Hello everyone and welcome to the Quorum podcast.
This is where academic medicine meets remote, austere and
resource limited areas. So welcome to the Quorum
conversations and we are going to hear from Zach Andrews, a
soft medic about one of his patients He he had and this is
an open conversation. So do please raise your hand and
ask any questions within the messaging and I'll keep an eye
on it. But Zach, looking forward to
this brother. All right.
Thanks a brick. Thanks everyone for logging on
today. So this is a clinical case that
had a profound effect on me and really shaping me as a younger
and trying to figure out kind of who I was and who I wanted to be
in the the world of medicine at this point.
And so this really isn't a textbook scenario.
This this patient actually presents quite a typical.
Then essentially what happened is a a man walked into a tent
under his own power in physiologic he shouldn't have
been able to. And that's one of the things
that had a significant shaping on me.
And the rest is how deep just in how rapid critical care medicine
can revolve around a patient. But the fact that he was walking
in is one of the most important teaching points that we have
through this entire session. It can be deceptive how severe
illnesses can be. And we can kind of be loped into
a false sense of security and and think that someone appears
relatively well. And this isn't just within
remotes. And this is what then, you know,
you could be at the emergency part or, or working EMS and you
know, doing calls. And so it's, it's a great lesson
to learn across. But most typically remote
medicine usually don't have the the time or the backup.
So remote medicine, you're, you're mine should be focused
more on what is hiding and what am I not seeing versus kind of
getting in that sense of security.
And we're going to walk through the clinical decision making
process for this patient, the drugs, the equipment where I was
in a general aspect. And we're going to get we're
going to go through settings. We're going to do a lot on here.
And I'd like this to be a conversation, not, not so much a
lecture. I don't have any trick
questions. I, you know, I really ask that
everything here has it like a clinical grounded evidence that
I, that I present then. And if you, if you have a
comment, you know, please jump in and defend your reasoning.
So what I will say is Abra, can there's a Word document that we
can we can post Maybe if we put this on YouTube, maybe there's a
way to post it in the description about to further
list learning out of this, whether you're a BSc or MSC
student, there's a Word document with questions that I have per
slide on here. And it's really just to help you
drill down and get some clinical reasoning going on.
If you're a BSc student, I just worry about the BSc side.
If you're MSC student, obviously it's going to take you that
further step, but maybe look at the BSc questions too and make
sure that you don't have any gaps that you need to work
through. So before we get into this, let
me just kind of frame what we're trying to achieve today.
The objectives are not just boxes to to check off.
Each of them represent a clinical skill that could save a
life. And by the time we finish, I
want you to be able to look at a patient in a remote environment
with limited resources and make sound defensible evidence based
decisions under pressure. And that's the standard that
we're going to work work for. For the BSc students, we're
focusing on recognition, location, a framework and
understanding a rationale behind clinical decisions for our
entity students, I want you to operate at a higher level.
I want you to critically evaluate evidence question
guidelines that maybe I used or maybe what you would use in
thinking about the and human factors that shape the clinical
outcomes. Both levels of thinking are
valuable and will the Word document directs questions in
that that area towards towards both.
OK so the scene let me let me paint this picture for you.
So we're in remote Africa, I mean room Africa.
There's not a hospital that is close by.
There's not a clinic, there's not a resuscitation bed.
There's not a crash trolley that is in the infrastructure of this
place. What you see atop is actually
out of it's you can tell it's the walls if you see the curve
there. It is a tent and the floor is
the covering on it, but it's just a plywood floor that's
under there. And over time we managed to get
a significant amount of equipment in there for a true
ICU. But there's no CT labs are very
lifted through, but there's, we did have X-ray in the the bottom
right is what a minutes or X-ray, but we had no X-ray.
So as a medic, I learned how to do labs.
I learned how to shoot X-rays. You really become a Jack of all,
all trades at that point. Now for this patient, the first
thing I will kind of put in front of you, this patient had
been unwell for three weeks in, in the last week of that, nobody
had actually really encountered him.
They, this is really kind of poor judgement in multiple
aspects of the company he worked for kind of just thought he was
on a Bender or needed a break. Unfortunately, that's that's
where they kind of work with them.
But really what was going on? Is he he, he actually had a
infectious disease and for three weeks without treatment when we
get to here, I won't break out to exactly what he had.
Hopefully I didn't put it on the slides already.
Once we built the differential, I'll kind of go into what he
actually had. But with this infection, every
day that passed, he was getting much worse.
And So what really caught the attention, he was on the
outstation that was actually little bit further away.
It was a good day's drive through the Bush.
I mean, it was a hard day's drive through the Bush to get
there, ideally moving by some, you know, rotor wing or fixed
wing aircraft to, to be able to move in between places.
But he ended up walking into the dining tent and as the dining
tent looked much like the resuscitation tent that you see
there, and he actually lost incontinence in front of his
colleagues there. And then they started
questioning him. Of course, you know of what's
what's going on. And he's like, I just, I just
don't feel well. And they determined, yeah,
something's off here. And so there was a medic who was
out there, had a much smaller aid station, much less
equipment. But he wasn't a joke of a, of a
medic. Actually he was experienced RN
who worked in a emergency department and the learning
points here is he was actually hesitant to send the patient to
me even though my clinic had much more capability and was
actually closer in the links to definitive care.
