Normal anion gap acidosis is an acidosis that is not accompanied by an abnormally increased anion gap.
The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second.
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Transcription
Differential diagnosis
The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis):
- Hyperalimentation (e.g. from TPN containing ammonium chloride)
- Chloride administration, often from normal saline
- Acetazolamide and other carbonic anhydrase inhibitors
- Renal tubular acidosis[1]
- Diarrhea: due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl−; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl−, results in a decrease in the plasma Na+ concentration relative to the Cl−concentration. This scenario can be avoided if formulations such as lactated Ringer’s solution are used instead of normal saline to replace GI losses.[2]
- Ureteroenteric fistula – an abnormal connection (fistula) between a ureter and the gastrointestinal tract
- Pancreaticoduodenal fistula – an abnormal connection between the pancreas and duodenum
- Spironolactone
- High ostomy output[1]
- Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap.[3]
As opposed to high anion gap acidosis (which involves increased organic acid production), normal anion gap acidosis involves either increased production/administration of chloride (hyperchloremic acidosis) or increased excretion of bicarbonate.
See also
References
- ^ a b "Metabolic Acidosis: Acid-Base Regulation and Disorders: Merck Manual Professional". Retrieved 2008-12-04.
- ^ Jean-Louis Vincent; Abraham Edward; Kochanek Patrick (8 July 2011). "Acid-base disorders". Textbook of Critical Care. Elsevier. ISBN 143771367X.
- ^ Coe FL (August 1974). "Magnitude of metabolic acidosis in primary hyperparathyroidism". Arch. Intern. Med. 134 (2): 262–5. doi:10.1001/archinte.1974.00320200072008. PMID 4843192.
External links
This page was last edited on 2 August 2022, at 04:36