Difference between revisions of "Starvation ketoacidosis"

(Differential Diagnosis)
 
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==Background==
 
==Background==
Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis.
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*Etiology: prolonged fasting, eating disorders, severely calorie-restricted diets, restricted access to food
 
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*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.
<big>'''Pathogenesis'''</big>
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*When Kreb's cycle oversaturated by excessive adipose breakdown, acetyl-CoA enters ketogenic pathway, resulting in ketone body production
 
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*Mild ketosis (1mmol/L) occurs  after fasting for ~12 to 14 hours.  
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.
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*Ketoacidosis rises with continued fasting, peaks 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).  
 
  
 
==Clinical Features==
 
==Clinical Features==
*Nausea and vomiting
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*[[Nausea/vomiting]]
*Abdominal pain
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*[[Abdominal pain]]
*Dehydration
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*[[Dehydration]]
*Altered mental status
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*[[Altered mental status]]
 
*Fatigue
 
*Fatigue
*Kussmaul breathing
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*[[Tachypnea]], Kussmaul breathing
  
 
==Differential Diagnosis==
 
==Differential Diagnosis==
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*[[Alcoholic ketoacidosis]]
 
*[[Alcoholic ketoacidosis]]
 
*[[Lactic acidosis]]
 
*[[Lactic acidosis]]
*[[Toxic alcohol]] (methanol or ethylene glycol) ingestion
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*[[Toxic alcohols]] (methanol or ethylene glycol) ingestion
 
*[[Uremia]]
 
*[[Uremia]]
 
*[[Salicylate toxicity]]
 
*[[Salicylate toxicity]]
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==Evaluation==
 
==Evaluation==
 
*Serum chemistry (elevated anion gap)
 
*Serum chemistry (elevated anion gap)
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*VBG
 
*Glucose (usually euglycemic or hypoglycemic)
 
*Glucose (usually euglycemic or hypoglycemic)
*Urinalysis (ketonuria)
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*[[Urinalysis]] (ketonuria)
 
*Serum beta-hydroxybutyrate
 
*Serum beta-hydroxybutyrate
 
*Lactate
 
*Lactate
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==Management==
 
==Management==
Dextrose and saline solutions
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*[[Dextrose]]
*Dextrose
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**Resultant increased insulin/decreased glucagon secretion to halt ketone production and facilitate ketone metabolism  
**Will cause increase in insulin and decrease in glucagon secretion, which will reduce ketone production and increase ketone metabolism
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**Correct hypokalemia PRIOR to glucose administration (insulin stimulated by dextrose will drive K+ into cells and worsen hypokalemia)
**Beta-hydroxybutyrate and acetoacetate will regenerate bicarbonate, causing partial correction of metabolic acidosis
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*Volume resuscitation with [[Normal saline]] or lactated ringers
*Saline or lactated ringer
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*Correct any concomitant [[electrolyte abnormalities]]
**Will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis)
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*Consider risk of [[refeeding syndrome]]
 
 
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
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*If severe, admit  
  
 
==See Also==
 
==See Also==
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<references/>
 
<references/>
  
 
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[[Category:Endocrinology]]
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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[[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

Differential Diagnosis

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

See Also

External Links

References