I was really the last stop before we get you to some really
nice high quality care. And you know with that with that
hesitation that that medic had it has clinical consequences
with it and as capable as he was in kind of the first question
that I have to put in front of US students.
If if you were the medic at that out station and he yeah though
lost incontinence was still a no times for GCS of 15 was able to
communicate freely with you move under his own control.
What would you have done? You know, and and you have to be
honest there. What are you actually assuming
by keeping them and what's your red flag that you're going to
send him out or what are you kind of explaining away in your
mind to hold on or would you have sent him?
And so essentially he stayed there about 24 hours before I
was able to convince that medic that you need to get them over
here. And we were able to spin up an
asset to be able to get them to me.
But that was a whole 24 hours that had elapsed and it was a
delay in in care for that patient.
So the patient arrives at my location.
What I see is again, 24 hours later, it's a man who's he's
alert and oriented to in place time event GCS of 15.
He's talking by the most bait neurological assessment we have.
He appears intact, but if you look a little bit more
carefully, he's pale, he's retic, you know, just sweaty.
He's shaking a bit and this isn't kind of a subtle tremor.
What I noticed is he had this large cup and we get from from
gas stations, you know, as we call them the US or you know, I
guess pet stations probably elsewhere are the same.
But they had this big goal. It's made to just put a
egregious amount of soda to cause diabetes in it over your
lifetime. And he had it full of ice.
And as he was walking in, I just distinctly remembered the ice
rattling inside of it. And I can actually, I can still
hear it to this day. And so that's just one of those
subtle signs. The body is working
extraordinarily hard just to maintain its basic function.
Now let's look at those vital signs.
And this is really where it started clicking with me that
something is wrong. A blood pressure of before over
50 how he walked in with that I'm impressed A heart rate in
the waist temperature was approximately 100 and
Fahrenheit. Sorry, I didn't do the oh, I did
do it. It's 39.4°C two of 97%.
You know some of those are concerning, but overall some of
those that are not too bad. 97% body is trying to maintain its
cardiac by increasing that heart because of the stroke volume on
this patient is failing and we know it's failing because look
at that blood pressure that's not a good blood pressure.
That temperature tells us there's a significant infectious
process driving a systemic inflammatory response during
We'll kind of come back to that because when we see some some
blood gas results that I had, that number will take on a very
different set that in mind. SPU 2 and 90s.
So what would you say is this is this patient in shock?
So what type of shock? He walked in under his own
power. GCS of 15.
It's deceptive, but yeah, the patients in shock, patients in
distributive, a septic shock. I didn't tell you what I already
knew at this point because I don't want to break down your
differential and kind of lead you with that.
Patients in septic shock here. So if this patient walked into
your austere clinic or your emergency department or wherever
it is that you work with these vital signs, what would your
first three actions be? You know, let that kind of
process in your mind? What would those first three
actions be? What would you do immediately to
make this patient better or what processes would you put in
motion to get this patient to a better situation?
So now let This is why I love remote medicine because now we
have a problem within a problem. Now you're in a tent in Africa.
What changes the way you approach this patient or the
problems that you have? We have comments of do a news
score, do a fluids, do a malaria test, take three, give three.
I'm not sure what that is. So here those are the comments
coming in so far. Great, great comments.
I like where you went news score.
Unfortunately, at this time, I actually wasn't familiar with
the news score, but that's great.
That's a great score to be to be grabbing the malaria test.
Hey, everything's malaria in Africa, so it's proven
otherwise. So good on you for that one.
The take three goes three. I'm not sure what that is, but.
Dimitro raised his hand. What do you got?
Thank you for this opportunity. I would say this patient is very
lucky cause having malaria for three weeks with the fever most
likely the parasitemia was very high.
So if this guy would be present in my clinic, I would try to
stabilise his blood pressure as soon as possible and find the
reason for this kind of symptoms of fever.
Do the malaria test definitely and urinalysis.
This and depends what kind of laboratory capabilities you had
there. Investigate deeper for the
septic shock. Yeah, great, great.
So what to drill down further on that?
So I had microscopy, I could do staining and then I had some RDS
with that. What?
Where do you think you'd go with that?
RDS being a rapid detection test?
What do you mean about RDTS? Yeah, we'll get into it.
So for RDTS, is the the rapid blood test similar to like a
rapid like influenza or you know, rapid strep test, the
things along that line, but they have some for malaria
specifically and we had some for various different diseases that
were tropical in nature. We have a question for Dimitro
Petra. Hi guys.
It wasn't the question is I wrote the take 3 and give 3.
So you really with the news score you take 3 diagnostics and
give 3 treatments. But again I wasn't, I was just
thinking about the septic shock, not the malaria issue.
