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Causes of Metabolic Acidosis

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Metabolic acidosis is a process that causes a primary decrease in the plasma HC03- concentration. Metabolic acidosis is generated by either a gain of acid or a loss of HC03-.

Metabolic acidosis is a process that causes a primary decrease in the plasma HC03- concentration. Metabolic acidosis is generated by either a gain of acid or a loss of HC03-.

Gain of acid may result from:

  •  Increased endogenous hydrogen ion production, as in ketoacidosis, L-lactic acidosis, D-lactic acidosis and salicylate intoxication.
  •  Metabolism of ingested toxins such as methanol, ethylene glycol, and paraldehyde.
  • Decreased renal excretion of hydrogen ion as in uremic acidosis and distal renal tubular acidosis.

Loss of HCO3- may result from:

  • Renal loss in proximal renal tubular acidosis.
  • Gastrointestinal loss in diarrhea.

Typically, metabolic acidosis is classified according to whether or not there is an increase in the anion gap.

High Anion Gap Metabolic Acidosis

A high anion gap acidosis results from either the production of an endogenous acid (ketoacidosis, lactic acidosis, uremic acidosis, salicylate intoxication) or the addition of certain exogenous compounds (ethylene glycol, and methanol). A high anion gap acidosis is caused by the addition of a hydrogen ion plus an unmeasured anion. The H+ is buffered by HCO3-, and therefore the HCO3- concentration falls. The unmeasured anion increases the term UA and therefore increases the anion gap according to:

AG = UA-UC = [Naf] - ([Cl-] + [HC03-I)

Diabetic ketoacidosis (DKA)

Patients with severe diabetic ketoacidosis typically present with

  • High anion gap metabolic acidosis
  • Severe acidemia (pH C 7.15)
  • Hyperglycemia
  • ECFV depletion
  • Potassium depletion despite serum potassium concentrations that may be normal or elevated.

In DKA, the anion gap acidosis is due to the generation of ketoacids, which are produced by the incomplete oxidation of fatty acids. Typically, diagnosis of diabetic ketoacidosis is made in the setting of uncontrolled insulindependent diabetes mellitus with tachypnea, polyuria, polydipsia, severe acidemia, and a urine dipstick positive for ketones. Serum ketones are generally strongly positive in diabetic ketoacidosis. Occasionally in diabetic ketoacidosis, a dipstick test for ketones may underestimate the degree of ketosis because of a marked increase in the beta-hydroxy butyratelacetoacetate ratio. This is because the test reagents of the dipstick do not detect beta-hydroxy butyrate.

L-lactic acidosis

L-lactic acidosis is by far the most common form of lactic acidosis. The most common cause of L-lactic acidosis is tissue hypoxia. L-lactic acidosis is typically divided into those disorders associated with hypotension or severe hypoxemia and all other causes . The latter can be further divided into:

  • Common conditions including sepsis, severe liver disease, diabetes mellitus, and various malignancies
  • Lactic acidosis caused by toxins or medications, including phenformin and ethanol
  • Rare hereditary forms

D-lactic acidosis

D-lactic acidosis is a very uncommon metabolic disturbance. It occurs in patients with a short-bowel, typically several months or a few years after a small bowel bypass created for the treatment of refractory massive obesity. Patients with D-lactic acidosis have episodes of neurological dysfunction characterized by ataxia, slurred speech, and confusion, in association with a high anion gap metabolic acidosis.

The acidosis is caused by fermentation of incompletely digested carbohydrate by anaerobic bacteria, resulting in the production of D-lactic acid which is poorly metabolized in animals. The preliminary diagnosis of Dlactic acidosis must be based on the clinical presentation, because routine clinical laboratories only detect L-lactate, which will be normal.

Alcoholic ketoacidosis

Alcoholic ketoacidosis is a common, serious condition that occurs in some chronic alcoholics, especially after prolonged binge drinking with diminished caloric intake. Accelerated ketogenesis results from the combined effects of starvation and ethanol. The patients may have nausea, vomiting, and abdominal pain. Metabolic alkalosis from vomiting and respiratory alkalosis may also be present in addition to the high anion gap acidosis. There is often ECFV depletion, hypoglycemia, and GI bleeding or acute pancreatitis. Because of prolonged poor food intake, phosphorous and magnesium are often depleted, even though the serum concentrations of phosphate and magnesium at presentation may be within the normal range.

Uremic acidosis

High anion gap metabolic acidosis does not usually occur in renal failure until the GFR declines below 20% of normal. The patient with mild to moderate chronic renal failure frequently has a normal anion gap acidosis rather than a high anion gap acidosis. The normal anion gap acidosis results from failure of renal elimination of hydrogen ion by production and excretion of NH4+. As the GFR falls, there is an increase in the anion gap due to retention of unmeasured anions such as sulfate, phosphate, and organic anions.

Salicylate intoxication

Although salicylate intoxication may produce a high anion gap acidosis, the most common and earliest manifestation is respiratory alkalosis due to the effect of salicylate on the respiratory center. The metabolic acidosis, which may develop after the respiratory alkalosis appears, is caused by the salicylate

interfering with certain metabolic processes. This interference leads to the increased accumulation of organic acids, such as lactic acid and ketoacids, which cause the acidosis and the increase in the anion gap. The salicylate itself makes up only a small part of the increased anion gap.

Ethylene glycol intoxication

Ethylene glycol intoxication may result from drinking antifreeze or radiator fluid. There is usually, but not always, a background of chronic alcoholism. Ethylene glycol is metabolized by alcohol dehydrogenase to a number of very toxic compounds which produce:

  • A high anion gap acidosis.
  • Acute central nervous system dysfunction: ataxia, confusion, seizures, and coma
  • Acute renal failure
  • Calcium oxalate crystals in the urine (one of the toxic compounds is oxalic acid)

Methanol intoxication

Methanol is metabolized to formic acid by alcohol dehydrogenase. Formic acid contributes to the high anion gap acidosis seen in this serious intoxication. Optic neuritis with blindness, and pancreatitis may develop in methanol intoxication.

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Clara L.

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