cytopathic effect' mentioned in the autopsy?
-Viral cytopathic effect refers to the changes in the appearance of cells that have been infected by a virus. Infected cells often appear abnormal and different from healthy cells, which can be observed under a microscope.
What was the patient's cardiac condition?
-The patient was diagnosed with reverse takotsubo cardiomyopathy, also known as 'broken heart syndrome,' which is not an ischemic type of cardiomyopathy. She also experienced cardiogenic shock and had elevated cardiac markers indicating concern about her heart function.
What was found regarding the patient's kidney condition?
-The patient had acute kidney injury with evidence of acute tubular injury and necrosis, which could be related to severe hypoxia due to her lung injury.
What is the role of hydroxychloroquine in the treatment of COVID-19 as mentioned in the script?
-Hydroxychloroquine was mentioned as a treatment the patient received. However, it's noted that it's not a benign drug and requires close monitoring due to its narrow therapeutic window, meaning the margin between effective dosage and toxicity is small.
What was the patient's vascular condition as observed during the autopsy?
-There was a perivascular lymphocytic infiltrate observed around the blood vessels in the lungs, which in some areas resembled vasculitis. However, the patient tested negative for ANCA, which is typically associated with vasculitis.
What are the implications of the autopsy findings for the understanding of COVID-19 pathology?
-The autopsy findings provide detailed pathological insights into the effects of COVID-19, particularly the extensive lung damage, which aligns with the clinical presentation of acute respiratory distress syndrome (ARDS). It also suggests potential cardiac and renal involvement.
What is the importance of not jumping to conclusions about micro thrombi in COVID-19 cases?
-The importance is to avoid misinterpretation of findings that could lead to inappropriate treatment. Micro thrombi can occur in the context of diffuse alveolar damage with acute lung injury, not necessarily indicating a systemic prothrombotic state.
What was the patient's age and medical history?
-The patient was a young to middle-aged woman with a past medical history significant for obesity and a questionable history of possible asthma.
What was the patient's condition that led to the autopsy?
-The patient passed away due to complications from COVID-19 infection, which resulted in acute respiratory distress syndrome (ARDS), septic shock, cardiogenic shock, and acute kidney injury.
Outlines
👩⚕️ Introduction to a Special Presentation on COVID-19 Autopsy Findings
Dr. Andrea Gilbert, a board-certified pathologist, introduces a special presentation on the autopsy findings of a patient who died from COVID-19. She emphasizes the importance of sharing such pathology data, which is scarce compared to the abundant clinical reports, to better understand the disease's impact on the body and to assist medical professionals in managing the pandemic.
📋 Clinical Presentation and Autopsy Findings of a COVID-19 Patient
The video presents the case of a young to middle-aged woman with obesity and possible asthma, who died from COVID-19 after experiencing fever, cough, and dyspnea. The autopsy revealed severe lung damage, including dullness, redness, and consolidation, with pleural effusion and lymphocytic pleuritis. Microscopic examination showed diffuse consolidation and air space filling, indicating impaired gas exchange due to fluid and cellular infiltrate.
🔬 Viral Cytopathic Effects and Lung Tissue Analysis
The autopsy findings suggest extensive pulmonary edema and the presence of viral cytopathic effects, which are visible changes in cell morphology due to viral infection. The video highlights the severe impact on the lungs, with cells appearing abnormally enlarged and reactive, indicative of the virus's effect on lung tissue. The desquamation pattern observed suggests a significant loss of normal lung function.
🩺 Lung Pathology and Gas Exchange Impairment
The video discusses the lung pathology observed in the autopsy, including areas of blocked alveoli and a desquamation pattern where pneumocytes are falling off, preventing gas exchange. The presence of hyaline membranes, a characteristic feature of diffuse alveolar damage, is also noted. These membranes line the alveolar spaces and further impede gas exchange, contributing to the patient's severe hypoxia.
🧫 Diffuse Alveolar Damage and Inflammatory Response
The autopsy case shows evidence of diffuse alveolar damage with edema, fibrin exudates, and a significant inflammatory response characterized by the presence of numerous neutrophils and lymphocytes. The patient's lung tissue exhibited features consistent with viral pneumonia, including lymphocytic infiltration and the formation of hyaline membranes, indicating an active inflammatory process.
🩸 Caution Regarding Thrombosis and Coagulopathy in COVID-19
Dr. Gilbert advises caution regarding the use of anticoagulant therapy in COVID-19 patients, given the risk of thrombosis and the potential for diffuse alveolar damage to cause microthrombi formation. She did not observe microthrombi in this particular case but acknowledges the need for further research on the topic. The discussion also touches on the vascular findings within the lung, including perivascular lymphocytic infiltrates and possible vasculitis.
