The potassium composition of LR is physiologically closest to human serum and is typically slightly lower. It would take a significant amount of fluid to have any effect on raising overall serum potassium level since the potassium equilibrates between intracellular and extracellular fluid spaces.
One subgroup analysis from the SALT-ED trial evaluated critically ill adults with hyperkalemia who received balanced crystalloids LR or plasma-lyte vs. Overall, eight 8. While this is not statistically significant, it does show that the higher level of potassium that is administered from LR or plasma-lyte vs.
NS 0 is closer to physiologic plasma and does not lead to worsening hyperkalemia. Pearl: LR is a safe fluid to use in resuscitation of patients with elevated potassium levels. Lactic acidosis is a result of failed oxidative metabolism, leading to an anion-gap metabolic acidosis. This can be secondary to decreased metabolism of naturally generated lactate in the body such as in liver disease or increased production of lactate when there is decreased oxygen available for aerobic metabolism.
The most common etiologies of lactic acidosis in the ED are from sepsis, trauma, and dehydration. In reality, this lactate is in the form of sodium lactate which our bodies metabolize to products that prevent cellular death.
It is not the same lactate that is generated during anaerobic metabolism, which causes metabolic acidosis. One double-blind RCT evaluated the change in lactate between LR and NS groups while also looking at the overall change in pH, bicarbonate, sodium, and chloride levels.
It is theorized that the lactate infused in the LR group may be metabolized under ischemic conditions and decrease overall cell death and is less likely to worsen an acidosis when compared to the hyperchloremic acidosis that results from NS. Pearl: Though LR contains sodium lactate, this is generally metabolized by the body and does not contribute to worsening lactic acidosis. In fact, the acidosis associated with NS likely has more clinically harmful effects.
Which fluids can be administered concomitantly with medications such as antibiotics or blood transfusions? The precipitates were noted as early as when infusions of ceftriaxone were mixed with varying doses of LR in the IV lines. It was postulated that the sodium concentration within ceftriaxone contributes to the formation of calcium precipitates and therefore the mixture of these solutions in the same line should be avoided. An additional study evaluated compatibility of LR with 94 medications by in vitro visual observation, particle counting testing, and light obscuration particle count testing.
Eight drugs were considered incompatible with lactated ringers including ciprofloxacin, cyclosporine, diazepam, ketamine, lorazepam, nitroglycerin, phenytoin, and propofol and are recommended against administering through the same IV line as lactated ringers.
In both studies, there was on statistically significant difference in clot formation when NS or LR was infused or used as a diluent in emergent transfusions. In order to avoid this, a separate line should be considered or alternative fluid should be chosen if limited access is available.
If possible, a separate line should be used to avoid potential precipitation. In patients with DKA, the body responds to low insulin levels by burning fatty acids and producing ketone bodies, leading to an anion-gap metabolic acidosis. Often overall body potassium is low; however, it may appear to be falsely elevated due to hydrogen ions shifting intracellularly and potassium moving extracellularly.
Fluids, in addition to insulin and potassium, are the main treatment for this disease process. Given the sheer volume of fluid required to treat this disease process, on average, 4. This study found a significant decrease in both time to resolution of DKA 13 hours vs This is hypothesized to be due to the concentrations of sodium lactate in LR and acetate in plasma-lyte which metabolize into bicarbonate helping to close the anion gap metabolic acidosis. However, this study was in contrast to prior work on the subject which failed to show any significant difference.
Pearl: Several studies balanced crystalloids are associated with improved outcomes in patients with DKA, dehydration, and pancreatitis. It is theorized that due to hyperosmolarity of the solution and ability to decrease cerebral edema, NS is the preferred resuscitation fluid in patients with Traumatic Brain Injuries TBI when compared with LR.
Additionally, LR is thought to increase neutrophil and inflammatory responses. There is limited data around LR causing hyponatremia or the use of LR in treating acute hypovolemic hyponatremia in the Emergency Department setting. One study evaluated post-operative hyponatremia and cited quantity of fluid resuscitation as the cause of hyponatremia versus use of LR itself. The theory is that increased extracellular volume leads to ADH release and worsens hyponatremia.
In acute burns, there is concern for both dehydration and electrolyte imbalances such as hyponatremia and hypoglycemia secondary to evaporative losses and changes in cellular permeability.
Burn patients treated with LR and DNS had statistically significant less evidence of hyponatremia and hypoglycemia. Pearl: In patients presenting with hyponatremia and acute burns, LR is not necessarily the sole fluid choice for resuscitation, and NS is preferred in patients with concern for TBI. The year-old female is febrile with signs of dehydration and hypotension in the setting of sepsis due to a urinary tract infection. She also has a lactic acidosis and hyperkalemia on her initial workup.
