S17C221 - Alcoholic ketoacidosis

Question 1

AK overview

Answer 1

• WAGMA/HAGMA
• assoc with cessation of EtOH
• b/c of low glycogen reserves
• results in increased ketoacids
• can be seen in non-alcoholics

Question 2

AK: pathophys

Answer 2

• EtOH metabolism uses NAD, it becomes depleted and results in inhibation of aerobic metabolism in the kreb cycle, depletion of glycogen stores, ketone formation and lipolysis stimulation
• when glycogen stores are depleted insulin secretion is suppressed
• increased catecholamines, glucagon, growth hormone which inhibits aerobic metabolism and stimulates lipolysis
• acetyl coenzyme A from EtOH metabolism is converted to ketones (beta-hydroxy and acetoacetate)
• beta-hydroxybutyrate predominates b/c not enough NAD to convert it to acetoacetate (AcAc)
• there is also increased lactate production

Question 3

AK - Dx

Answer 3

CRITERIA

• low, normal or only slightly elevated serum glucose
• binge drinking ending in n/v, decr intake
• WAGMA/HAGMA
• positive serum ketones (however if not present this doesn’t exclude AK)
• HAGMA w/o better explanation

other findings:

• hypophos, hyponatremia, hypokalemia
• AG is usually 16-33 mostly secondary to ketonemia
• osmolal gap may be elevated from acetone but these pts are not hyperosmolar

Question 4

AK: symptoms

Answer 4

• n/v
• abdo pain
• tachy, tachypnea
• SOB, tremulous, hepatomegaly, aLOC, HoTN

Question 5

AK: Ddx

Answer 5

• lactic acidosis
• uremia
• sepsis
• ASA
• toxic alcohols
• DKA
• starvation ketosis
• concomitant dx: methanol, ethylene glycol, isopropronaol, pancreatitis, gastritis, UGIB, Sz, withdrawal, PNA, sepsis, hepatitis

Question 6

AK: Tx

Answer 6

• hydrate with D5NS
• giving sugar increases insulin and suppresses glucagon thereby reversing the AK and halting further ketone production
• thiamine
• replace lytes
• give bicarb if severe and unresponsive to fluids and glucose

Question 7

AK: dispo

Answer 7

-may go home if acidosis resolved and pt can tolerate oral fluids