🫀 Cardiac Findings in the Autopsy Patient
The video describes cardiac findings in the patient, including a thin right atrium with areas lacking myocardium and suspected congenital issues. Despite concerns for viral myocarditis, the autopsy did not reveal evidence of inflammation indicating the presence of the virus in the heart tissue. However, edema and rare focal lymphocytic infiltrates were observed, raising questions about the cause of the cardiac abnormalities.
💊 Considerations on Hydroxychloroquine and Cardiac Function
Dr. Gilbert discusses the potential effects of hydroxychloroquine, noting that it is not a benign drug and requires close monitoring due to its narrow therapeutic window. She suggests that the drug's administration might have influenced the cardiac findings, but there was no clear evidence of myocarditis in the patient. The video emphasizes the importance of considering all factors when managing patients with COVID-19.
🧵 Kidney Pathology and Acute Tubular Injury
The autopsy revealed unremarkable kidney tissue with no signs of primary infection or inflammatory disorders. However, focal areas of acute tubular injury were identified, which could explain the patient's elevated creatinine levels and acute kidney injury. The video suggests that severe hypoxia due to lung injury might have contributed to this renal damage, but a direct viral effect on the kidneys was not evident.
📝 Conclusion and Thanks for the Educational Presentation
Dr. Gilbert concludes the presentation by thanking the family for allowing the case to be shared and emphasizing the educational value of the autopsy findings. She highlights the importance of understanding the pathogenesis of COVID-19 through pathology and encourages healthcare professionals to stay informed about the disease's effects on various organs.
Mindmap
Keywords
💡Neuropathology
💡Autopsy
💡COVID-19
💡Acute Respiratory Distress Syndrome (ARDS)
💡Viral Cytopathic Effect
💡Pulmonary Edema
💡Lymphocytic Infiltrate
💡Vasculitis
💡Takotsubo Cardiomyopathy
💡Acute Kidney Injury
💡Hydroxychloroquine
Highlights
Andrea Gilbert, a pathologist, discusses an autopsy of a COVID-19 positive patient to provide insights into the pathology of the virus.
The patient was a young to middle-aged woman with obesity and possible asthma, presenting with fever, cough, and dyspnea.
The patient experienced severe respiratory failure, hypotension, and hypoxia, leading to intubation and ventilation.
Laboratory findings included low lymphocyte count, elevated cardiac markers, and positive antinuclear antibody (ANA), with negative ANCA.
Autopsy revealed extensive lung damage with consolidation, pulmonary edema, and desquamation, impeding gas exchange.
Microscopic examination showed viral cytopathic effects in lung cells, indicating direct damage from the virus.
Diffuse alveolar damage was present, characterized by hyaline membranes and fibrin exudates, typical in acute lung injury.
Perivascular lymphocytic infiltrates were observed, suggesting a possible vasculitis associated with COVID-19.
The patient had acute kidney injury with evidence of acute tubular necrosis, potentially linked to severe hypoxia from lung injury.
Heart pathology showed no signs of viral myocarditis, but there was evidence of edema and areas of the right atrium with thinned myocardium.
The patient's cardiac issues might be related to the lung involvement and not directly to viral myocarditis.
Andrea Gilbert emphasizes the importance of ventilators in treating severe respiratory failure in COVID-19 patients.
The case highlights the severe clinical course and potential for acute organ damage in patients without significant comorbidities.
Hydroxychloroquine treatment in the patient is discussed, noting the need for close monitoring due to its narrow therapeutic window.
The autopsy findings provide valuable data for understanding the pathogenesis of COVID-19 and its impact on various organs.
Gilbert dispels myths about the dangers of ventilators, stressing their necessity in life-threatening respiratory conditions.
The presentation concludes with a reminder of the seriousness of COVID-19 for all age groups and the importance of taking preventive measures.
