Linking To And Embedding “POCUS In Acute Kidney Injury” From MetroHealth Emergency Ultrasound By Dr. Abhilash Koratala

In this post, I link to and embed POCUS in Acute Kidney Injury from MetroHealth Emergency Ultrasound, 1:18:02, Jun 17, 2021, by Dr. Abhilash Koratala.

Note to myself and my readers: The best way to quickly review this excellent teaching video is to watch the video on YouTube. By doing this, you can follow the video using the transcript. And as you go through the transcript you will be automatically reviewing the slides.

I put these resources on my medical education blog because the blog’s WordPress search function easily allows me to quickly find and access my study resources.

And copying and pasting the slides and transcript excerpts in a blog post (like this one) helps me reinforce my learning. But again, I recommend my readers review the video on YouTube so that they can follow along with the autogenerated (but usually very accurate) transcript.

 

This discussion is part of our weekly ultrasound education series. Here we have a guest speaker. Dr. Abhilash Koratala is talking about the use of ultrasound to evaluate patients with acute kidney injury. Follow us on Social Media: Twitter: https://twitter.com/MH_EMultrasound Instagram: https://www.instagram.com/MH_EMUltras...

Here are some of the slides from this excellent lecture.

Fig 2, 0:27

Fig 3, 2:07

In this first section, Dr. Koratala discusses acute kidney injury due to obstruction.

,Fig 4, 3:56

Fig 5, 5:19

Fig 6, 6:02

Fig 7,  6:56. Below the arrow points to a mass  surrounding the left kidney.

Fig8, 7:39. Below the arrows show a mass encircling the kidney causing the hydronephrosis.

Fig9, 8:40. Below, the initial kidney ultrasound shows no evidence of hydronephrosis.

Fig10, 9:20. Pt’s creatinine was not improving and so Pt had a CT Scan of the abdoman which showed peri-aortic fibrois and peri-ureteral fibrosis. So the patient had retroperitoneal fibrosis which was compressing the uteters.

Fig11, 9:50. The pt recieved bilateral stents and the creatinine rapidly improved within 4 days. Note that a patient can have obstructive nephropathy without demonstrating hydronephrosis as in this patient. This fact is very important to remember.

Fig12, 10:04. Also you can see this
similar phenomena in patients who are like severely volume depleted representation [but who have obstruction] and who
may develop hydronephrosis on repeat scans [when re-hydrated].

Fig13, 11:22–Below. A non-contrast CT in the ED was unrevealing. Dr .Katala, the lecturer, states that a non-contrast CT is insuficiennt to evalute AKI.

Fig14, 11:55 Below. Because the patient was septic and no source could be found, she underwent laparoscopy which was non-diagnostic.

Fig15, 12:08. Below. When a contrast CT was performed after non-diagnostic surgery, the etiology was determined, pyonephrosis [arrows] with hydronephrosis.

Fig16, 13:48, below.  Another example. The oval shows a staghorn calculus (could also be air in the collecting duct- CT would show which it was). The green arrow shows layering of pyonephrosis.

Fig17, below. This is a parapelvic cyst rather than hydronephrosis because there is no branching of hydronephrosis.

Fig18, below. A kidney ultrasound is never complete without a bladder ultrasound. Here we see, on the left, the way the bladder should look with a functioning foley catheter. On the right, there is an obstructed foley catheter.

Now we come to the intrinsic causes of kidney injury.

Fig3, below.

Fig19, 16:38 Ultrasound is pretty non-specific. It cannot diagnose any particular cause of kidney injury. But what it can tell you, especially when you have no baseline serum creatinine available, is whether this is more likely acute kidney injury [normal size kidneys] or more likely chronic kidney disease [small kidneys]. For that, you look at renal length and parenchymal thickness.

Fig20, 19:02 The next factor is cortical echogenicity that’s another thing you would look at is cortical. When we say cortical echogenicity we are comparing the relative echogenicity or how bright the kidney cortex is compared to the liver on the right and spleen on the left and renal cortical echogenicity increases in in many things. It’s pretty non-specific.

Fig21, 20:29 Here is an example of a patient on dialysis with esrd kidney. the length is only 7 centimeters and you can see that there is pretty much no visible cortex and it’s pretty bright all over. And here is a transverse section of the kidney that shows the increased echogenicity better and a very thin parenchyma so this is definitely esrd kidney

Fig22, 20:56 Below. And here is an example obtained from a patient with lupus nephritis [a type of glomerulonephritis] and presenting with acute kidney injury. Here you can see the very significantly elevated echogenicity compared to that of adjacent liver and here is the left kidney you can see that the kidneys are thick and the parenchymal thickness is very much preserved and the length of the kidney is also very much preserved it’s about 12 centimeters. So in any kind of active glomerulonephritis you can have  increased cortical echogenicity

Fig23, 21:28 below.

Here is another case of a biopsy provem atn. This was  a young patient who presented with influenza and had prolonged icu stay requiring ecmo and all that and so required crrt in the interim and the kidneys look like this. So a big  preserved parenchmal thickness [with] increased echogenicity. The length is preserved.

