Approach to postoperative acute kidney injury: Clinical sciences

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Introduction0:00–0:54

Postoperative acute kidney injury, or AKI, is defined as a decrease in kidney function within 7 days after surgery. It is relatively common, as fluid shifts occur in the preoperative disease state, during surgery, and in the postoperative recovery period.
The most common cause of postoperative AKI is inadequate fluid resuscitation. Similar to nonsurgical AKI, postoperative AKI is divided into three types: prerenal, intrinsic renal, and postrenal.
Prerenal AKI occurs when there is a decrease in blood flow to the kidneys; while intrinsic renal AKI is caused by direct damage to the renal parenchyma; and postrenal AKI often reflects an obstruction of urinary outflow.

Unstable patient0:54–1:22

Your first step in evaluating a patient presenting with signs and symptoms suggestive of postoperative AKI is to assess their ABCDE.
Now, if the patient is unstable, start with acute management like ensuring adequate airway, providing supplemental oxygen, and obtaining IV access right away.
Remember that AKI in an unstable patient can be a consequence of postoperative shock which would require immediate management.Alright, now that the acute management for unstable patients has been started, let’s talk about stable patients.

Stable patient1:22–2:37

If the patient is stable, the next step is to obtain a focused history and physical exam. One of the first things you’ll notice is decreased urine output or oliguria.
However, keep in mind that postoperative AKI can be asymptomatic and often presents with abnormal lab values, so keep an eye on serum creatinine during the postoperative observation.
If you notice that it increased by 0.3 milligrams per deciliter or 1.5 times a patient’s baseline, that’s indicative of postoperative AKI.
It is also important to identify all underlying risk factors in addition to the type of operation performed, any significant intraoperative events, and on what postoperative day the AKI developed.
Remember to ask the anesthesiologist for the intraoperative intake and output to determine the fluid status of the patient during surgery.
If there are signs of oliguria, consider placing an indwelling urinary catheter, also known as Foley, if the patient doesn’t already have one to accurately track their urine output.During the physical examination, if your patient has an indwelling catheter, be sure to assess for catheter dysfunction.

Urinary catheter dysfunction2:37–4:29

First, inspect the catheter to make sure it isn’t kinked. If the catheter isn’t kinked, but you still notice a low urine output, order a bladder scan.
If you see urine within the bladder that isn’t draining, you should be concerned about an obstructed or a malpositioned catheter, which needs to be removed.
On physical exam, suprapubic discomfort with a palpable full bladder can support your diagnosis. After removing the catheter, have the patient do a voiding trial to see if they can urinate on their own.
If they can, there is no need to replace the catheter. However, if they are unable to void, you might need to replace the catheter.
Now, once you've ruled out urinary catheter dysfunction, your next step is to calculate the urine output, and obtain labs like a CBC, CMP including BUN, serum creatinine, and the BUN/creatinine ratio.
In addition, if your patient is making urine, you should get urine studies, like urinalysis, electrolytes, creatinine, and urea nitrogen; you may also calculate the fractional excretion of sodium or FENa.
The combination of the patient’s history, laboratory findings, and if available, FENa will help you determine the type of AKI and narrow your differential diagnoses.Here’s a clinical pearl to keep in mind!
FENa might not always be highly reliable, and it takes at least 24 hours of urine collection followed by lab analysis. Moreover, it can't be calculated if the patient is not making urine.
For these reasons, calculating the FENa might not be feasible to diagnose the type of AKI in postoperative settings.Okay, let’s start with prerenal AKI, which is the most common one, and occurs when there’s inadequate renal perfusion.

Prerenal AKI4:29–6:10

This is most often caused by hypovolemia, which in the postoperative setting can be due to significant perioperative blood or fluid loss, which is more common after high-risk operations like emergent surgery, cardiovascular procedure, burn surgery, and even sepsis or adrenal insufficiency.
However, some patients with hypervolemia may also develop prerenal AKI, particularly in the setting of cardiac dysfunction or hepatic dysfunction.
In these patients, you can expect to find decreased urine output, elevated BUN and serum creatinine, as well as a BUN/creatinine ratio typically over 20.
Urinalysis might show an elevated specific gravity of urine, indicating increased concentration of blood and urine. An additional clue to suspect prerenal AKI is a FENa of less than 1%.
Based on these, you should consider prerenal AKI.Your next step is a fluid challenge, meaning you give your patient IV fluids and assess their response by rechecking their urine output and labs 8 to 12 hours later.
If your patient’s urine output and lab values improve, you can confirm that the cause of your patient’s prerenal AKI was hypovolemia.
On the other hand, if your patient’s urine output and lab values don’t improve, then you should consider other causes, such as cardiac or hepatic dysfunction, and address the underlying cause.Alright, now that we’ve found the cause of prerenal AKI, let’s go back to history and labs to talk about intrinsic renal AKI.

Intrinsic renal AKI6:10–7:59

In history, you might find some risk factors for intrinsic renal disease like chronic kidney disease, glomerulonephropathy, diabetes, hypertension, and peripheral vascular disease.
As part of your history taking, make sure to check the anesthesia records for perioperative use of medications like NSAIDs, antibiotics and IV contrast, as well as intraoperative periods of hypotension that can cause ischemic renal injury.
On labs, you can expect to see elevated BUN and creatinine, with a BUN to creatinine ratio below 15. If obtained, FENa will likely be greater than 2%.Here’s a clinical pearl!
FENa between 1 and 2 % wouldn’t help you determine if AKI is prerenal or not, since it can happen in all AKI types. If you see this, make sure you obtain a detailed history about the operation your patient had, or any conditions they might have, as it can guide you to the likely diagnosis!Alright, now that you have your lab results, your next step is to obtain a bilateral renal ultrasound.
Because labs can be similar between intrinsic renal and post renal AKI, renal ultrasound is used to differentiate between the two.
If the ultrasound shows grossly normal kidneys with mild atrophy, which is a sign of CKD, without signs of hydronephrosis, you can consider intrinsic renal or parenchymal AKI.
Make sure you also assess the renal arteries and the blood flow to the kidneys.Okay, let’s now talk about specific findings that can help you narrow down your differential diagnoses for intrinsic renal AKIs.
History may reveal advanced kidney disease, atherosclerotic disease with moderate to severe hypertension, and even a kidney transplant.
On exam, you see acute worsening of hypertension, especially with the administration of ACE-inhibitors or ARBs. Urinalysis shows proteinuria; and on ultrasound, you see decreased blood flow to the kidney and narrowing of the renal artery.

