Difference between revisions of "Starvation ketoacidosis"

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==Background==
 
==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.  
+
    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.  
+
    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).  
  
Eating disorders, prolonged fasting, severely calorie-restricted diet, restricted access to food (low socioeconomic and elderly patients)
+
    Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis.
  
 
==Clinical Features==
 
==Clinical Features==
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==Differential Diagnosis==
 
==Differential Diagnosis==
*Diabetic ketoacidosis
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*[[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==
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==See Also==
 
==See Also==
 
+
*[[Alcoholic ketoacidosis]]
 +
*[[Diabetic ketoacidosis]]
  
 
==External Links==
 
==External Links==
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<references/>
 
<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.
 
Owen OE, Caprio S, Reichard GA Jr, et al. Ketosis of starvation: a revisit and new perspectives. Clin Endocrinol Metab 1983; 12:359.

Revision as of 22:58, 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). 
   Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis.

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


Owen OE, Caprio S, Reichard GA Jr, et al. Ketosis of starvation: a revisit and new perspectives. Clin Endocrinol Metab 1983; 12:359.