Fig24, 23:17 Here is an example where you would see actually white or bright pyramids and not more blackish pyramids as you would see in a case of increased echogenicity. This is a nice example of medularry calcinosis and another interesting case of intrinsic renal cause.

Fig25, 23:21 Here is an elderly gentleman. I saw this patient in the clinic uh very recently he’s otherwise healthy. [This case is] about 70 year old caucasian male hypertension is also very well controlled. [He had] no hypotensive episodes or anything [else].

[But he presented] with acute kidney injury. The creatinine rose to like three point something. When i initially saw him and the baseline was about one 1.1 ish. And the kidney showed markedly increased echogenicity on clinical ultrasound.
So in my clinic note I wrote: I suspect the two primary differentials.
It would be either: It’s a deposition disease. That’s a common thing that elderly patients present to nephrology clinic with
unexplained aka and found to have like multiple myeloma.
Or i think it’s something else though i cannot say based on this non-specific features

Fig26, 23-36

so it turns out that the biopsy showed this so so what you see here is first
you see a lot of blue things here so blue things are cells so that means there is a lot of uh cellular infiltrate in the

interstitium that’s one thing so my prediction about having interstitial nephritis is correct and on top of that

you see something more interesting that these arrows point to here so you notice this glassy structure is better

seen on this polarized microscopy here so they light up here so these are calcium oxalate crystals

and remember i mentioned he was taking vitamin c and d for covid19 prophylaxis poor guy because somebody said

they can boost the immune system so what happened is oxalate nephropathy is seen as a complication of

too much vitamin c and ascorbic acid gets converted into oxalate and that can get deposited in the kidney

and cause oxalate nephropathy this is very unfortunate situation and simultaneously if you’re taking vitamin d

and you don’t have vitamin deficiency it can it causes uh hypercalceuria and that calcium and

oxalate passing through the kidney um probably led to all this calcium oxalate uh

formation this is very unfortunate scenario because uh this anecdotally has you know poor prognosis and this patient

um like i mean i started him on steroids for the inflammation component but didn’t really respond and ended up in

hospital we initiated him on dialysis i hope he recovers but but that’s a bad thing

so you need to be aware of this thing like i mean especially in er setting or even in the icu setting there are case

reports where in some icos patients received iv vitamin c and patients developed

oxalate nephropathy okay so based on my experience i would just

say in in general in clinic if you are seeing a patient with relatively preserved parenchymal

thickness and hyperechoic kidneys the first differential would be an acute interstitial nephritis

most likely from some over the counter medications or paraprotanemia then some kind of

glomerulonephritis or you would also want to rule out hiv because hiv induced nephropathy um can have big hyperechoic kidneys we

don’t see that often these days because patients present early and we have better treatments but

that used to be like a very common differential uh previously and if you are seeing impatient with similar picture with big

hyperechoic kidneys most of the time it’s atn and the second differential would be a n

because in inpatient setting most most likely the patient experiences hypotension and is subjected

to drug therapy so these are the two common causes it’s very rare that some kind of acute gn is presenting in the inpatient

Fig27, 26:05

so based on my experience i would just

say in in general in clinic if you are seeing a patient with relatively preserved parent chemical

thickness and hyperechoic kidneys the first differential would be ain acute interstitial nephritis

most likely from some over the counter medications or paraprotanemia then some kind of

glomerulonephritis or you would also want to rule out hiv because hiv induced nephropathy um can have big hyperechoic kidneys

 if you are seeing impatient with similar picture with big

hyperechoic kidneys most of the time it’s atn and the second differential would be a n

because in inpatient setting most most likely the patient experiences hypotension and is subjected

to drug therapy so these are the two common causes it’s very rare that some kind of acute gn is presenting in the inpatient

setting uh except for maybe post-infectious gn

Fig28, 27-14

this is the last case of

intrinsic kidney disease so this is a patient with right flank pain otherwise young female

no known comorbidities like just had like severe flank pain came to the er and uh is there anything suspicious for

intrinsic cause i mean there was really the urinalysis was remarkable i mean really uh unremarkable meaning

there there was no blood in the urine no white cells in the urine

did have some subjective fever but there was no measured fever um or elevated temperature so

it looks pretty normal and there is no obstruction there are no obvious stones um i mean maybe there is

some like hypoechoic area in this region maybe it gives little bit of heterogeneous appearance to the

parenchyma but nothing uh really right so what’s the next step you do

Fig29, 28:15

 kidney ultrasound again is never complete without bladder ultrasound and also never complete without um you

you doing one at least one color doppler image so the color doppler image shows

this spectacular pattern where the there was blood flow only to one part of the kidney and the the top portion of the kidney is

completely bloodless so and the ct scan eventually showed a massive renal infarction

i mean it’s it’s strange that like we couldn’t find any cause of renal infection despite doing uh

angiogram and all the hypercoagulable workup and all this all that stuff and it is said that about 30 percent of

the patients can have idiopathic renal infarction so this is one important thing i think especially for uh in the ed setting uh

never finish without

[a color power doppler] image

And now we come to the third section of causes of acute kidney injury. In the first part, Doctor Koratala went over obstructive causes. In the second part, he reviewed some intrinsic causes. And in this section, the doctor reviews hemodynamic causes of acute kidney injury.

Fig29, 28:53

 

 

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