Demand a code for demand myocardial infarction
Association of Clinical Documentation Improvement Specialists, July 9, 2009
by Robert S. Gold, MD
Each year, the Cooperating Parties make changes to various ICD-9 code sets. Most recent changes will help us transition to ICD-10. Most of the time, the recommendations are an improvement; however, sometimes they are not.
I have written extensively about heart muscle injuries. My primary reason for doing so is because I am concerned with the pervasive use of the term “acute coronary syndrome” (ACS) when the event may be totally different from what is expected with the term.
Causes of ACS
ACS is a term specifically developed to describe a coronary event of some type in which there is reduced supply or increased demand on the heart muscle to ensure circulation.
The most common cause of ACS is occlusion caused by something that blocks blood flow through a coronary artery or one of its branches; however, there are several levels of severity and many causes, each of which is different and requires different treatment than the classic presentation.
Since 2005, ICD-9 codes differentiated between the levels of severity. Code 411.1 denoted general unstable angina regardless of cause as well as a breakdown of ST-elevation myocardial infarction (MI) and non-ST- elevation MI (NSTEMI), regardless of cause.
Here’s the first issue. In 2001, the American College of Cardiology and the American Heart Association published practice guidelines. Dr. Braunwald led the effort and discussed the guidelines for management of patients with unstable angina and NSTEMI. These guidelines, which were designed to create uniformity among cardiologists, were also a classification of conditions that could lead to unstable angina and NSTEMIs.
As described, in differentiating between unstable angina and NSTEMI, when there was a documented bump in cardiac markers, it was an NSTEMI. When this was not the case, it was unstable angina.
Importance of noncoronary causes
When working up these patients, it is important to determine as quickly as possible the presence of noncoronary causes. Toward that end, the practice guidelines divided the etiologies of these events as follows:
- Class A: Secondary unstable angina (e.g., an identified extrinsic cause such as anemia, infection, fever, thyrotoxicosis, or uncontrolled hypertension)
- Class B: Primary unstable angina
- Class C: Postinfarction unstable angina (within two weeks of documented infarction)
A physician is supposed to work with a patient who presents with unstable angina or an NSTEMI by first ruling out the secondary causes (Class A) because although the patient may have some mild, moderate, or severe coronary artery disease or no coronary artery disease whatsoever, the secondary causes are the ones that need the treatment.
These specific causes demonstrate no change in blood flow through the coronaries. There are no spasms, no embolisms, and no ruptured plaque. In other words, there is no acute coronary occlusion. Treating such patients should involve treating the offending cause.
When an end-stage renal disease patient with an erythropoietin deficiency develops anemia so severe that the coronaries cannot supply the heart with sufficient oxygen and the heart becomes anoxic when the patient is active, the patient will develop angina. Some myocardial cells may die when the patient exercises and increase his or her heart rate, thereby increasing the demand for oxygenated blood.
The cardiac markers will increase in response to the dead cells. Physicians should not treat this angina with nitroglycerine, aspirin, and cardiac catheterization. They should use a blood transfusion.
When a patient with atrial fibrillation develops significant tachycardia, often referred to as atrial fibrillation with rapid ventricular response, the increased work that the heart performs to pump rapidly may exceed the coronaries’ capability to supply sufficient blood to the heart itself. When this takes place, hypoxia occurs, and the patient develops angina. When the heart pumps so rapidly that the blood supply is significantly hindered, some subendocardial cells of the myocardium will die. Physicians should not use beta-blockers to treat this. They should reduce the heart rate instead.
There has been no change in the coronary arteries themselves, regardless of whether the heart is working harder, as in significant tachycardia or accelerated hypertension; the compromised oxygenated blood exceeds the existing state of the coronaries due to a lack of red blood cells, as in significant anemia; or there is not enough blood pressure to perfuse the coronaries, as may occur in septic shock. These do not represent acute coronary occlusive disease. They each represent supply-and-demand mismatch. And they are each unstable angina NSTEMI, by definition.
Limitations of practice guidelines
This is all well and good. However, the practice guidelines pay little attention to this differentiation beyond introducing the concept. They do state that physicians must identify it and deal with it, but the rest of the article talks about how to proceed when the etiology is, indeed, coronary occlusion and how to work up and treat the occluded coronary artery.
In October 2007, the American Heart Association and the heart associations of almost all civilized countries came up with a consensus definition of MI. The definition includes the following five types and provides identifying criteria for each:
- Type 1: Acute occlusive disease of the coronary
- Type 2: A supply-and-demand mismatch
- Type 3: Sudden cardiac death, when one doesn’t know whether a significant tachyarrhythmia led to the heart’s development of asystole or whether a coronary occlusion led to the fatal arrhythmia
- Type 4: Divided into two categories representing death of some myocardial cells immediately at the time of angioplasty or late after angioplasty
- Type 5: Occurs during or after a coronary artery bypass
Here we go again. This really does a good job at specifying that there are some MIs that represent acute coronary occlusion and some that don’t. The issue is that a physician must determine which one a patient has as soon as possible. If it is acute coronary occlusion, there are guidelines (i.e., Core Measures) recommending how to work up and treat that patient. If this is a supply-and-demand mismatch, the treatment is directed toward the cause and not toward the coronaries.
With our current coding system, we have no way of determining which is which. We have no way of identifying MIs that are due to coronary occlusion and those that are not. We have no way of telling whether treatment for an MI should follow guidelines for treating an acute coronary occlusive MI. We have no way of determining the incidence of heart attacks caused by coronary occlusion and the incidence of heart attacks that are caused by something else, which is a serious flaw in our data.
I have recommended that the Cooperating Parties pursue one of the following two options:
- Create a new code to describe a supply-and-demand mismatch NSTEMI. My suggestion is to create new code 411.71. Code category 411 denotes “Other acute and subacute forms of ischemic heart disease.” Leave the 410 code series for occlusive MIs. The suffix .71 or .72 parallels the 410 series for NSTEMI as it exists.
- Create an E-code to represent a 410 series code that is not due to acute coronary occlusion.
Either option would answer all of the questions I’ve raised above. That’s not a bad goal, is it?
When workup reveals that a patient had a true acute coronary occlusive MI, the code for the true acute coronary occlusive MI can be the principal diagnosis (if that was the reason for admission). The patient’s hospital course would be predicated by the Core Measures guidelines.
When a physician determines that the MI was a supply-and-demand mismatch, the MI code would not be assigned as a principal diagnosis. Instead, coders would assign it as a secondary diagnosis, along with whatever mechanism caused the principal problem. The MI code will be secondary and a major complication/comorbidity.
When the patient’s workup demonstrated that he or she required considerable coronary workup and maybe even treatment such as coronary artery bypass graft or angioplasty (even though it was a supply-and-demand issue), the coronary artery disease or MI code could be a principal diagnosis. This is because utilization would have been greater in dealing with that problem.
If anyone has other ideas or would like to support this initiative, we have time to act before the next Coordination and Maintenance meeting.
Editor’s note: Dr. Gold is CEO of DCBA, Inc., a consulting firm in Atlanta that provides physician-to-physician programs in clinical documentation improvement. The goals are data accuracy, profile management, and compliance for physicians and hospitals in the inpatient and outpatient arenas. Reach him by phone at 770/216-9691 or by e-mail at DCBAInc@cs.com.
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