SCGIM Acute Kidney Injury 4 23 19


– Hello everyone. Sanjay Saint here and I’m really glad that you could join me for a discussion of acute kidney injury. This is based on the book,
The Saint-Chopra Guide to Inpatient Medicine, that I
worked on with my colleague, Vineet Chopra. So let me just give you
some background information about acute kidney injury. The definition is a rapid
decrease is glomerular filtration that results in abnormal
fluid and electrolyte balance and azotemia. And the diagnosis is
usually made when the serum creatinine level rises abruptly. There’s many different
types of definitions. I’ll first give you
the formal definitions, then I’ll give you the practical one that we tend to use in
hospitalized patients. The formal definitions is
that acute kidney injury is defined by either an
increase in serum creatinine by 0.3 in 48 hours or an increase in serum
creatinine by one and a half times baseline within seven days, or a decrease in urine output
to less than 0.5 milliliters per kilogram per hour for six hours. I’ll tell you, practically,
what we usually do is if we see, because we get QAM labs, if the patient’s creatinine
increases by roughly 0.3 or 0.5 in a 24 hours period, we think to ourselves this
person has acute kidney injury. Most of the time patients
with acute kidney injury, which happens about 2% of
all hospitalized patients, will be asymptomatic. Most of the time they will be asymptomatic unless their BUN starts approaching 100. At which times they may
have symptoms of uremia and those symptoms can be remembered, kind of, from the head to the gut. CNS would be coma, confusion, seizures. Cardiovascular would be pericarditis with an overload, arrhythmias, and then GI would be
anorexia, nausea, vomiting, GI bleeding because of
dysfunctional platelets, which sometimes occurs in uremic patients. And as we will talk about at the end, these non-specific findings should, especially in a patient who’s got a BUN that approaches 100, should make you think, ah, they’re uremic and therefore they need
acute hemodialysis. The best way to approach
acute kidney injury is anatomically. Thinking about it as prerenal,
intrarenal, and postrenal and we’ll kinda go through
that one at a time. The first and the most common cause of acute kidney injury are prerenal causes and prerenal causes really
are preglomerular causes, but we just call them prerenal. And I think of this anatomically
from the left ventricle all the way to the
level of the glomerulus. Anything that decreases
profusion at the level of the glomerulus can lead to prerenal acute kidney injury. So that’s decreased filling
of the left ventricle because of dehydration,
due to diarrhea or vomiting or third spacing. Poor forward flow
because of heart failure, critical aortic stenosis leading to decreased forward flow. Renal artery stenosis either
due to atherosclerosis or fibromuscular dysplasia. And then issues related to the afferent and efferent arterial where you can have perturbations there that leads to decreased profusion, such as sepsis or contrast
dye, hepatorenal syndrome or certain medications like NSAIDs. That’s all under the category of prerenal acute kidney injury and clues that someone
has prerenal would be that they have a high
BUN to creatinine ratio. Rather than 10 to one it would
be 15 to one or 20 to one. Their urinalysis is bland. Their fractional excretion of sodium shows that they’re very sodium avid. So they’re FENa is less than 1%. If they’re on diuretics
we would then use FEurea that’d be less than 30 or 35%. And, but one of the best approaches though is that we tend to give
these patients fluids and see if they respond. The exception to this rule
would be cardiorenal syndrome where patients are
already fluid overloaded and they’re on the other
end of the Starling curve so fluids would be contraindicated. In these types of patients, you would actually diurese
them which would improve their Starling dynamics,
increase cardiac output, and therefore improve profusion
at the level of the kidney. Prerenal accounts for a large percentage of acute kidney injuries and the first thing that you think about when someone has acute kidney injury. The other extreme are postrenal causes. These are relatively unusual. They account for a small number, but they’re important to
rule out after a few days in order to avoid long
standing kidney damage. And again, we approach these anatomically. Start with the urethra, work your way up to the bladder, the ureters,
and then the renal pelvises. Blockage along all that path, anywhere on that pathway can
lead to obstructive uropathy or postrenal acute kidney injuries. So this would include urethral strictures, in male, a large
prostate, bladder problems that lead to mechanical obstruction, like bladder tumor, bladder
