00:01
So, once our patient has ATN,
what is our diagnostic workup
and how can we actually
come to that conclusion?
Just as we have in every other
portion, we're gonna be a good detective.
00:13
We're gonna look at that history
and do a very thorough chart review.
00:15
So we wanna see, has our patient
had any period of time where they've had
prolonged hypotension in the
ICU or in any other circumstance?
Did they have any evidence of ischemic
hits to the kidney or low blood pressures?
Have they been exposed to radiocontrast?
Now with the advent of electronic
medical record, that's very easy to see.
00:35
We can just look under our diagnostic
imaging, under our cardiac cast
and see if those patients were actually administered
iodinated contrast from either an angiogram or CT scan.
00:45
And then , we also want to see if
our patient had a period of sepsis.
00:48
Did they have septic physiology?
Were they in the ICU for a period of time?
These are all things that can
lead us to the right direction
of more risk factors that can be
involved in acute tubular necrosis.
01:00
We're also looking for drugs so looking under
medication administration record in our AMR,
we're able to see was that patient actually
administered aminoglycosides for a bacterial infection?
Amphotericin B for a fungal infection?
or did they have a crush injury or were
they found down for a prolonged period of time.
01:16
It's not uncommon for us to see at
our hospital patients that are brought in
because of the fact that they've been
found down either from a drug overdose
or another phenomena where
they're down for a long period of time
and they end up with a
crush injury to muscle.
01:30
And that would be rhabdomyolysis.
01:34
So, there's some laboratory evaluations
that make it very helpful to see what's going on.
01:38
So when we look at our serologies,
we're looking at BUN and creatinin.
01:42
And specifically oftentimes with
pure ATN, you could really see
that BUN to creatinine ratio
being less than 10-15:1
This is as opposed to pre-renal, remember
we talked about that being greater from 20:1.
01:54
This is about 10-15:1.
01:56
And if you think about why that's happening, remember
what we said pathophysiologically what's happening.
02:01
We have that patch necrosis in the S3 segment
and the thick ascending limb in the loop of Henle.
02:05
This is also areas where we're going be
reabsorbing urea, so if we don't have that
because these tubules are damaged,
then we see less urea nitrogen in our blood.
02:15
So that's why the BUN to
creatinine ratio is a little bit less.
02:18
Our urine sodium and chloride are going
to be high, typically greater than 20 mEq/L again
because we are spilling sodium into our
urine because we are not absorbing that
at that proximal tubule and the thick
ascending limb of the loop of Henle.
02:32
When we calculate our FENa which
we learned about in our pre-renal section,
it's going to be greater than 2% and
that's important because that tells us that
that patient most likely is not going to
be responsive to volume resuscitation.
02:45
Then of course, we
want to look at the urine.
02:47
And the urine always tells a lot so
typically these patients are isosthenuric,
They have a specific gravity
that's relatively normal.
02:54
They can't really concentrate
because they've lost that ability.
02:57
Why? because the medullary
gradient is really washed out
and not maintained because again if you
think about where the injury is, it's at that
thick ascending limb of the loop of Henle and that's
critical in order to maintain your medullary gradient.
03:10
And the urine osmolality in our patients
because of this is typically less than 450 mOsm/kg
oftentimes it's isoosmolar
to the serum osmolarity.
03:22
Our patients may also
have low-grade proteinuria,
typically it's between 500 (mg) to 1
gram within a 24-hour period of time.
03:31
And that's oftentimes because of impaired
reabsorption of protein at thst proximal tubule.
03:36
So it's not necessarily glomerular damage
but we do absorb proteins other than albumin
at that proximal tubules so again
if proximal tubule is damaged,
we're gonna see some proteinuria.
03:46
And then my favorite part being a
nephrologist which I talked about before
is I get to look at the urine
underneath a microscope
and that's exciting because there
are clues there for me that tell me
and that can tell you whether
or not your patient has ATN.
03:59
In this situation, we get to see these really
wonderful cellular cast called pigmented granular cast.
04:06
And they look just like this,
this is from one of our patients
who had ATN and you can see you have
these kind of beautiful brown cylindrical cast
that are granular in quality
and they populate the entire field,
this is looking at the 10x view.
04:19
And that's great because the specificity is high and it
tells us that that patient does have a tubular injury
Sometimes if you're lucky enough, you
can actually see a tubular epithelial cell
free-floating in the urine as well.
04:32
And these are all things that ar e gonna tell you
that this patient likely has acute tubular necrosis.
