Metabolic acidosis is a process that results in excessive generation of H+ or consumption of serum HCO3. It may or may not be associated with acidemia (low plasma pH). This can occur by the addition of an acid, direct loss of bicarbonate from the gastrointestinal tract or the kidney, or rapid dilution of the ECF by a nonbicarbonate-containing solution. The physiologic response to acidemia is an increase in ventilation that returns serum pH towards normal (Table 2). In clinical practice, metabolic acidosis is divided into two functional categories—increased anion gap and normal anion gap

(Table 3). With high anion gap acidosis, it is important to measure the serum osmolality and compare it to the estimated osmolality (Calculated osm = 2 x plasma Na + [Glucose]/18 + BUN/2.8). A markedly elevated serum osmolal gap (the difference between the actual and calculated serum osmolality) >10 mosm would indicate the presence of unaccounted osmoles, suggesting ethylene glycol or methanol as possible causes. If the osmolal gap is less than 10 mosm in the setting of a high-anion-gap acidosis, the differential diagnosis primarily consists of ketoacidosis, lactic acidosis, renal failure, salicylate ingestion, and D-lactic acidosis.

Table 3. Common Causes of Metabolic Acidosis in the Elderly

High Anion Gap (AG) Metabolic Acidosis Normal AG Metabolic Acidosis
L-Lactic acid (tissue hypoxia) Renal tubular acidosis
D-Lactic acid (altered Gl flora, blind loop syndromes) Diarrhea
Ketoacids (insulin deficiency, alcohol, starvation) Renal failure (reduced acid excretion)
Renal failure (inorganic acids) Ureterogastrointestinal fistulas
Acetosalicylic acid (salicylates, organic acids) HCI acids
Intoxicants (check serum osmolal gap): Dilution
methanol, ethylene glycol, paraldehyde

By contrast, normal anion-gap metabolic acidosis is related to a loss or reduced synthesis of bicarbonates either through the gastrointestinal tract (e.g., diarrhea) or the kidney (e.g., renal tubular acidosis), rather than generation or addition of acid (with the exception of chloride-based acid, such as HCL or arginine HCL in total parenteral nutrition supplements). A helpful step to the diagnosis of renal vs. nonrenal cause of normal anion-gap metabolic acidosis is the measurement of random urinary electrolytes and calculating the urinary anion gap, the difference between positive and negative charges (Une+Uk-Uci). An excess of negative charges (a negative urinary anion gap) suggests high levels of ammonium excretion. Ammonium is cation that is excreted with chloride in the urine. A negative urinary anion gap indicates an intact renal response, suggesting a nonrenal cause for the acidosis (e.g., GI bicarbonate loss with diarrhea). The absence of excess calculated negative charges indicates a renal origin to the acidosis since the kidney is not able to acidify the urine through generation of ammonium. The differential diagnosis is then narrowed to renal tubular acidosis, early stages of chronic kidney disease, use of carbonic anhydrase inhibitor, and ureteral diversion.
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CLINICAL PRESENTATION

The patient with mild acidemia may exhibit no acute symptoms. With severe acidemia nausea, vomiting, anorexia, lethargy, and Kussmaul respirations may develop. Severe acidemia is associated with decreased myocardial contractility, hypotension, pulmonary edema, and tissue hypoxia. These affects are less well-tolerated in older individuals and are more likely to lead to acute medical emergencies. Chronically, it can produce a negative nitrogen balance and result in bone loss, which may exacerbate osteopenia and osteoporosis. Animal studies suggest acidemia associated myocardial impairment is more severe with advancing age.
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Therapy

Initial treatment is directed toward correcting the underlying disease process. Oral НСОз or precursors, such as citrate, can be administered to treat mild and chronic metabolic acidosis. Severe acidemia, pH <7.10, necessitates treatment with intravenous sodium bicarbonate to help maintain normal cardiac function and cellular integrity. While the use of bicarbonate in the treatment of lactic acidosis remains controversial, it is generally recommended that bicarbonate be administered to patients with severe lactic acidosis to assist survival while addressing the underlying problem. Caution must be used in the elderly to avoid iatrogenic volume overload, which can occur with vigorous НСОз replacement. In general, half of the НСОз deficit should be replaced over the first 24 hours and half over the following 24-48 hours (НСОз (meq/1) deficit = 60% body weight (kg) x [24 – НСОз (meq/1) observed]). Close monitoring is important, as this formula may underestimate the bicarbonate deficit in severe acidosis.