Meeting Criteria for AKI, Sepsis

Many, many years ago, I was working on a clinical documentation (CDI) implementation project at an acute-care facility when I stumbled on what would be a huge impasse in capturing “acute renal failure” (nowadays it’s more appropriately called acute kidney injury, or AKI). There appeared to be a huge difference on which surgeons and medical practitioners were basing it. The surgeons would only call it when creatinine hit 2.0 mg/dl, but the medical providers would call it at 1.5!

Most current studies have shown that when the creatinine jumps up 1.5 times from baseline, injury to the kidney has occurred. So if the patient’s normal baseline is 1.0 and it rises to 1.5, this would reflect a patient having acute renal failure (or AKI). (Disclaimer: patients’ baselines would be different in the face of chronic kidney disease. With higher baselines, smaller increases may be integral to the natural progression of the chronic disease process; thus, 1.5 times a baseline would be a more accurate representation of an acute kidney injury on top of a chronic kidney disease. For example, in a patient with Cr baseline of 2.0, 1.5 times that figure is 3.0.)

One after another, surgeons would convey that they only made a diagnosis of acute renal failure if the increase was 2.0 or higher. They did not care even if nephrologists called it that at 1.5-1.9. Currently, many nephrologists would call a 0.3 increase from a baseline of 1.0 as indicative of injury. A caveat, though, is that if a small rise like that occurs due to dehydration/hypovolemia and it resolves within 4-6 hours of volume repletion, this would only indicate hemoconcentration and not true injury. So what would it be then? Just dehydration/hypovolemia. Get it? The small rise is a false positive! It would be the reverse of dilutional anemia, when Hb/Hct drops due to a high plasma volume from fluid replacement in the face of regular amounts of RBC (though “dilutional anemia” is a misnomer, because it is not really anemia.)

Nevertheless, capturing the diagnosis only at thresholds of 2.0 meant that the facility would miss out on the capture of this diagnosis among its surgical patient population. It was perplexing until a couple of surgeons expressed that it was what ACS-NSQIP (American College of Surgeons National Surgical Quality Improvement Program) was capturing for its quality measure. (By the way, current the ACS-NSQIP threshold for risk calculation pre-operatively is two creatinine values of greater than 3.)

Because the surgeons were going by what they thought defined acute renal failure, based on what was being abstracted and collected by their specialty, they also thought that going by any other criteria would distort their data and their quality measures. And that is the moral of the story! One needs to know what specific screening criteria are meant to capture. Different objectives will change this. When the surgical specialty was looking for a threshold that would affect their outcomes, it came to the conclusion that a creatinine of 2.0 made sense. It did not mean that the nephrologists were wrong in their criteria. It just made sense to the surgeons that this certain threshold accounted for what generally would impact their outcomes.

How do you resolve this kind of conundrum? By educating the surgeons that the lower threshold does not take away from NSQIP measures! Providers, both surgical and medical, can name the diagnosis. It just does not get abstracted for the NSQIP measure because it specifically calls for higher creatinine values.

This applies to all other screening criteria that are out there. Core measures have their own criteria. Folks should not go into a tizzy because some providers called a diagnosis and it fell off the facility’s core measure basket. What’s most important is that the condition is clinically valid. Clinical screening protocols have their own criteria for the purposes of making an impact on patient morbidity and mortality. Sepsis screening protocols’ objective, in particular, is to cast a wide net to capture sepsis cases in order to make the most impact in intervention and save lives. It does not mean that SOFA-1, -2, or even -3 criteria are the last word in defining sepsis. There will be false positives and false negatives. Patients may fulfill criteria but not have sepsis. qSOFA criteria consists of new or worsened altered mentation, respiratory rate greater than 22, and systolic blood pressure of less than 100.

High risk by qSOFA. Assess for evidence of organ dysfunction with blood testing including serum lactate and calculation of the full SOFA score.

It may change, depending on new information from the patient’s circumstances and results of workup. The response to treatment and its time continuum will confirm or negate the initial impression. This needs to be documented on a concurrent basis. One needs to see how the story unfolds. Things may not be fully apparent until at least a day into the admission.

Providers often ask me, “what diagnosis should I then document in the beginning?” I respond with the following example. The initial impression can be, “sepsis with altered mental status, leukocytosis, hypotension in a patient with UTI. Place patient on sepsis protocol.” The next progress note could say, “sepsis ruled out because of quick return to baseline mental status and blood pressure with volume repletion. Dehydration (or hypovolemia) ruled in, in this patient with UTI. Off sepsis protocol.” By preserving the clinical story of the patient encounter, true clinical information is communicated forward, thereby ensuring the best care that can be afforded the patient and improving healthcare for all. In return, this kind of documentation will withstand any scrutiny. Furthermore, appropriate optimal reimbursement will be secured. There will be fewer DRG denials and even when such claims are denied, documentation that is clinically valid will always persevere. It’s a win-win for everyone! There is really no justifiable reason for hustling for severity of illness, because it meets criteria but it fails clinical validity.

Meeting two of the criteria, as above, is considered high risk by qSOFA. Yet clinical studies have shown that elderly patients who are hypovolemic/dehydrated will manifest with altered mental status, with or without hypotension. They may be thought of as being septic initially, especially in the presence of an infection, e.g., a UTI. But volume repletion will bring them back to normal mental baseline and blood pressure within four to six hours! Does it mean that the SOFA criteria are erroneous? No; it has done its job by casting a wide net and made tremendous improvement in patient outcomes! Subsequently, it’s up to providers to weed out the false positives and take them off the sepsis protocol. Yes, providers may push back on the extra work needed to document what’s true and what’s not. But it also clears up the confusion on whether a patient really has the condition or not. Transparency will save the day and eliminate misrepresentation, medical errors, as well as fraud and abuse.

Lactic acidosis can be a helpful tool in assessing for sepsis, but one needs to be aware that it is also inherent in severe dehydration, acute hemorrhage, heart failure, diabetic ketoacidosis, drug toxicity, liver disease, regional hypoperfusion, genetic diseases, lymphomas, and even in excessive exercise. Thus, providers need to be proactive in determining and documenting its significance. There are other sepsis markers that one can look at, e.g., procalcitonin and other pro-inflammatory cytokines (in the hyperinflammatory phase, a.k.a. cytokine storm) and anti-inflammatory cytokines (in the compensatory anti-inflammatory response syndrome phase).

I am sure that, at this point, you certainly appreciate that nothing is black and white in medicine. Patients can present with a myriad of presentations in different circumstances. A skillful provider does not go by criteria alone, but needs to exclude all other conditions and circumstances that can account for the patient presentation and what is shown in the laboratory findings.

Making a diagnosis definitely involves exhaustive investigative work that goes beyond meeting criteria. Diagnoses follow certain clinical courses and respond accordingly to therapy.

Provider documentation should have transparency in showing the clinical support for the diagnosis.