Step 1 Recognizing its Acute Kidney injury
Step 2 : differentiating between Prerenal (hypotensive) azotemia and Ischemic ATN
From the vignette , Patient is "fully volume restored " ( not hypotensive anymore) but yet he still has a low urine output
Note: Failure of AKI to correct after patient is once again euvolemic - would suggest either another prerenal cause such as Heart Failure , Nephrotic syndrome etc or an intrinsic cause like Ischemic ATN
A side note from medscape : Ischemic ATN is a continuum of Prerenal Azotemia . Indeed the cause of the two conditions are the same , ischemic ATN resulting when hypoperfusion overwhelms the kidneys autoregulatory defenses leading to cell death
I think of it as a reversible cause vs an Irreversible one .
Failure of Prerenal Azotemia to correct after fluid resuscitation means it has progressed to the point of cell death ; Acute Tubular Necrosis .
(These cells will eventually regenerate with time )
imgdocThe key in this question is that he is FULLY volume repleted, and YET he still continues to have oliguria. This is why it is AKI and NOT prerenal azotemia. +1
The patient has ATN secondary to renal ischemia. Due to tubular necorsis, the patient will have an elevated FeNa. The patient's urine will also be dilute, but this will be reflected by the low urine osmolality, not the FeNa
mousieHypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia? +19
sympathetikeyI had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself.+3
ajoThis might help clarify why the pt. has ATN rather than pre renal azotemia.
The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong. +53
ajoIn addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption! +21
gh889Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN+1
sugaplumfor anyone who wants to see it: FA 2019 pg591 +2
divyai'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too?+1
osler_weber_renduLets all take a moment to admire how shit this question is
"Bp 90/60.""Repeated episodes of hypotension in the OR" and still the answer is ATN+5
step1dreamteamMaybe it's a brainer, but I think the key point here is to understand that episodes of pre-renal AKI are REVERSIBLE, if you correct the cause of ischemia (in case of the vignette, stopped bleeding + corrected volemia). Hence, what remains as a viable option is only ATN due to previous episodes of ischemia (the damage to the tubules happened during the episodes of bleeding). Again, this thing about the reversibility of pre-enal AKI state is my idea, not read anywhere else, but it would be awesome if someone would confirm this. +
kcyanide101This question is a lil unfair.... First aid mentions that ATN begins 1 to 3 weeks after injury. The main problem here was distinguishing between ATN and Pre renal azotemia :(+
stsfytProlonged prerenal injury leads to intrinsic injury, as decreased renal perfusion causes tubular necrosis. (e.g., hypovolemia, hypotension, diuretics etc etc)+
submitted by โandro(269)
Step 1 Recognizing its Acute Kidney injury
Step 2 : differentiating between Prerenal (hypotensive) azotemia and Ischemic ATN
From the vignette , Patient is "fully volume restored " ( not hypotensive anymore) but yet he still has a low urine output Note: Failure of AKI to correct after patient is once again euvolemic - would suggest either another prerenal cause such as Heart Failure , Nephrotic syndrome etc or an intrinsic cause like Ischemic ATN
ATN Stages : 1. prodrome
2. Low urine output (Oliguric phase )
3. High urine output (Polyuric phase)
A side note from medscape : Ischemic ATN is a continuum of Prerenal Azotemia . Indeed the cause of the two conditions are the same , ischemic ATN resulting when hypoperfusion overwhelms the kidneys autoregulatory defenses leading to cell death
I think of it as a reversible cause vs an Irreversible one .
Failure of Prerenal Azotemia to correct after fluid resuscitation means it has progressed to the point of cell death ; Acute Tubular Necrosis . (These cells will eventually regenerate with time )