Transcripts
[Music]
hello and welcome to Adventures in
neuropathology
I have a very special presentation for
you all today a little bit of background
my name is Andrea Gilbert I am a
pathologist I am a physician I am board
certified in anatomic pathology clinical
pathology and neuropathology and usually
on this platform I share with you guys
the neuropathology part of my practice I
am also the autopsy director at my
institution and I wanted to share with
you the results of an autopsy that we
did for a patient who was positive for
kovat 19 I think that this is very
important because we don't have a lot of
pathology data out there regarding kovat
19 we do have quite a few clinical
reports coming out of how these patients
are doing in a clinical perspective but
we don't really have a lot of reports
out there based on pathology studies and
so I just want to say thank you so much
to the family for allowing me to present
this I think it gives a lot of
information to our clinical colleagues
in the ICUs and in the emergency
departments so that we have a more
informed position when trying to fight
this virus on the on the global stage
okay so let's get started okay this is a
clinical presentation fortunately we
haven't had
that many deaths yet in the San Antonio
area so I don't want to share with you
her exact age but she was a young to
middle-aged woman and she presented six
days before she passed away with a
one-week history of fever cough and
dyspnea which means difficulty breathing
her past medical history was significant
for just obesity there was a
questionable history of possible asthma
my impression was that she would puff on
an inhaler every once in a while
especially during allergy season but as
far as having pulmonary function testing
that she didn't have that official
diagnosis in the emergency room she was
noted to have severe respiratory failure
and hypotension she had some serious
hypoxia meaning that her oxygen levels
were very low and so she immediately had
a breathing tube stuck down her throat
to help her breathe and was put on a
ventilator so here are some labs and
again this is a pathology presentation
so this is going to be very brief to the
non pathologist non-medical folks out
there her white blood cell count had a
normal range but the peripheral
lymphocyte count the absolute lymphocyte
count was a little bit low and this has
been described in other patients with
Kovan and the reason for that is not
clear her cardiac markers which is the
troponin and the BNP her cardiac markers
were elevated so there was concern about
her heart function the d-dimer was
elevated interleukin 6 was undetectable
that did increase throughout her stay of
note ANCA was negative
I will show you a little bit of
vasculitis in the future here in just a
little bit but ANCA was negative she did
have a positive a na for the non-medical
folks we see a na in disease processes
like SLE lupus and a few other things so
the the meaning for this as far as how
much it was implicated in her disease
process that is unclear but ultimately
throughout her medical admission she was
diagnosed with a RDS which is acute
respiratory distress meaning you're
having some severe difficulty breathing
requiring ventilation requiring her to
be on a ventilator and this was believed
to be secondary to
Kovan 19 infection and she was positive
for the the kovat 19 virus which is
called the SARS copa 2 virus she did
have an instant me what that means is a
myocardial infarction she had not enough
oxygen getting to the muscle tissues she
developed septic shock
cardiogenic shock and she also had this
reverse tuck asobu cardiomyopathy
colloquially this is called broken heart
syndrome it means that it's not an
ischemic type cardiomyopathy she also
had shock liver acute kidney injury and
then the possibility of SLE with the
positive a na so this patient passed
away and she had an autopsy done for the
non-medical folks out there as part of
an autopsy what we do is we open the
chest and we open the abdomen and we
look at the the organs and looking at
them with the naked eye this is called
the gross examination and then we take
small little pieces of tissue and we cut
them very small and we put them under a
microscope okay so let's take a look at
her lung this is what it looks like here
on the outer surface
where the lung should look like is a
lung should be very very shiny and we've
got a bit of glare here but we can see
that this if you look in the areas of
this lung that does not have the glare
to it we can see that there is a
dullness to it here on the pleural
surface and then if we look right around
here this area of the lung is very red
it's very eerie thinness and it was
actually this area of the pleura that
I'm showing here was underlying large
areas of consolidation and when we took
little sections of this long to look for
to look at under the microscope I'd see
that there was a lot of pleural deema
that had this blood-tinged fluid to it
on the surface of the lung we could see
that there were these flat tan smooth
little lesions kind of like macules on
the on the pleural surface
microscopically these did correlate with
a lymphocytic pleuritis the lungs were
very heavy
they were very boggy they were very
consolidated and and so what that means
is that when when you feel the lungs it
should have this very kind of spongy
like consistency to it because it's full
of air but this month was not it was
very very much of a firm or kind of a
rubbery consistency and then when you
cut into it there's all this pleural
edema so if we take a look at what the
lung tissue looked like on the the lung
on the left side of the screen this is
what generally lungs should look like
relatively speaking we see that there's
a lot of these clear looking spaces here
and those clear looking spaces they
should have air in them so what we've
done is we've taken this this big piece
of tissue and we've sliced it into these
very very very very thin slices and when
we take those thin slices and we
down on the glass slide and we look at
