Fluid Choice in Resuscitation aka The Myths of LR
Case 1: A 30 year old woman presents to the ED with severe diarrhea for 3 days.
Case 2: A 65 year old man present with septic shock and a lactate of 8.
Case 3: A 22 year old man with type 1 diabetes presents to the ED with altered mental status and a finger stick glucose of 660.
What is your go-to resuscitation fluid in each of these instances? As ED doctors, we tend to use what is most familiar, whether it be due to availability bias, or ease, or habits. Most of us would choose normal saline (NS) boluses in each of the above case scenarios as our initial fluid resuscitation. But I’d like to make a case for more thoughtful ED fluid administration – what about lactated Ringers (LR)?
One way to think about what fluid to give is to consider where the patient is losing fluid. In a patient with vomiting who has vomited themselves into a hypochloremic metabolic alkalosis – NS makes perfect sense. At 154 mEq of Na and 154 mEq of Cl per L, we are replacing the lost chloride and providing an acidic solution for the likely alkalotic patient. In the patient with dehydration secondary to profuse diarrhea, LR is likely a good choice. In diarrhea, almost every electrolyte is lost, predominantly potassium, chloride, and bicarbonate, and LR at 130mEq of Na (as NaLactate and NaCl), 4 mEq of K, 2.7 mEq of Ca, 109 mEq of Cl and 28 mEq of lactate per liter is full of the stuff lost in explosive diarrhea.
But where is the bicarbonate in LR you ask? Think back (way back) to basic science…and SEPSIS (you can never escape). Think of a muscle cell. In the cell, glycolysis ends with the creation of pyruvate. In the presence of oxygen (as in a happy, healthy functioning cell) the cell continues aerobic respiration and pyruvate becomes acetyl coA and so on until a bunch of baby ATP is born. In the absence of O2, pyruvate is metabolized to lactate, and it accumulates.
In the healthy liver, lactate is converted back to glucose in the Cori Cycle, but this takes a lot of ATP and in septic shock, you just don’t have much of it to go around. In normally functioning cells, or when sepsis is corrected with fluid volume and perfusion to the tissues, the lactate present in now oxygenated cells can get converted back to pyruvate and continue on its way down the TCA cycle making a bunch of NADH and CO2. Recall that CO2 hangs out with water and tends to take some protons from it, meaning CO2 hangs out in solution in your body as HCO3– (bicarb). So in a normal body, lactate can become glucose and be stored as glycogen in the liver, or it is converted to pyruvate and proceeds down aerobic respiration to become bicarbonate and ultimately gets excreted in the kidneys, the stool and as exhaled CO2. (Whew!)
What if the patient has lactic acidosis?
Lactic acid is different from sodium lactate. LR contains sodium lactate, not lactic acid (acids contribute that extra proton or H+).
OK, let’s say you are treating severe sepsis or you have a patient in HHS or DKA severely fluid down. Lactate is accumulating in cells because of poor tissue perfusion. Can you give a lactate containing fluid to these patients? First, the concentration of sodium lactate in LR is miniscule. Remember, lactate is present in 28 mEq/L in LR – compared to 15 L of extracellular fluid present in a normal 70kg human (even in a critically ill person – there is more than 1 L of extracellular fluid in the body!). Second, once perfusion is corrected, lactate should begin to be metabolized in the liver and in aerobic respiration to bicarb and excreted.
But what about hyperkalemia?? What if your academic patient is hiding a potassium of 6?
The blog Pulm Crit (EMCrit) goes into this discussion nicely. https://emcrit.org/pulmcrit/myth-busting-lactated-ringers-is-safe-in-hyperkalemia-and-is-superior-to-ns/
The potassium concentration of LR is 4mEq per L. Remember that a normal human has about 15 L of extracellular fluid. In a patient with a potassium of 6mEq/L, adding 1 L of LR may negligibly increase the potassium level – but in reality, remember that potassium likes to hang out inside cells. If you start to correct the acidosis present from shock or DKA with IV fluid, you will likely decrease the measured extracellular potassium. Cellular shifts in potassium homeostasis are an important component of its management. In DKA, a person is likely total body potassium down. They will be needing some potassium repletion with IV fluid anyways. Why not start with gentle potassium containing fluid? Consider then treating an acidemic hyperkalemic patient with the acidic solution of NS – you may ultimately worsen the hyperkalemia by worsening the acidic extracellular environment.
NS might not be the best choice for every patient. NS is an acidic solution and in excess, i.e. when you’re into giving your 4th and 5th liters of NS in a patient in septic shock or with severe DKA, you are creating a hyperchloremic metabolic acidosis, working against your resuscitative efforts by creating an acidic environment.
Case Fluid Choices
Case 1: LR all the way!
Case 2: LR! Or if you’re wary – start with 1 L NS and then switch to LR when they have a little volume in their system. The patient will likely need more potassium repletion then the LR provides anyways. Can start this fluid while waiting for lab results. Again, PulmCrit is all over this: https://emcrit.org/pulmcrit/four-dka-pearls/
Case 3: NS or LR – I’d probably do no more than 2 L NS then switch to LR
Does LR infusion increase serum lactate lab measurements? Jury is still out, it may. But we need a better marker for sepsis anyway! Procalcitonin anyone?
Be wary of using LR in profound liver failure or in patients on hemodialysis or with advanced stage CKD who may not excrete many electrolytes well. But also consider that the negative effects of NS will be much more pronounced in these patients as well!
Pancreatitis- Patients given LR were shown to have decreased systemic inflammatory response compared to NS, however it is unclear in additional studies if this improves patient outcomes.
Eye irrigation- When performing eye irrigation using a Morgan lens, there is evidence that LR has decreased patient discomfort compared to NS
*image via Kruse, Ole & Grunnet, Niels & Barfod, Charlotte. (2011). Blood lactate as a predictor for in-hospital mortality in patients admitted acutely to hospital: a systematic review. Scandinavian journal of trauma, resuscitation and emergency medicine. 19. 74. 10.1186/1757-7241-19-74.