Difference between revisions of "Starvation ketoacidosis"

(Created page with "==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...")
 
 
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==Background==
 
==Background==
 
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*Etiology: prolonged fasting, eating disorders, severely calorie-restricted diets, restricted access to food
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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*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.
 
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*When Kreb's cycle oversaturated by excessive adipose breakdown, acetyl-CoA enters ketogenic pathway, resulting in ketone body production
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.
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*Mild ketosis (1mmol/L) occurs  after fasting for ~12 to 14 hours.  
 
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*Ketoacidosis rises with continued fasting, peaks after 20 to 30 days (8-10mmol/L).  
Eating disorders, prolonged fasting, severely calorie-restricted diet, restricted access to food (low socioeconomic and elderly patients)
 
  
 
==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
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*Fatigue
Kussmaul breathing
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*[[Tachypnea]], Kussmaul breathing
  
 
==Differential Diagnosis==
 
==Differential Diagnosis==
Diabetic ketoacidosis
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*[[Diabetic ketoacidosis]]
Alcoholic ketoacidosis
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*[[Alcoholic ketoacidosis]]
Lactic acidosis
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*[[Lactic acidosis]]
Toxic alcohol (methanol or ethylene glycol) ingestion
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*[[Toxic alcohols]] (methanol or ethylene glycol) ingestion
Uremic acidosis
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*[[Uremia]]
Aspirin toxicity
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*[[Salicylate toxicity]]
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*[[Sepsis]]
  
 
==Evaluation==
 
==Evaluation==
Serum chemistry (elevated anion gap)
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*Serum chemistry (elevated anion gap)
Glucose (usually euglycemic or hypoglycemic)
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*VBG
Urinalysis (ketonuria)
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*Glucose (usually euglycemic or hypoglycemic)
Serum beta-hydroxybutyrate
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*[[Urinalysis]] (ketonuria)
Lactate
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*Serum beta-hydroxybutyrate
Salicylate level (if overdose suspected)
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*Lactate
Serum osmolality (if toxic alcohol ingestion suspected)
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*Salicylate level (if overdose suspected)
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*Serum osmolality (if toxic alcohol ingestion suspected)
  
 
==Management==
 
==Management==
Dextrose and saline solutions
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*[[Dextrose]]
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)
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**Resultant increased insulin/decreased glucagon secretion to halt ketone production and facilitate ketone metabolism  
Saline- will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis)
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**Correct hypokalemia PRIOR to glucose administration (insulin stimulated by dextrose will drive K+ into cells and worsen hypokalemia)
Rate of infusion dependent on volume status
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*Volume resuscitation with [[Normal saline]] or lactated ringers
If hypokalemic, need to correct before administering glucose (as glucose stimulates insulin production which will drive K into cells and worsen hypokalemia)
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*Correct any concomitant [[electrolyte abnormalities]]
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*Consider risk of [[refeeding syndrome]]
  
 
==Disposition==
 
==Disposition==
If mild, can be discharged after correction of acidosis, electrolytes, and hypovolemia
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*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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*[[Alcoholic ketoacidosis]]
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*[[Diabetic ketoacidosis]]
  
 
==External Links==
 
==External Links==
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<references/>
 
<references/>
  
https://www.uptodate.com/contents/fasting-ketosis-and-alcoholic-ketoacidosis/abstract/4
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[[Category:Endocrinology]]
 
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[[Category:FEN]]
Owen OE, Caprio S, Reichard GA Jr, et al. Ketosis of starvation: a revisit and new perspectives. Clin Endocrinol Metab 1983; 12:359.
 

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