it through the microscope what we're
seeing is a lot of clear spaces because
those clear spaces should be filled with
air in the living person so on the right
side of the screen what we're seeing is
that there is this diffuse consolidation
the air spaces that we see on the left
side of the screen on the right side of
the screen they're completely filled up
and so I'm gonna focus in right about
here in the center here and so on the
left side of the screen it's relatively
less involved on the right side of the
screen we can see that the air spaces
are really really filled up and they've
got a lot of cells in them which I'll go
into in just a second for the
non-medical people out there take a look
at the the septal walls here at the
alveoli the alveoli are supposed to be
very very thin essentially they contain
a capillary vessel running through with
blood and then the Numa site which is
the lung cell that the cell lining of
the alveoli and that is a very very thin
border and the reason why it's so thin
is that it allows for the diffusion of
oxygen coming from the alveolar space
into the capillaries where the blood is
so that we can oxygenate the blood the
way that that should normally work is
that the alveolar spaces the alveolar
sacs and the alveolar ducts they should
be clear they should be full of air on
the left side of the screen it's
relatively what we should be seeing on
the right side of the screen it is not
okay so let's take a look here what
we're seeing here is a really markedly
severe and very extensive edema so if
you take a closer look here you can see
that there's this kind of reticulated
pattern here what we're seeing there is
that is where the alveolar septa are
this this is where the alveoli are we
can make out these little circles here
and here and here and here and here and
basically what that is show
this is where the alveolar spaces were
and that is the alveolar wall bordering
that space but instead of seeing the
clear space like we should be seeing
we're seeing that it's filled massively
filled up with this pulmonary edema and
so for the for the non-medical folks out
there what this means is that that she
was unable to perform gas exchange in
the alveolar spaces because they were
they were filled up with fluid and this
cellular infiltrate which we'll see in
just a second okay so we've got a lot of
findings here and I'm just gonna list
these as we go through them so we're
seeing large areas of consolidation
there's markedly severe pulmonary edema
again filling up those air spaces with
that fluid and so if we think back to
her clinical presentation of how she
presented before she passed away
you will remember that she had a really
bad hypoxia in hypoxemia which means
that there's not enough oxygen in the
blood and this is why because her her
alveolar sacs and the air spaces were
filled up with fluid and you're not able
to get oxygen and carbon dioxide out so
if we continue on here we can see we'll
go back to this example that we just
looked at previously let's zoom in in
this area right here and we already saw
this slide there's a relatively
uninvolved lung on the left side and
much more involved lung on the right
side and let's zoom in right here where
that box is some of you might be
wondering what this is we can see that
there are these little cilia here this
is respiratory epithelium it probably
got lodged in there during section so
don't worry about that the thing that I
really want to point out here is this
cell right here now if you take a
comparison between this cell and the
cell
around it you can see that this cell is
massively enlarged we've got a scale bar
right here to me this is very convincing
for viral cytopathic effect so for a
viral psychopathic effect well what is
that it is the effect that the virus has
on the cytologic appearance of a cell so
if you think about things like herpes
add no virus
cytomegalovirus there's a bunch of
different viruses out there that when
the virus infects the cells it looks
abnormal so the the cell that is
infected by the virus looks very
different from the cells that are not
affected by the virus and so this I
believe is a Numa site and I believe
that this it may be a very reactive Numa
site but I think it's very convincing
for viral psychopathic effect another
cell that's very convincing Perseid
viral psychopathic effect is this one
look at the size here it's a massively
enlarged cell now this cell is really
prominent it catches the eye you can see
it from a mile away but if you look
around you can see that there's other
cells very similar to it that aren't are
not as enlarged or not as prominent but
they do have what looks like to be an
abnormal appearance to them this guy
over here and so I think what we have
here is a viral psychopathic effect with
there being some cells that are
massively affected but other cells they
do show this this change to the to the
nuclear appearance and to the
cytoplasmic appearance that is is very
suspicious very very suspicious so okay
so if we take a closer example we can
see here's another example of what I
believe to be a viral psychopathic
effect other people out there might
think that oh maybe that's just a really
reactive Numa site and that's totally
possible but to me that this is very
convinced
so just to recap what have we seen so
far I've put the new findings in red
here in here that we just described as
this viral psychopathic effect and some
people might think is a really reactive
Newman site but I think it's very
convincing okay so moving on here we've
moved to another part of the lung we can
see here here is the pleura here if this
is the peripheral aspect of the lung
here and I'm gonna focus in in just a
little bit but I want to show how on the
bottom left-hand side of the screen we
can see that there's a lot of clear
space this is where the air is able to
get into and on the bottom right-hand
part of the screen we can see that
there's really no spaces there and those
alveoli have been blocked up and are not
able to do gas exchange here let's take
