From Saline to Balanced: My Shift as an Intensivist, and What DKA Taught Me About Acid-Base

A few years ago, I was what you’d call a “saline intensivist.” Like many of us trained in the fast-paced world of critical care, I reached for normal saline as my default resuscitation fluid. It was reliable, familiar, and widely available. But over time—and with a growing body of evidence—I’ve come to understand that “normal” saline isn’t always physiological, especially when it comes to complex acid-base disorders like diabetic ketoacidosis (DKA).

Today, I practice more as a “balanced intensivist,” and DKA is one of the classic cases that illustrates why fluid choice matters.

DKA: The Classic High-Anion Gap Acidosis

In DKA, the absence of insulin drives the body to burn fat for energy, leading to the accumulation of ketone bodies like beta-hydroxybutyrate and acetoacetate. These organic acids overwhelm the buffering capacity of the body, consuming bicarbonate and resulting in a high-anion gap metabolic acidosis (HAGMA).

At this stage, the acidosis is caused by too many acids, not the loss of base.

The Shift: From HAGMA to NAGMA During Recovery

As we begin treatment—with insulin and fluids—the production of ketones stops. The kidneys then begin to excrete the excess ketone anions in the urine. But here’s the catch: those ketones are actually bicarbonate precursors. If retained, they would eventually regenerate bicarbonate as they are metabolized.

When they’re lost in the urine—along with sodium or potassium—we also lose the potential to regenerate bicarbonate. This is functionally equivalent to losing base, not adding acid.To maintain electrical balance, the kidneys start retaining chloride.

And if we’re giving large volumes of 0.9% normal saline, which already contains 154 mmol/L of chloride, we’re further loading the system with chloride.

The result? A normal anion gap metabolic acidosis (NAGMA)—also called hyperchloremic acidosis. The original ketone-driven HAGMA has resolved, but the patient now has a new, iatrogenic acidosis driven by bicarbonate loss and chloride gain.

Balanced Crystalloids: More Than Just a Trend

Balanced salt solutions like Ringer’s lactate have a lower chloride content and include buffering agents like acetate or lactate that are metabolized to bicarbonate. They’re less likely to cause or worsen hyperchloremic acidosis, especially in the DKA recovery phase.

Several studies—including SPLIT, SALT-ED, and SMART—have consistently shown benefits of balanced fluids in terms of acid-base balance, kidney outcomes, and even mortality in some subgroups. While not DKA-specific, the logic applies cleanly here.

So Why Did I Switch?

Because I saw it with my own eyes.

I saw patients recover from DKA only to remain acidotic from fluids we gave them. I saw chloride levels climb while bicarbonate remained stubbornly low. And I saw that simply switching from saline to a balanced solution often helped correct that persistent acidosis faster—and more physiologically.

Key Takeaways for Clinicians

In early DKA, acidosis is due to ketone accumulation (HAGMA). During recovery, renal loss of ketone salts (which are bicarbonate precursors) leads to bicarbonate depletion. Chloride retention, especially from normal saline, replaces the lost bicarbonate, causing a normal anion gap metabolic acidosis (NAGMA). Balanced fluids reduce this risk by supplying less chloride and offering bicarbonate precursors.

Final Thoughts

We often think of fluids as neutral tools, but in critical care, fluids are drugs. Their composition, volume, and timing all matter. In DKA, understanding the physiology of acid-base balance during recovery can help us choose fluids more wisely—and avoid replacing one problem with another.

I used to be a saline intensivist.

Now, I’m balanced.