What happens to lactate when infusing Ringer (lactated Ringer's solution) in a patient, particularly those with liver disease or critically ill?

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What Happens to Lactate When You Infuse Ringer's Lactate

Lactate from Ringer's lactate solution is rapidly metabolized to bicarbonate in the liver, kidneys, and skeletal muscle, providing buffering capacity without clinically increasing circulating lactate levels in hemodynamically stable patients with normal or even moderately impaired liver function. 1

Metabolism and Buffering Mechanism

The lactate in Ringer's lactate (28 mEq/L) serves as a bicarbonate precursor that undergoes hepatic and extrahepatic metabolism 2:

  • Lactate is converted to bicarbonate through the Cori cycle, where it serves as a substrate for gluconeogenesis in the liver, ultimately generating bicarbonate and providing alkalinizing effects 1
  • The liver, kidneys, and skeletal muscle all metabolize lactate, meaning metabolism is not solely dependent on hepatic function 1
  • Each liter of Ringer's lactate provides 9 calories from lactate metabolism and delivers 28 mEq of lactate that converts to bicarbonate 2

Clinical Impact on Measured Lactate Levels

In hemodynamically stable patients, rapid infusion of Ringer's lactate does NOT falsely elevate circulating lactate concentrations 3:

  • A prospective, randomized, double-blind trial demonstrated that 1 liter of Ringer's lactate infused over 1 hour in healthy adults produced no clinically or statistically significant increase in blood lactate levels (all values remained <2 mmol/L) 3
  • Clinicians should NOT disregard elevated lactate concentrations in patients receiving Ringer's lactate infusions, as elevated levels indicate true tissue hypoperfusion or metabolic derangement, not the infusion itself 3

Special Populations and Caveats

Patients with Liver Disease

Even in severe liver disease, lactate from Ringer's lactate can be metabolized, though interpretation requires nuance 2, 4:

  • The FDA label warns that "solutions containing lactate ions should be used with great care where there is an increased level or an impaired utilization of lactate ions, as in severe hepatic insufficiency" 2
  • However, in acute liver failure, hyperlactatemia is associated with shock and mortality, not simply from impaired lactate clearance 4
  • In critically ill patients with liver disease and shock, maximal lactate levels averaged 9.6 mM (range 1.2-30 mM), while those without shock averaged only 1.3 mM (range 0.6-2.0 mM), demonstrating that elevated lactate reflects tissue hypoperfusion rather than inability to metabolize infused lactate 4
  • The acidifying effect of elevated lactate in acute liver failure is often neutralized by the alkalinizing effect of hypoalbuminemia, explaining why metabolic acidosis may be absent despite hyperlactatemia 5

Critically Ill Patients on Vasopressors

Epinephrine infusions independently increase plasma lactate through stimulation of the Cori cycle, making lactate interpretation more difficult 1:

  • Epinephrine stimulates gluconeogenesis and increases the shuttle of lactate to the liver as a substrate for glucose production 1
  • Patients on epinephrine have increased plasma lactate concentrations independent of changes in organ perfusion, so elevated lactate in these patients may not solely reflect inadequate resuscitation 1
  • This effect is specific to epinephrine and represents a metabolic phenomenon rather than tissue hypoxia 1

Patients on Kidney Replacement Therapy

High-lactate replacement fluids during continuous renal replacement therapy can provide substantial energy (up to 1300 kcal/day) that must be accounted for in nutritional calculations 1:

  • Lactate provides 3.62 kcal/g when metabolized 1
  • Energy gain from lactate-containing dialysis/hemofiltration solutions ranges from 115-1300 kcal/day depending on lactate content and flow rates 1
  • This energy provision should be included in total daily energy calculations to avoid overfeeding 1

Comparison to Other Buffered Solutions

Acetate-buffered solutions (like Ringer's acetate) may provide superior buffering compared to lactate in patients with compromised liver function 6:

  • In a rat model of hemorrhagic shock with 70% partial liver resection, Ringer's acetate and PlasmaLyte restored pH and bicarbonate better than Ringer's lactate or saline 6
  • Acetate is metabolized regardless of liver function and may be the most efficient bicarbonate precursor, while lactate infusion tends to overwhelm the metabolism capacity of residual liver 6
  • However, both L-lactate and racemic lactate (DL-lactate) are metabolized at nearly the same rate in patients with normal liver function 7

Key Clinical Pitfalls

Do not attribute rising lactate levels to Ringer's lactate administration in patients with adequate hemodynamics 8:

  • If lactate is rising despite adequate resuscitation, investigate for ongoing shock, inadequate source control, liver failure, medications (especially epinephrine), or seizures 8
  • Lactate-guided resuscitation improves mortality in septic shock (RR 0.67; 95% CI 0.53-0.84), so trending lactate remains valuable even when using Ringer's lactate 8

Avoid Ringer's lactate in severe traumatic brain injury due to its hypotonic nature (273-277 mOsm/L), which can worsen cerebral edema—use 0.9% saline instead 9, 8, 10

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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