a focus in here and let's take a closer
look there so what we can see here is
this is a higher power image and I've
made a an outline of the alveolar
linings here okay so this is where the
alveolar wall is these little black
areas so that everybody can see what I'm
talking about so if we take a look here
here's the little capillaries it's a
little bit congested within the alveolar
wall and look at the pneuma sites that
have come off of the alveolar wall so
this is kind of a desquamation type
pattern so for the non-medical folks out
there if you if you rub your hand up
against your skin you'll see it gets
really ashy because there's little skin
cells that are falling off
that's called desquamation so basically
the the cells of the that normally lined
the lung tissue they seem to be falling
off of their basilar attachments which
is not a good thing
you don't want those cells to be falling
off because you're not going to be able
to get good gas exchange so in this area
where we actually have air within this
area within the alveolar spaces but
there's no gas
going on here because the cells have
come off of their baler attachment so
here is where the alveolar wall should
be and then here is where the pneuma
sites are so basically what I'm saying
here is that the the large areas of the
lung were filled up with this fluid this
pulmonary edema and then even in the
areas of lung that we're able to get air
into them you're not able to get gas
exchange because of this desk womate of
type pattern that we're seeing with the
pneuma sites that seem to be falling off
of their alveolar walls and as we go
through here we if you take a look at
the nuclear features of these cells we
can see that some of these cells they
have these very eosinophilic nuclei that
are very suspicious for viral cytopathic
effect okay
so if we move forward we can see in a
higher power view that these Numa sites
were disassociating from the alveolar
wall and they form these sensational
aggregates if you look through the
medical literature of the very few
autopsy cases that have been reported
for the current novel coronavirus that
we're seeing today and then you also
look at the literature for the SARS
virus we can see that there are these
multinucleated giant cells that have
been reported in the literature
multinucleated giant cells when you
typically see that you typically think
about TB fungus foreign body reaction
sarcoid etc etc but I don't think that's
any of the processes that we're seeing
here in my opinion what has been
reported as multinucleated giant cells
are actually these social groups of Numa
sites that have been decimated their
work come off of of the alveolar wall
and if we look further if we look a
little bit closer some of these are very
suspicious for a viral site
Pathak effect if we correlate our lung
findings that we've seen thus far the
the areas that are listed in light we've
already talked about the the areas that
are listed in red these are new findings
that we're discussing so the new Messiah
desquamation are swapping off where
those the the lining of the lung alveoli
are just kind of coming off in droves
kind of like in a DI pee sort of pattern
but not really
and then the multinucleated giant cells
like aggregations which I believe are
just these soft Numa sites that form
these sensational groups what we were
also seeing was bona fide Highland
membranes so this is a characteristic
feature of diffuse alveolar damage also
notice that we've got a ton of
inflammatory cells here and here and
here and here and so this is a
characteristic of diffuse alveolar
damage where we get the formation of
these highland membranes that line the
alveolar spaces and of course you can't
get any gas exchange through these
highland membranes so that kind of
worsens the picture here's another
example of the highland membranes is
this very eosinophilic kind of dense
looking material that lines the alveolar
walls this image is also showing how
these Numa sites that are just kind of
falling off of their basilar attachments
they're filling up into the alveolar
spaces some of them have kind of
enlarged nuclear features and ample
cytoplasm very suspicious for a viral
psychopathic effect
this is alveolar fibrin and again this
was a very prominent finding throughout
the the lung this this amorphous pink
material they were quite a few areas
that were looking like maybe it was
Highland membranes versus fiber and
deposition
it was a little bit hard to tell which
was which so this was a pretty extensive
finding all right so basically what we
were seeing is conducive or congruent
with what is so far reported in the
literature this is just another example
showing that there is edema here here's
the Hyland membranes associated with
diffuse alveolar damage and I'd like to
take a moment just to point out the
massive amount of inflammatory cells so
to the medical folks out here all of
these little purple dots here this is
all inflammatory cells inflammatory
cells so this is a this is a very
extensive inflam inflammatory process so
when we think about inflammation in the
lung if you see a whole bunch of
neutrophils in the lung then we call
that in acute pneumonia and that's
usually associated with bacteria and
things like that
for pneumonias that have a lot of
lymphocytic infiltration which is what
we see here the lymphocytic infiltration
goes along more with a viral pneumonia
and so that's what we have here so far
what we've been seeing is very
consistent with a viral pneumonia so
just going back to the diffuse alveolar
damage to the pathology residents out
there diedi can be basically separated
into two parts an early phase in the
later stage the early phase is called
the exudative stage because you get
these edema and the fibrin s exudates
that we've just been talking about the
later stage is called a proliferative
phase or organizing phase and then a
fibrosis stage so in this and and these
are not completely black and white it's
a spectrum so what we're seeing here is
the early stage of diffuse alveolar
damage with these Highland membranes and
