What are the causes of non-anionic gap metabolic acidosis?

From the Guidelines

Non-anionic gap metabolic acidosis is primarily caused by the replacement of ketoanions with chloride from intravenous fluids, as seen in patients recovering from diabetic ketoacidosis (DKA) who receive excessive saline for fluid and electrolyte replacement 1. This condition can also be caused by other factors such as gastrointestinal bicarbonate loss, renal tubular acidosis, and the use of certain medications.

• Key causes of non-anionic gap metabolic acidosis include:
  • Gastrointestinal bicarbonate loss through diarrhea or fistulas
  • Renal tubular acidosis (types 1,2, and 4)
  • Use of certain medications like carbonic anhydrase inhibitors (acetazolamide)
  • Administration of chloride-containing solutions such as normal saline (dilutional acidosis)
  • Recovery from ketoacidosis, as noted in the study published in Diabetes Care in 2003 1 The study published in Diabetes Care in 2003 1 highlights that patients recovering from DKA may develop hyperchloremia and transient non–anion gap metabolic acidosis due to the use of excessive saline for fluid and electrolyte replacement.
• It is essential to note that these biochemical abnormalities are usually transient and not clinically significant, except in cases of acute renal failure or extreme oliguria, as mentioned in the study 1.

From the FDA Drug Label

Metabolic acidosis and electrolyte imbalance may occur. The cause of non-anionic gap metabolic acidosis is not directly stated in the drug label.

• The label mentions metabolic acidosis as a possible adverse reaction, but it does not specify the type of metabolic acidosis.
• There is no information about the specific cause of non-anionic gap metabolic acidosis. 2

From the Research

Causes of Non-Anionic Gap Metabolic Acidosis

• Loss of large quantities of base secondary to diarrhea 3
• Administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states 3
• Gastrointestinal bicarbonate loss 4
• Renal tubular acidosis 4
• Drugs-induced hyperkalemia 4
• Early renal failure 4
• Administration of acids 4
• High-volume ileostomy output causing large bicarbonate losses 5

Mechanisms

• The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes 3
• The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate 3

Diagnosis

• A complete clinical history and physical examination are critical initial steps to begin the evaluation process 5
• Measuring serum electrolytes with a focus on potassium level, blood gas, urine pH, and either direct or indirect urine ammonium concentration 5