Ringer's Lactate

Shashank Singh; David Davis.

Indications
Ringer’s lactate solution, or lactated Ringer’s solution, is a type of isotonic, crystalloid fluid further
classified as a balanced or buffered solution used for fluid replacement. The contents of Ringer’s
lactate include sodium, chloride, potassium, calcium, and lactate in the form of sodium lactate,
mixed into a solution with an osmolarity of 273 mOsm/L and pH of about 6.5. In comparison,
normal saline (NS) has an osmolarity of about 286 mOsm/L. Ringer’s lactate is largely used in
aggressive volume resuscitation from blood loss or burn injuries; however, Ringer’s lactate is a
great fluid for aggressive fluid replacement in many clinical situations, including sepsis and acute
pancreatitis.[1]

Mechanism of Action
Understanding the metabolism of lactate and briefly reviewing its biochemistry and physiology is
important to recognize the specific benefits of Ringer’s lactate utilization. Often confused with
lactic acid, lactate is the compensatory base of lactic acid. Under aerobic physiologic conditions,
the metabolism of glucose leads to the production of pyruvate into cellular respiration. However,
there is always a small state of anaerobic metabolism taking place at any given time, causing
pyruvate to undergo an oxidation-reduction reaction with NADH which leads to oxidation of
NADH to NAD+ and the formation of lactate via the enzyme lactate dehydrogenase (LDH). This
reaction maintains NAD+ levels, even in anaerobic metabolism, to allow further glycolysis to
occur in the absence of oxygen. Normally, through cellular respiration, there is always a balanced
ratio of NADH/NAD+ with the transfer of protons and electrons to finally make ATP, water
(H2O), and carbon dioxide (CO2) as the final products. If this aerobic system shuts down, the
protons have nowhere to go. Lactate is formed and shuttled out of the cells to keep NADH/NAD+
ratio constant. The increased production of lactate, in turn, acts as a buffer system as it takes up
the H+ forming lactic acid. Furthermore, lactate can be metabolized back into pyruvate via LDH
and through cellular respiration, forming CO2 and H2O. This CO2 and H2O form carbonic acid
(H2CO3) via carbonic anhydrase, rapidly dissociating to form HCO3. Lactate can be metabolized
to form bicarbonate.[2]

Administering a liter of Ringer’s lactate does 2 important things:

1. Volume resuscitation: In that intravascular volume expands increasing preload and thus,
perfusion

2. Provides the body with sodium lactate: Sodium lactate is a bioenergetic fuel that the human
body is designed to metabolize under ischemic conditions thus decreasing cellular death
from ischemia.[3]
Volume kinetics is a complex topic but can be simplified with the following fluid characteristics,
osmolarity, and tonicity. To review, the intracellular fluid compartment is about 67% of total body
water while extracellular fluid compartment is about 33%. The extracellular fluid compartment
can further be broken down into the interstitial fluid, approximately 75% to 80% of the
extracellular compartment, and intravascular, approximately 20% to 25% of the extracellular
compartment. Osmolarity among all fluid compartments at any given time will remain equal, or
actively equalizing, as water free flows between all compartments. Tonicity is a measure of the
osmotic (water) gradient between 2 fluids across a semipermeable membrane and is a relative
concept between these 2 fluids. When describing a fluid in terms of tonicity, in other words,
hypotonic, isotonic, or hypertonic, the tonicity refers to the osmotic gradient between the
intracellular and extracellular compartments. Thus, an isotonic fluid is given intravenously (IV)
does not move across into the intracellular compartment but does distribute across the entire
extracellular compartment (interstitial and intravascular), usually proportionally to the
compartment volumes (interstitial 75% to 80%, intravascular 20% to 25%).

Administration
Ringer’s lactate is administered most commonly via IV route but may be safely administered
intraosseously as well. The goal of administration is to replenish the intravascular volume to permit
adequate organ perfusion.[4]

Adverse Effects
There is a fear of Ringer’s lactate causing hyperkalemia and worsening lactic acidosis. To put it
in perspective, Ringer’s lactate does include a concentration of potassium 4 mEq/L. Logically, if
giving a patient who is hyperkalemic additional potassium would worsen hyperkalemia; however,
this is not correct. A patient's potassium volume of distribution is larger than the extracellular
compartment and equilibrates between the intracellular and extracellular compartments.
Therefore, giving a patient, even a patient in renal failure, 4 mEq/L of potassium is not an additive
effect.[5] In fact, giving Ringer’s lactate to a patient with hyperkalemia will trend the patient’s
potassium level to 4 mEq/L.[6][7] Furthermore, patients' hyperkalemia may worsen with
metabolic acidosis. Consequently, large-volume IV administration of normal saline may give
patients a hyperchloremic non-anion gap metabolic acidosis. Ringer’s lactate does not have this
effect.

