Starvation ketoacidosis

Background

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). The main ketone body that accumulates in beta-hydroxybutyrate.

Eating disorders, prolonged fasting, severely calorie-restricted diet, restricted access to food (low socioeconomic and elderly patients)

Clinical Features

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

Differential Diagnosis

Diabetic ketoacidosis
Alcoholic ketoacidosis
Lactic acidosis
Toxic alcohol (methanol or ethylene glycol) ingestion
Uremic acidosis
Aspirin toxicity

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

External Links

References

https://www.uptodate.com/contents/fasting-ketosis-and-alcoholic-ketoacidosis/abstract/4

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

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