Starvation ketoacidosis

Revision as of 23:04, 6 October 2017 by Hirokoa33 (talk | contribs) (Differential Diagnosis)

Background

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

Pathogenesis

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

Evaluation

  • 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)

Management

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)

Considerations

  • 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)

Disposition

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

See Also

External Links

References


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