Metabolic Acidosis

A primary metabolic acidosis is characterized by low arterial pH (< 7.35), reduced plasma HCO3- concentration, and compensatory alveolar hyperventilation resulting in decreased PCO2.

It can be induced by either increased endogenous acid production, increased exogenous acid administration, loss of HCO3-, or by decreased ability to excrete the normal dietary H+ load.

Differential Diagnosis

The differential diagnosis of metabolic acidosis is vast and is best approached if one breaks down the causes of metabolic acidosis into normal vs elevated anion gap metabolic acidosis. See below.

Elevated Anion Gap (>16 meq) Normal Anion Gap (8-16 meq)

Increased Endogenous production:


Ketoacidosis (Alcohol, Starvation, DKA)


Lactic Acidosis


Uremia

Loss of Bicarbonate:
Diarrhea
Carbonic anhydrase inhibitors
Type 2 RTA (proximal)
Pancreatic ileostomy
Pancreatic, biliary, intestinal fistula

Exogenous Administration: ammonium chloride or HCL

Decreased Renal Acid Excretion:
Type 1(distal) ,4 RTA
Renal Failure

Intoxications:
Methanol, Ethylene Glycol, Paraldehyde, Salicylates, INH

Miscellaneous:
Hyperkalemia
Recovery from DKA

 

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