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Metabolic Acidosis

Metabolic Acidosis. Alex Flaxman, MD, MSE. Presentation. 50 yo M, 4d h/o vomiting & R inf chest/RUQ pn Wife adds 10-15 lb wt loss x4d and lethargic , sleeping “23 hrs/day” Vomiting:

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Metabolic Acidosis

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  1. Metabolic Acidosis Alex Flaxman, MD, MSE

  2. Presentation • 50 yo M, 4d h/o vomiting & R inf chest/RUQ pn • Wife adds 10-15 lb wt loss x4d and lethargic, sleeping “23 hrs/day” • Vomiting: • After eating, but also when doesn’t eat, NBNB. Has been able to tolerate Gatorade, and has increased his intake of Gatorade. • Pain: • R-sided, underneath ribs, occ rad to L

  3. “Prior’s” • Pt in ED  MICU 8/04 for same • S/p CTAP, UGI & LGI endoscopy • Investigated for toxidrome • Denies EtOH, home-made alcohol, antifreeze, ethylene glycol, MeOH, pica, or other tox exposures. DOH visit to home. • EGD 6 wks ago for N/V, neg as per pt • Travel 3 wks ago to Palm Beach, FL

  4. ROS • General: -chills, +fatigue • CV: CP • Resp: SOB, Cough • GI: N/V, abd pn, -diarrhea, -blood • GU: -freq/hematuria/urgency

  5. All: NKDA • PMH: Depression x2yrs, hyperchol, disc herniations L3, L4, L5 s/p bk inj • PSH: Laminectomy x2, UGI, LGI, EGD 6 wks ago • Meds: Compazine x1d, Nexium, Zoloft, Vicodin, Somma • PMD: @BI

  6. Tobacco: 1 ppd, h/o 2-3 ppd • EtOH: Denies • Drugs: Denies

  7. Vital Signs BP 161/103 P 129 R 24 O2 97% T 99.4 PR Pn 10/10

  8. Exam • General: WDWN, NAD, tachypneic • Pul: CTAB • CV: Tachy, reg, S1, S2, -m/r/g • Abd: NABS, RUQ tend, epig tend, +masses- liver edge ~ 9 cm inf to costal margin • Rectal: Guaiac neg w/ no stool • Ext: -edema, hyperpig L foot cool R PT 2+ DP +Doppler L PT +Doppler DP +Doppler

  9. EKG SR @ 124 w/ LAE ? Q II, aVF (new from 8/31/04) ? ST elev V2, V3 Sinus tach new from 8/21/04 • CXR NAD, -free air • NG Lavage Yellow-green material, no blood

  10. What labs do you want?

  11. 13.6 1.2 31.5 136 112 3 179 4.3 6 1 N 96L 3M 3 17.1 10.3 465 16.3 50.9 Labs Lipase 159Troponin 0.02

  12. More Labs AST 74ALT 6Alk 163TB 3.6DB 0Alb 5.2TP 9.7 UACloudyProt 100WBC 0-5RBC 0-3Hyaline Casts 0-5 Lactate 2.2 Acetone neg EtOH 0 Serum osmolarity 290

  13. Now What?

  14. 136 112 6 7.12 / 18 / 105 / RA / 8.3 Recall ABG

  15. Rule 1: Acidosis or Alkalosis Acidosis 7.12 / 18 / 105 / RA / 8.3

  16. Rule 2: Metabolic, Respiratory, Both Metabolic 7.12 / 18 / 105 / RA / 8.3

  17. 136 112 6 Rule 3: Anion Gap 7.12 / 18 / 105 / RA / 8.3 • AG = ? = Na – Cl – HCO3 = 136 – 112 – 6 = 18 • So we have an… Anion Gap Metabolic Acidosis

  18. Rule 4: Degree of Compensation For metabolic acidosis, Expected PCO2 = 1.5(HCO3) + 8 ± 2 = 1.5(6) + 8 ± 2 = 9 + 8 ± 2 = 17 ± 2 = 15, 19 7.12 / 18 / 105 / RA / 8.3 Actual PCO2 is 18  appropriate compensation

  19. 136 112 6 Rule #5: δ/δ 7.12 / 18 / 105 / RA / 8.3 • Any takers? AG = 18 (nl 6.6-10.6) HCO3 = 6 (nl 24)

  20. Rule #5: δ/δ • AG should be 10 but is now 18, for a difference of 8 • The AG went up by 8, so the HCO3should go down by 8. • So HCO3 should be 24 – 8 = 16 but is really 6. The HCO3 is lower than predictedso there is also a concurrent non-AG metabolic acidosis.

