Q&A: Coding lactic acidosis and sepsis

Q: I recently came upon this article, but it’s several years old at this point. What are your thoughts on coding lactic acidosis (E87.2-) and sepsis together? 

A: This is a common question and one that still creates a bit of confusion. I can appreciate the substantive response that was provided in the article you cited.

It really comes down to provider discretion and whether the lactic acidosis is considered a condition in and of itself or whether it is considered a clinical indicator of the organ dysfunction or some other etiology.

According to Coding Clinic, fourth quarter 2017, pp. 98–99, which deals with severe sepsis and acute organ dysfunction/failure, “Code assignment is based on the provider’s documentation, the instructions in the classification, as well as the current coding guidelines.”

The best option is to discuss this with your hospitalist/nephrology and infectious disease providers as to whether they consider it a separate condition and how it would be supported/treated outside of the realm of the underlying condition.

Coding Clinic does provide some indication on how this should be handled as referenced in Coding Clinic, second quarter 2000, pp. 3–4, which includes it in the hypoperfusion/organ dysfunction indicators. Hypoperfusion/organ dysfunction may include, but is not limited to lactic acidosis, oliguria, and/or acute alteration in mental status.

Sepsis syndrome comprises septicemia with evidence of inadequate organ perfusion with at least some degree of one or more of the following: hypoxemia (PaO2< 75 mmHg); elevated lactate (>5 meq/L); oliguria (< 30mL/hr urine); altered mentation (Glasgow coma score); disseminated intravascular coagulopathy (DIC); decreased platelets; increased INR; and/or increased fibrin split products (FSP).

Lactic acidosis occurs as a cascade effect from hypoperfusion and metabolic dysfunction creating higher concentrations of lactic acid and lower concentrations of plasma bicarb (see https://www.ncbi.nlm.nih.gov/books/NBK470202/).

It can have many etiologies and that is the difference. You need to identify the underlying etiology and whether lactic acidosis is inherent to the condition. Is it sepsis or respiratory failure? Is it due to medication?

The other consideration is whether it is supported by UHDDS (MEAT criteria—Monitored, Evaluated, Assessed, Treated). Where are the resources specifically for that condition? Are there serial labs? Anion gap measures? Nephrology being consulted? What does albumin reflect? Is there a clearance/kidney issue? Liver dysfunction? How are fluids being handled differently than the underlying condition?

The difficulty is that to treat lactic acidosis, you must treat the underlying etiology. Therefore, it is difficult to reflect additional resources to support lactic acidosis as a separate reportable condition.

For documentation and CDI context, lactic acidosis can be:

• A clinical indicator supporting sepsis or shock
• A marker of severity
• Supportive evidence in medical necessity reviews

It should not be assumed to represent organ dysfunction unless the provider links it to hypoperfusion, shock, or metabolic derangement.

Bottom line: it is the provider’s discretion if they believe the lactic acidosis is a significant condition that required additional medical decision making and meets the definition of other reportable condition. My recommendation is to have those conversations with providers on whether they see it as an indicator or a separate condition.

Editor’s note: Deanne Wilk, MPS, BSN, RN, CCDS, CCDS-O, CDIP, CCS, CDI education director at ACDIS/HCPro, answered this question. Contact her at deanne.wilk@hcpro.com