Pocket Pediatrics: The Massachusetts General Hospital for Children Handbook of Pediatrics (Pocket Notebook Series), 2 Ed.

METABOLIC ACIDOSIS

Definition (Pediatr Rev 2004;25:350; Pediatr Rev 2011;32:240)

• Net gain of H⁺ or loss of HCO₃ and can be divided into AG or NAG

• AG acidosis: Implies presence of unmeasured anions; ↑ organic acids from ingestion, production, inborn errors of metab, or ↓ excretion 2/2 renal failure

• AG = [Na⁺] − ([Cl⁻] + [HCO₃⁻]); normal defined as 8–12 w/ normal values believed to be higher in pts <2 yo (some use 16 +/− 4 mEq/L as normal for this group)

• Figge formula corrects AG for albumin: Adjusted AG = observed AG + 2.5 (nl albumin − observed albumin)

• NAG acidosis: 2/2 inability to excrete H⁺ or loss of HCO₃ from GI or urinary tracts

• Severe met acidosis: HCO₃ ≤ 8 mEq/L (if nl resp compensation)

Clinical Manifestations (Pediatr Rev 1996;17:395; Pediatr Rev 2011;32:240)

• Nl response to met acidosis is hyperpnea (deep, pauseless respirations) w/ resultant 4–8×’s increase in minute ventilation. As acidosis worsens, resp muscle strength decreases and WOB increases → resp failure

• At pH <7–7.1, cardiac contractility can be impaired and the risk of malignant arrhythmias is increased. Can p/w arteriolar dilation, HoTN, pulmonary edema

• CNS: Cerebral edema, lethargy, coma

• Other: Oxyhemoglobin dissociation curve shifts right, hyperK, insulin resistance, protein denaturing

Etiologies (Rose & Post. Clinical Physiology of Acid-Base & Electrolyte Disorders 2001:535; Pediatr Rev 2011;32:240)

• AG acidosis: Due to exogenous and endogenous H⁺ excess: MUD PILES

• Methanol: Found in wood alcohol, varnishes, shellac, and sterno, metabolized to formaldehyde, Osm gap >10; p/w sx 12–36 hr after ingestion w/ weakness, N/V, can result in blindness, coma, and death

• Uremia (2/2 renal failure w/ decreased clearance of sulfate, urate, phosphate)

• Diabetic ketoacidosis, starvation ketosis

• Paraldehyde (solvent, anticonvulsant and hypnotic, not available in the United States but still used elsewhere)

• Iron, isoniazid, and ingestions (other): Toluene (glue sniffing), sulfur, etc.

• Lactic acidosis: Most common, 2/2 anaerobic metab, can be 2/2 ↑ production (severe hypoxia, ischemia, shock, CO or cyanide poisoning, szr, inborn errors of metab) or ↓ clearance (hypoperfusion, liver disease)

• Ethylene glycol (in antifreeze, w/ glycolate, oxalate, and Osm gap >10; Ethylene glycol ingestion p/w drunkenness or even coma, then pulmonary edema and then renal failure, consider fomepizole and/or dialysis for rx), Ethanol (alcoholic ketoacidosis)

• Salicylate: Results in combination resp alkalosis and met acidosis, tinnitus

• If concern for ingestions, check Osmolar gap = Measured Osm − Calculated Osm

• Calculated Osm = 2[Na⁺] + [glucose]/18 + [BUN]/2.8 + [EtOH]/4.6

• If Osm gap >10, presence of unmeasured Osm; methanol, ethylene glycol, etc.

• W/ +AG; to check if >1 cause for low HCO₃ can check Δ/Δ = Δ AG/Δ HCO₃

• Δ/Δ <1; loss of HCO₃ greater than expected (AG acidosis + NAG acidosis)

• Δ/Δ = 1–2; typical AG acidosis as almost 1:1 buffering of H⁺ w/ HCO₃

• Δ/Δ >2; loss of HCO₃ less than expected (AG acidosis + metabolic alkalosis)

• NAG acidosis: 2/2 ↑ GU or GI loss of HCO₃ or inability to excrete H⁺: HARD UP

• Hyperalimentation, Hypoaldosteronism, HyperPTH

• Acetazolamide, Ammonium chloride

• RTA (see later), Renal loss 2/2 rapid correction of chronic resp alkalosis

• RTA II (proximal RTA): Dec HCO₃ reabsorption, p/w normal or low serum [K⁺], variable urine pH, fractional excretion of HCO₃ (Fe_HCO3) >15–20%

• Can result in rickets or osteomalacia

• Carbonic anhydrase inhibitors (e.g., acetazolamide) impair HCO₃ reabsorption

• Treat w/ 10–15 mEq/kg HCO₃ divided multiple times a day

• Renal dysfunction: Some cases of renal failure and RTA

• RTA IV (hypoaldosteronism): W/ normal or inc serum [K⁺], urine pH < 5.3, Fe_HCO3 < 3%, check serum aldo; treat w/ HCO₃ 1–3 mEq/kg qd

• RTA I (distal RTA): Dec H⁺ secretion w/ urine pH >5.3, low serum [K⁺], and fractional excretion of HCO₃ <3% in adults but can be 5–10% in children

• Can be 2/2 autoimmune process, hyperPTH, amphotericin

• Can result in nephrocalcinosis or nephrolithiasis

• Treat w/ daily HCO₃ 4–14 mEq/kg qd in children, 1–2 mEq/kg qd in adults

• Diarrhea (most common cause) and other GI losses (ostomy, etc.)

• Ureteral diversion (ureteroenterostomy/ureterosigmoidostomy → intestinal HCO₃⁻ loss)

• Parenteral NaCl (common cause, due to rapid dilution of HCO₃⁻ by Cl⁻; similar effect from KCl or MgCl₂), Pancreatic fistula

• Urine AG can distinguish between situations w/ intact NH₄⁺ secretion (GI losses RTA II, rapid correction of chronic resp alkalosis) vs. those where secretion of NH₄⁺ is impaired (renal failure, RTA I, and IV)

• UAG is inaccurate w/ high AG acidosis or w/ significant volume depletion

Management (Pediatr Rev 2004;25:350)

• Correct underlying abnormalities as described above

• Sodium-bicarb is the agent of choice for severe metabolic acidosis (especially NAG) but controversial as evidence of improved outcomes is weak

• Amt bicarb to infuse = (weight in kg) × (15 − [measured HCO₃]) × (0.5)

• Mix amount calculated in hypotonic solution and infuse over 1 HR

• Provides enough bicarb to correct pH >7.2 or bicarb concentration >15 mEq/L

• Rapid correction can result in acidification of CSF (w/ worsening symptoms); volume overload; development of alkalemia, hypocalcemia, and respiratory depression