CD
Alcoholic Ketoacidosis
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Alcoholic Ketoacidosis
See Also
Starvation Ketosis
Ketoacidosis
Alcohol Intoxication
Alcohol Toxicity
Alcohol Withdrawal
Alcohol Detoxification
Chemical Dependency
Pathophysiology
See
Ketoacidosis
Develops in baseline chronic
Alcohol Abuse
and associated poor nutrition, in combination with an acute stressor
Identifying the acute stressor is key to effective management (see causes below)
Most common triggers are infection and
Pancreatitis
Causes
Intraabdominal Disorder
Cholecystitis
Appendicitis
Pancreatitis
Small Bowel Obstruction
Bowel
Perforation
Mesenteric Ischemia
Other
Alcohol
related disorder
Alcohol Withdrawal
Delirium Tremens
Other metabolic disorder
Diabetic Ketoacidosis
Rhabdomyolysis
Other Systemic Disorders
Hypothermia
Acute Coronary Syndrome
Pulmonary Embolism
Sepsis
Toxic Ingestion
Salicylate Toxicity
Toxic Alcohol
Ingestion (e.g.
Ethylene Glycol Poisoning
)
Symptoms
Nausea
Vomiting
Generalized Abdominal Pain
Signs
Red Flags
Significant intraabdominal findings suggest a possible underlying trigger (see causes above)
Peritoneal signs
Abnormal bowel sounds
Abdominal Distention
or significant tenderness
Significant
Altered Level of Consciousness
(expect only mild alteration in Alcoholic Ketoacidosis)
See
Altered Level of Consciousness
Consider
Unknown Ingestion
(coingestion)
Consider
Wernicke Encephalopathy
Toxic Alcohol
Ingestion (e.g.
Ethylene Glycol Poisoning
)
Consider in severe
Lactic Acidosis
,
Altered Mental Status
,
Osmolal Gap
Labs
Comprehensive Metabolic Panel
Increased
Anion Gap
Decreased serum bicarbonate
Serum Glucose
is typically low or normal (elevated in 10% of cases)
Other
Electrolyte
abnormalities may be present
Hyponatremia
Hypomagnesemia
Hypokalemia
Hypophosphatemia
Venous Blood Gas
Metabolic Acidosis
Mixed acid base findings are common (75% of cases)
Serum Ketone
s
Increased Beta Hydroxybutyrate in addition to other
Ketone
s
Ketone
s are elevated more than
Lactic Acid
in uncomplicated Alcoholic Ketoacidosis
Serum Lactate
Lactic Acid
is mildly elevated (rarely >4 mmol/L) in uncomplicated Alcoholic Ketoacidosis
Significantly increased (>4 mmol/L) in
Toxic Alcohol
ingestion (
Methanol
or
Ethylene Glycol Poisoning
)
Osmolar Gap
Consider
Toxic Alcohol
ingestion (
Methanol
or
Ethylene Glycol Poisoning
)
Serum
Alcohol
Level
Alcohol
level is independent to
Ketoacidosis
development (may be high or low)
Management
Similar to
Starvation Ketosis
Most common cause of
Metabolic Acidosis with Anion Gap
in
Alcohol
ics (poor nutrition)
However, exclude
Toxic Alcohol
ingestion (e.g.
Ethylene Glycol Poisoning
)
As with
Diabetic Ketoacidosis
,
Serum Beta Hydroxybutyrate
is increased
Urine Ketone
s are unreliable for detection
Administer IV fluids containing dextrose (e.g. D5LR)
Emergent correction of
Hypoglycemia
(
Serum Glucose
<60 mg/dl)
Give
Thiamine
100 mg before dextrose (
Wernicke Encephalopathy
)
Dextrose infusions stop
Ketone
formation, whereas simple crystalloid will not
However, assess
Potassium
and replace before significant dextrose aministered (
Hypokalemia
risk)
Anticipate
Ketone
clearance and acidosis resolution within 8 to 12 hours of starting fluid and dextrose infusion
Replace other
Electrolyte
s as needed
Potassium Replacement
Magnesium Replacement
Alcoholism Management
See
Alcoholism Management
See
Alcohol Dependence Management
See
Alcohol Withdrawal
See
Substance Addiction Aftercare
References
Long and Swaminathan in Swadron (2022) EM: Rap 22(9): 13-5
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