So that that's why I said the septic shock in my opinion that
should be treated first. So the take 3 is like for
example, like blood cultures, blood tests and I don't know,
urine output, for example. And then give three oxygen in
case, in case his sats were not good, but he had 97 IV fluids
and IV antibiotics. That would be my first course of
action. But then again, we are talking
about Africa. So I would go with the malaria
test as well. Yeah, very good.
I like it. I like where you're thinking
with that. I like to take three, give
three. I'm going to have to remember
that one. So what's what's the difference?
We talked about area, so let's just put that up the top of the
differential. What else?
You're in Central Africa, this patient immediately what's what
else is hitting your mind? Yellow fever, Typhoid, Cholera.
Yeah, yeah. If I can throw in though, the
remote, you know, there is travel between, you know, urban
and rural places. So I'd be thinking of things
like dengue fever. Thinking of gastrointestinal was
common for us at this point. We got wrecked by poor food
choices multiple times. Yeah.
So there's a few other we can add in there, but areas.
Comment on dysentery Dysentery as a different diagnosis.
Yeah, yeah. So it and that's great because
we actually did have a couple bouts of dysentery.
I was those that fell casualty to dysentery while we were out
there. So we'll talk about the, the
diagnosis here after this patient got to me.
It was, it was suscept infected malaria.
And so I, I used what's a brand called Bionex Bionex now.
And the only reason I use that brand is because that's what was
FDA approved and you know, from the, the US, that's, that's what
I had. It's not the only one.
There's actually a better and cheaper fantastic tests that are
that are out there too. But I had that and I ran it in
the results and I have a picture that shows it a bit next and we
can talk about it was so immediate and unambiguous, so
strongly positive for Plasmodium falciparum that actually had to
do another test because I thought well, maybe something is
wrong with this. So usually that has to develop
over 10 to 15 minutes to show a pop.
And as you could see the sample moving towards the line, it was
positive immediately. And so I went and actually got
our newest batch just to make sure the the latest to expire
and grabbed it open. It ran it an exact same thing.
And so I think that's something to, you know, bit I ran a second
test. I didn't just grab it and move
on. And why?
Because it wasn't typical in the way that presented as a
positive. And I wanted to be sure.
And in the resource limited environment, you can't afford to
be wrong very long, OK, because you're going to paint yourself
into a corner and then to be able to get out of that be
impossible. If if it was a fault positive,
would I have been treating this patient for something they
didn't have? It was a false negative, which
is less likely, but you know it it could be mean missing the
diagnosis entirely. So I ran a second test, you
know, from a different batch and it just eliminates the
possibility of a specific manufacturing error.
That is it, it sound clinical government, you know, you do
have to worry about your resources, but I was fine with
that. And this is a kind of thinking
that that you should put on a bit in these situations.
Now if we applied the sepsis framework for this patient which
I applied the sepsis framework back then I didn't do the new
score, which is a great one too. This is patient meet the
criteria for sepsis septic shock, suspected infection.
Yes, we we have that organ dysfunction with a sofa score of
two or more. I will actually we'll see some
evidence in the labs for the and then for this patient they're
going to end up needing vasopressant or vasopressor
actually ended up needing norepinephrine.
So this page falls in there and is lactate was enormous.
You'll see it here or it's actually here in the second to
last one, lactate a 14.36. He he wasn't just sick.
He exceeds all those criteria by a significant margin.
So if you're unfamiliar with the rapid diagnostic test, we can,
we'll chat about that here. Again, you know, I have no stock
in Bionax malaria and actually I took a charcoal medicine course
years ago in the Gates Foundation deputy director of
malaria was giving the presentation on malaria.
According to him, he actually said the tests that you get in
Africa are are better than the vionax test.
So I, I don't, I don't stay this is what you need use this is
what I had and what I was allowed to use and very easy
simple test if not good at microscopy, it's quicker it
gives buys you a little bit of time.
You can get a a blood simple sample on a capillary tube or
for for you over in the UKA capillary tube.
As I've been corrected. It's just that a card in a
reagent in the reagent is a little bottle with the A on
there and you end up transferring blood to the card
with the capillary tube. And then you put the prescribed
amount of drop and it's all labelled within the card when
you open it step by step. How to do it and you should have
a result within 10 to 15 minutes.
And really phenomenal. They take up very little space.
I mean, even if you're working out of an aid bag, you could
carry a couple of these and you probably wouldn't notice that
you had it. The little, the developer, the
little dropper, it's the size of an eye drop.
And so that's what I used two of them and immediate results as
soon as that sample hit that test line that was positive.
So what I will show you here, I went too far there.
So actually the blood gas on the left is is actually from my
patient now on the right is this is an I stat.
I didn't have a picture of the I stat I used.
That's not my patient. Please don't confuse the two.
But that's what I stat looks like.
So I end up getting a blood gas on this patient to treat them.
I did before I got here, I did get IVX.
It was pretty painful to be able to get IV access on this
patient. But after that I was able to
start a fluid resuscitation of 30 MLS per kilogramme and which
he was a rather large guy. So it was a kind of fluid.
And while that was going, I grabbed this, this VBG.
