Metabolic acidosis: Etiology
Basic, Clinical Sciences: Anesthesia Procedures, Methods, and Techniques
Metabolic acidosis refers to the increased hydrogen ion concentration and decreased bicarbonate that can result from one of three abnormalities: 1) Increased generation of acid, 2) Decreased excretion of acid, or 3) Loss of bicarbonate.
Increased generation of acid occurs in processes such as lactic acidosis, ketoacidosis, and exposure to certain drugs/toxins. Lactic acidosis is the most common etiology in hospitalized patients and arises from increased anaerobic metabolism, which is triggered by either a defect in oxygen delivery to tissue, or a defect in oxygen utilization (at the level of the mitochondria). Ketoacidosis may be caused by underlying issues of diabetes, starvation, or alcohol use, and results from the breakdown of fatty acids for energy when glucose is unavailable. Toxins that can result in increased acid include methanol, ethylene glycol, acetaminophen, aspirin, and toluene.
Decreased acid excretion in the kidneys can cause metabolic acidosis by two mechanisms. The lowered GFR of renal failure results in less hydrogen ion excretion. Alternatively, distal renal tubular acidosis (type 1) can cause acidosis due to decreased hydrogen ion excretion in the collecting duct, even if GFR is preserved.
Loss of bicarbonate is the last broad mechanism of metabolic acidosis. Diarrhea typically results in loss of both bicarbonate and the salts of organic acids, which represent “potential bicarbonate.” Proximal renal tubular acidosis (type 2) can also cause bicarbonate loss as its reabsorption from the urine is impaired. Lastly, when urine is exposed to the GI mucosa (e.g. with a ureterosigmoidostomy) it can reabsorb metabolites excreted by the kidneys and thus thwart the renal acidification of urine.
Metabolic acidosis is of course also often divided into categories of increased anion gap versus “non-gap.” The following is one of numerous mnemonics outlining several etiologies by this distinction:
Anion Gap Metabolic Acidosis: “MUDPILES ”
U remia of CKD
D iabetic ketoacidosis
P ropylene glycol
I nfection or isoniazid
L actic Acidosis
Type A: Tissue hypoxia- systemic shock, decreased O2 delivery, or ischemia
Type B: cellular respiration impaired at mitochondria
E thylene glycol
Non-gap Metabolic Acidosis: “HARDUPS ”
H yperalimentation (TPN)
A cetazolamide, topiramate
R TA or CKD
U reterosigmoid conduit
P ancreatico-enteric fistula
S aline (expansion acidosis)