Balance salt solutions

Ringer Lactate (RL) vs Plasma-Lyte

Ringer Lactate

• Lactate is metabolized to bicarbonate.Mild alkalinizing effect.
• Large volumes generally produce less hyperchloremic acidosis than normal saline.
• In severe liver failure, lactate metabolism may be slower, although clinically RL rarely causes significant lactate accumulation.

Why sodium lactate does not cause lactic acidosis

The concern arose because Ringer lactate contains sodium lactate, and people assumed giving lactate would increase “lactic acidosis.” However:

• Lactic acidosis is caused by the accumulation of lactic acid due to tissue hypoxia or impaired metabolism—not by administration of sodium lactate.
• In RL, the lactate is present as sodium lactate (Na⁺ + lactate⁻), not lactic acid (H⁺ + lactate⁻).
• Sodium lactate is the conjugate base of lactic acid and therefore does not release hydrogen ions (H⁺) into the blood.
• After infusion, lactate is rapidly metabolized (primarily in the liver, but also in the kidneys, heart, and skeletal muscle) to bicarbonate (HCO₃⁻).
• Thus, RL has a mild alkalinizing effect, rather than causing metabolic acidosis.

Simplified reaction

Sodium lactate → Lactate⁻ → CO₂ + H₂O → HCO₃⁻ (bicarbonate)

Net effect:

• ✔ No increase in hydrogen ions
• ✔ Generation of bicarbonate
• ✔ Mild correction of metabolic acidosis

Does RL increase serum lactate?

Yes, but usually only slightly and transiently:

• Serum lactate may rise by ~0.5–1 mmol/L after large-volume RL infusion.
• This reflects the exogenous lactate load, not tissue hypoxia or worsening shock.
• Clinicians should interpret lactate trends in the context of recent RL administration, especially after massive resuscitation.

Contraindications

• Raised intracranial pressure/TBI
• Metformin-associated lactic acidosis

 Relative Avoidance

• Severe hyponatremia
• Severe hypercalcemia
• Simultaneous infusion with citrated blood products through the same line
• Severe metabolic alkalosis

Lactated Ringer’s is safe in hyperkalemia and is generally preferable to normal saline.

Despite containing 4 mmol/L of potassium, RL does not increase serum potassium to a clinically significant extent. In fact, it may result in lower potassium levels than normal saline.

Why?

1. The potassium content is very low

• RL contains 4 mmol/L K⁺, which is close to the normal plasma concentration (3.5–5.0 mmol/L).
• Infusing RL does not substantially increase the body’s potassium load.

2. Normal saline can worsen hyperkalemia

• NS (154 mmol/L chloride) may cause hyperchloremic metabolic acidosis.
• Acidosis promotes potassium movement from the intracellular to the extracellular space, increasing serum K⁺.
• Thus, NS can paradoxically increase serum potassium more than RL.

3. RL has an alkalinizing effect

• Lactate is metabolized to bicarbonate.
• Correction of acidosis promotes intracellular potassium uptake, helping to lower serum potassium.

Clinical evidence

• Multiple perioperative and ICU studies have shown no increase in serum potassium with RL compared with NS, even in patients with renal impairment.
• In patients undergoing kidney transplantation, RL or other balanced crystalloids resulted in less metabolic acidosis and similar or lower serum potassium than NS.
• Large ICU trials (SMART, SALT-ED, BaSICS, PLUS) found no increased risk of hyperkalemia with balanced crystalloids.

STEROFUNDIN VS KABILYTE

*May vary slightly depending on country-specific formulation.

Buffer System

Sterofundin

• Acetate → rapidly metabolized in muscle, heart, liver → bicarbonate.
• Malate → enters the Krebs cycle → bicarbonate generation.
• Does not depend primarily on hepatic metabolism.

Kabilyte

• Acetate → bicarbonate.
• Gluconate → metabolized with minimal effect on acid-base beyond serving as a buffer precursor.
• Similar alkalinizing effect to Plasma-Lyte.

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