Q&A: Lactic acidosis and sepsis

CDI Strategies - Volume 13, Issue 24

Q: Is lactic acidosis considered integral to the diagnosis of sepsis?

A: First, let’s spend some time talking about hyperlactatemia, defined as a persistent, mild to moderate (2-4 mmol/L) increase in blood lactate concentration without metabolic acidosis.  Whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually greater than 5 mmol/L) in association with metabolic acidosis.

Hyperlactatemia can occur in the setting of adequate tissue perfusion, intact buffering systems, and adequate tissue oxygenation.

Lactic acidosis, on the other hand, is associated with major metabolic dysregulation, tissue hypoperfusion, the effects of certain drugs or toxins, and congenital abnormalities in carbohydrate metabolism. It also occurs as a result on markedly increased transient metabolic demand (e.g., post seizure lactic acidosis). Lactic acidosis is a high anion gap metabolic acidosis due to elevated blood lactate. Lactic acidosis results from overproduction of lactate, decreased metabolism of lactate, or both.

Type A lactic acidosis, the most serious form, occurs when lactic acid is overproduced in ischemic tissue—as a byproduct of anaerobic generation of adenosine triphosphate (ATP from pyruvate) during oxygen deficit via anerobic glycolysis. Overproduction typically occurs during global tissue hypoperfusion in hypovolemic, cardiac, or septic shock and is worsened by decreased lactate metabolism in the poorly perfused liver. It may also occur with primary hypoxia due to lung disease and with various hemoglobinopathies.

Type B lactic acidosis occurs in states of normal global tissue perfusion (and hence aerobic ATP production) and is less ominous. Causes include local tissue hypoxia (e.g., as with vigorous muscle use during exertion, seizures, hypothermic shivering), certain systemic and congenital conditions, cancer, and ingestion of certain drugs or toxins (seethe Merck Manual’s  Causes of Metabolic Acidosis). Drugs include the nucleoside reverse transcriptase inhibitors and the biguanides phenformin and, less so, metformin. Metabolism may be decreased due to hepatic insufficiency or thiamin deficiency.

Lactic acid is an essential carbohydrate within cellular metabolism and its levels rise with increased metabolism during exercise and with catecholamine stimulation. Glucse-6-phospate is converted anaerobically to pyruvate via the Embden-Meyerhof pathway. Pyruvate is in equilibrium with lactate with a ratio of about 25 lactate to 1 pyruvate molecules. Thus, lactate is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle.

However, all tissues can use lactate as an energy source, as it can be converted quickly back to pyruvate and enter into the Krebs cycle. In the setting of decreased tissue oxygenation, pyruvate is not readily metabolized, and its intracellular levels rise, causing lactate levels to rise proportionally. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from long-term dysfunction or excessive production), hyperlacticaemia and metabolic acidosis ensue, commonly referred to as lactic acidosis.

Remember, there is no separate code in ICD-10 for “lactic acidosis.” You simply get the generic “acidosis” code here with no differentiation as to type.

In light of all this, your question has multiple answers:

  1. From a coding standpoint, ICD-10 code A41.x series do not have Excludes 1 notes for acidosis and the acidosis E codes do not have Excludes 1 notes for sepsis. From a strictly coding standpoint, these codes may be reported together.
  2. From a clinical standpoint, any patient with severe sepsis would be expected to have elevated lactate levels, they would not, however, be expected to always have a large anion gap and persistent levels of lactate > 5mmol/l after hydration. In fact, such a patient would be considered by many definitions (Sepsis-3 included) to be in septic shock.

If the patient simply has an elevated lactate, I believe this would invoke the general guideline that additional codes that are “routinely associated” with an existing code are not reported separately, and elevated lactate is a routine finding in severe sepsis. Furthermore, if you’re using a Sepsis-3 definition, all sepsis is severe sepsis which would render all cases with elevated lactate as expected findings. Additionally, I believe lactic acidosis would be an integral (routinely associated) finding in nearly all cases of septic shock.

  1. If the lactic acidosis is due to an unrelated event in tandem with sepsis such as respiratory failure, severe anemia, asphyxia, limb ischemia, poisoning, hemorrhage, alcohol, etc., then it would be separately reportable as a “multifactorial” metabolic event, but only if documented as such. The unfortunate reality here is that physicians do not routinely document the pathology for cause-and-effect relationships to the detail that the ICD-10 requirements and reporting guidelines seem to suggest they would.

In summary, vanilla sepsis would be code A41x with no R65 code in a patient with an elevated lactate. You’ll have questions and likely need to issue a query here. Why is the lactate elevated? Perhaps the patient actually has severe sepsis? Is it septic shock? Do they have some other organ or metabolic problem raising the lactate levels and if so, what is it?

  • Mild levels of elevated lactate with a documentation of sepsis: This is clinically a routine finding which would make it not separately reportable under ICD-10.
  • Severe elevated levels of lactate with mild sepsis and an A41x code, but no R65.x code and no organ/metabolic disruptions to explain the lactate levels is a disconnect that requires a query. The clinical circumstance is incongruent with the code assignment you are looking at. Continued severely elevated lactate levels indicates you are missing the severity of the sepsis, additional organ failures, other metabolic problems or all of the above.
  • Septic shock with severely elevated lactate levels, anion gap, etc. would again be a routinely associated finding in septic shock and therefore not reportable by basic coding guidelines.
  • Severely elevated lactate levels with acidosis in a patient with documented causes for the lactate other than sepsis would create a situation where the additional acidosis may be reportable (assuming it is not an expected finding for the other diagnoses as well).

To illustrate a little further, let’s use respiratory failure as an example.

Since respiratory failure can be hypoxic, hypercapnic, or both, acidosis is not an integral portion of the ICD-10 code for unspecified respiratory failure, but it would be an integral part of the ICD-10 code for hypercapnic respiratory failure.

Unspecified respiratory failure may receive both ICD-10 codes, but you would have more questions than answers. Is it really just hypercapnic respiratory failure or is hypercapnia a component of the respiratory failure? If not, what is causing the acidosis?

On the other hand, if the physician had already documented hypercapnic respiratory failure, I would not expect to be adding acidosis as an additional diagnosis. It simply isn’t necessary.

Editor’s note: Allen Frady, RN, BSN, CCDS, CCS, CRC, CDI education specialist for HCPro in Middleton, Massachusetts, answered this question. Contact him at AFrady@hcpro.com. For information regarding CDI Boot Camps, click here.

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