Monday, April 09, 2007

Case Reports

Here's an interesting little case that I saw recently....
CC: Alcohol withdrawal
HPI: 54 yo WF presents w/ EtOH w/drawal. Last drink was 48 hours prior. + H/o w/drawal and a possible Sz in the past (unsure if due to DT's). Did later admit to having just a "swig" of listerine 24 hours PTA. Denies methanol, ethylene glycol, etc. No h/o DM
PMHx: Hypercholesterolemia; EtOH abuse
Meds: Denies
PSHx: Denies
SHx: + EtOH abuse; Denies drug use
ROS: Pertinent for anxiety
V/S: BP: 149/61 HR: 96 RR: 20 Temp: 97.8 Sats: 96% RA
PE: Pertinent findings- tachy in low 100's, anxious, slightly tremulous; Slight epigastric TTP
Hospital Course:
Obviously EtOH w/drawal is number 1-3 on the DDx. I checked a CBC, CMP, lipase. I gave her some Ativan to prevent full-blown w/drawal, monitors, etc. Here's where it gets a little interesting....
Pertinent Labs:
Glucose: 224
H/H: 10.8/32.3
MCV: 100.5
BUN/Cr: 15/0.9
K: 5.0
Cl: 92
Lipase: 179
Bicarb: 9
AG: 41
So why would this patient, who is not diabetic, have such a large AG and profound acidosis? I asked again about co-ingestants (methanol, ethylene glycol, etc). She again adamantly denied these except for the "swig" of listerine 24 hours before. I went ahead and ordered a couple labs with the thought that she might have an interesting condition that I used to see back at the Copa. What would you order and what do you think this might be?
I ordered an ABG, serum acetone, Beta-hydroxybutyrate, lactate and here are the results...
ABG: pH: 7.158 pCO2: 26 pO2: 95 Bicarb: 8.9 Base Excess: -18.5
Acetone: 3+
B-hydroxybutyrate: 76.2 (normal 0-3)
Methanol: neg
Ethylene Glycol: neg
Lactate: 6.3 (Normal 0-2.2)
So what is the diagnosis?
I diagnosed this patient with Alcoholic ketoacidosis (AKA). In review AKA is due to a decrease in fatty acid oxidation in association with poor PO intake or recurrent emesis. There will be a significant increase in serum ketones, mildly elevated glucose, large gap, mild to moderate increase in lactate and a beta-hydroxybutyrate:lactate ratio of 5:1 to 10:1 (normal is 1:1). In this patient the lactate came back soon, but the BHB is a send-out lab (but w/ a ratio of 12:1 helps confirm the diagnosis).
AKA can be seen in first-time binge drinkers or chronic alcoholics. The general starvation results in a decrease in glycogen and insulin stores w/ an increase in catecholamines, glucagon, growth hormone and cortisol levels. Lipolysis and hepatic ketogenesis is stimulated resulting in ketoacidosis.
Of note, AKA typically happens after an acute DECREASE in EtOH consumption (like this patient). They will often show tachycardia, tachypnea, mild to moderate abdominal pain (as seen in this patient, NV, etc. The initial AG will be 21 but elevate later.
Also interestingly, pH may be normal or even alkalemic early in the course. A contraction metabolic alkalosis secondary to protracted N/V may obscure the acidosis.
You want to make sure you also rule out other causes of a metabolic acidosis (methanol, ethlylene glycol, isopropyl etc).
Treatment is symptomatic. Volume repletion and glucose are mainstays of therapy. Glucose will stimulate insulin production which helps alleviate the lipolysis and ketone formation. Insulin is of no proven benefit. Make sure you also evaluate patients for hypophosphatemia and hypomagnesemia (both often seen in alcoholics). You can give the usual thiamine, folate and MVI as well. The acidosis will usually clear within 24 hours.
Hope this was of some educational benefit. Now have a drink...


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