Basics
Description
- Increased production of ketone bodies due to:
- Dehydration (nausea/vomiting, ADH inhibition) leads to increased stress hormone production leading to ketone formation
- Depleted glycogen stores in the liver (malnutrition/decrease carbohydrate intake)
- Elevated ratio of NADH/NAD due to ethanol metabolism
- Increased free fatty acid production
- Elevated NADH/NAD ratio leads to the predominate production of β-hydroxybutyrate (BHB) over acetoacetate (AcAc)
Etiology
- Malnourished, chronic alcohol abusers following a recent episode of heavy alcohol consumption:
- Develop nausea, vomiting, or abdominal pain
- Leading to the cessation of alcohol ingestion
- Presentation usually occurs within 12-72 hr
Diagnosis
Signs and Symptoms
- Dehydration
- Fever absent unless there is an underlying infection
- Tachycardia (common) due to:
- Dehydration with associated orthostatic changes
- Concurrent alcohol withdrawal
- Tachypnea:
- Common
- Deep, rapid, Kussmaul respirations frequently present
- Nausea and vomiting
- Abdominal pain (nausea, vomiting, and abdominal pain are the most common symptoms):
- Usually diffuse with nonspecific tenderness
- Epigastric pain common
- Rebound tenderness, abdominal distension, hypoactive bowel sounds uncommon
- Mandates a search for an alternative, coexistent illness
- Decreased urinary output from hypovolemia
- Mental status:
- Minimally altered as a result of hypovolemia and possibly intoxication
- Altered mental status mandates a search for other associated conditions such as:
- Head injury, cerebrovascular accident (CVA), or intracranial hemorrhage
- Hypoglycemia
- Alcohol withdrawal
- Encephalopathy
- Toxins
- Visual disturbances:
- Reports of isolated visual disturbances with AKA common
History
Chronic alcohol use:
- Recent binge
- Abrupt cessation
Physical Exam
- Findings of dehydration most common
- May have ketotic odor
- Kussmaul respirations
- Palmar erythema (alcoholism)
Essential Workup
- Presence of an increased anion gap metabolic acidosis secondary to the presence of ketones
- Differentiate from toxic alcohol ingestion and other causes of anion gap metabolic acidosis.
Diagnosis Tests & Interpretation
Lab
- Acid-base disturbance:
- Increased anion gap metabolic acidosis hallmark
- Mixed acid-base disturbance common:
- Respiratory alkalosis
- Metabolic alkalosis secondary to vomiting and dehydration
- Hyperchloremic acidosis
- Mild lactic acidosis common
- Due to dehydration and the direct metabolic effects of ethanol
- Profound lactic acidosis should prompt a search for other disorders such as seizures, hypoxia, and shock.
- Positive urine and serum nitroprusside reaction tests for ketoacids
- May not reflect the severity of the underlying ketoacidosis, since BHB predominates and is not measured by this test.
- May become misleadingly more positive during treatment as more AcAc is produced.
- Electrolytes:
- Decreased serum bicarbonate
- Hypokalemia due to vomiting
- Hypocalcemia
- Hypophosphatemia may worsen with Tx
- Hypomagnesemia
- Initially, can see hyperkalemia and/or hyperphosphatemia which will correct with treatment of the acidosis
- Glucose:
- Usually mildly elevated
- Should be monitored frequently as per DKA
- Hypoglycemia may be present
- Alcohol level may be negative
- BUN and creatinine mildly elevated due to dehydration unless underlying renal disease.
- CBC:
- Mild leukocytosis-neither sensitive nor specific
- Thrombocytopenia and anemia commonly due to chronic alcoholism
- Urinalysis:
- Ketonuria without glucosuria
- Amylase/lipase:
- Elevated with associated pancreatitis
- LFTs:
- May have mildly elevated LFTs
- Osmolal gap:
- May be elevated
- Elevation >20 mOsm/kg should prompt evaluation for other ingestions (methanol and ethylene glycol)
- Correct for ethanol level in osmolal gap by dividing ethanol level by 4.6
Imaging
- CXR if suspect associated pneumonia
- Abdominal films for free air if an acute abdomen is present
- CT scan of the head if associated trauma or unexplained altered mental status
Differential Diagnosis
- Elevated anion gap metabolic acidosis: ACAAT MUDPILES:
- Alcoholic ketoacidosis
- Cyanide, CO, H2S, others
- Acetaminophen:
- Rare in acute ingestion
- Rare in chronic ingestion
- Fulminant hepatic failure
- Antiretrovirals (NRTI)
- Toluene
- Methanol, metformin
- Uremia
- Diabetic ketoacidosis
- Paraldehyde, phenformin, propylene glycol
- Iron, INH
- Lactic acidosis
- Ethylene glycol
- Salicylate, acetylsalicylic acid (ASA; aspirin), starvation ketosis
- Hypovolemia:
- Abdominal pain, nausea, vomiting:
- Pancreatitis
- GI bleeding
- Gastritis
- Hepatitis
- Perforated ulcer
- Alcohol withdrawal
- DKA
- Viral illness
- Obstruction/Ileus
Treatment
Pre-Hospital
- Supportive measures including IV access with 0.9 NS, oxygen, and cardiac monitoring
- Search for historical clues that may suggest other etiologies such as toxic ingestions or diabetic history, consider scene search
- Attend to other possible coexistent illnesses such as GI bleeding.
