Starvation ketoacidosis: Difference between revisions
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==Clinical Features== | ==Clinical Features== | ||
Nausea and vomiting | *Nausea and vomiting | ||
Abdominal pain | *Abdominal pain | ||
Dehydration | *Dehydration | ||
Altered mental status | *Altered mental status | ||
Fatigue | *Fatigue | ||
Kussmaul breathing | *Kussmaul breathing | ||
==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== | ||
Serum chemistry (elevated anion gap) | *Serum chemistry (elevated anion gap) | ||
Glucose (usually euglycemic or hypoglycemic) | *Glucose (usually euglycemic or hypoglycemic) | ||
Urinalysis (ketonuria) | *Urinalysis (ketonuria) | ||
Serum beta-hydroxybutyrate | *Serum beta-hydroxybutyrate | ||
Lactate | *Lactate | ||
Salicylate level (if overdose suspected) | *Salicylate level (if overdose suspected) | ||
Serum osmolality (if toxic alcohol ingestion suspected) | *Serum osmolality (if toxic alcohol ingestion suspected) | ||
==Management== | ==Management== | ||
Dextrose and saline solutions | Dextrose and saline solutions | ||
Dextrose | *Dextrose | ||
Saline | **Will cause increase in insulin and decrease in glucagon secretion, which will reduce ketone production and increase ketone metabolism | ||
Rate of infusion dependent on volume status | **Beta-hydroxybutyrate and acetoacetate will regenerate bicarbonate, causing partial correction of metabolic acidosis | ||
If hypokalemic, need to correct before administering glucose (as glucose stimulates insulin production which will drive K into cells and worsen hypokalemia) | *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== | ==Disposition== | ||
If mild, can be discharged after correction of acidosis, electrolytes, and hypovolemia | *If mild, can be discharged after correction of acidosis, electrolytes, and hypovolemia | ||
If severe, admit for close monitoring | *If severe, admit for close monitoring | ||
==See Also== | ==See Also== | ||
Revision as of 22:53, 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). 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
See Also
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.