Gap Acidosis

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  • 1. Interesting Case Conference
  • 2. THE CASE
    • 70 y/o CF admitted to the ICU for ataxia and change of mental status. Was found to be in high anion gap metabolic acidosis with AG 25 and HCO3 10 and a Ph of 7.25.
    • Workup was negative for any cause of HAGMA.
    • Pt was given NaHCO3 and experienced rapid resolution of her symptoms with spontaneous closure of the AG in 24h.
    • Relevant PMH include gastric bypass surgery
  • 3. THE CASE
    • Exam was unremarkable
  • 4. THE ANION GAP
  • 5. THE ANION GAP
    • Low anion gap
      • relatively rare
      • the most common causes of a low anion gap is a low albumin level
        • which constitutes ~80% of the unmeasured anions
      • increase in the number of cations
        • organic paraproteins
        • inorganic bromide, lithium, Iodine or polymyxin B can lead to low anion gap values.
  • 6. KETOACIDOSIS
  • 7. KETOACIDOSIS
  • 8. KETOACIDOSIS
  • 9. KETOACIDOSIS
  • 10. KETOACIDOSIS
  • 11. LACTIC ACIDOSIS
  • 12. LACTIC ACIDOSIS
  • 13. Increased lactate production
    • A. Increased pyruvate production
      • 1. Enzymatic defects in glycogenolysis or gluconeogenesis (as with type 1 glycogen storage disease)
      • 2. Respiratory alkalosis, including salicylate intoxication
      • 3. Pheochromocytoma
  • 14. Increased lactate production
    • B. Impaired pyruvate utilization
      • 1. Decreased activity of pyruvate dehydrogenase or pyruvate carboxylase
        • a. Congenital
        • b. Possibly a role in diabetes mellitus, Reye's syndrome
  • 15. Increased lactate production
    • C. Altered redox state favoring pyruvate conversion to lactate
      • 1. Enhanced metabolic rate
        • a. Grand mal seizure
        • b. Severe exercise
        • c. Hypothermic shivering
        • d. Severe asthma
      • 2. Decreased oxygen delivery
        • a. Shock
        • b. Cardiac arrest
        • c. Acute pulmonary edema
        • d. Carbon monoxide poisoning
        • e. Severe hypoxemia (P O2 <25 to 30 mmHg)
        • f. Pheochromocytoma
  • 16. Increased lactate production
    • C . Altered redox state favoring pyruvate conversion to lactate
      • 3. Reduced oxygen utilization
        • a. Cyanide intoxication
        • b. Drug-induced mitochondrial dysfunction due to zidovudine or stavudine
    • D. D-Lactic acidosis
  • 17. Primary decrease in lactate utilization
    • A. Hypoperfusion and marked acidemia
    • B. Alcoholism
    • C. Liver disease
  • 18. Mechanism uncertain
    • A. Malignancy
    • B. Diabetes mellitus, including metformin in the absence of tissue hypoxia
    • C. Acquired immune deficiency syndrome
    • D. Hypoglycemia
    • E. Idiopathic
  • 19. UREMIA
  • 20. TOXINS
  • 21. TOXINS
  • 22. Toxins Isopropanol is primarily metabolized via alcohol dehydrogenase to acetone
  • 23. TOXINS
  • 24. TOXINS
  • 25. Clinical course in acute ethylene glycol intoxication
    • 30 minutes to 12 hours
      • Central nervous system
        • Inebriation
        • euphoria
        • ataxia
        • slurred speech
        • drowsiness
        • irritation
        • restlessness
        • disorientation    
    • Gastrointestinal
    • Nausea and vomiting    
    • Metabolic
    • Elevated osmolal gap
  • 26. Clinical course in acute ethylene glycol intoxication 12 to 24 hours Cardiovascular Mild hypertension, tachycardia, and shock     Pulmonary Tachypnea adult respiratory distress syndrome pulmonary edema pneumonitis     Metabolic Metabolic acidosis with elevated anion gap decreased osmolal gap possible tetany from hypocalcemia, and hyperventilation
  • 27.
    • 24 to 72 hours
      • Renal
        • Flank pain
        • costovertebral angle tenderness
        • oliguric renal failure, hyperkalemia, and hypocalcemia    
      • Metabolic
        • May have normal anion and osmolal gaps
  • 28. TOXINS
  • 29. TOXINS
  • 30. TOXINS
  • 31. TOXINS
  • 32. Conclusion
    • D Lactic Acid is under diagnosed.
    • Usually reversible
    • Avoid large Carbohydrate Loads