  21. Methanol: wood alcohol, grain alcohol (moonshine), paint thinners, windshield washer fluid Uremia DKA, AKA Paraldehyde, propylene glycol Ingestions (INH, iron, XTC, cocaine) Lactic Acidosis EtOH, Ethylene glycol Salicylates Causes of AG Metabolic AcidosisMUD PILES

  22. Other causes • “P” – Phenformin • Toluene poisoning (glue sniffing) • Other organic acids • Lactic acid • Acetone • Ketoacids: hydroxybutyrate / acetoacetate • Hippuric Acid • 5-oxyproline • Salicylates

  23. Lactic Acidosis • Usually increase in the L isomer • Type A • 2° to hypoxia (hypoperfusion, sepsis) • Type B • Not d.t. hypoxia: seizures, liver failure, thiamine deficiency • D-Lactic Acidosis- increase in the D isomer

  24. D-Lactate

  25. D-Lactate: External Sources • Ingestion of fermented fruits and vegetables: pickles, yogurt, sauerkraut • LR and dialysate contain dl-lactate (50/50) • Propylene glycol ?metabolism?

  26. D-Lactate: Internal Sources • In the gut, glucose is metabolized by flora to lactate: l-Lactate d-Lactate • Produced via the methyl-glyoxal pathway (part of threonine catabolism) (threonine is an essential amino acid)

  27. D-Lactate: Internal Sources Pyruvate ↔ dl-Lactate via Lactate Dehydrogenase BUT Pyruvate ↔ l-Lactate requires l-LDH Pyruvate ↔ d-Lactate requires d-LDH Mammals do not have d-LDH

  28. D-Lactate: Getting rid of it • Slowly metabolized? Not. • d-hydroxy-acid-dehydrogenase • Mitochondrial enzyme • In many tissues (especially liver and kidney) • Converts d-lactate (and other substrates) to pyruvate • But overall, d-lactate is metabolized more slowly than l-lactate

  29. D-Lactic Acidosis An increase in D-Lactate (duh)

  30. AMS Slurred speech Confusion Inability to concentrate Somnolence Hallucinations Clumsiness Weakness Ataxia / unsteady gait Nystagmus Irritable Abusive behavior Ptosis Asterixis Symptoms • Tachypnea

  31. Risk Factor Anything that results in increased delivery of undigested carbohydrates to the colon

  32. Risk Factors • Short Bowel Syndrome #1 Surgical resection #2 Intestinal bypass (bariatric surgery) • Feeding tube placement • Intestinal malabsorption? • Chronic pancreatitis

  33. Risk Factors Not from the H&P • Alteration of normal colon flora to a predominance of Gm+ anaerobes (lactobacillus) • ? Colonic stagnation • Impaired metabolism

  34. Precipitating Factors • Excessive oral food intake • Especially carbohydrates (like Gatorade) • Change in enteral feeding formula

  35. Labs • Renal function normal or abnormal • AG Metabolic acidosis • Can have non-AG metabolic acidosis • Elevated serum or urine D-lactate • Serum level > 3 mmol/L

  36. Ancillary Tests • LP: CSF D-lactate levels same as serum • EEG: b/l diffuse, high-voltage slow waves without focal abnormality • Stool culture: predominance of Gm+ anaerobic organisms • Lactobacillus • Bifidobacterium • Eubacterium

  37. Immediate Treatment • A-B-C • NPO • IV dextrose (e.g. D5NS)

  38. Treatment • Supportive • Adjust feeding tube • Adjust enteral feeding formula • Change diet to starch instead of carbohydrates  recurrent attacks • Surgical: reanastomosis • Oral abx: neomycin, vanco, kanamycin, metro • Bicarb- unclear

  39. Treatment • Increase luminal pH • CaCO3, MgCl2 • HCO3 • Abx • Oral vanco, metro, or neomycin Although can cause overgrowth of lactobacillus • Dialysis • Corrects acidosis • Clears d-Lactate

  40. Other Interesting Points • d-Lactate levels correlate poorly with symptoms • Normal humans infused with d-lactate do not develop symptoms • Other acidoses to the same pH do not cause similar symptoms

  41. 136 112 6 Final dorky Interesting Point 7.12 / 18 / 105 / RA / 8.3 • AG metabolic acidosis and concurrent non-AG metabolic acidosis • Why?

  42. Final dorky Interesting Point • In D-lactate acidosis the increase in the AG tends to be less than the decrease in the HCO3. • In L-lactic acidosis where the increase in the AG tends to be greater than the reduction in the bicarb.

  43. Final dorky Interesting Point • Much lower renal threshold for d-lactate than for l-lactate • Loss of the sodium salt of D-lactic acid in the stool (the H+ is resorbed from the lumen or reacts with secreted HCO3) but the organic ion does not

  44. Take Home Points- General • Consider ABG’s more often • Look for causes of metabolic acidosis • In unclear cases, or cases where MUD PILES fails, send tests for organic acids (e.g. d-lactate and ß-hydroxybutyrate) • Involve intensivist early

  45. Take Home Points- d-Lactate • For patients with short bowel (or other malabsorption risks), consider D-lactic acidosis. • Also consider when AG acidosis and: • Nl “lactate” levels and no acetone • Short bowel or other malabsorption syndrome • Preceded by food ingestion (and symptoms improve after discontinuation) • Characteristic neurological findings

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