Difference between revisions of "Starvation ketoacidosis"

(Differential Diagnosis)
Line 20: Line 20:
*[[Alcoholic ketoacidosis]]
*[[Alcoholic ketoacidosis]]
*[[Lactic acidosis]]
*[[Lactic acidosis]]
*Toxic alcohol (methanol or ethylene glycol) ingestion
*[[Toxic alcohol]] (methanol or ethylene glycol) ingestion
*Uremic acidosis
*[[Salicylate toxicity]]
*[[Salicylate toxicity]]

Revision as of 23:04, 6 October 2017


Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis.


When insulin levels are low and glucagon levels are high (such as in a fasting state), long chain fatty acids and glycerol from triglycerides are released from peripheral fat stores and are transported to the liver. The fatty acids undergo beta-oxidation and generate acetyl-CoA. However, with excessive amounts of acetyl-CoA, the Krebs cycle may become oversaturated, and instead the acetyl-CoA enter the ketogenic pathway resulting in production of ketone bodies.

Mild ketosis (1mmol/L) results after fasting for approximately 12 to 14 hours. However, the ketoacid concentration rises with continued fasting and will peak after 20 to 30 days (8-10mmol/L).

Clinical Features

  • Nausea and vomiting
  • Abdominal pain
  • Dehydration
  • Altered mental status
  • Fatigue
  • Kussmaul breathing

Differential Diagnosis


  • Serum chemistry (elevated anion gap)
  • Glucose (usually euglycemic or hypoglycemic)
  • Urinalysis (ketonuria)
  • Serum beta-hydroxybutyrate
  • Lactate
  • Salicylate level (if overdose suspected)
  • Serum osmolality (if toxic alcohol ingestion suspected)


Dextrose and saline solutions

  • Dextrose
    • Will cause increase in insulin and decrease in glucagon secretion, which will reduce ketone production and increase ketone metabolism
    • Beta-hydroxybutyrate and acetoacetate will regenerate bicarbonate, causing partial correction of metabolic acidosis
  • Saline or lactated ringer
    • Will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis)


  • Rate of infusion dependent on volume status
  • If hypokalemic, need to correct before administering glucose (as glucose stimulates insulin production which will drive K into cells and worsen hypokalemia)


  • If mild, can be discharged after correction of acidosis, electrolytes, and hypovolemia
  • If severe, admit for close monitoring

See Also

External Links


Owen OE, Caprio S, Reichard GA Jr, et al. Ketosis of starvation: a revisit and new perspectives. Clin Endocrinol Metab 1983; 12:359.