Metabolic Acidosis

A condition characterized by a primary decease in extracellular fluid bicarbonate; serum pH and carbon dioxide content are decreased.

The serum anion gap, which may help identify the cause of metabolic acidosis (see Table 59-1), is determined as follows: Serum sodium - (serum chloride + total CO₂) = ± 2. The urine anion gap is calculated as follows: (urine sodium + urine potassium) - urine chloride <= 0.

A non-anion gap metabolic acidosis (NAGMA) is due to a failure of bicarbonate homeostasis and is characterized by a compensatory retention of the other main body anions, which results in hyperchloremia. NAGMA results from renal tubular acidosis or from a loss of bicarbonate or organic acid anions in patients with diarrhea.

If there is a serum NAGMA and the urine anion gap is <= 0, gastrointestinal loss of bicarbonate (diarrhea) is the cause of the metabolic acidosis. A NAGMA with a urine anion gap >= 0 suggests type 1 (distal) or type 4 renal tubular acidosis. A urine pH > 5.5 with metabolic acidosis suggests distal tubular inability to acidify the urine and occurs with type 1 or type 4 renal tubular acidosis. In the elderly, type 1 renal tubular acidosis may be caused by amphotericin therapy or by tubular dysfunction due to the myeloma protein in multiple myeloma. Type 2 (proximal) renal tubular acidosis is uncommon in the elderly as a primary defect of tubular function but can result from the bicarbonate diuresis caused by carbonic anhydrase inhibitors used to treat glaucoma. In this disorder, there is NAGMA, but after the bicarbonate diuresis, urine pH is < 5.5 during acidosis due to normal distal hydrogen ion urine acidification capability.

Type 4 renal tubular acidosis is caused by urinary tract obstruction, diabetes mellitus, or drugs that interfere with aldosterone (eg, distal angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers). Acidosis with an increased anion gap (such as occurs with lactic acidosis, diabetic ketoacidosis, salicylate toxicity, toxic alcohol ingestion, and renal failure) is more common. Type 4 renal tubular acidosis is characterized by tubular dysfunction that is worse than that in type 1. The added tubular dysfunction is suggested by concomitant hyperkalemia.

Diagnosis is usually established by the history, physical examination findings (eg, hyperpnea), and laboratory findings (eg, blood gas determinations; urine pH; and blood urea nitrogen [BUN], creatinine, blood glucose, and ketone levels).

Initial treatment aims to correct the underlying disease process. When severe acidosis (pH < 7.2) is accompanied by anorexia, nausea, lethargy, hyperventilation, and decline in cardiac output, treatment should be started with IV sodium bicarbonate. Acute complete correction of arterial pH is not a goal of therapy, and caution must be used to avoid volume and sodium overload. Commonly, 2 to 3 ampules (44 mEq/L each) of sodium bicarbonate are dissolved in 5% dextrose in water and administered at a rate of 50 to 100 mL/h.