Starvation ketoacidosis: Difference between revisions

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

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

External Links

References

Authors:

@@ Line 1: / Line 1: @@
 ==Background==
+*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.
+*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) 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) occurs  after fasting for ~12 to 14 hours.
+*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==
-Nausea and vomiting
+*[[Nausea/vomiting]]
-Abdominal pain
+*[[Abdominal pain]]
-Dehydration
+*[[Dehydration]]
-Altered mental status
+*[[Altered mental status]]
-Fatigue
+*Fatigue
-Kussmaul breathing
+*[[Tachypnea]], Kussmaul breathing
 ==Differential Diagnosis==
-Diabetic ketoacidosis
+*[[Diabetic ketoacidosis]]
-Alcoholic ketoacidosis
+*[[Alcoholic ketoacidosis]]
-Lactic acidosis
+*[[Lactic acidosis]]
-Toxic alcohol (methanol or ethylene glycol) ingestion
+*[[Toxic alcohols]] (methanol or ethylene glycol) ingestion
-Uremic acidosis
+*[[Uremia]]
-Aspirin toxicity
+*[[Salicylate toxicity]]
+*[[Sepsis]]
 ==Evaluation==
-Serum chemistry (elevated anion gap)
+*Serum chemistry (elevated anion gap)
-Glucose (usually euglycemic or hypoglycemic)
+*VBG
-Urinalysis (ketonuria)
+*Glucose (usually euglycemic or hypoglycemic)
-Serum beta-hydroxybutyrate
+*[[Urinalysis]] (ketonuria)
-Lactate
+*Serum beta-hydroxybutyrate
-Salicylate level (if overdose suspected)
+*Lactate
-Serum osmolality (if toxic alcohol ingestion suspected)
+*Salicylate level (if overdose suspected)
+*Serum osmolality (if toxic alcohol ingestion suspected)
 ==Management==
-Dextrose and saline solutions
+*[[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)
+**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)
+**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
+*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)
+*Correct any concomitant [[electrolyte abnormalities]]
+*Consider risk of [[refeeding syndrome]]
 ==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
+*If severe, admit
 ==See Also==
+*[[Alcoholic ketoacidosis]]
+*[[Diabetic ketoacidosis]]
 ==External Links==
@@ Line 52: / Line 55: @@
 <references/>
-https://www.uptodate.com/contents/fasting-ketosis-and-alcoholic-ketoacidosis/abstract/4
+[[Category:Endocrinology]]
+[[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.