Column: AKI and the mess we're in

In March 2008, the National Kidney Foundation sent a letter to the National Centers for Health Statistics and asked that the term “acute kidney injury” (AKI) be an optional phrase for assigning ICD-9-CM code 584.9 (i.e., that it was the current terminology for what used to be called “acute renal failure.”) The request was granted.

 

CDI specialists and coders looked at the definitions published through the Acute Kidney Injury Network and noted the criteria of stages 1, 2 and 3 of AKI. They began to ask physicians to document AKI whenever a patient’s labs or urine output met those criteria. But in so doing we hurt ourselves—and we hurt “acute renal failure.” And it’s a shame. Now, with CMS’ resulting reduction of acute renal failure to CC, it now has no more severity attached to it than a simple urinary tract infection.

 

Let’s see where we went wrong and where we have to go to get it right.

Long ago, in a galaxy far, far away, we had the terms “acute renal insufficiency” and “acute renal failure,” and we had advice as to when each was appropriate terminology to use in order to assign the codes that were designed for those conditions. These codes included 593.9 for renal insufficiency and 584.9 for acute renal failure (notice I didn’t use the term “acute” in the description of 593.9—it was a nonessential modifier then).

 

In the medical textbooks and within the medical community there was confusion in the terminology. For example, one medical textbook called the disease “renal insufficiency” and talked about “progressive renal failure,” and another textbook had a chapter entitled “renal failure” and spoke of “anemia of renal insufficiency.”

 

AHA’s Coding Clinic for ICD-9-CM, First Quarter 1993, p. 17, gave us the following definitions as guidance:

 

 

 

And on p. 18, Coding Clinic states:

 

 

Back then, we looked for more than dehydration. We looked at more than a minor bump in creatinine. We looked for a sick patient. Sure, there may have been obstruction due to prostate cancer associated with a high creatinine level which returned to normal soon after suprapubic tube insertion.

 

Yes, there may have been a patient found down for three days at home who came in with depressed mental status and rhabdomyolysis and responded to a couple of liters of IV fluids in a couple of days. And these patients came back, at least measurably, to normal. But they were sick and they had acute renal failure. And if a patient had two days of diarrhea “altered mental status” and responded to a glass of water to return the creatinine level to normal, we were happy with dehydration or prerenal azotemia or acute renal insufficiency—because that’s what is was.

 

During this time, the renal world recognized the problems with lack of consistency and did some studies of acute decrease in renal function. It came up with mortality rates, rates of need for Renal Replacement Therapy (RRT – or dialysis) and identified three pretty distinct levels of change in creatinine, change in Glomerular Filtration Rate (GFR) and change in urine production. It also identified two levels of long-term outcome: Return of measurable function, or no return of measurable function. They published their results and findings and called the system RIFLE. And all rejoiced.

 

But there were two issues of massive importance that somehow didn’t get into the subsequent evolution of acute damage to the kidneys. First, all of the studies were done in critical care units on critically ill patients. Certainly there was mortality—but it was not clear whether the mortality came either from the renal damage or from the other conditions that the patients had at the time of death. 

 

It was merely an observation of mortality, regardless of the cause, in patients with measurable changes in renal function. Secondly, and they were very specific about this—RIFLE only applied to intrarenal damage and did NOT apply to prerenal causes or postrenal causes. Basically, they said that the patients who actually had what they believed was acute tubular necrosis or hemorrhage of the kidney or infectious or immune destruction of renal parenchyma counted, and that the patients with elevations of creatinine due to dehydration without ATN or elevations of creatinine due to obstructing bladder cancer did not count.

 

Several iterations of acute kidney injury studies followed to validate the results and recommendations above and the Acute Kidney Injury Network was formed. Again, all of the studies were done on critically ill patients on critical care units. But this group changed some of the rules. They eliminated GFR change as a valid measure and that was reasonable, especially if one didn’t know what the patient’s creatinine was before the insult and didn’t know if the end result was a decrease in function or not. And other less important issues could impact GFR than the renal destructive condition.

 

And then they said that their new staging of “AKI” was applicable to prerenal and postrenal causes because, in critically ill patient in critical care units, many had intrarenal damage because of prerenal and postrenal causes. The problem is that all of their patients again were critically ill and on critical care units. They did not look at creatinine change or urine output change in patients who didn’t make it to the ICU.