the fitness exudates and lots of edema
and then in the later stages you'll
start to get organization proliferation
and fibrosis now we don't have any
fibrosis here but we do have a few areas
that had increased mitosis ie
proliferation and things like that so so
I think we're starting to move into the
organizing phase but this for the vast
majority this patient was kind of in the
early stages of the proliferative phase
and very much in the exudative stage
again we can see these kind of
multinucleated giant cells like groups
of the numa sites here is a nice
alveolar wall here and all of the numa
sites are just kind of falling off and
in these newest sites they they're much
thicker they have this reactive
appearance so basically what I'm saying
here is that there is a really bad viral
type pneumonia and even though there
were some parts of her lungs that were
aerated they weren't getting good gas
exchange because of the damage to the
pneuma sites that we were seeing okay so
what are lung findings so far we had the
Highland membranes which is a very very
characteristic of the diffuse alveolar
damage and this is consistent with her
clinical presentation of the acute
respiratory distress syndrome or a RDS
okay so when I was first looking through
this lung and scanning in at 10,000 feet
I thought that originally I thought that
this was a fibrin thrombus but when you
get up on higher power you can see that
no it's not a fibrin thrombus
it's just coagulum and you can see
separation of the erythrocytes here and
the fibrin there so to the pathologist's
in the group if you're looking at these
things from 10,000 feet before you start
calling micro thrombi please go in and
take a closer look I know that
obvious but please do that okay and then
to the clinicians in the group there
have been some very convincing reports
of a possible coagulopathy type
situation associated with a throat
prothrombotic propensity of these
patients forming clots and things like
that so as far as whether or not micro
thrombi are present in covent 19
patients I think the jury is still out I
didn't see any in this autopsy case but
that's not to say that it's not present
in other patients so I would offer a
word of caution to the clinicians out
there who are managing these patients as
you all know by Brent oolitic therapy is
not an innocuous thing and it does have
its risks so before administering that
you know you just gotta take it in
context of the of what's going on with
your patient so I do want to make a note
though that any time you have a diffuse
alveolar damage type situation with
acute lung injury that in and of itself
can cause can cause fibrin thrombi to
form so you can always get a little bit
of micro thrombi anytime you have a
diffuse alveolar damage situation with
acute lung injury and so you have to
take that with a grain of salt if you're
only seeing micro thrombi within the
lung tissue that doesn't necessarily
mean that is a pro thrombotic since
systemic situation there so that's
something to be taken into account okay
so this is an extensive evaluation of
the lung findings here we just have the
the lung parenchymal findings I want to
move forward with you guys and talk
about the vascular findings within the
lung and so this is the blood vessels
and I've labeled it here the the blood
vessels are filled up with red blood
cells as the oxygen carrying cells but
notice on the periphery of these blood
cells the periphery of the blood vessels
we can see that there
a somewhat of a concentration of these
little purple dots which are lymphocytes
and other inflammatory cells and so this
is a peri vascular distribution so if we
look in another section here we can see
that again I've labeled the vessels here
and here and we can see that there's a
little bit of an accentuation of the
inflammatory cells right around the
blood vessels so this is a peri vascular
distribution a lymphocytic peri vascular
infiltrate and in some areas it really
starts to look like vasculitis and so we
can see here that the peri vascular
inflammatory infiltrate and what we can
appreciate here on higher power is how
these inflammatory cells they look like
they're really extending through the
wall now I wasn't seeing anything that
looked like fibrin oeid necrosis which
would be a slam-dunk vasculitis but I
think it is pretty convincing where we
have these perivascular lymphocytes and
some of them look like they're really
starting to go through the walls here
and so this is on higher power if we
look on lower power we can see that in
and I've circled this for the for the
non-medical folks but we can see on
lower power we can see how the blood
vessels here and here and here and here
are surrounded by these little purple
dots which are the lymphocytes the
inflammatory cells and so we've got this
pretty prominent peri vascular
lymphocytic infiltrate we can see the
exact same thing here and I've circled
these for you
this peri vascular lymphocytic
infiltrate in in an area of the lung
that's a little bit more aerated than
what we were seeing in other areas in
addition we can also see lymphocytes
inflammatory cells within the pleura and
and this corresponds to what we're
seeing on the gross examination with the
little flat tan Mac you'll like lesions
on the gross surface okay so in addition
to everything that we've just talked
about there were large areas of a
pulmonary infarction and so basically
what we can see here is that
there are these really consolidated
areas that are not aerated they don't
have any air in them and and this tissue
has has died so we've got a pulmonary
infarction if you look up close there
isn't a necrosis there and so we've got
a necrotizing infarction with hemorrhage
in addition to what I believed to be is
vasculitis a lymphocytic vasculitis with
a very prominent and very extensive
perivascular lymphocytic huffing i don't
think that this has been described in
other
Cobin 19 patients in addition of note
she did have a positive a na so i don't
know what exactly that means as far as
