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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*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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*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.  
<big>'''Pathogenesis'''</big>
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*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).  
 
 
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).  
 
  
 
==Clinical Features==
 
==Clinical Features==
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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]]

Revision as of 23:26, 6 October 2017

Background

  • Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis.
  • 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).

Clinical Features

  • Nausea and vomiting
  • Abdominal pain
  • Dehydration
  • Altered mental status
  • Fatigue
  • Kussmaul breathing

Differential Diagnosis

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