Starvation ketoacidosis - Revision history

ClaireLewis at 00:58, 27 January 2019

2019-01-27T00:58:01Z

← Older revision		Revision as of 00:58, 27 January 2019
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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.~~		*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.
	*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 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==		==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==		==Differential Diagnosis==
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	*[[Alcoholic ketoacidosis]]		*[[Alcoholic ketoacidosis]]
	*[[Lactic acidosis]]		*[[Lactic acidosis]]
	*[[Toxic ~~alcohol~~]] (methanol or ethylene glycol) ingestion		*[[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)
			*VBG
	*Glucose (usually euglycemic or hypoglycemic)		*Glucose (usually euglycemic or hypoglycemic)
	*[[Urinalysis]] (ketonuria)		*[[Urinalysis]] (ketonuria)
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	==Management==		==Management==
	~~Dextrose and saline solutions~~		*[[Dextrose]]
	*Dextrose		**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		**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~~		*Volume resuscitation with [[Normal saline]] or lactated ringers
	*Saline or lactated ringer		*Correct any concomitant [[electrolyte abnormalities]]
	**Will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis)		*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~~		*If severe, admit

	==See Also==		==See Also==

Rossdonaldson1: Text replacement - "Urinalysis" to "Urinalysis"

2018-10-21T01:05:47Z

Text replacement - "*Urinalysis" to "*Urinalysis"

← Older revision		Revision as of 01:05, 21 October 2018
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	*Serum chemistry (elevated anion gap)		*Serum chemistry (elevated anion gap)
	*Glucose (usually euglycemic or hypoglycemic)		*Glucose (usually euglycemic or hypoglycemic)
	*Urinalysis (ketonuria)		*[[Urinalysis]] (ketonuria)
	*Serum beta-hydroxybutyrate		*Serum beta-hydroxybutyrate
	*Lactate		*Lactate

Mholtz at 23:26, 6 October 2017

2017-10-06T23:26:41Z

← Older revision		Revision as of 23:26, 6 October 2017
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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.		*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.
	~~<big>'''Pathogenesis'''</big>~~		*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/>

			[[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.~~		[[Category:FEN]]

Hirokoa33: /* Differential Diagnosis */

2017-10-06T23:04:10Z

Differential Diagnosis

← Older revision		Revision as of 23:04, 6 October 2017
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	*[[Alcoholic ketoacidosis]]		*[[Alcoholic ketoacidosis]]
	*[[Lactic acidosis]]		*[[Lactic acidosis]]
	*Toxic alcohol (methanol or ethylene glycol) ingestion		*[[Toxic alcohol]] (methanol or ethylene glycol) ingestion
	*~~Uremic acidosis~~		*[[Uremia]]
	*[[Salicylate toxicity]]		*[[Salicylate toxicity]]
	*[[Sepsis]]		*[[Sepsis]]

Hirokoa33 at 23:03, 6 October 2017

2017-10-06T23:03:05Z

← Older revision		Revision as of 23:03, 6 October 2017
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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.		Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis.

	'''Pathogenesis'''		<big>'''Pathogenesis'''</big>

	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).		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==

Hirokoa33 at 23:02, 6 October 2017

2017-10-06T23:02:29Z

← Older revision		Revision as of 23:02, 6 October 2017
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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.

	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.		'''Pathogenesis'''

	~~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.

	~~Eating disorders~~, ~~prolonged~~ fasting~~, severely calorie-restricted diets, restricted access~~ to ~~food~~ (~~low socioeconomic and elderly patients~~) ~~may be causes of starvation ketoacidosis~~.		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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	*Toxic alcohol (methanol or ethylene glycol) ingestion		*Toxic alcohol (methanol or ethylene glycol) ingestion
	*Uremic acidosis		*Uremic acidosis
	*[[~~Aspirin~~ toxicity]]		*[[Salicylate toxicity]]
			*[[Sepsis]]

	==Evaluation==		==Evaluation==

Hirokoa33 at 22:58, 6 October 2017

2017-10-06T22:58:58Z

← Older revision		Revision as of 22:58, 6 October 2017
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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		*[[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.

Hirokoa33 at 22:53, 6 October 2017

2017-10-06T22:53:31Z

← Older revision		Revision as of 22:53, 6 October 2017
Line 8:		Line 8:

	==Clinical Features==		==Clinical Features==
	Nausea and vomiting		*Nausea and vomiting
	Abdominal pain		*Abdominal pain
	Dehydration		*Dehydration
	Altered mental status		*Altered mental status
	Fatigue		*Fatigue
	Kussmaul breathing		*Kussmaul breathing

	==Differential Diagnosis==		==Differential Diagnosis==
	Diabetic ketoacidosis		*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==
	Serum chemistry (elevated anion gap)		*Serum chemistry (elevated anion gap)
	Glucose (usually euglycemic or hypoglycemic)		*Glucose (usually euglycemic or hypoglycemic)
	Urinalysis (ketonuria)		*Urinalysis (ketonuria)
	Serum beta-hydroxybutyrate		*Serum beta-hydroxybutyrate
	Lactate		*Lactate
	Salicylate level (if overdose suspected)		*Salicylate level (if overdose suspected)
	Serum osmolality (if toxic alcohol ingestion suspected)		*Serum osmolality (if toxic alcohol ingestion suspected)

	==Management==		==Management==
	Dextrose and saline solutions		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)		*Dextrose
	Saline~~- will~~ provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis)		**Will cause increase in insulin and decrease in glucagon secretion, which will reduce ketone production and increase ketone metabolism
	Rate of infusion dependent on volume status		**Beta-hydroxybutyrate and acetoacetate will regenerate bicarbonate, causing partial correction of metabolic acidosis
	If hypokalemic, need to correct before administering glucose (as glucose stimulates insulin production which will drive K into cells and worsen hypokalemia)		*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==		==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 for close monitoring

	==See Also==		==See Also==

Hirokoa33: 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..."

2017-10-06T22:47:43Z

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..."

New page

==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). The main ketone body that accumulates in beta-hydroxybutyrate.

Eating disorders, prolonged fasting, severely calorie-restricted diet, restricted access to food (low socioeconomic and elderly patients)

==Clinical Features==
Nausea and vomiting
Abdominal pain
Dehydration
Altered mental status
Fatigue
Kussmaul breathing

==Differential Diagnosis==
Diabetic ketoacidosis
Alcoholic ketoacidosis
Lactic acidosis
Toxic alcohol (methanol or ethylene glycol) ingestion
Uremic acidosis
Aspirin toxicity

==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- will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis)
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==
<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.