Approach to postoperative acute kidney injury: Clinical sciences

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.

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. 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. 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. 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. 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%.