Chapter 048. Acidosis and Alkalosis (Part 8)

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Methanol (See also Chap. e34) The ingestion of methanol (wood alcohol) causes metabolic acidosis, and its metabolites formaldehyde and formic acid cause severe optic nerve and central nervous system damage. Lactic acid, ketoacids, and other unidentified organic acids may contribute to the acidosis. Due to its low molecular weight (32 Da), an osmolar gap is usually present. Metabolic Acidosis: Treatment This is similar to that for ethylene glycol intoxication, including general supportive measures, fomepizole or ethanol administration, and hemodialysis. Isopropyl Alcohol Ingested isopropanol is absorbed rapidly and may be fatal when as little as 150 mL of rubbing alcohol, solvent, or de-icer is...

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Chapter 048. Acidosis and Alkalosis (Part 8) Methanol (See also Chap. e34) The ingestion of methanol (wood alcohol) causes metabolic acidosis, and its metabolites formaldehyde and formic acid cause severe optic nerve and central nervous system damage. Lactic acid, ketoacids, and other unidentified organic acids may contribute to the acidosis. Due to its low molecular weight (32 Da), an osmolar gap is usually present. Metabolic Acidosis: Treatment This is similar to that for ethylene glycol intoxication, including general supportive measures, fomepizole or ethanol administration, and hemodialysis.
Isopropyl Alcohol Ingested isopropanol is absorbed rapidly and may be fatal when as little as 150 mL of rubbing alcohol, solvent, or de-icer is consumed. A plasma level >400 mg/dL is life threatening. Isopropyl alcohol differs from ethylene glycol and methanol in that the parent compound, not the metabolites, causes toxicity, and acidosis is not present because acetone is rapidly excreted. Alcohol Toxicity: Treatment Isopropanol alcohol toxicity is treated by watchful waiting and supportive therapy; IV fluids, pressors, ventilatory support if needed, and occasionally hemodialysis for prolonged coma or levels >400 mg/dL. Renal Failure (See also Chaps. 273 and 274) The hyperchloremic acidosis of moderate renal insufficiency is eventually converted to the high-AG acidosis of advanced renal failure. Poor filtration and reabsorption of organic anions contribute to the pathogenesis. As renal disease progresses, the number of functioning nephrons eventually becomes insufficient to keep pace with net acid production. Uremic acidosis is characterized, therefore, by a reduced rate of NH 4+ production and excretion, primarily due to decreased renal mass. [HCO 3–] rarely falls to 20 mmol/L. The acid retained in chronic renal
disease is buffered by alkaline salts from bone. Despite significant retention of acid (up to 20 mmol/d), the serum [HCO3–] does not decrease further, indicating participation of buffers outside the extracellular compartment. Chronic metabolic acidosis results in significant loss of bone mass due to reduction in bone calcium carbonate. Chronic acidosis also increases urinary calcium excretion, proportional to cumulative acid retention. Renal Failure: Treatment Because of the association of renal failure acidosis with muscle catabolism and bone disease, both uremic acidosis and the hyperchloremic acidosis of renal failure require oral alkali replacement to maintain the [HCO 3–] between 20 and 24 mmol/L. This can be accomplished with relatively modest amounts of alkali (1.0– 1.5 mmol/kg body weight per day). Sodium citrate (Shohl's solution) or NaHCO 3 tablets (650-mg tablets contain 7.8 meq) are equally effective alkalinizing salts. Citrate enhances the absorption of aluminum from the gastrointestinal tract and should never be given together with aluminum-containing antacids because of the risk of aluminum intoxication. When hyperkalemia is present, furosemide (60–80 mg/d) should be added. Hyperchloremic (Nongap) Metabolic Acidoses Alkali can be lost from the gastrointestinal tract in diarrhea or from the kidneys (renal tubular acidosis, RTA). In these disorders (Table 48-5), reciprocal
changes in [Cl–] and [HCO3–] result in a normal AG. In pure hyperchloremic acidosis, therefore, the increase in [Cl–] above the normal value approximates the decrease in [HCO3–]. The absence of such a relationship suggests a mixed disturbance. Table 48-5 Causes of Non-Anion-Gap Acidosis I. Gastrointestinal bicarbonate loss A. Diarrhea B. External pancreatic or small-bowel drainage C. Ureterosigmoidostomy, jejunal loop, ileal loop D. Drugs 1. Calcium chloride (acidifying agent) 2. Magnesium sulfate (diarrhea) 3. Cholestyramine (bile acid diarrhea)
II. Renal acidosis A. Hypokalemia 1. Proximal RTA (type 2) 2. Distal (classic) RTA (type 1) B. Hyperkalemia 1. Generalized distal nephron dysfunction (type 4 RTA) a. Mineralocorticoid deficiency b. Mineralocorticoid resistance (autosomal dominant PHA I) c. Voltage defect (autosomal dominant
PHA I and PHA II) d. Tubulointerstitial disease III. Drug-induced hyperkalemia (with renal insufficiency) A. Potassium-sparing diuretics (amiloride, triamterene, spironolactone) B. Trimethoprim C. Pentamidine D. ACE-Is and ARBs E. Nonsteroidal anti-inflammatory drugs F. Cyclosporine and tacrolimus IV. Other A. Acid loads (ammonium chloride, hyperalimentation)
B. Loss of potential bicarbonate: ketosis with ketone excretion C. Expansion acidosis (rapid saline administration) D. Hippurate E. Cation exchange resins Note: RTA, renal tubular acidosis; ACE-I, angiotensin-converting enzyme inhibitors; ARB, angiotensin receptor blocker; PHA, pseudohypoaldosteronism.