Identify opportunities from audits

 

It's great, identifying opportunities to teach. Whenever I do medical record audits, I always look for chances to educate coders, physicians, and/or clinical documentation improvement (CDI) specialists about areas of misunderstanding by coding professionals or elements of patient experience that require specific documentation for proper code assignment.

 

These misunderstandings can be either in application of guidelines or clinical approach, but addressing them can lead to greater accuracy in the future. After all, the most important part of the patient record is the patient. (Unless you're the chief financial officer of a hospital.)

 

Here's some tidbits from recent reviews I've done. See if you've come across any of these in the past. 

 

A patient with end-stage renal disease (ESRD) comes into the ED with volume overload, identified by increased swelling of the legs and slight shortness of breath. Chest x-ray shows some pulmonary edema. Studies show a creatinine level of 9.8 that went down to 4.5, hemoglobin of 10.5 and BNP of 25,000. The patient is admitted for dialysis, gets rapid relief, and is discharged the next day.

 

Coders assigned the following, among other codes:

 

Somewhere in the chart we had noticed history of congestive heart failure, so the CDI team member approached the PA with the evidence of a BNP of 25,000 and previous echo demonstrating ejection fraction of 65%. The CDI specialists asked whether these two pieces met the criteria needed for acute on chronic diastolic (heart failure with preserved ejection fraction) heart failure.

 

Other conversations included that the creatinine dropped from 9.8 to 4.5, a greater than 0.3 drop and certainly a 50% improvement in renal function, so obviously AKI must have existed.

 

The patient's hemoglobin was only 10.5, so it was probably anemia of the patient's chronic disease.

And the pulmonary edema documented in the ED physician's note, having been seen on the chest x-ray and copied and pasted on every progress note, must be 514.

 

Wrong!

 

You don't jump at numbers. You look at the patient and the evidence and use clinical thinking.

 

People with ESRD and who are on dialysis, people who don't have renal function, can't go into acute renal failure. There's nothing left to fail. The change in creatinine level was caused by dialysis removing nitrogenous products from the bloodstream. That's all. Renal function didn't change at all.

 

People with ESRD constantly have higher-than-normal levels of fluid in the bloodstream. Why? They can't get rid of the fluid in the urine—they're not making urine. So the venous circulation fills up with fluid.

When the right atrium gets stretched by volumes of fluid in the right side of the circulation, it stretches every day. And when the atria of the heart stretch, BNP is produced so that the body can try to urinate the extra fluid. That's the normal mechanism in everybody.

 

But the kidneys don't work, so the stretch stays there and it gets worse. The BNP level rises and rises. These people walk around with BNP levels in the thousands, ten thousands, hundred thousands every day, and they're not in acute congestive heart failure at all. It's their new baseline. Get over it. Check their last 20 BNP levels; it's the same high level.

 

Are you kidding about 514? I have ranted enough about 514. I'm tired of ranting about 514. But I'll keep on ranting about 514 until someone gets it.

 

Pulmonary congestion and hypostasis was invented in the early 1800s (it was called 94 at that time). It defined a finding at postmortem exam of some people who had lain without moving with minimal nutrition for extended periods of time while they died of something, whether cancer or tuberculosis or leprosy. The pathologists who performed the autopsies on these patients gave it several descriptive names, including pulmonary congestion, pulmonary edema, hypostatic pneumonia, and apoplexy of the lung. Here is an excerpt from the Manual of the International List of Causes of Death from 1909:

 

 

None of these terms were ever designed to be diagnoses. They were all ways that pathologists described the lungs in these patients. The instructions for codes, which represented signs and symptoms and findings on autopsy of patients who died, were to never assign such codes for a patient.

 

Here again is a quote from the instructions on coding for death certificates from that time (emphasis added):

 

 

In our case, pulmonary edema was an x-ray finding and not a diagnosis at all. It was evidence of volume overload, which the physician diagnosed.

 

And finally, the anemia of chronic disease. We have no code for anemia of chronic disease. Code 285.29 is not anemia of chronic disease. We have code 285.21 for anemia of CKD (which is what the physicians were actually talking about, but somebody told them of "anemia of chronic disease"), 285.22 for anemia of neoplastic disease, and 285.29 for anemia of other chronic disease—you tell us which other chronic disease the patient has. If you can't, it's not 285.29, period.

 

Sometimes in reviewing a medical record, we can see different physicians referring to the left ventricular status of a heart failure patient in totally different ways. Sometimes, that's the way the status is and sometimes it's a misunderstanding by the docs.

 

There are two basic models of left ventricular heart failure. One is referred to as heart failure with reduced ejection fraction (HFrEF) and is synonymous, according to the American College of Cardiology and the American Heart Association, with systolic heart failure. The other is referred to as heart failure with preserved ejection fraction (HFpEF) and is synonymous, for coding and continued classification purposes, with diastolic heart failure. Okay? That's it.

 

Now we have another conundrum. A patient can move from one to the other. Oops! Or, even more oops, a patient with one can have it resolve totally and have no chronic heart failure at all.

 

Here's part of the issue. Heart failure can be an acute event with no chronicity associated with it at all and heart failure can be a chronic condition with no acute decompensation ever.

 

A patient who has a viral myocarditis can develop dilation of the left ventricle associated with severe reduction in ejection fraction (EF) to the 12% levels with severe, debilitating symptoms and then occasionally have the dysfunction resolve totally (although most retain functional disability and do become chronic systolic failure patients).

 

A patient with left ventricular hypertrophy due to chronic hypertensive disease (hypertensive cardiomyopathy) or aortic valvular stenosis (valvular cardiomyopathy) with the development of severe diastolic dysfunction and chronic diastolic heart failure can evolve in time to a dilated left ventricle situation and systolic heart failure (with ongoing significant diastolic dysfunction).

 

A patient who has an acute myocardial infarction with an echo demonstrating dilation and severely reduced EF (acute systolic failure), which developed due to stunning of the surrounding myocardium, can have this resolve totally and be left with no dysfunction at all and never develop chronic failure.

 

So one has to look at the clinical circumstances. In truth, a patient with chronic heart failure due to valvular cardiomyopathy from aortic stenosis can suffer stress cardiomyopathy (Takotsubo syndrome) and develop acute systolic heart failure, which then resolves totally and the patient is left with chronic diastolic heart failure.

 

If you see an old echo showing an EF of 30% and a new one showing 70%, it seems as though the episode with the 30% EF was a temporary one and there is either no chronic heart failure at all or the patient had an acute systolic heart failure on top of a chronic diastolic heart failure. Don't shoot for systolic if it's only a history and the current EF is normal.

 

The current EF should line up to some extent with the systolic or diastolic status.

 

Many cardiologists recognize that an acute heart failure event with backup of fluid into the lungs is really, physiologically, acute diastolic dysfunction, whether the patient has chronic systolic failure or chronic diastolic failure or no chronic heart failure whatsoever. 

 

Editor's note: Dr. Gold is CEO of DCBA, Inc., a consulting firm in Atlanta that provides physician-to-physician CDI programs, including needs for ICD-10. Contact him at (770) 216-9691 or rgold@DCBAInc.com.