Morning Report! Julie McGregor 1/18/06

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!!!!

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

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.

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

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)

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

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)

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.

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

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

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

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