Thursday, May 18, 2017

Introduction to Metabolic Acidosis

A physiologic state of excess acid accumulation and deficient base bicarbonate, metabolic acidosis is produced by an underlying pathologic disorder. Symptoms result from the body’s attempts to correct the acidotic condition through compensatory mechanisms in the lungs, kidneys, and cells.
Metabolic acidosis is more prevalent among children, who are vulnerable to acid-base imbalance because their metabolic rates are faster and their ratios of water to total body weight are lower. Severe or untreated metabolic acidosis can be fatal.

Metabolic acidosis usually results from excessive burning of fats in the absence of usable carbohydrates. This can be caused by diabetic ketoacidosis, chronic alcoholism, malnutrition, or a low-carbohydrate, high-fat diet—all of which produce more keto acids than the metabolic process can handle.

Other causes include:
  • anaerobic carbohydrate metabolism: a decrease in tissue oxygenation or perfusion, as occurs with pump failure after myocardial infarction, or when pulmonary or hepatic disease, shock, or anemia forces a shift from aerobic to anaerobic metabolism, causing a corresponding rise in the lactic acid level
  • renal insufficiency and failure (renal acidosis): underexcretion of metabolized acids or the inability to conserve base
  • diarrhea and intestinal malabsorption: loss of sodium bicarbonate from the intestines, causing the bicarbonate buffer system to shift to the acidic side. For example, ureteroenterostomy and Crohn’s disease can also induce metabolic acidosis.
Less frequently, metabolic acidosis results from salicylate intoxication (overuse of aspirin), exogenous poisoning, or Addison’s disease with an increased excretion of sodium and chloride and the retention of potassium ions (due to a deficiency of glucocorticoids and mineralocorticoids).

Signs and symptoms
With mild acidosis, symptoms of the underlying disease may obscure any direct clinical evidence. Metabolic acidosis typically begins with headache and lethargy, progressing to drowsiness, central nervous system depression, Kussmaul’s respirations (as the lungs attempt to compensate by “blowing off” carbon dioxide), stupor and, if the condition is severe and goes untreated, coma and death.
Associated GI distress usually produces anorexia, nausea, vomiting, and diarrhea and may lead to dehydration. Underlying diabetes mellitus may cause fruity breath from catabolism of fats and excretion of accumulated acetone through the lungs.


Arterial pH below 7.35 confirms metabolic acidosis. With severe acidotic states, pH may fall to 7.10 and partial pressure of arterial carbon dioxide may be normal or less than 34 mm Hg as compensatory mechanisms take hold. The bicarbonate level may be less than 22 mEq/L.

Supportive findings include:
  • urine pH: < 4.5 in the absence of renal disease
  • serum potassium levels: > 5.5 mEq/L from chemical buffering
  • glucose level: > 150 mg/dl in those with diabetes mellitus
  • serum ketone body level: elevated in those with diabetes mellitus
  • plasma lactic acid level: elevated in those with lactic acidosis
  • anion gap: > 14 mEq/L, indicating metabolic acidosis.
Treatment for metabolic acidosis consists of administration of sodium bicarbonate I.V. for severe cases, evaluation and correction of electrolyte imbalances and, ultimately, correction of the underlying cause. For example, in patients with diabetic ketoacidosis, a low-dose continuous I.V. infusion of insulin is recommended.

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