Based on the data above, lactated ringers are a safe and appropriate approach to fluid resuscitation in combination with antibiotics. Broad spectrum antibiotics were started and the patient was admitted to the medical intensive care unit for further workup and care. Lactate does not cause hagma. It can be a marker of a process that does cause hagma. Agree with the section about LR not causing lactic acidosis, just wanted to be clear that neither does lactate.
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Detailed Description:. Drug Information available for: Sodium chloride Ringer's lactate Ringer's lactate solution. FDA Resources. Arms and Interventions. Participants in this arm will receive two liters of IV 0. Outcome Measures. Seven days after study enrollment, participants were asked by text message, "Have you filled any prescriptions from the emergency department?
Seven days after study enrollment, participants were asked by text message, "Have you returned to the emergency department for the same problem? Seven days after study enrollment, participants were asked by text message, "Have you seen another medical provider for the same complaint? Eligibility Criteria. Information from the National Library of Medicine Choosing to participate in a study is an important personal decision. Venous oxygen content was also decreased for 6 h after hemorrhage and resuscitation with LR or NS Table 2.
Oxygen extraction was increased for 6 h after resuscitation with LR solution or NS. Oxygen delivery was reduced after resuscitation with LR, with no significant changes observed in the NS group Figure 3 A. Oxygen consumption remained unchanged in all three groups during the study Figure 3 B. Oxygen demand did not change after NS resuscitation, but doubled immediately after LR resuscitation, but returned to baseline values by 3 h Figure 3 C.
Oxygen delivery to oxygen demand ratio, an index of oxygen debt, was decreased after NS resuscitation but returned to baseline value within 3 h, whereas a larger drop was observed after LR resuscitation and remained low over the course of the study Figure 3 D. No significant changes in Hct, base excess, or lactate concentrations were observed in the control group over the entire experimental period. Total protein dropped from baseline value of 5. There were no significant differences in Hct Table 1 or total protein between LR and NS groups during the 6 h after resuscitation.
Base excess fell below zero after hemorrhage and returned to pre-hemorrhage levels with LR resuscitation by 3 h but remained below pre-hemorrhage levels for 6 h with NS resuscitation Figure 4. Plasma lactate levels rose about 4.
Bicarbonate HCO 3 - levels were decreased by hemorrhage but returned to pre-hemorrhage values by 3 h after LR resuscitation, whereas no return was observed with NS resuscitation Figure 4. Arterial pH was decreased from a pre-hemorrhage value of 7. No significant changes in arterial pH occurred in the control or LR group during the study.
Cl - was elevated for 6 h after NS resuscitation, with no changes shown after LR resuscitation Table 3. Plasma fibrinogen concentration in control pigs remained unchanged during the study. There were no significant differences between LR and NS groups in fibrinogen concentrations or platelet count during the 6 h after resuscitation.
There were no changes in TEG measurements in the control group during the study Figure 5. R time and K times were shortened by hemorrhage but returned to near pre-hemorrhage values after resuscitation with LR or NS Figure 5.
Clot strength MA was not changed by hemorrhage but was similarly reduced by resuscitation with LR or NS, followed by return to baseline values within 3 h after resuscitation Figure 5. No significant changes in fibrinolysis LY 60 were observed in any group during the study data not shown. R time: latency time for initial fibrin formation. K time: a measure of speed to reach a certain level of clot strength.
Angle a: the rapidity of fibrin build up and cross-linking. MA: maximum strength of the developed clot. PT was similarly prolonged by resuscitation with LR from Using a large-animal model with severe hemorrhage and 6 h follow-up, we performed a comprehensive assessment of the physiologic and biochemical effects of LR and NS. Hemodilution, however, was not different between groups indicating that that the additional NS did not stay in the vascular, as supported by the greater urine output in the NS group.
In addition, NS resulted in a lower peripheral resistance and a higher stroke volume, possibly due to its vasodilation effects. Despite similar oxygen extraction and oxygen consumption, NS resuscitation resulted in better oxygen delivery and oxygen delivery-to-oxygen demand ratio as an index of oxygen debt. This better response appears to be primarily due to vasodilation effects as suggested by the large increase in cardiac output compared to the LR group.
Thus, in the current severe hemorrhage model, NS had better tissue perfusion and oxygen metabolism than LR. However, since the oxygen delivery to demand ratio was 1 or higher in the LR and NS groups at 6 hrs, both fluids seemed adequate in maintaining survival at least through 6 h. Significant separation was observed between LR and NS in acid base balance in this study, as expected.
LR resuscitation returned BE and bicarbonate to pre-hemorrhage levels within 3 h, but no return of BE or bicarbonate was observed for 6 hr with NS resuscitation.
Similar changes of BE and bicarbonate from LR or NS have been shown in different animal models and in patients [ 18 , 19 , 28 ]. The impact of acid base status from resuscitation fluids on survival has been assessed by Traverso et al.