Initial Stabilization/Therapy
- Cardiac monitor and supplement oxygen
- Naloxone, thiamine, and dextrose if altered mental status
- Initiate 0.9 NS IV fluids
- 500 mL-1 L bolus
- Fluid resuscitation as necessary
- Promotes renal excretion of ketone bodies
Ed Treatment/Procedures
- Antiemetic for vomiting-ondansetron, promethazine, or prochlorperazine
- Benzodiazepines for symptoms of alcohol withdrawal
- Start dextrose containing solutions (D5NS):
- More rapid resolution of the metabolic abnormalities than saline alone
- Rate higher than maintenance as tolerated until acidosis resolves
- Avoid with significant hyperglycemia
- Help replete glycogen stores
- Decreases production of ketone bodies by stimulating the production of endogenous insulin
- Thiamine repletion (IV) prior to glucose administration to avoid precipitating Wernicke encephalopathy
- Sodium bicarbonate rarely indicated:
- Consider in severe acidosis with associated cardiovascular dysfunction or irritability
- Electrolyte replacement:
- Hypokalemia occurs with treatment and should be anticipated.
- Hypophosphatemia may occur with treatment.
- Magnesium replacement as indicated for both hypomagnesemia and hypokalemia
- Insulin is not indicated and may precipitate hypoglycemia.
Medication
- D50W: 1 ampule of 50% dextrose (25 g) IVP
- Lorazepam (benzodiazepine): 2 mg IV and titrate to effect
- Narcan: 2 mg IVP
- Ondansetron: 4-8 mg IVP
- Prochlorperazine: 5-10 mg IVP slowly (not >5 mg/min)
- Promethazine: 12.5-25 mg IVP
- Thiamine: 100 mg IVP
Follow-Up
Disposition
Admission Criteria
- Persistent metabolic acidosis
- Persistent signs of hypovolemia
- Persistent nausea and vomiting
- Abdominal pain of uncertain etiology
- Comorbid illness requiring admission for treatment
- Need for monitored bed due to electrolyte abnormalities requiring continued treatment
Discharge Criteria
- Many patients can be managed in observation unit over 12-24 hr.
- Tolerating oral fluids well
- Resolution of metabolic abnormalities
- No other associated illnesses requiring additional therapy
- Most will warrant at least observation
Followup Recommendations
Counseling regarding alcohol cessation
Pearls and Pitfalls
- Aggressive volume repletion with dextrose containing fluid is key.
- Volume resuscitate with NS as necessary
- Thiamine repletion
- Monitor electrolytes before and after treatment.
- Unrecognized increased osmolal gap
- Inadequate monitoring of glucose levels
- Failure to recognize initial electrolyte abnormalities and electrolyte shifts caused by treatment.
- Must be placed on monitor:
- Cases of sudden death in AKA:
- Possible alcoholic cardiomyopathy
- Dysrhythmias
- Electrolyte derangements
Additional Reading
- Cartwright MM, Hajja W, Al-Khatib S, et al. Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes. Crit Care Clin. 2012;28(4): 601-631.
- Diltoer M, Troubleyn J, Lauwers R, et al. Ketosis and cardiac failure: Common signs of a single condition. Eur J Emerg Med. 2004;11(3):172-175.
- McGuire L, Cruickshank A, Munro P. Alcoholic ketoacidosis. Emerg Med J. 2006;23:417-420.
- Yanagawa Y, Kiyozumi T, Hatanaka K, et al. Reversible blindness associated with alcoholic ketoacidosis. Am J Opthalmology. 2004;137(4):775-777.
- Yanagawa Y, Sakamoto T, Okada Y. Six cases of sudden cardiac arrest in alcoholic ketoacidosis. Intern Med. 2008;47(2):113-117.
See Also (Topic, Algorithm, Electronic Media Element)
- Acidosis
- Diabetic Ketoacidosis
Codes
ICD9
276.2 Acidosis
ICD10
E87.2 Acidosis
SNOMED
- 55571001 alcoholic ketoacidosis (disorder)