Rosen & Barkin's 5-Minute Emergency Medicine Consult (41 page)

• Ethylene Glycol, Poisoning
  
• Methanol, Poisoning
  

CODES

• 303.00 Acute alcoholic intoxication in alcoholism, unspecified
  
• 305.00 Alcohol abuse, unspecified
  
• 980.0 Toxic effect of ethyl alcohol
  

BASICS

• 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)
  

• 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

• 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
    

Chronic alcohol use:

• Recent binge
  
• Abrupt cessation
  

• Findings of dehydration most common
  
• May have ketotic odor
  
• Kussmaul respirations
  
• Palmar erythema (alcoholism)
  

• 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.
  

• 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
    

• 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
  

• Elevated anion gap metabolic acidosis:
  ACAAT MUDPILES:
  
  • A
    lcoholic ketoacidosis
    
  • C
    yanide, CO, H
    ₂
    S, others
    
  • A
    cetaminophen:
    
    • Rare in acute ingestion
      
    • Rare in chronic ingestion
      
    • Fulminant hepatic failure
      
  • A
    ntiretrovirals (NRTI)
    
  • T
    oluene
    
  • M
    ethanol, metformin
    
  • U
    remia
    
  • D
    iabetic ketoacidosis
    
  • P
    araldehyde, phenformin, propylene glycol
    
  • I
    ron, INH
    
  • L
    actic acidosis
    
  • E
    thylene glycol
    
  • S
    alicylate, acetylsalicylic acid (ASA; aspirin), starvation ketosis
    
• Hypovolemia:
  
  • GI bleeding
    
  • Sepsis
    
• Abdominal pain, nausea, vomiting:
  
  • Pancreatitis
    
  • GI bleeding
    
  • Gastritis
    
  • Hepatitis
    
  • Perforated ulcer
    
  • Alcohol withdrawal
    
  • DKA
    
  • Viral illness
    
  • Obstruction/Ileus
    

TREATMENT

• 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.
  

• 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 (D
  ₅
  NS):
  
  • 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.