With equal volume resuscitation from NS pH 5. But BE and pH from LR and Plasmalyte-A resuscitation were similar and higher than those from NS [ 18 ], suggesting a better acid base status was not necessarily attributable to a better survival. Nevertheless, as an index of shock, improved BE should be a goal to improve outcome and acidosis is associated with well-known detrimental effects on the cardiovascular system and coagulation [ 29 , 30 ].
Clinical trials have failed to show significant differences in outcomes of LR and NS resuscitation. In comparative trials of LR and NS performed in patients who underwent abdominal aortic aneurysm repair or renal transplant, Waters et al. Using a rat model with hemorrhage and simultaneous resuscitation, Healey et al.
Thus, it appears that the separation of outcomes from LR and NS becomes apparent only under extreme circumstance, such as when greater than 1 blood volume of fluid is given. The recovery rates, however, were different: NS returned lactate to pre-hemorrhage level within 15 min, but lactate did not return to near pre-hemorrhage level for at least 3 h after resuscitation. At 15 min after resuscitation, lactate levels were 8. This difference could result from lactate load from LR resuscitation or from a larger-volume dilution from NS resuscitation.
Calculation of fluid inflow and outflow suggested that the latter is unlikely. From the start of resuscitation to 15 min after the completion of resuscitation, a total of 4. During the same period a total of 6. Thus, the difference of lactate levels at 15 min after resuscitation may relate to the lactate load from LR resuscitation, at least in part.
However, this difference gradually disappeared within 6 h with a simultaneous increase of HCO 3 - in the LR group, suggesting that an ongoing lactate metabolism in pigs and the production of bicarbonate may contribute to the better acid-base status from lactate resuscitation.
In addition, current blood bank guidelines state that LR should not be mixed with blood to prevent the risk of clot formation from calcium included in LR, which can diminish the anti-coagulation effect in stored blood. Thus, LR resuscitation should not be given with blood through the same iv-line and crystalloids should be avoided in patients with blood transfusion. Hemorrhage and resuscitation caused disturbances in the coagulation process. PT and aPTT were prolonged for 6 h after hemorrhage and resuscitation, suggesting a hypocoagulable states.
In contrast, the TEG data suggested a hypercoagulable states. These differences between TEG and standard plasma assays were also observed in burn and trauma patients [ 32 , 33 ]. Clotting initiation was shortened, and clotting speed was accelerated by hemorrhage; but both returned to pre-hemorrhage values after resuscitation.
Clot strength was compromised after resuscitation but returned within 3 h. Despite these dynamic changes in the coagulation profile, there were no differences between LR and NS resuscitation during the study, suggesting the equivalent effects of the two fluids on coagulation.
In contrast, a faster clotting speed and better clot strength from LR resuscitation were reported by Kiraly et al. This discrepancy is likely due to the differences in study design. In addition, a sham control group was included in the present study and our data showed that coagulation profiles from LR and NS resuscitation returned to pre-hemorrhage values and became similar to those of the control values.
Thus, potential thrombotic risk from LR resuscitation is unlikely. In order to make a valid comparison, a common physiological endpoint after resuscitation is needed to assess the effects of resuscitation. In this study, we used post-resuscitation MAP as the physiological endpoint to compare the effects of LR and NS on hemodynamics, coagulation and metabolism.
If the same volume of resuscitation was used in LR and NS groups, we suspected that the blood pressure after NS resuscitation would be lower than that of LR due to its vasodilator effects.
A fixed volume controlled hemorrhage model was used in this study to investigate metabolic, hemodynamic and coagulation effects of hypovolemia and fluid resuscitation. This model mimics situations where trauma patients bleed an amount of blood before hemorrhage is controlled [ 34 ]. However, it is limited in reflecting coagulation changes under a clinical scenario of continued bleeding or rebleeding.
It is likely the on-going bleeding from uncontrolled hemorrhage will exaggerate the impact of vasodilation effects from NS, with higher volumes infused and more hemodilution and coagulation impairment. Considering that restriction on resuscitation fluid has been shown improving survival in uncontrolled bleeding patients [ 35 ] and animals [ 36 ], a larger volume of NS, as compared to LR, would increase bleeding with resultant higher morbidities and mortality in trauma patients.
These differences are possibly due to the vasodilator effects from NS. It is worth emphasizing that these effects are likely to be exaggerated under uncontrolled hemorrhage, resulting in more fluid volume, a larger hemodilution, and more severe impairment in coagulation. Consistent with our current results, clinically significant hyperkalemia from NS administration has been reported in patients during renal transplantation [ 16 , 28 ]. Thus, NS is associated with vasodilator effects and the risks of metabolic acidosis and hyperkalemia.
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