Transcript Morning Report! - University of North Carolina at Chapel Hill

Morning Report!
Julie McGregor
1/18/06
Fun with Acid Base! Day of
admission:
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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:
 2(Na) + (gluc/18)+ (BUN/2.8)
 280+ 0.72+ 9.6= 290
 Measured Osm= 317
 Osm Gap= 27
Last Acid Base PageThe 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!