 

I think that this overlooked the 80+% of patients who have changes in creatinine or urine output that falls within their established criteria—particularly of Stage 1.

 

As an aside, let’s take a quick look at the term “injury” as it has pertained to other organs. There was a time that the pulmonology groups spoke of “acute lung injury” and there were a ton of publications talking about “acute lung injury.” What these investigators recognized is that the myriad of diseases that fall into the category of “acute lung injury” included the range of the most mild to the most severe and that the identification of the particular disease was more important than the vague term of “injury.” Thank goodness for that. 

 

Acute lung injury due to viral pneumonia is a totally different animal than acute lung injury from ARDS due to amniotic fluid embolism. And they now continue to clarify “acute respiratory failure” and distinguish it by pathologic change rather than dwelling on a new term that has no specificity for risk. Should the renal world follow this lead? It’s not for me to say.

 

 

So we are left with a term, “acute kidney injury,” that has a myriad of levels of severity, and entering a reimbursement world where classification of failure of an organ—the kidney – is not an MCC at all. It’s the only failure of an organ that is not a major condition. Why? I believe it’s because the proper homework wasn’t done. 

 

Because of the approved definition of 584.9 to include AKI, all levels of AKI were included in the statistics generated through coding and CDI initiatives. And patients with a creatinine bump of 0.3 mg% due to dehydration who were treated with a glass of water were reported with 584.9—and they went home in six hours when they cleared up mentally.

 

We have met the enemy and they is us (with fond memories to the critters of the Okeefenokee swamp).

 

Certainly, patients with stages 2 and 3 AKI are pretty darned sick—and I would guess that a significant portion of patients with stage 1 are sick, as well. But it may not be from the renal disease specifically. They do have other organs!

 

 

I see a couple of options to fix the problem and I’ve worked with some of the authorities in renal disease medicine on this. The first is to create individual codes for the three stages of AKI (if we’re going to stay with AKI). And with these levels, we could perform some analysis on all patients with the identified stages, not only on patients on ICUs. We could run statistics from ICU patients only, non-ICU patients only, and all patients, just to see if there is an identifiable difference in mortality or in long term damage of renal function between the groups. By examining mortality, the rate of RRT, and cost, we would have a viable way to identify which patients are sick—who has a major disease—and who isn’t.

 

The second option is to follow the lead of the pulmonologists and dump AKI. From a coding, resource utilization, and CMS perspective, that’s a great option. From the perspective of statistical analysis of risk of mortality, we need the breakdown of “acute renal failure” or “acute kidney injury” to be studied, analyzed, and classified appropriately. This cannot be accomplished by repeating the flawed studies of the past. Let’s open it up to all comers. If the definition of the disease applies to all comers, the studies have to be done on all comers.

 

In the meantime, CDI specialists and coders who are dealing with the rules as they exist must look at how sick the patient was and how the patient was treated. If the cause of a bump in creatinine is dehydration and the patient’s treatment consists of a bolus of 500 cc of crystalloid in the ED and then regular diet, or consists of IV fluids at a normal rate of 75 – 100 cc/hour with no efforts at real resuscitation of vital signs and perfusion, and if the patient responds rapidly to these treatments, the patient should be considered to have the old acute renal insufficiency and not coded to 584.9 because it was not failure and it did not entail “kidney injury.” If we’re going to use “AKI,” we have to be able to validate injury, reversible or not. There has to be some consequence.

 

In fact, Mehta and his group of international nephrologists unanimously agreed that the “that application of the diagnostic criteria would be used only after an optimal state of hydration had been achieved.” (Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury, Critical Care, volume 11, issue 2)

 

Some consultants are now advising their clients to tell the docs to document “acute tubular necrosis” rather than AKI across the board. That’s a very questionable practice and can do nothing but get you into trouble. If the case is one in which the patient probably has measurable injury of the kidneys, after fluid resuscitation, with acute tubular necrosis due to salicylate poisoning or sepsis or shock, sure—call it acute tubular necrosis, because that’s what it likely is. Even severe dehydration with significant hypovolemia can cause ATN—but it should be significant. Got it?