relating that to this vasculitis here
her ANCA was negative and is it possible
that maybe there might be an autoimmune
sort of situation here I'm not sure so
so the lung findings were really really
extensive and very severe so I just want
to get on a soapbox for a little bit and
and let you guys know that there have
been some reports out there especially
in the lay media talking about how
ventilators cause harm and that
ventilators are bad etc etc and I just
want to say that that is not the case so
ventilators do have the capacity to
cause Barrow trauma but as with anything
you have to weigh the risks and the
benefits in patients who are basically
drowning in their own fluids and they're
not able to breathe and they're gasping
for breath ventilator is absolutely
necessary to be clear I didn't see
anything in this lung that looked like
Barrow trauma I didn't see anything in
this patient that looked like there was
injury from the ventilator all of this
is associate
with the with the with the virus with
the inflammatory infiltrate and with the
infection of the virus and another
interesting thing about this case is
that this patient was not an older
patient she was not elderly she had
obesity maybe this possible history of
asthma but really didn't have much in
the way of comorbidities and she was
relatively young and and she had a very
severe a very severe clinical course so
just a note to all of you young people
out there if you think that you're
invincible you're not so please take it
seriously okay so I'm off my soapbox
let's continue so these were the lung
findings that I was showing you guys I
wanted to continue on to some other
aspects of this case and so if we move
forward here's the peripheral smear this
comes back to the discussion about the
possibility of micro thrombi and a
prothrombotic sort of situation here
basically what we're seeing were these
atypical lymphocytes and then a left
shift so what does that mean the left
shift is where the cells are getting
pushed out of the bone marrow a little
bit earlier than when they're ready and
usually you see this when a person is
fighting an infection and they're trying
to get as many of those an infection
fighting immune cells out as quickly as
possible so we were seeing the left
shift and some atypical lymphocytes and
we can see that here so basically what I
wanted to point out is that this blood
smear is really not all that super
exciting there's there's some atypical
lymphocytes and the left shift but for
the most part we weren't seeing anything
that looked like thrombosis we weren't
seeing shifts the sites we weren't
seeing di sea we weren't seeing anything
like that so alright and so there's some
more okay now we get into the heart okay
so I will remind you
that this patient had a reverse
takotsubo cardiomyopathy she had severe
hypokinesis of part of the the wall of
her heart and so that means that the
heart was not able to beat properly and
to the point where there was actually
quite the question of whether or not
this represented a viral myocarditis so
I wanted to show with you the heart
findings here and these are the coronary
vessels we can see that the coronary
vessels are really clear they're widely
open widely paitent and so whatever
cardiomyopathy issues that she was
having was not due to an ischemic type
injury and on cuts section the heart
looked pretty good there was a little
bit of staining here but that wasn't
anything microscopically and then here
what we have is a little bit of formalin
fixation artifact but for the most part
she didn't have any areas of ischemic
looking injury the right ventricle is a
little bit dilated she did have a lot
going on in her lungs and so the right
ventricle pumps blood to the lungs so if
you've got a lot of increased pressure
in the lungs that can cause a back up in
the in the right ventricle so it's not
able to pump blood out as well but for
the most part the the gross impression
of the heart was not all that it wasn't
that bad this was really interesting
though this heart the right atrium this
is the right atrium it was very thin and
there were areas of the right atrium
that looked like the the myocardium was
partially missing here and here and so
there were areas where the epicardium
was basically bare and did not have
myocardium underlying it and so I think
that this is probably a congenital
process for this patient where can Jenna
congenitally she didn't have enough
myocardium with
the right ventricle but that never
really caused her any problems because
she was relatively healthy but when you
have a severe lung injury and a severe
lung involvement that right ventricle
sorry that right atrium would not be
able to contract as as as well as it
should have so I think that this
probably contributed some to her cardiac
abnormalities that were noted in the
ante-mortem time period okay so let's
take a closer look at the myocardium
just as a reminder the the clinicians in
this case were very concerned about a
viral myocarditis she had this very
severe hypokinesis or decreased wall
movement of the of the wall of her heart
she wasn't able to push blood as well as
she should have been and so the the
clinicians in this case were very
concerned about a fulminant viral
myocarditis we did not see that what we
did find was edema so there was this
very interesting mix oeid edema that we
were seeing in the heart and I don't
know if this is an intrinsic part of the
covent process or if this was something
different so just as a bit of background
there have been increased reports of
koban 19:00 and patients with kovin 19
having a cardiomyopathy cardiac issues
and for the most part this has been
complicated because a lot of the the
patients who have been passing away they
have other cardiac issues that were
pre-existing prior to them getting sick
so it's kind of hard to say okay what
was the pre-existing cardiovascular
disease compared to the the current
COBIT infection and but in this patient
this patient had no history of
underlying cardiovascular disease this
patient had
very clear coronary arteries that
