NSTEMI Clinical Guidelines
Does anyone have NSTEMI Clinical Guidelines? We have physicians with different opinions on whether patients are NSTEMI's or not. Some of the physicians are just charting elevated troponin, they won't even diagnose demand ischemia. There is a great deal of discrepancy in the documentation from physician to physician. What to do??
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This is some of the information that we use at our facility---our physicians feel that the telling marker to determine if it is demand ischemia or NSTEMI type 2, is if the troponin elevation is above or below the 99th percentile.
With the new ICD-10-CM codes, we finally have codes to identify type 2 MI and make the important distinction between it and type 1 MI. In the past, type 2 MI was coded as NSTEMI, creating many practical problems, especially since these two types of MI have completely different causes, implications for management, implications for quality measures, and outcomes.
The new code for Type 2 MI is I21.A1. This code includes the following:
Type 2 MI
Myocardial infarction due to demand ischemia
Myocardial infarction secondary to ischemic imbalance
If known, the underlying cause should be documented, such as:
Anemia/Acute blood loss anemia
COPD exacerbation
Acute systolic/diastolic heart failure
Paroxysmal tachycardia
Shock
Other
How do these changes affect the provider’s use of the term “demand ischemia”?
“Demand ischemia” is supposed to be reserved for supply/demand mismatch causing ischemia without necrosis where biomarkers remain below the 99th upper reference limit (Troponin I of less than 0.035 in our lab), and has a code that is different (I24.8) than that of Type 2 MI. However, this term has recently been used to describe what is technically a type 2 MI. A clinically correct distinction between demand ischemia and type 2 MI is crucial because demand ischemia has far less impact on severity classification.
It is also important to remember that in order to establish the diagnosis of MI, a dynamic pattern needs to be present with troponin values. As the Third Universal Definition states: “The demonstration of a rising and/or falling pattern is needed to distinguish acute from chronic elevations in Troponin concentrations that are associated with structural heart disease.” Chronic troponin elevations can be seen, for instance, in patients with heart failure or advanced renal disease.
I agree with the above.
Is it possible the physicians you are talking to have never heard of the Third Universal Definition of an MI consensus statement? It has only been around since 2012 and is recognized by both the American heart Association and the American College of Cardiologists. The post above largely covers the content.
Troponin > 99th percentile (after eliminating false positives and in the presence of an identifiable troponin curve [not a sustained chronic elevation]) and at least one of the below:
http://circ.ahajournals.org/content/126/16/2020
https://www.medscape.com/viewarticle/769921
It is essential to confirm what the 99th percentile for troponin is at your facility. The lab director should be able to tell you.
A diagnosis of MI requires a clinical picture consistent with "myocardial ischemia". For NSTEMI there is usually no uncertainty. With type 2, when a provider documents "demand ischemia" or "supply/demand mismatch", he/she has confirmed an "ischemic" setting.
Finally, the Index and Tabular indicate that a myocardial infarction "due to" demand ischemia or ischemic imbalance is assigned code I21.A1 (type 2). The Official Coding Guidelines "With" rule states that terms related by ICD-10 using the words "due to" assumes the relationship between the 2 conditions unless otherwise specified by the provider. Therefore whenever NSTEMI or just "MI" is documented together with demand ischemia or ischemic imbalance, type 2 MI should be assigned without further clarification.
Richard D. Pinson, MD, FACP, CCS
Pinson & Tang
CDI Educators and Advisers
Authors of the CDI Pocket Guide
www.pinsonandtang.com