And I want to start with something critically kind of
important here too, before we look at single number.
So this is a VBG, it's not arterial, it's it is Venus.
So if you're going to do this, understand that your baseline is
going to be different for what a normal value and that can be a
common source of error in practise.
So make sure that you label it as a VBG too, if you ended up
and out to somebody to read. And so we're sampling the blood.
The important thing with the VBG, it's already delivered its
oxygen to the tissue and it's returning to the heart.
So the values we see reflect what the tissue has already done
with that, that blood with that oxygen, right, Not what the
lungs have really put into it. So the venous pH is typically
about 0 point 03 to 0.05 to lower than the arterial in the,
the Venus PCO 2 is typically 4 to 5 millimetres higher of
Mercury than arterial. And the Venus PO2 is essentially
it's, it's not really useful for assessing oxygenation.
We, we can't use it to tell how how well the lungs are really
working. But with that in mind, let's
look at these numbers. The pH is 7.0.
Even accounting for the venous correction of on the high side
of .04, the estimated arterial pH is approximately 7.06.
This is catastrophic acidemia. If you're not aware, anytime you
get below 7.2, you don't work the same way that you were.
Especially the cardiac tissue doesn't work the same way.
And that's probably a great indication of why he was not
able to maintain a blood pressure and was decompensating.
So now let's look at the PCO 2:00.
It's at 30.4 millimetres in a venous sample.
The normal range is 41 to 51 and so this is quite a bit lower
than the normal range and that's extraordinary.
It means that his arterial PCO 2 is approximately 25 to 26
millimetres of mercury. His body is hyperventilating so
aggressively right now trying to blow off CO2 and compensate for
that veer metabolic acidosis that his venous PCO 2 was
paradoxically low. And yet, as we'll look in a
moment, even the extreme hyperventilation was not enough
to fully compensate. The lactate as we talked about
earlier was 14.36 millimols per litre.
Normal is is less than two. A lactate above 10 is associated
with extremely high mortality and in most published series
that past 10 is is really kind of unseen to live through in
with his we're we're in a territory that's you know, it's
it's really it's it's incompatible with this is not a
number that tells you the patient sick.
This is a number that tell you that tells you the patient's
tissues are done. Now if we look at the venous Sao
2, it's 20%. Normal venous Sao 2 is 70 to
75%. So the tissues normally extract
about 25% of the oxygen delivered to them.
She's we're extracting about 8%. So the body's an extremis here,
stripping every every bit of oxygen that it can from the
blood because delivery has collapsed so catastrophically.
So remember back to the Spo 2 of 97 and now the venous Sao 2 on
the blood gas was 20%. How do you reconcile those two
numbers? What what we just talked about
it, but think in your mind, what does each of those tell you what
is truly happening to this patient?
Here I said it earlier, I want you to really understand of what
has happened and you need to understand what is not spoken in
those numbers. So here's chemistry panels and
these are all on the ISTAT and these are my actual patients
panels. And this is where this full
picture of multi organ dysfunction becomes undeniable.
The sodium is 122 millimoles per litre, which normal if you're
not tracking is 135 to 140. Best way I remember the last two
numbers of each of those is because your pH is normally 7.35
to 7.4. That makes that a little easier
to remember. So severe hyponatremia at this
level and the sodium effects the patient's neurological function,
cerebral edoema, confusion and in severe cases, seizures in a
coma. And yet this man still within
these numbers, he still walked in with Agcs of 15.
Again, going back to patient didn't present how we would have
expected this patient to. His brain was functioning
outside of having a sodium below.
And it really tells you about the remarkable resilience of the
human body and also how close to the AT she was.
Now the blood urea nitrogen or the BUN was at 96 and the
creatine at 5. Those two numbers paint a
picture of severe acute kidney injury.
The kidneys were not being perfused and therefore they
weren't filtering. They were weren't really
producing much urine at this point either.
We, I did get a Foley on them at some point to be able to check
urine output. Very minimal.
But that's where the waste products should be cleared and
they're accumulating in the blood.
This is acute tubular necrosis driven by prolonged
hypoperfusion. The CKNB is at 39.8 nanograms
per millilitre against the normal which is less than 5.
Tells us that his heart is under significant stress in the septic
shock. This is cardiomyopathy radiators
released during sepsis directly impair myocardial contraction
cardiac event. This is the heart being damaged
as a bystander. It's it's a secondary effect on
this patient. So the eye or the international
normalisation ratio is 1.8 and the prothrombin time is point
1.3 second. So even the clotting system of
this patient is beginning to fail.
This is the early picture DIC or disseminated intravascular
coagulation, an inflammatory cascade that is destroying the
kidneys in the lungs and is consuming clotting factors.
If this patient has survived longer without treatment, we
would expect to actually see frank bleeding from multiple
mucosa sites on this patient. In the anion gap on here, is 28
millimoliter normal? It is 8 to 12.
That gap is almost entirely explained by that lactate of
14.36. And the body is producing acid
faster than it can clear it and that acid is accumulating and
it's in the paste blood. So we just talked about it.
But looking at this chemistry panel as a whole, how many organ
systems are failing? In any that I missed in here
that you think are failing, which one do you think is most
life threatening? Multiple liver is a answer from
Alfredo. Yeah, I multiple, multiple are
going, this patient is in mods, right, Organ dysfunction
syndrome didn't have liver panels on here, but I would
assume that the liver is failing also.
Well, but we did have the prothrombin time and INR.
So I back up like, yeah, we, we are assuming that the liver is
failing because it's, it's not keeping up the kidneys and the
heart and in the heart being the most vulnerable here, it's
additive process of months and struggle.
So this, this patient's not in a good situation right now.
And if you do get in your Word document, I do have a question
that it walks you through the chelation of anion gap in the
BSc level questions. I recommend a little bit proud
of myself, but I think I give you good questions.
If you're not familiar, reading some chemistry panels that will
help lead you into some conclusion.
So put the link to that document in the messages guys so you can
download it from the quorum Google.
Perfect. Thanks, Sabre.
Let's talk about the vascular access.
So I did give a hint and you, you were all right on the money
that we had this patient and we needed to recipitate this
patient. The vascular access in this
patient needs to be talked about because it was not straight.
When a patient is in septic shock, the the peripheral veins,
they have no pressure. I mean, they just collapse.
You try to you put on a band and it's just nearly impossible to
get anything on this patient. But he is shunting blood away
the best it can and truly it's distributed.
So it really can't in this one that well.
And the ones that you'd normally cannulate easily, they're flat,
they're fragile, they're difficult to find.
And this does a frustrating time critical challenge in managing a
shock patient in here. So eventually did achieve
peripheral access and immediately commenced
crystalloid resuscitation. And after that ID stick is when
we got labs. So you know, that's excellent
practise. That's how you don't need to
wait on lab before you necessarily start treating your
patient, especially the hypoperfuge.
Every minute of delay without fluid resuscitation is
associated with work worse outcomes and peripheral access
of one line really isn't enough. If you've ever managed a true
ICU worthy patient, you know that you need multiple lines and
drips see them in the hospitals and there's pumps things on
these patients and so not confident to be able to get
another line. What was actually inserted is a
gay under ultrasound. If you've not used ultrasound to
place IV catheters, I highly recommend it.
It gets you out of a pickle. It gets you out of the way of
having to default to an I/O I I much rather prefer getting
ultrasound guided IV if I can over IO.
Now the the IG is not a routine app does require a bit of skill
and confidence, but overall if you can do Ivs under ultrasound,
you could, you could do this patient, but it was the the
right call. It gave a reliable large or
central access for the vase suppressor which was was going
to be placed in this patient. It was needed after 30 MLS per
kilogramme of crystalloid was the surviving sepsis campaign
recommendation. The blood pressure had only
slightly improved. Patient's vasculature was so
profoundly dilated that the fluid alone could not restore
perfusion pressure. And so norepinephrine was was
convinced and it did bring the map up to some degree.
But overall the urine output still remained relatively low,
telling us despite the improved blood pressure, the kidneys are
still not being adequately perfused.
And the the organ damage at this point was already likely to
advance upping at 30 miles per kilogramme.
When I think it's, it's important for you to recognise
that the nature of the shock when they get to here, but also
to understand the risk of more fluid.
So I'm taught by one of the best physicians, very unlikely
physician to be working with me at the time told me the first
press or in septic shock is fluids, the second is fluids and
the third is fluids. Your backstop at a minimum
IS30ML per kilogramme or really at the maximum IS30ML per
kilogramme. Apologise.
Why is that? What are we?
What are we risking here if we continue to do more?
Alfredo mentioned artisanate for the malaria as well as your your
fluids. Yeah, Artisanate is the answer.
Actually. I did not have artisan and I'll
get to it in a little bit of what I actually had was IV
quinidine and that's all I had. But what you have is better than
what you don't have at the time. So pushing the patient past 30
miles per kilogramme of crystalloid fluid really start
to risk fluid overload for this patient, which could stress the
heart further and also most importantly the pulmonary
system. We could have a shift pulmonary.
In fact, many remote practitioners starting to be on
the Shire side of crystalloid fluid resuscitation in starting
to to re evaluate the patient at about 20 MLS per kilogramme.
There's multiple studies you can look at, but the one I recall
was done in Vietnam and they actually stopped a bit earlier
because in their IC US they did not have the same capability
that many other IC US had that were successful with 30 mills
per kilogramme. Typically they write ventilator
to patient ratio and things like ECMO and respiratory therapist
and touch in their clinics. And so they actually had a
better outcome of patients in the long run to limiting fluids
a bit more. I believe Kenya did a similar
study on that. It's something some I should
have put that in my notes here to tell you so I apologise to
that one pressed into Tory body had been working so hard to to
compensate for metabolic acidosis.
Breathing fast and deep trying to blow off that seat that
eventually with that PA with everything going on with just
the the sheer fatigue, the muscles could not sustain the
effort. So when venol failure occurs in
a patient with a degree of metabolic acidosis, it's a pre
terminal event and that's something that was recognised.
