Starvation ketoacidosis: Difference between revisions
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==Background== | ==Background== | ||
*Etiology: prolonged fasting, eating disorders, severely calorie-restricted diets, restricted access to food | |||
*Low insulin/high glucagon in fasting state leads to increased lipolysis. Fatty acids initially converted to acety-CoA, which is then oxidized by the Kreb cycle. | |||
*When Kreb's cycle oversaturated by excessive adipose breakdown, acetyl-CoA enters ketogenic pathway, resulting in ketone body production | |||
Mild ketosis (1mmol/L) | *Mild ketosis (1mmol/L) occurs after fasting for ~12 to 14 hours. | ||
*Ketoacidosis rises with continued fasting, peaks after 20 to 30 days (8-10mmol/L). | |||
==Clinical Features== | ==Clinical Features== | ||
*Nausea | *[[Nausea/vomiting]] | ||
*Abdominal pain | *[[Abdominal pain]] | ||
*Dehydration | *[[Dehydration]] | ||
*Altered mental status | *[[Altered mental status]] | ||
*Fatigue | *Fatigue | ||
*Kussmaul breathing | *[[Tachypnea]], Kussmaul breathing | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
*Diabetic ketoacidosis | *[[Diabetic ketoacidosis]] | ||
*Alcoholic ketoacidosis | *[[Alcoholic ketoacidosis]] | ||
*Lactic acidosis | *[[Lactic acidosis]] | ||
*Toxic | *[[Toxic alcohols]] (methanol or ethylene glycol) ingestion | ||
* | *[[Uremia]] | ||
* | *[[Salicylate toxicity]] | ||
*[[Sepsis]] | |||
==Evaluation== | ==Evaluation== | ||
*Serum chemistry (elevated anion gap) | *Serum chemistry (elevated anion gap) | ||
*VBG | |||
*Glucose (usually euglycemic or hypoglycemic) | *Glucose (usually euglycemic or hypoglycemic) | ||
*Urinalysis (ketonuria) | *[[Urinalysis]] (ketonuria) | ||
*Serum beta-hydroxybutyrate | *Serum beta-hydroxybutyrate | ||
*Lactate | *Lactate | ||
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==Management== | ==Management== | ||
*[[Dextrose]] | |||
*Dextrose | **Resultant increased insulin/decreased glucagon secretion to halt ketone production and facilitate ketone metabolism | ||
** | **Correct hypokalemia PRIOR to glucose administration (insulin stimulated by dextrose will drive K+ into cells and worsen hypokalemia) | ||
** | *Volume resuscitation with [[Normal saline]] or lactated ringers | ||
*Correct any concomitant [[electrolyte abnormalities]] | |||
*Consider risk of [[refeeding syndrome]] | |||
==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 | *If severe, admit | ||
==See Also== | ==See Also== | ||
*[[Alcoholic ketoacidosis]] | |||
*[[Diabetic ketoacidosis]] | |||
==External Links== | ==External Links== | ||
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<references/> | <references/> | ||
[[Category:Endocrinology]] | |||
[[Category:FEN]] | |||
Latest revision as of 00:58, 27 January 2019
Background
- Etiology: prolonged fasting, eating disorders, severely calorie-restricted diets, restricted access to food
- Low insulin/high glucagon in fasting state leads to increased lipolysis. Fatty acids initially converted to acety-CoA, which is then oxidized by the Kreb cycle.
- When Kreb's cycle oversaturated by excessive adipose breakdown, acetyl-CoA enters ketogenic pathway, resulting in ketone body production
- Mild ketosis (1mmol/L) occurs after fasting for ~12 to 14 hours.
- Ketoacidosis rises with continued fasting, peaks after 20 to 30 days (8-10mmol/L).
Clinical Features
- Nausea/vomiting
- Abdominal pain
- Dehydration
- Altered mental status
- Fatigue
- Tachypnea, Kussmaul breathing
Differential Diagnosis
- Diabetic ketoacidosis
- Alcoholic ketoacidosis
- Lactic acidosis
- Toxic alcohols (methanol or ethylene glycol) ingestion
- Uremia
- Salicylate toxicity
- Sepsis
Evaluation
- Serum chemistry (elevated anion gap)
- VBG
- 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
- Resultant increased insulin/decreased glucagon secretion to halt ketone production and facilitate ketone metabolism
- Correct hypokalemia PRIOR to glucose administration (insulin stimulated by dextrose will drive K+ into cells and worsen hypokalemia)
- Volume resuscitation with Normal saline or lactated ringers
- Correct any concomitant electrolyte abnormalities
- Consider risk of refeeding syndrome
Disposition
- If mild, can be discharged after correction of acidosis, electrolytes, and hypovolemia
- If severe, admit