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Morning Report!

Morning Report!. Julie McGregor 1/18/06. Fun with Acid Base! Day of admission:. HCO 3 20; 7.336/39/203/21 Acidemia- pH 7.336 Metabolic Acidosis pCO 2 = 1.5(20)+ 8 +/-2 = 36-40

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Morning Report!

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  1. Morning Report! Julie McGregor 1/18/06

  2. Fun with Acid Base! Day of admission: • HCO3 20; 7.336/39/203/21 • Acidemia- pH 7.336 • Metabolic Acidosis • pCO2= 1.5(20)+ 8 +/-2 • = 36-40 • pCO2= 39 …appropriate compensation!!! • AG 25, • delta gap= 25-12/24-20= 3.25 …concominent metabolic alkalosis!!!!

  3. Osmolal Gap • Calculated Osm: • 2(Na) + (gluc/18)+ (BUN/2.8) • 280+ 0.72+ 9.6= 290 • Measured Osm= 317 • Osm Gap= 27

  4. Last Acid Base Page- The next day • HCO3 17; 7.34/29/89/15 • Acidemia • Metabolic Acidosis • pCO2= 1.5(17)+8 +/-2 • = 31.5-35.5 • pCO2= 28…Compensation plus additional Respiratory alkalosis • Anion Gap of 13 • delta gap of 0.14 so there was a Nongap acidosis on day after admission.

  5. Alcoholic ketoacidosis • Alcoholics- decreased carbohydrate intake reduces insulin secretion and increases glucagon production • Low insulin leads to lipolysis and free fatty acid delivery to the liver • Glucagon excess promotes conversion of free fatty acids into ketoacids in the liver

  6. Additionally… • Alcohol inhibits gluconeogenesis and itself stimulates lipolysis • Metabolism of ethanol into acetaldehyde and then acetic acid contributes to acid production • AKA is the causative factor in 20% of patients presenting with ketoacidosis. (Tanaka, Intern. Med. 2004, Oct, (10): 955-9)

  7. Clinical Presentation • History of alcohol abuse. Infact, AKA only affects chronic alcoholics. Case reports have also shown that “classic” patients are heavy drinkers who have a binge episode followed by abrupt cessation of alcohol consumption (Tanaka, Intern. Med. 2004, Oct, (10): 955-9) • Anion Gap metabolic acidosis • Ketonemia • Elevated osmolal gap thought to be due to acetone accumulation and presence of ethanol

  8. Plasma Glucose in AKA • Plasma glucose can be low, normal, or high • Hyperglycemia is not well understood (hyperglycemia should lead to insulin production) • Theory that the stress response eventually triggers hyperglycemia or patients may have undiagnosed DM • Case report of AKA associated hypoglycemia leading to irreversible encephalopathy (Jain, Med Sci Monit. 2002, Nov; 8(11): CS77-9)

  9. Complications of Acid Base in Alcoholic ketoacidosis • Hypoperfusion induced lactic acidosis- present in 50% of cases • Metabolic alkalosis resulting from concurrent vomiting. Acidosis and alkalosis can be of comparable severity leading to a relatively normal pH but an elevated AG marking underlying ketoacidosis. • Chronic respiratory alkalosis induced by underlying hepatic disease • A relatively normal anion gap (compared to fall in bicarb) due to urinary ketoacid anion loss.

  10. Diagnosis • Confirmation with ketonemia or ketonuria (if possible measure b-hydroxybutyrate in the blood) • Differential diagnosis of the alcoholic patient with a high anion gap metabolic acidosis and an osmolal gap: ethanol, methanol, and ethylene glycol toxicity, lactic acidosis and diabetic ketoacidosis

  11. Diagnostic Evaluation • History • Assessmet for ketonemia or ketonuria • U/A for calcium oxalate crystals • Measurement of serum levels of suspected toxins

  12. Treatment • Dextrose to increase insulin and reduce glucagon secretion • Saline to repair fluid deficit • EtOH rehab, MVI, thiamine, folate, CIWA • Nutrition consult • Acidemia and ketoacidosis largely correct spontaneously

  13. References: • Tanaka, Intern. Med. 2004, Oct, (10): 955-9 • Jain, Med Sci Monit. 2002, Nov; 8(11): CS77-9 • Up to date!

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