Starvation ketoacidosis: Difference between revisions
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==Background== | ==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. | 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) | 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). | ||
Eating disorders, prolonged fasting, severely calorie-restricted | Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis. | ||
==Clinical Features== | ==Clinical Features== | ||
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==Differential Diagnosis== | ==Differential Diagnosis== | ||
*Diabetic ketoacidosis | *[[Diabetic ketoacidosis]] | ||
*Alcoholic ketoacidosis | *[[Alcoholic ketoacidosis]] | ||
*Lactic acidosis | *[[Lactic acidosis]] | ||
*Toxic alcohol (methanol or ethylene glycol) ingestion | *Toxic alcohol (methanol or ethylene glycol) ingestion | ||
*Uremic acidosis | *Uremic acidosis | ||
*Aspirin toxicity | *[[Aspirin toxicity]] | ||
==Evaluation== | ==Evaluation== | ||
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==See Also== | ==See Also== | ||
*[[Alcoholic ketoacidosis]] | |||
*[[Diabetic ketoacidosis]] | |||
==External Links== | ==External Links== | ||
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<references/> | <references/> | ||
Owen OE, Caprio S, Reichard GA Jr, et al. Ketosis of starvation: a revisit and new perspectives. Clin Endocrinol Metab 1983; 12:359. | Owen OE, Caprio S, Reichard GA Jr, et al. Ketosis of starvation: a revisit and new perspectives. Clin Endocrinol Metab 1983; 12:359. | ||
Revision as of 22:58, 6 October 2017
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).
Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis.
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
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.