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concentration, and a compensatory reduction in the PaCO2. The etiologies of metabolic acidosis are divided into those that lead to an increase in the anion gap and those associated with a normal anion gap and are listed in Table 28-4. Although there are numerous mnemonics to recall the differential diagnosis of the metabolic acidosis, two simple ones are shown in Table 28-3. High anion gap metabolic acidosis is most frequently caused by lactic acidosis, ketoacidosis, and/or renal failure. Although there is considerable variation, the largest anion gaps are caused by ketoacidosis, lactic acidosis, and methanol or ethylene glycol ingestion.14

Table 28-4 Common Causes of Metabolic Acidosis

Elevated Anion Gap

Normal Anion Gap1'

Intoxications Methanol Ethylene glycol Salicylates Paraldehyde Isoniazid Ketoacidosis Diabetic Ethanol Starvation Lactic acidosis Carbon monoxide poisoning Drugs

IV lorazepam (due to vehicle)'

Metformin6

Nitroprusside (due to cyanide accumulation)6

Nucleoside reverse transcriptase inhihirnrs'1

PropofoK Seizures

Severe hypoxemia Shock Renal failure

Bowel fistula Diarrhea

Dilutional acidosis Drugs Arera7olamide& Ammonium chloride4' Amphotericin B6 Arginine hydrochloride0 Cholestyramine41 Hydrochloric acid" Lithium6

Parenteral nutrition6 Topiramate6 Zonisamide6 Lead poisoning Renal tubular acidosis Surgical drains Ureteral diversion Villous adenomas (some)

"Anion gap = serum sodium concentration - (serum chloride concentration + serum bicarbonate concentration). Under normal circumstances, the anion gap should be 10 mEq/L (mmol/L) or less.

6May be observed with therapeutic doses or overdoses.

Typically observed only with overdoses.

Symptoms of metabolic acidosis are attributable to changes in cardiovascular, musculoskeletal, neurologic, or pulmonary functioning. Respiratory compensation requires marked increases in minute ventilation and may lead to dyspnea, respiratory fatigue, and respiratory failure. Acidemia predisposes to ventricular arrhythmias and reduces cardiac contractility, each of which can result in pulmonary edema and/or systemic hypotension.15 Neurologic symptoms range from lethargy to coma and are usually proportional to the severity of the pH derangement. Chronic metabolic acidosis leads to a variety of musculoskeletal problems including impaired growth, rickets, osteomalacia, or osteopenia. These changes are believed to be caused by the release of calcium and phosphate during bone buffering of excess H+ ions.

As previously discussed, in anion gap metabolic acidosis, the isoelectric state is maintained because unmeasured anions are present. With a normal anion gap metabolic acidosis, the isoelectric state is maintained by an increase in the measured chloride. Because of this, normal anion gap metabolic acidosis is often referred to as hy-perchloremic acidosis.

In patients with a normal anion gap metabolic acidosis, it is often helpful to calculate the urine anion gap (UAG).16 The UAG is calculated as follows:

The normal UAG ranges from 0 to 5 mEq/L (mmol/L) and represents the presence of unmeasured urinary anions. In metabolic acidosis, the excretion of NH4+ and concurrent Cl- should increase markedly if renal acidification is intact. This results in UAG values from -20 to -50 mEq/L (mmol/L). This occurs because the urinary Cl concentration now markedly exceeds the urinary Na+ and K+ concentrations. Diagnoses consistent with an excessively negative UAG include proximal (type 2) renal tubular acidosis, diarrhea, or administration of acetazolamide or hydrochloric acid (HCl). Excessively positive values of the UAG suggest a distal (type 1) renal tubular acidosis.

In order to effectively treat metabolic acidosis, the causative process must be iden-

tified and treated. The precise role of adjunctive therapy with sodium bicarbonate (NaHCO3) is not universally agreed upon. However, most practitioners accept that NaHCC>3 is indicated when renal dysfunction precludes adequate regeneration of 1 3 or when severe acidemia (pH less than 7.10) is present. The metabolic acidosis seen with lactic acidosis and ketoacidosis generally resolves with therapy targeted at the underlying cause and NaHCO3 may be unnecessary regardless of the pH. The metabolic acidosis of renal failure, renal tubular acidosis, or intoxication with ethylene glycol, methanol, or salicylates is much more likely to require NaHCO3 therapy.

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