Ringer’s lactate is often avoided in septic patients secondary to the fear of worsening lactic
acidosis. This is also untrue, as the content of Ringer’s lactate is sodium lactate, not lactic acid.
Administration of Ringer’s lactate will cause an excess of lactate, which will be utilized by the
body for energy. However, in today’s practicing culture, there tends to be an emphasis on blood
lactate levels.[3] This emphasis can lead to confusion in the interpretation of lactic acid levels. The
adverse effect of worsening a lactic acid is not seen with Ringer’s lactate.
Ringer’s lactate also has a calcium concentration which prohibits its use as a diluent for blood
transfusions. Some blood products use citrate as an anticoagulant and when mixed with calcium
leads to the precipitation of calcium citrate which may cause clotting and obstruction of the IV
line. Patients can receive blood products and Ringer’s lactate simultaneously, however, not within
the same line.

As with any IV fluid administration, there is a possibility of swelling and edema. At-risk patients
are those with congestive heart failure, chronic kidney disease, liver cirrhosis, and
hypoalbuminemia. These patients must be monitored during IV administration with serial physical
exams to determine if they are becoming clinically hypervolemic.

Further adverse effects may include allergic reactions ranging from mild local redness and itching
to generalized symptoms, local infection, redness, and even regional cellulitis which can progress
to systemic infection if not intervened. Many of these symptoms may be secondary to the actual
intravenous site access rather than the contents of Ringer’s lactate itself. Allergic reactions are
more common with adhesive dressings to secure IV access rather than the contents of Ringer’s
lactate itself. IV infiltration is also a possibility, which can cause localized swelling, redness and
pain and ultimately is treated with conservative management and replacement of the IV access.
Infection therapy can include local to systemic antibiotic therapy depending on the severity.

Contraindications
Not an absolute contraindication, but more of a consideration, is the administration of Ringer’s
lactate in patients with liver dysfunction. Most of the lactate is metabolized in the liver, and any
dysfunction there will be an accumulation of lactate. This can confuse interpretation of lactate
levels.

Patients with cerebral edema requiring osmotic therapy should avoid all hypotonic or isotonic
fluid, including Ringer’s lactate, in the acute setting. The goal of therapy is to draw out free water
from brain parenchyma using hypertonic fluid administration. Although studies have compared
the 2, a single study compared conventional fluid resuscitation versus hypertonic saline in
hypotensive patients with traumatic brain injury in the prehospital setting. Findings were nearly
identical neurological function 6 months after the injury between the 2 groups; however,
conventional therapy is to avoid isotonic saline in the acute setting.[8]

Monitoring
Patients on any intravenous fluid replacement need to be monitored for fluid overload. As stated
above, any crystalloid fluid distributes across the extracellular fluid compartment equally in an
approximately 3:1 ratio (interstitial: intravascular) under normal physiologic conditions. That is to
say, giving 1 L of Ringer’s lactate causes only 250 mL to remain in the intravascular fluid
compartment. Giving too much crystalloid fluid causes fluid overload that can present as a
progressively worsening peripheral and pulmonary edema. Patients at high risk for fluid overload
are those with congestive heart failure, renal disease, and liver cirrhosis. In these cases, IV fluid
administration should be done cautiously.

Additionally, monitoring of electrolytes may be warranted with Ringer’s lactate administration.

Given that Ringer’s lactate contains sodium and potassium, in some cases, it may be warranted to
check these levels frequently. The concentration of sodium in Ringer’s lactate is less than the
physiologic range in plasma, and large amounts of administration can drive sodium levels to
hyponatremic ranges. With a concentration of 130 mEq/L, administration of this fluid brings the
plasma sodium concentration closer to 130 mEq and depending on the clinical situation,
hyponatremia should be avoided.

Monitoring of the site of infusion and IV access is necessary to make sure that the fluid is, in fact,
being delivered into the vein. IV sites should be monitored for any signs of infiltration, redness,
pain, swelling or discomfort. If present, the infusion should be stopped, and other IV access should
be established. Infusion-site monitoring holds true across all IV access sites with any drug
administration, not just to Ringer’s lactate.

Toxicity
Toxicity of Ringer’s lactate is more so associated with volume overload due to IV fluid
administration rather than the contents of Ringer’s lactate itself. As previously stated, excessive
IV fluid administration can cause fluid overload. Patients may present anywhere on the
spectrum from mild peripheral edema to respiratory distress secondary pulmonary edema.
Symptomatic patients should be given diuretic therapy for and have serum electrolytes monitored
closely. In the most severe cases of respiratory distress, patients may require noninvasive positive
pressure ventilation or even intubation. Asymptomatic fluid overload can be managed
conservatively with fluid restriction and continued monitoring.

Enhancing Healthcare Team Outcomes

All healthcare workers including nurse practitioners should be familiar with ringers lactate and its
indications. Ringer’s lactate is a versatile IV-fluid choice for resuscitation. Ringer’s lactate is
superior to normal saline in many ways; however, at times avoided by clinicians due to the stigma
of containing lactate. Again, the lactate contained in Ringer’s lactate is only a problem in patients
who have liver dysfunction. In many clinical scenarios, lactate is a beneficial molecule given its
metabolism. Ringer’s lactate is surprisingly cost-effective, better understood and much more
studied than the newer buffered solution, and has a role in many illnesses as a strong choice for
physiologic fluid replacement. The solution is safe; the only drawback is not the electrolyte
changes but the fluid overload that occur. Hence attention should be paid to the amount of volume
infused.