Surgeons use lactated ringers.
Its a cultural difference, perpetuated by dogma.
Here's how Burton Rose characterized Ringer's solution in his classic Clinical Physiology of Acid-Base and Electrolyte disorders:
This what I was taught. That is what I teach and this is what I believed, but I'm turning.
Last week's JAMA published Association Between a Chloride-Liberal vs Chloride-Restrictive Intravenous Fluid Administration Strategy and Kidney Injury in Critically Ill Adults.
The Study was a bundle-of-care study, in which a number of practices were changed all at once. The study was conducted in a single ICU at the University of Melbourne. For six months outcomes were tracked with usual care to act as the control group, then the bundle was phased-in and after 6 months, they tracked a second 6 month block to represent the experimental group. By spacing the control experimental groups as they did, they eliminated seasonal variation in illnesses.
During the control phase, physicians were able to prescribe IV fluids per personal preference. During the experimental period, chloride rich solutions were restricted to specific clinical conditions: hyponatremia, traumatic brain injury and cerebral edema. Otherwise patients were given low chloride solutions: Hartman's solution, plasma-Lye 148 and 4% albumin.
The primary outcome was the change in creatinine and incidence of AKI, using RIFLE criteria. Secondary outcomes included need for acute dialysis, length of of ICU and hospital stay and survival.
The study consisted of 1644 admissions to the ICU, 760 in the control period and 773 in the experimental period. The two cohorts were well matched with significant differences only with metabolic diagnosis being more common in the control period (7 vs 4.4%) and neurologic disorders being more common in the experimental period (6.2 vs 8.8%).
The difference in the fluids being used was dramatic and this resulted in significant differences in electrolyte exposure:
The authors demonstrated a statistically significant difference in the change in serum creatinine,(increase of 0.25 in the control group vs 0.16 experimental group) which is of questionable clinical significance. More impressive was the decrease in AKI by RIFLE criteria.
With Cox proportional hazards model adjustment they found a hazard ratio of 0.52 (P=0.01) for AKI.
The authors actually use a modified RIFLE criteria as they only used changes in serum creatinine and ignore changes in urine output. This is convenient as most of the studies that have validated the RIFLE criteria have likewise used creatinine limited criteria. As a refresher for those of you sleeping in AKI class here is how the RIFLE criteria grades AKI:
The most important finding was a decreased need for acute dialysis: 78 patients during control versus 49 with the low chloride bundle (P=0.005).
There was no difference in length of ICU or hospital stay, and no change in survival.
In the discussion the authors acknowledge that their study design precludes a deep analysis of what was responsible for the reduction in AKI. By changing nearly all of the fluids at the same time it is difficult to assign blame to any one change. Was it the decrease in chloride? Or the increase in alkali? Increased potassium? Despite this limitation the authors provide the rational for blaming chloride for AKI.
They point out that chloride in normal saline is no where near physiologic at 154 mEq/L. They point to observational study data showing decreased dialysis with Plasmalyte compared to saline. Animal studies showing better cortical perfusion with decreased chloride exposure. They suggest that Tubulo-glomerular feedback maybe responsible for this.
Tubulo-glomerular Feedback is the driving principle behind the theory of Acute Renal Success. Acute renal success is a theory which attempts to explain the conundrum of oliguria in ATN. Patients with ATN have intact glomeruli, yet in some cases they have a GFR of zero. Why do normal appearing glomeruli cease to filter? They cease to filter because if the they did, the damaged tubules would not be able to reabsorb the filtrate and the kidney would excrete all of the body's plasma in about half an hour.
The glomeruli can only safely filter 100 ml per minutes if the tubules reabsorb 99+% of that fluid. In ATN that reassurance is lost and the intact glomeruli need a way to detect the failure of reabsorption. Chloride sensors in the thick ascending loop of Henle signal the glomeruli to decrease filtration when activated. So in cases of ATN, the glomeruli initially filter normally but when the proximal tubule and Loop of Henle fail to reabsorb the chloride, chloride floods these receptors triggering a feedback mechanism to shutdown the glomeruli associated with that tubule.
In this article the authors suggest the non-physiologic, high chloride solutions we use in patients may result in excess chloride delivery to the thick ascending limb of the loop of Henle triggering tubulo-glomerular feedback decreasing GFR.
This is an intriguing paper and I look forward to more data, even if it means the surgeons were right.
Update: Jim Smith and I had a great back-and-forth on this. Open this link to follow all of the fireworks.