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: Measured Osm= 317 Osm Gap= 27
2(Na) + (gluc/18)+ (BUN/2.8)
= 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 =
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!