Renal artery stenosis7:59–8:51

Based on these findings, you can make your diagnosis of renal artery stenosis. Although most renal artery stenosis is chronic, any acute changes in blood pressure or volume status within the perioperative setting can cause ischemic parenchymal injury to the kidneys.Another common cause of intrinsic renal AKI is acute tubular necrosis, or ATN, which can be caused by nephrotoxicity or ischemic injury.
Nephrotoxic injury refers to renal parenchymal damage often caused by medications like NSAIDs, IV antibiotics, or agents like IV contrast.
Because these medications or agents are often administered to surgical patients, it is an important factor to identify when obtaining the patient’s history.

Acute tubular necrosis8:51–10:16

Keep in mind that nephrotoxic injury is not only caused by medications, but also from myoglobinuria associated with crush injuries and rhabdomyolysis.
On the other hand, ischemic injury involves periods of intraoperative or ongoing hypotension, which can compromise renal perfusion enough to cause ischemia and necrosis of the tubular cells.
So, keep in mind that even if the patient has recovered from hypotension, the damage might already be done. On urinalysis, you can expect to find renal tubular epithelial cells and muddy-brown casts, which can help you confirm your diagnosis of acute tubular necrosis.
For rhabdomyolysis induced ATN, urinalysis will show myoglobin; and of note, serum CK level will be greatly elevated.Alright, the next diagnosis to consider is urinary tract infection or pyelonephritis.
Postoperative patients, much like any hospitalized patient, are at a greater risk for developing UTIs, especially if an indwelling urinary catheter was used during the course of their hospital care.
If the patient reports dysuria, and you find fever and costovertebral tenderness on exam, consider genitourinary infection as the cause of AKI.

UTI/Pyelonephritis10:16–11:05

Laboratory findings like leukocytosis on CBC, as well as urinalysis revealing white blood cells and bacteria should further raise your clinical suspicion.
Make sure to obtain a urine culture to identify the bacteria and confirm your diagnosis of urinary tract infection or pyelonephritis.Okay, now that the causes of intrinsic renal AKI have been identified, let’s go back to the ultrasound and talk about postrenal AKI.
In general, most postrenal causes are related to the obstruction of the urinary system distal to the kidneys. History will include risk factors like benign prostatic hyperplasia, genitourinary surgery such as kidney resection, transplant, ureteral reconstruction, or stent placement, in addition to other abdominopelvic operations, and neurogenic bladder from diabetes mellitus.

Postrenal AKI11:05–12:19

You can expect similar laboratory findings to intrinsic renal AKI, such as elevated BUN and creatinine, and a BUN-creatinine ratio lower than 15.
Similarly, if you obtain a FENa, it will likely be greater than 2%.So here, the ultrasound findings will be the differentiating factor between intrinsic and postrenal AKI.
If you see signs of hydronephrosis, like dilated renal calyces on ultrasound, you should be concerned for postrenal AKI.
Then, your next step is to obtain a bladder scan to determine if the obstruction is within the upper or lower urinary tract.
Let’s talk about upper GU obstruction first. If the bladder scan is normal, meaning that there are less than 100 ccs of urine within the bladder, the obstruction is likely proximal to the bladder, so you should consider an upper genitourinary tract obstruction.
In this case, you need to obtain a CT scan of the abdomen and pelvis to locate the obstruction. If you see a stone, ureter stricture, compression from a mass, hematoma or urinoma, or a migrated ureteral stent proximal to the bladder, your diagnosis is confirmed.On the other hand, if the bladder scan reveals that there are more than 100 ccs of urine, the patient has a lower genitourinary tract obstruction.

Upper GU obstruction12:19–12:56

Some common causes include benign prostatic hyperplasia, neurogenic bladder, or Foley malfunction.Alright, as a quick recap… Postoperative AKI is a common complication that occurs within 7 days after any operation.
The three types of postoperative AKI include prerenal, intrinsic renal, and postrenal. Prerenal AKI is most commonly caused by hypovolemic states, but can also be caused by hypervolemia associated with cardiac or hepatic dysfunction.

Lower GU obstruction12:56–13:13

Intrinsic renal AKI reflects renal parenchymal damage that can occur from renal artery stenosis, acute tubular necrosis, and infection.
Lastly, postrenal AKI is caused by an obstruction of the genitourinary tract from a stone, stricture, mass, or chronic conditions like BPH, neurogenic bladder, or Foley malfunction.

Review13:13–13:59

days after any operation The three types of postoperative A K I include prerenal intrinsic renal and post renal prerenal AKI is most commonly caused by hypovolemic states but can also be caused by hypervolemia associated with cardiac or hepatic dysfunction Intrinsic renal AKI reflects renal parenchymal damage that can occur from renal artery stenosis acute tubular necrosis and infection Lastly post renal A K is caused by an obstruction of the genitourinary tract from a stone stricture mass or chronic conditions like BPH neurogenic