04:38
So in terms of the the clinical
course and how people do with ATN,
they oftentimes go through
kind of a 3-phase approach.
04:47
So they have the initiation phase where
injury occurs and sometimes gets augmented,
And then the maintenance phase,
this is where the creatinine plateaus.
04:57
Typically, it occurs anywhere
from 7-10 days after the injury
And then the recovery phase,
where the excess solutes and water
tend to be excreted as
the tubule undergoes repair.
05:08
And that oftentimes will mark the polyuric
phase, anywhere from days 10-14 of ATN
And this important because our patient's
actually changed in their clinical appearance .
05:17
Instead of being oliguric, they are now
polyuric - they're making lots of urine.
05:22
3 liters or more of urine.
05:23
And again, part of this is because they're just
removing these extra solutes that they built up
when when they have renal failure.
05:29
But part of this too is that they've lost that
concentration gradient in their medullary interstitium
and so because of that again, they are quite polyuric
and they're unable to concentrate their urine.
05:41
Recovery in the typical phase will usually
occur somewhere between 14-21 days.
05:46
I do want to say that this is textbook approach and it
would be wonderful if our patients always behave this way,
but oftentimes, ATN can either be
shortened or it could be much longer.
05:56
And sometimes it takes up to 3 months for
our patients to recover from their tubular injury.
06:04
Okay, so what do we do once
our patient is diagnosed with ATN,
How can we treat them or what can
we do to prevent that from happening?
We just said that this is one of the most serious types
of AKI because of the mortality association with it.
06:17
So it's important to really
identify people who are at risk,
so people who are
undergoing major surgery, why?
Because there's a real chance for a drop in
mean arterial pressure during surgical cases.
06:29
People who are in shock, right?
They might have these dilatory
shock, cardiogenic shock,
our patients who have comorbid
conditions that would put them at risk.
06:38
That would be patients with chronic
kidney disease, we already talked about
how they're really vulnerable
to having an acute tubular injury.
06:46
People who have peripheral vascular
disease, diabetes is coming up once again,
people with malignancies, heart
failure and malnourished patients.
06:54
So people who have these comorbid
conditions really are at an increased risk
when they're coming into the
hospital to develop acute tubular injury.
07:03
So things that we can do to decrease that
risk in addition to identifying those people
who are at risk is we want to really optimize
volume status and maintain hemodynamic stability.
07:12
That's really critical, we want
to avoid any points of ischemia.
07:17
We want to avoid nephrotoxic exposures.
07:20
I definitely do not want to be giving
my patients NSAIDs during their stay
if I feel that they are a population who
are at risk of developing a tubular injury.
07:28
Similarly, I don't want to give them nephrotoxic
medications like Amphotericin or aminoglycosides,
and then contrast-induced nephrotoxicity.
07:37
There's a couple of things that
we can do to mitigate that injury.
07:40
So I know that my patient has to have
contrast because the CT scan is critical
and being able to diagnose what's
happening with them or they need an angiogram
because they're coming in with acute
coronary syndrome and they have to have dye
in order to place a stent or diagnostically
see what's going on with them
And then I'm gonna do a couple of things.
07:59
I want to make sure that their
volume status is really optimized.
08:03
They can't go into that
procedure hypovolemic.
08:05
So I'm gonna volume expand them with
crystalloids, something like normal saline
pre and post contrast in order to maintain
the hemodynamics and dilute that contrast
and try to wash that
away as soon as possible.
08:18
I also am going to be talking to my radiology
colleagues as well as my cardiology colleagues
and I'm gonna ask them to minimize the amount
of contrast that they're using for my patient.
08:26
Sometimes, we can get away with using much less
or we could even use an alternative contrast agent
like CO2 in order to light up our
vessels, and that could really help us.
08:35
I do just want to make one comment because
there's been some thought processes in the past
that perhaps if we gave
diuretics at the same time
when our patients were getting
these contrast that they would do better,
We know that definitively evidence has shown that
diuretics are not helpful in the course of ATN.
08:52
We do use them if our patient is volume
overloaded and we have to mobilize volume.
08:57
But we're not using them in order to essentially
convert their renal failure to a non-oliguric state
or essentially see urine
output, so do keep that in mind.
09:08
Okay so that's ATN.
09:10
And again the big things that
I really want to stress is that
this is such a serious injury because
of its association with mortality.
09:17
And there's a lot of things that we can
do in terms of identifying populations at risk
and then being able to mitigate or
prevent some of the things from happening.