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 AlcoholIngested 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) Chapter 048. Acidosis and Alkalosis (Part 8) Methanol (See also Chap. e34) The ingestion of methanol (wood alcohol) causesmetabolic acidosis, and its metabolites formaldehyde and formic acid cause severeoptic nerve and central nervous system damage. Lactic acid, ketoacids, and otherunidentified organic acids may contribute to the acidosis. Due to its low molecularweight (32 Da), an osmolar gap is usually present. Metabolic Acidosis: Treatment This is similar to that for ethylene glycol intoxication, including generalsupportive measures, fomepizole or ethanol administration, and hemodialysis. Isopropyl Alcohol Ingested isopropanol is absorbed rapidly and may be fatal when as little as150 mL of rubbing alcohol, solvent, or de-icer is consumed. A plasma level >400mg/dL is life threatening. Isopropyl alcohol differs from ethylene glycol andmethanol in that the parent compound, not the metabolites, causes toxicity, andacidosis is not present because acetone is rapidly excreted. Alcohol Toxicity: Treatment Isopropanol alcohol toxicity is treated by watchful waiting and supportivetherapy; IV fluids, pressors, ventilatory support if needed, and occasionallyhemodialysis for prolonged coma or levels >400 mg/dL. Renal Failure (See also Chaps. 273 and 274) The hyperchloremic acidosis of moderaterenal insufficiency is eventually converted to the high-AG acidosis of advancedrenal failure. Poor filtration and reabsorption of organic anions contribute to thepathogenesis. As renal disease progresses, the number of functioning nephronseventually becomes insufficient to keep pace with net acid production. Uremicacidosis is characterized, therefore, by a reduced rate of NH 4+ production andexcretion, primarily due to decreased renal mass. [HCO 3–] rarely falls to 20 mmol/L. The acid retained in chronic renaldisease is buffered by alkaline salts from bone. Despite significant retention ofacid (up to 20 mmol/d), the serum [HCO3–] does not decrease further, indicatingparticipation of buffers outside the extracellular compartment. Chronic metabolicacidosis results in significant loss of bone mass due to reduction in bone calciumcarbonate. Chronic acidosis also increases urinary calcium excretion, proportionalto cumulative acid retention. Renal Failure: Treatment Because of the association of renal failure acidosis with muscle catabolismand bone disease, both uremic acidosis and the hyperchloremic acidosis of renalfailure require oral alkali replacement to maintain the [HCO 3–] between 20 and 24mmol/L. This can be accomplished with relatively modest amounts of alkali (1.0–1.5 mmol/kg body weight per day). Sodium citrate (Shohls solution) or NaHCO 3tablets (650-mg tablets contain 7.8 meq) are equally effective alkalinizing salts.Citrate enhances the absorption of aluminum from the gastrointestinal tract andshould never be given together with aluminum-containing antacids because of therisk of aluminum intoxication. When hyperkalemia is present, furosemide (60–80mg/d) should be added. Hyperchloremic (Nongap) Metabolic Acidoses Alkali can be lost from the gastrointestinal tract in diarrhea or from thekidneys (renal tubular acidosis, RTA). In these disorders (Table 48-5), reciprocalchanges in [Cl–] and [HCO3–] result in a normal AG. In pure hyperchloremicacidosis, therefore, the increase in [Cl–] above the normal value approximates thedecrease in [HCO3–]. The absence of such a relationship suggests a mixeddisturbance. 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 diseaseIII. ...