Starvation ketoacidosis
Background
- Etiology: prolonged fasting, eating disorders, severely calorie-restricted diets, restricted access to food
- Low insulin/high glucagon in fasting state leads to increased lipolysis. Fatty acids initially converted to acety-CoA, which is then oxidized by the Kreb cycle.
- When Kreb's cycle oversaturated by excessive adipose breakdown, acetyl-CoA enters ketogenic pathway, resulting in ketone body production
- Mild ketosis (1mmol/L) occurs after fasting for ~12 to 14 hours.
- Ketoacidosis rises with continued fasting, peaks after 20 to 30 days (8-10mmol/L).
Clinical Features
- Nausea/vomiting
- Abdominal pain
- Dehydration
- Altered mental status
- Fatigue
- Tachypnea, Kussmaul breathing
Differential Diagnosis
- Diabetic ketoacidosis
- Alcoholic ketoacidosis
- Lactic acidosis
- Toxic alcohols (methanol or ethylene glycol) ingestion
- Uremia
- Salicylate toxicity
- Sepsis
Evaluation
- Serum chemistry (elevated anion gap)
- VBG
- Glucose (usually euglycemic or hypoglycemic)
- Urinalysis (ketonuria)
- Serum beta-hydroxybutyrate
- Lactate
- Salicylate level (if overdose suspected)
- Serum osmolality (if toxic alcohol ingestion suspected)
Management
- Dextrose
- Resultant increased insulin/decreased glucagon secretion to halt ketone production and facilitate ketone metabolism
- Correct hypokalemia PRIOR to glucose administration (insulin stimulated by dextrose will drive K+ into cells and worsen hypokalemia)
- Volume resuscitation with Normal saline or lactated ringers
- Correct any concomitant electrolyte abnormalities
- Consider risk of refeeding syndrome
Disposition
- If mild, can be discharged after correction of acidosis, electrolytes, and hypovolemia
- If severe, admit
External Links
References
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