But RSI in a shock patient is is a high risk procedure in
emergency medicine. The drugs used to facilitate
innovation can cause cardiovascular collapse in a
patient who's already hemodynamically compromised in
the act of innovation itself that learns about the positive
pressure ventilation can cause a precipitous drop in blood
pressure. And if we take over the
patient's ventilation without matching the rate and depth that
they were achieving spontaneously, we can actually
cause a catastrophic worsening of the acidosis.
This is not a procedure to rush into it out preparation and to
prepare for RSI, you can use the SOAP mnemonic.
There's also the MIS made mnemonic which is similar to
whatever you remember. Everything was was checked and
confirmed before a single drug was given, right?
And that's the standard that you should be doing.
And ideally you recognise as we did, this patient was going to
go into respiratory failure before we get there.
So for induction, ketamine was chosen.
Ketamine is the choice for sign hemodynamically compromised
patient. Another common one use is
atomidate and unlike propofol or midaz which causes that case of
dilation and myocardial depression, ketamine actually
stimulates the sympathetic gosh sympathetic nervous system.
It maintains a heart rate and blood pressure and it's also a
bit of a bronchodilator which is useful in that pulmonary edoema
and critically in this environment, it is it's
temperature stable too, very important for us.
Not needing refrigeration in a tent in Africa matters for the
paralytic Vecaronium was chosen over sexsenocholine and
sexsenocholine can cause a transient rise in serum
potassium, typically about .5 to .1 millimoles per litre.
And in a healthy patient, that is inconsequential.
In a patient with severe AKI, though a kidney injury, a
potassium that may already be higher than the measured 4 point
because of a pair's potassium excretion, the measured value
may not reflect that true intracellular burden.
And that rise could trigger a fatal arrhythmia.
So vecuronium was safer choice. And it also like ketamine is
temperature stable, which again, it it matters.
So here's my question to you for this slide.
You're about to intubate a patient with APH of 7.02 who is
breathing at 30 breath per minutes.
To compensate, you intubate and you set the say you end up
setting the ventilator to 12 breaths per minute.
What'd you just do to that patient?
So what you did to that patient is you forced them to to stop
compensating. The one thing that was though
they were way outside of tolerance, The one thing that
was really stopping them from just going off the Cliff, you
turned it off. So now we could expect that pH
to decrease even more and really put the patient in a dangerous
situation. So once the patient was
inhibited and the tube was confirmed and positioned by by
of course, a good direct visualisation, we also had in
title and a chest X-ray. So the ventilator that I had is
the the Zol EMV plus. It's a transport ventilator and
we used a lung protective strategy.
Now here where the ventilator management of this patient
becomes genuinely complex. And I want you to think
carefully about this standard's approach to birds patient.
Birds patient is the ARDS net protocol something to become
very familiar with if you if you're not, they recommend 4 to
8 millilitres per kilogramme, but really starting in the
middle at six millilitres per kilogramme of ideal body weight.
If you're not familiar with that, please go look that up
because it's not just based on height or based on their actual
weight. So it's it gives a low tidal
volumes and it can allow a little bit of permissive hyper
cadmium, but you accept that is maybe slightly higher CO2 in
exchange for protection of the lungs from barrel trauma.
And that's a standard in these patients.
But in this patient permissive hypercapnia was was not so much
as of an option. And we place this patient on a
very high respiratory rate to try to maintain that
complication. And again, we talked about this
because the patient's pH just pointed.
I didn't talk about his bicarbonate earlier, meant to I
apologise, but his bicarbonate was at 7.9, which a normal is is
bicarbonate 22 to 26. His entire acid base system was
on the edge of collapse. The only keeping him from
failing further was his respiratory compensation.
That hyperventilation is just off that CO2 as quickly as it
possibly could let them fall anymore, really risking cardiac
compromise. We we already talked about the
cardiac effect of 7.2 of APH. 7.2 is where that starts to
disrupt it. The further you go the worse
that gets away from there. Ventilator rate as I said was 20
to 24 breaths per minute and it is higher than standard.
A lot of people using lung protective strategy shoots for
about 15 at a volume 6 somewhere between 8:00 to 12:00 to recruit
some collapsed alveoli and improve oxygenation.
And the F IO 2 was was at 100% starting for this patient and it
was going to be titrated down based on AB GS.
The chest X-ray confirmed correct entitled or ET2
placement and it did show a little bit of pulmonary edoema
consistent with developing ARD. And actually lung ultrasound
confirmed that there was no pneumothorax in this patient,
which is a critical check after an inhibation in case you got
too vigorous with their. We all saw the curly B lines
within that also. So that also confirmed pulmonary
edoema. All right.
And I will move to my anti malarial treatment of this
patient. Now I guess before I move, since
we hit on the lung protective strategy, there is a obstructive
pathology strategy of your patients and that is used for
COPD and asthma and patients of the like there.
But if it's usually not those, we're usually going to move to a
lung protective strip. So my anti malarial treat.
So alongside the resuscitation, as I talked about earlier, I
administered IV quinidine. It was the drug I had and the
best drug you can treat it with is the one you have.
Quinidine was historically the drug of choice in the US for
intravenous treatment for severe fuss.
It works by actually disrupting the parasite's ability to
detoxify the heme byproduct of the haemoglobin digestion and
it's toxic to the parasite if it accumulates and blocking this
process, phenidine kills the parasite inside the red blood
cell. However, that globe has already
shifted. The World Health Organisation
recommends Nate as the first line treatment of severe
falciparum now. It was based on the Aquamat
trial, which superior surviving outcome compared to 9 and and
African children and the the sequel map trial and adults in
Southeast Asia. So I will say Artestinate is
faster acting and it has a better safety profile and is
more effective in in reducing parasite clearance time in
remote field environment. You know, Dean may will have
been what was it or what the imperfect beats the perfect when
you don't have perfect every time.
We'll see. Quinidine carries a significant
risk that requires monitoring. Does anyone remember the effect
that quinidine may have on the patient?
And actually I'll give you a hint.
You need to use AECG to find this.
It's OK. If not, it prolongs the QT
interval which can precipitate the life threatening arrhythmia
of torsods or so it it also stimulates insulin secretion.
It's another thing to look for and that can cause hypoglycemia
further hypertension. So all all these risks are
compound in a patient who is all hemodynamically they're unstable
in mods, they're acidotic and they have a vasopressor infusion
going on. Now one thing we are expecting
cerebral malaria with this patient and actually an autopsy
did have and steroids not indicated in cerebral malaria
and actually they show I didn't have the study off top of my
head, but the steroids worse enough comes in in cerebral
malaria. So question why IV treatment
versus oral or antimalarials. Maybe if he walked in and write
he actually wasn't intubated the four clinidine today we gave him
a oral anti malaria. What would be the risk with this
patient? Dimitro, you have your hand up,
bro. Yeah, because this is the severe
malaria, you can treat it only these the four medications or I
am medications like you mentioned quinidine or artisanet
Artematar. So oral medications are not
useful for severe malaria type and because of the low
absorption level and most likely most of these patients, they're
not able to swallow medications. This one was, but I would also
move to IV medications in this case.
Yeah, Yeah, very good. Yeah.
And giving, giving a oral medication to a patient who is
in multi organ dysfunction, the likelihood of that absorbing as
you pointed out is is very low. It's not going to you need to
move to IV medications on this patient.
So we'll talk a little bit about point of care ultrasound in the
field. 1 of abrix favourite topics here, but it was used
significantly and 1 and critically in in this patient a
few times. It's an indispensable tool in
pre hospital and austerity medicine.
Oram has a great course with it. I recommend that you you get
your hands on it. It's becoming more and more
affordable. Yeah, at this point the size
wise you can fit it almost anywhere.
So first it was used to guide the the internal jugular
cannulation and without ultrasound, central venous
access in a in a shocked patient, it's a blind procedure
and there's significant complications.
You can only imagine, you know, arterial Sure you can.
Actually, if it's a long enough needle, you can actually cause a
hematorax hematoma occur and you can actually disrupt blood
perfusion or or increase ICP by inhibiting venous return
ultrasound. You can see the vein, confirm
its patency. You can watch the needle enter
the vein in real time and dramatically reduce the
complication in a tent in Africa with no backup that that's
enormous. Second, it was used to confirm
lung sliding after innovation, which confirms that both lungs
were being ventilated and that no pneumothorax had been
created. And this is a critical safety
check and is particularly important after the IG.
On that same side, as I talked about earlier, a lung ultrasound
also identified the curly B lines, the sound signature for
pulmonary edoema, which is consistent with that developing
ARDS. And yeah, we did get a chest
X-ray. So someone may say, well, why
don't you just get the chest X-ray earlier when you're alone
and doing, you're getting the cassette behind the patient, you
have all this. It's much quicker to get the
view of what's going on with the patient with ultrasound actually
moving to X-ray but not going to be sweating in the back of your
mind. Wonder if you actually have good
on this patient. So other things, if I was more
developed at the point, I could have had a good cardiac view of
the patient. I could have looked at the left
and right ventricular function. Is the really telling me is the
heart failing as a pump or is it being overwhelmed by fluid?
I could look at the IVC collapsibility, it give a real
dynamic assessment of fluid status.
There's really quite a bit that can can be done here with the
the low fluid urinary output. I could have done a bladder scan
to see if maybe there was something more distal in line
with this patient to make sure that they were able to pass
urine. So it doesn't replace clinic
judgement, but ends your your reach significantly.
Yeah, I'll move on to, to the next piece of here.
I have some good questions that ask about POCUS if you're if
you're wanting to look at that a bit further.
So this patient was evacuated in with the critical care team
unabated ventilated norepinephrine infusion and as
stable as you could have hoped to have made them, though truly
they still weren't stable, but they were just a little bit
better than prior in the handover was comprehensive, but
even in the arms of the receiving team, the patient
passed the patient died just patient was not compatible with
surviving. So and I want that to sit with
you for a minute too. This was a hard thing to to
think about as the young medic and someone dies very much will
blame yourself may have done everything right and and as I
believe a good job was done on this patient and they were the
patient was diagnosed rapidly. The guidelines were followed
pretty comprehensive care, more comprehensive care than probably
was within hundreds of kilometres from this patient.
