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Alcoholic Ketoacidosis, Emergency Medicine

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

- Dehydration - Fever absent unless there is an underlying infection - Tachycardia (common) due to: - Dehydration with associated orthostatic changes - Concurrent alcohol withdrawal

- 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

- 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

- 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

- 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

- 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

- 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

- 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

- 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

  • Increased production of ketone bodies due to:Dehydration (nausea/vomiting, ADH inhibition) leads to increased stress hormone production leading to ketone formationDepleted glycogen stores in the liver (malnutrition/decrease carbohydrate intake)Elevated ratio of NADH/NAD due to ethanol metabolismIncreased 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 painLeading 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 changesConcurrent alcohol withdrawal
  • Tachypnea:CommonDeep, rapid, Kussmaul respirations frequently present
  • Nausea and vomiting
  • Abdominal pain (nausea, vomiting, and abdominal pain are the most common symptoms):Usually diffuse with nonspecific tendernessEpigastric pain commonRebound tenderness, abdominal distension, hypoactive bowel sounds uncommonMandates a search for an alternative, coexistent illness
  • Decreased urinary output from hypovolemia
  • Mental status:Minimally altered as a result of hypovolemia and possibly intoxicationAltered mental status mandates a search for other associated conditions such as:Head injury, cerebrovascular accident (CVA), or intracranial hemorrhageHypoglycemiaAlcohol withdrawalEncephalopathyToxins
  • 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 hallmarkMixed acid-base disturbance common:Respiratory alkalosisMetabolic alkalosis secondary to vomiting and dehydrationHyperchloremic acidosisMild lactic acidosis commonDue to dehydration and the direct metabolic effects of ethanolProfound lactic acidosis should prompt a search for other disorders such as seizures, hypoxia, and shock.Positive urine and serum nitroprusside reaction tests for ketoacidsMay 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 bicarbonateHypokalemia due to vomitingHypocalcemiaHypophosphatemia may worsen with TxHypomagnesemiaInitially, can see hyperkalemia and/or hyperphosphatemia which will correct with treatment of the acidosis
  • Glucose:Usually mildly elevatedShould be monitored frequently as per DKAHypoglycemia 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 specificThrombocytopenia 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 elevatedElevation >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 ketoacidosisCyanide, CO, H2S, othersAcetaminophen:Rare in acute ingestionRare in chronic ingestionFulminant hepatic failureAntiretrovirals (NRTI)TolueneMethanol, metforminUremiaDiabetic ketoacidosisParaldehyde, phenformin, propylene glycolIron, INHLactic acidosisEthylene glycolSalicylate, acetylsalicylic acid (ASA; aspirin), starvation ketosis
  • Hypovolemia:
  • Abdominal pain, nausea, vomiting:PancreatitisGI bleedingGastritisHepatitisPerforated ulcerAlcohol withdrawalDKAViral illnessObstruction/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 fluids500 mL-1 L bolusFluid resuscitation as necessaryPromotes 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 aloneRate higher than maintenance as tolerated until acidosis resolvesAvoid with significant hyperglycemiaHelp replete glycogen storesDecreases 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 cardiomyopathyDysrhythmiasElectrolyte 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)