polyp, bladder hematoma, bladder cancer, bladder stone, or non-mechanical or neurogenic causes, like multiple sclerosis,
injured spinal chord, diabetes, and certain medications. Ureteral problems include things like renal stones, lymphadenopathy,
retroperitoneale fibrosis, for example the IGG4 related disease. And if you have two functioning kidneys, though one will be able to compensate, but many patients do not and therefore you can
see a rising creatinine even with a unilateral
kidney stone, for example. The approach here is to do an ultrasound to rule out hydronephrosis and if you see
hydronephrosis you get urolog or interventional radiology
involved for stenting or percutaneous nephrostomy tubes. And then finally, intrarenal causes. This is I realize an opaque box, but we can make this easier to understand by thinking about the
four things that live within the kidney. The first are tubules
that live in the kidney and this is ATN. ATN is usually due to something, some type of an insult, shock, severe hypotension,
ischemia, contrast dye, sepsis, hemoglobin urea, myoglobin
urea, medications, like immunoglycosides, and clues that someone has ATN will be that their BUN to creatinine
ratio is now normalized, their urine shows muddy brown
granular, tubular casts, their FENa is greater than 3%, their FEurea, if they’re on
diuretics, greater than 50%, and they don’t respond
or only partially respond to a fluid challenge. When I’m thinking someone has ATN, I always get nephrology involved so they can confirm the diagnosis. Most patients will then get better before they need dialysis. But it’s just something
that you want to think about because it’s a common cause
of acute kidney injury, especially in patients in the ICU. Glomerular causes, here
we’re talking about acute glomerular nephritis,
which is inflammation of the glomerulus and this can be
due to many different causes. Things such as lupus,
cryoglobulinemia, vasculitis, Goodpasture’s Disease, MPGN, and the like. Clues that someone has
glomerular nephritis is that they’re going to
have a rising creatinine, new hypertension. They’ll have a little bit of proteinuria, but usually not nephrotic
range proteinuria. So it’ll be less than three
or three and a half grams in a 24 hour period. They’ll see, you’ll see
red blood cell casts or dysmorphic red blood cells and sometimes patients
will even say that they’re urinating blood. You’ll wanna biopsy these patients early because we’ll need to give
them immunosuppressants and getting nephrology
to see this patient soon will be important. The third, or interstitial, causes here, it’s really acute or allergic
interstitial nephritis usually due to drugs or
sometimes a viral infection and because it’s allergic to something, the acidophils tend to proliferate. You can see it in the blood and you can see it in the urine, but you don’t always need to see it. Usually withholding the offending agent will cause this process to go away. And then finally, vascular causes and here I’m talking about vascular causes other than those that
involve the glomerular, the glomerulus. So this would be HUS TTP,
or hemolytic uremic syndrome and TTP, which are the
thrombotic microangiopathies. I’m lumping them together even though I know because
of Adams TS13 activity, they’re distinct, but HUS has a triad of
HUS, hemolysis, uremia, and sthrombocytopenia,
but the S is silent. And TTP has those three things plus fever and neurological changes and for TTP the management
is plasmapheresis. And then the final vascular cause are all the different vasculitides that can involve the kidney and there are many different types. Vasculitides, that are
involving different vessel size and that’ll be actually a
separate talk down the road, but when I think someone has a vasculitis, I’ll get a rheumatologist to
help me manage that patient. So finally, as I’d
mentioned at the beginning, there are some indications
for acute hemodialysis and they can be remembered
with the mnemonic AEIOU. A is for acidosis that is not
being managed appropriately with conservative measures. Electrolyte abnormalities,
especially hyperkalemia. Intoxication to certain drugs
that you need dialyze off. Volume overload states and then finally uremia, which involves, like we discussed, the
central nervous system, the cardiovascular
system, and the GI system. So thank you very much for
your time and attention. I appreciate you watching this video. Have a great day, bye.

3 thoughts on “SCGIM Acute Kidney Injury 4 23 19”

  1. I wish you're my lecturer. Ours keeps going on and on about their stupid research, not about what we need to know for exams

Leave a Reply

Your email address will not be published. Required fields are marked *