The anti malarial treatment was given, patient still died and
this is a reality of medicine in austerity environments.
Sometimes the disease has progressed too far beyond what
you or the patient or anyone else can see.
Three weeks of untreated Plasmodium farciferum malaria in
a man in his mid 50s or early 50s had caused irreversible
damage. This point.
The truth is is there was likely nothing I could do to fully
reverse this patient. The likelihood of the patient
actually oxygenating enough with the parasitic load was was very
low and the what was done gave the patient the best chance.
Still was was going to die unfortunately.
And that's something you know, as as a question to you is does
this patient die? Does that mean the clinical care
had failed? You know, how do you separate
the quality of the clinical decision making from the
outcome? And what does that distinction
mean for how we evaluate performance in austere medicine?
You know, something to something to give yourself as a as a
question and to kind of hold in the back of your mind that way
you don't have a moral injury, you know, especially one that
wasn't earned on a patient like this when doing the correct
thing. One thing I didn't talk about
was nursing care interventions for this patient, but what were,
what would some of the top nursing care interventions that
you would see need to be employed on this patient?
So if you're not familiar with nursing care interventions, I
truly I don't like calling it nursing care.
It's not my favourite term for it.
I think it kind of cheapens the role of what a nurse does.
It's care that can be performed by anyone and everyone.
It is predominantly performed by nurses, but some people feel
it's below them. Oh, it's nursing care and I they
may be a mid level practitioner or physician.
If you're all that's there and still your your care to do
specifically patients like this is you have to worry about the
oral care of these patients worry about suctioning.
You have to one thing to really pay careful attention to the
pressure within the ET tube of this patient.
If you just fill it up to 10 ML because that's what you were
taught in paramedic school or as you innovate, you're likely to
cause tracheal escape on these patients.
And that's a whole nother problem since you're, you're
creating an internal tourniquet in that trachea and the
pressures that can be administered through the ET tube
are four or five times the appropriate amount on their
nifty resource. They do have some really cool
syringes that have actual a manometer in them and you can
measure what it's at, but and it is the size of the ML syringe.
But to likely have that, I rarely see one and usually I
it's somebody brings one with them and there's usually only
one. Another way that you could do
this is actually after you confirm placement on this
patient and you come back, secure the tube, everything's in
place, deflate the cuff and reflate it with 10 MLS and then
hold the, the syringe onto the bulb and let it equalise in
pressure. And there is a CRNA programme in
the United States military out of a military hospital called
Womack and they showed that that is very closely getting on
target for what the right cuff pressure is supposed to.
And you just let that equalise. Once it equalisers, you
disconnect it from there and do continue to watch your patient.
But that's the recommendation they have.
So key learning points. Let me do this together.
Lots of learning points from one case.
The 1st and most important thing is disease is deceptive. 3 weeks
of flu like symptoms, talking under your your own power, DCS
of 50 and outrageous lack. Don't let that over assure you
that the patient isn't critically I'll just by initial
patient presentation look at that whole picture.
Second, your blood gas know that the difference between VB GS and
AB GS drug selection matters. It did not only in the austere
set the clinical course of our patient and what's going on them
and again back to the vectorium versus and also the ketamine
versus a drug like propofol in the patient in that ventilatory
management is not just about the lung.
So in a patient with severe metabolic acidosis that the
ventilator is also part of the acid base management and also we
didn't get too much to it, but venous return as the way we
normally breathe for negative pressure that help augment his
return in a hemodynamically unstable patient as we now put
positive pressure clear Tampa nodding venous return and and
actually impacting that a bit. Again, a patient that's
hemodynamically unstable, the one thing to augment cardiac
output is and that's exactly what we're disrupting.
All right. In most powerful intervention in
this case was not the innovation, it was not the vase
suppressor or the antimalarial. Most powerful intervention was
really the recognition that the moment that it the take this
patient and go all this patient is sick and not only sick but in
sepsis and they are on a razor thin edge here that recognition
is is everything it stops delayed treat.
It allows you to start culminating the resources you
need to getting things in motion and especially in the steer
environment to get a critical care team to me at that point in
the best of situation is minimum 6 hour and much likely many
times in that situation was actually 24 hours.
So even delaying the recognition by three to 4 hours can greatly
affect my on there. All right, I have some
references if you want to see some of where the, you know,
kind of read in on some of these things.
Ards net on here. There's kind of multiple other
publications that you can hunt down and read and I believe most
of them are open source at this point.
You can find them somewhere, but do give those a read and at that
point, I'm going to turn this back over to a brick and answer
any questions that you may have. Fantastic.
And that's one of the most difficult cases of malaria I've
ever heard someone present. So that's we have some time.
Who's got some questions. This has been a presentation
from the College of Remote and Offshore Medicine.
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