grossly and microscopically did not have
any [ __ ] erotic disease and she was a
young to middle-aged adult so we're
seeing this mix oeid type edema which is
kind of strange but I'm not sure the
exact cause of that is this a process of
the virus but we weren't seeing
inflammatory infiltrates that would
indicate presence of the virus in the
heart tissue perhaps maybe this might be
due to the hydroxychloroquine that she
received when she had about a leak of it
so let me take a moment to get on my
little soapbox about hydroxychloroquine
so hydroxychloroquine is not a benign
drug it's not like popping an aspirin or
taking an ibuprofen it's not a benign
drug so so people who take it they need
to be closely monitored the therapeutic
window for hydroxychloroquine is very
narrow so what does that mean it means
that the amount that it takes to have
effect versus the amount that it takes
to have toxicity is very close together
so that therapeutic range between having
an effect and then having toxicity is
very narrow and so these patients they
really need to be monitored it needs to
be under a physician's management okay
done with a hydroxychloroquine spiel
let's move on so this patient has a
relatively good-looking heart there was
this edema this kind of mix oeid edema I
apologize the blue really isn't coming
out but it had these kind of mix oyd
like spaces there and again the
clinicians were very concerned about a
fulminant viral myocarditis we were not
seeing a fulminant myocarditis we did
see very very rare areas of very focal
very mild lymphocytes and so these
little purple guys right here these are
little lymphocytes we did do an
immunohistochemical
saying that highlights lymphocytes and
this is as exciting as it gets a very
rare faux sigh of very few scattered
lymphocytes were present this was in the
papillary muscle of the left ventricle
we did not see lymphocytes anywhere else
and so that clinical impression of a
fulminant viral myocarditis was not
substantiated on the on the pathologic
findings so for the clinicians out there
who are in the ICUs and treating these
patients we're seeing that there's these
very abnormal kind of EKG functional
processes within the heart the hearts
not beating as well as it should be and
there's a question about a viral
myocarditis and that's not what we're
seeing in this autopsy patient so so
what is responsible for those cardiac
abnormalities I don't know but it's not
a viral myocarditis them and maybe
perhaps the virus is involving the
electrical conduction system within the
heart but I don't see evidence of a
viral myocarditis in this autopsy case
okay so moving on when it talked to you
about the kidneys here so this is the
kidneys the the kidneys grossly they
they looked pretty okay and
microscopically this is what we were
seeing it was a pretty unremarkable
kidney for the most part so so just a
brief review these are the glomeruli
here this is the the part that makes the
urine and it has a normal size normal
cellularity normal architecture okay and
so for this patient she did have
elevated creatinine that was going up
throughout the the hospital course and
so there was a concern for acute kidney
injury and looking through the remainder
of this kidney and browsing through we
saw a lot of autolytic change and this
is what autologous and the kidney looks
like where there's basically this kind
of
rotation of the the tissue here and what
autologous means is that after a person
passes away the the membranes start to
lose their structure the cells they
start to degrade and that's basically
what Hollis's is but what was very
interesting was in focal areas we could
see evidence of acute tubular injury and
so what we were seeing was these cells
the the tubules cells so here the TBL
cells here and here and here and here
okay and these tubular cells we start to
get this proteinaceous material the TAM
horsfall protein within the the to be
lumen we're also starting to get
granular casts within the tubular lumen
and then here is this necrotic debris
within the the tubules basically we were
seeing this very focal acute tubular
necrosis which would explain the
clinical impression of acute kidney
injury there have been reports out there
showing that patients are having kidney
disease sometimes the kidney disease
gets worse even after the pulmonary
disease gets better so I think the
jury's still out there on this one I
mean I could hypothesize that she did
have a very severe hypoxia due to her
sit very severe lung injury and so maybe
the severe hypoxia might be responsible
for this acute tubular necrosis that's
possible but I didn't see anything that
looked like a primary an infection
inflammatory disorder here I didn't see
anything that looked like a viral
nephritis or an interstitial nephritis
anything like that all right so that
completes the tour of this autopsy case
again I want to say thank you so much to
the family for allowing me to present
this case I think that it has the
potential to teach us a lot about what's
going on with the Co
19 virus and what are the pathologic
effects of this virus again we've had a
lot of clinical reports coming out
talking about what they're seeing in
patients and ICUs and emergency rooms
but I think it gives a lot of
information to us if we can look at the
pathology and see what's going on in the
pathogenesis of this disease so that
completes our discussion this is autopsy
findings I also present neuropathology
findings on adventures in their
pathology if you found this video
educational and you think that it helped
and you learn something please feel free
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website adventurous and nerve pathology
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Twitter okay so that's the longest video
that I've ever made before sorry about
the length but I think it's important to
present these findings so people know
what we're dealing with so that's it
join us next time on adventures in
neuropathology thanks
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