Alcoholic Ketoacidosis (AKA)
The most likely explanation for this patient's findings is carbohydrate starvation causing shift of metabolism to lipid ketogenesis—specifically, alcoholic ketoacidosis (AKA). This diagnosis is supported by the combination of severe alcoholism, high anion gap metabolic acidosis (anion gap = 13), profound ketosis (serum ketones 5.5), hypoglycemia (glucose 65), and the absence of an osmolar gap or toxic alcohol ingestion 1.
Why AKA is the Correct Diagnosis
The clinical presentation is pathognomonic for AKA in the context of chronic alcohol abuse:
Severe ketoacidosis with hypoglycemia distinguishes AKA from diabetic ketoacidosis, where glucose is typically >250 mg/dL 1, 2. The patient's glucose of 65 mg/dL with ketones of 5.5 is classic for AKA 3, 4.
High anion gap metabolic acidosis (calculated as 127 - [100 + 7] = 20, though the question states 13) with pH 7.1 and bicarbonate of 7 indicates severe ketoacidosis 1, 5.
Absence of osmolar gap and negative oxalate crystals effectively rules out toxic alcohol ingestion (methanol or ethylene glycol) 1.
Low blood ethanol level (10 mg/dL) indicates recent cessation of alcohol intake, which is typical for AKA—patients binge drink, then abruptly stop due to vomiting or gastric intolerance 6, 7.
Pathophysiology of AKA
AKA develops through a specific metabolic cascade in chronic alcoholics:
Acute starvation following alcohol cessation triggers enhanced lipolysis and ketogenesis 6, 5. The patient was found "soaked in vomit," indicating prolonged inability to maintain oral intake.
Elevated glucagon-to-insulin ratio combined with increased NADH/NAD ratio from alcohol metabolism drives β-hydroxybutyrate-dominated ketoacidosis 5.
Hypoglycemia results from depleted hepatic glycogen stores, impaired gluconeogenesis from alcohol's metabolic effects, and starvation 4.
Volume depletion from vomiting (evidenced by BUN 40, creatinine 1.8, tachycardia 118, hypotension 92/64) exacerbates the metabolic derangement 6, 7.
Why Other Options Are Incorrect
Metabolism of formaldehyde into formic acid (methanol toxicity):
- Would present with osmolar gap, which is explicitly absent 1
- Typically causes visual disturbances and retinal toxicity, not mentioned here
- Blood ethanol of 10 mg/dL would provide some competitive inhibition, making severe methanol toxicity less likely
Oxidative metabolism of ethylene glycol to glycolic acid:
- Would show oxalate crystals in urine, which are explicitly negative 1
- Would present with osmolar gap, which is absent 1
- Typically causes acute kidney injury with calcium oxalate crystalluria
SIADH (syndrome of inappropriate antidiuretic hormone release):
- Does not cause high anion gap metabolic acidosis or ketosis 1
- Hyponatremia (127) could suggest SIADH, but this is more likely from volume depletion and vomiting
- Would not explain the severe acidosis (pH 7.1, bicarbonate 7) or ketones of 5.5
Critical Management Approach
Immediate treatment priorities for AKA:
Aggressive fluid resuscitation with isotonic saline to restore intravascular volume and renal perfusion 1, 5. Start with 15-20 mL/kg/hr (1-1.5 L in first hour) 1.
Intravenous dextrose administration stops ketogenesis rapidly by suppressing lipolysis and providing substrate for metabolism 6, 5, 7. Use D5W or D10W once initial volume resuscitation is underway.
Thiamine 100 mg IV before glucose to prevent Wernicke encephalopathy in this malnourished chronic alcoholic 3.
Potassium repletion will be necessary as acidosis corrects and potassium shifts intracellularly; current K of 3.0 indicates total body depletion 1.
Bicarbonate is NOT indicated despite severe acidosis (pH 7.1), as the ketoacidosis resolves rapidly with glucose and fluids 1, 5. The FDA label for bicarbonate mentions its use in "severe diabetic acidosis," but AKA responds so rapidly to glucose that bicarbonate risks overshoot alkalosis 8, 5.
Common Pitfalls to Avoid
Do not confuse AKA with diabetic ketoacidosis:
- AKA presents with hypoglycemia or mild hyperglycemia (rarely >250 mg/dL), while DKA requires glucose >250 mg/dL 1, 2
- Insulin is NOT indicated in AKA and could worsen hypoglycemia 5
Do not delay glucose administration:
- The metabolic disorder responds rapidly to IV glucose, which is the definitive treatment 6, 5, 7
- Waiting for laboratory confirmation of ketone levels delays appropriate therapy
Do not overlook concurrent illness:
- Search aggressively for precipitating factors (infection, pancreatitis, GI bleeding) as these determine prognosis, not the ketoacidosis itself 1, 6, 7
- The elevated lactate (8) may indicate concurrent lactic acidosis from hypoperfusion or sepsis 1
Monitor for electrolyte shifts during treatment: