Rosen & Barkin's 5-Minute Emergency Medicine Consult (258 page)

• Boerhaave Syndrome
  
• Foreign Body, Caustic Ingestion, Esophageal
  
• Mallory–Weiss Syndrome
  

CODES

• 862.22 Injury to esophagus without mention of open wound into cavity
  
• 862.32 Injury to esophagus with open wound into cavity
  
• 935.1 Foreign body in esophagus
  

BASICS

• Peak serum concentration in 1–4 hr
  
• Half-life, 2.5–4.5 hr
  
• <20% excreted unmetabolized by kidneys
  
• Pathophysiology:
  
  • Metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase ultimately to oxalic acid
    
  • Results in aldehyde and acid metabolites
    
  • Directly toxic to CNS, heart, and kidneys
    

• Ethylene-glycol–containing products:
  
  • Antifreeze
    
  • Solvents
    
• Min. reported lethal dose is 30 mL of 100% ethylene glycol.
  

DIAGNOSIS

• Cardiovascular:
  
  • Tachycardia/bradycardia/other dysrhythmias
    
  • Hypertension/hypotension
    
• CNS:
  
  • Inebriation/irritability
    
  • Ataxia
    
  • Obtundation
    
  • Coma
    
  • Cerebral edema
    
  • Convulsions
    
  • Peripheral nervous system
    
  • Cranial nerve abnormalities
    
• GI:
  
  • Nausea/vomiting
    
  • Abdominal pain
    
• Pulmonary:
  
  • Hyperventilation/tachypnea/Kussmaul respiration
    
  • Pulmonary edema
    
• Renal:
  
  • Acute renal failure
    
  • Crystalluria
    
• 3 stages (may overlap):
  
  • 1st stage: 1–12 hr after ingestion:
    
    • CNS depression
      
    • GI symptoms
      
    • Worsening acidosis
      
    • Coma
      
    • Convulsions
      
    • Cerebral edema
      
    • Tetany and myoclonus secondary to hypocalcemia
      
  • 2nd stage: 12–36 hr after ingestion:
    
    • Cardiopulmonary symptoms
      
    • When most deaths occur
      
  • 3rd stage: 36–72 hr after ingestion:
    
    • Oliguria
      
    • Flank pain
      
    • Acute renal failure
      

• Intentional or unintentional ethylene glycol ingestion
  
• No history but a patient with an unexplained high anion gap metabolic acidosis
  
• Elevated unexplained osmol gap
  

• Tachypnea
  
• Altered mental status
  

• History of all substances ingested
  
• Drawn simultaneously:
  
  • Arterial blood gas
    
  • Serum ethylene glycol, methanol, isopropyl alcohol, and ethanol serum concentration
    
  • Electrolytes, BUN/creatinine, glucose
    
  • Measured serum osmolality (by freezing point depression)
    
  • Serum calcium, phosphorus, magnesium
    

• Determine the anion gap:
  
  • Anion gap = (Na
    ⁺
    ) – (Cl
    ⁻
    + HCO
    ₃
    ⁻
    )
    
  • Normal anion gap is 8–12.
    
• Determine osmol gap:
  
  • Osmol gap = measured osmolality – calculated osmolarity
    
  • Increased osmol gap: >10
    
  • Calculated osmolarity = 2(Na
    ⁺
    ) + glucose/18 + BUN/2.8 + ethanol (mg/dL)/4.6
    
  • Calculated to screen for ethylene glycol ingestion because toxic alcohol serum concentration are not commonly available in timely manner from most clinical labs
    
  • Most useful early in course of ethylene glycol poisoning or with concurrent ethanol ingestion
    
  • With concurrent ethanol ingestion, osmol gap tends to be larger and acidosis tends to be less severe because relatively less ethylene glycol has been converted to acid-producing metabolites.
    
  • Normal osmol gap does not rule out ethylene glycol ingestion.
    
  • Late presentation after ethylene glycol ingestion may manifest itself with only an elevated anion gap without a significant osmol gap.
    
• Ethylene glycol, methanol, isopropyl alcohol serum concentration
  
• Ethanol serum concentration:
  
  • Measured to determine amount of ethanol bolus necessary to attain therapeutic serum concentration, and to determine coingestants
    
• Urinalysis:
  
  • Envelope-shaped oxalate crystals: Insensitive but specific finding.
    
  • Absence of urine calcium oxalate crystals does not rule out ethylene glycol exposure.
    
  • Ketones may be due to isopropyl alcohol ingestion, starvation, or diabetic ketoacidosis.
    

Wood lamp inspection of urine or gastric contents:

• Detects presence of fluorescein, a common antifreeze additive
  
• Insensitive and not specific marker of antifreeze ingestion
  
• Absence of urinary fluorescence does not rule out ethylene glycol exposure.
  

• Increased osmol gap:
  
  • M
    ethanol
    
  • E
    thanol
    
  • D
    iuretics (mannitol, glycerin, propylene glycol, sorbitol)
    
  • I
    sopropyl alcohol
    
  • E
    thylene glycol
    
  • A
    cetone, ammonia
    
  • P
    ropylene glycol
    
• Elevated anion gap metabolic acidosis:
  A CAT MUDPILES
  :
  
  • A
    lcoholic ketoacidosis
    
  • C
    yanide, CO, H
    ₂
    S, others
    
  • A
    cetaminophen
    
  • Antiretrovirals (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
    

TREATMENT

• Bring containers of all possible substances ingested.
  
• Monitor airway and CNS depression.
  
• Dermal decontamination of an ethylene glycol chemical spill by removal of clothing and jewelry and irrigation with soap and water
  

• ABCs
  
• Supplemental oxygen, cardiac monitor, secured IV line with 0.9% NS
  
• D
  ₅₀
  W (or Accu-Check), naloxone, and thiamine for altered mental status
  

• Prevent further ethylene glycol absorption:
  
  • Gastric lavage with nasogastric tube:
    
    • If <1 hr since ingestion, if patient is in coma, or if history of large ingestion
      
  • Initial dose of activated charcoal for potential coingestants, but unlikely to help if only ethylene glycol:
    
    • Activated charcoal adsorbs ethylene glycol poorly.
      
• Prevent ethylene glycol conversion to toxic metabolites with fomepizole:
  
  • Fomepizole (4-MP, Antizol):
    
    • Initiate before ethylene glycol serum concentration returns, if accidental ingestion greater than a sip or intentional ingestion oraltered mental status associated with unexplained osmol gap or elevated anion gap acidosis.
      
    • Competitive inhibitor of alcohol dehydrogenase
      
  • Disadvantages:
    
    • Blurry vision
      
    • Transient elevation of LFTs
      
  • Advantages:
    
    • Easy dosing
      
    • No need for continuous infusion
      
    • No inebriation/CNS depression
      
    • No hypoglycemia, hyponatremia, or hyperosmolality
      
    • Not necessary to check ethanol serum concentration
      
    • Reduction in degree of nursing care and monitoring
      
• Ethanol therapy:
  
  • 2nd choice antidote if fomepizole is not available
    
  • Not FDA approved for treatment of ethylene glycol
    
  • Initiate before ethylene glycol serum concentration returns, if potentially toxic ingestion is suspected.
    
  • Ethanol: Greater affinity than ethylene glycol for alcohol dehydrogenase:
    
    • Slows conversion to toxic metabolites
      
  • Indications:
    
    • History of accidental ethylene glycol ingestion of greater than a sip or intentional ethylene glycol ingestion
      
    • Altered mental status associated with unexplained osmol gap or elevated anion gap metabolic acidosis
      
  • Goal: Serum ethanol serum concentration of 100–150 mg/dL
    
  • Continue ethanol therapy until ethylene glycol serum concentration is 25 mg/dL.
    
• Administer thiamine, pyridoxine, and magnesium:
  
  • Cofactors in metabolism of ethylene glycol that may promote conversion to nontoxic metabolites.
    
  • No human data supporting this theory
    
• Hemodialysis:
  
  • Decreases elimination half-life of ethylene glycol and removes toxic metabolites
    
  • Indications: Severe acidosis or osmol gap; persistent electrolyte or metabolic acidosis; renal insufficiency; pulmonaryedema; cerebral edema; serum ethylene glycol serum concentration >25 mg/dL
    
  • Continue hemodialysis until ethylene glycol serum concentration approaches 25 mg/dL and metabolic acidosis resolves.
    
• Correct secondary disorders:
  
  • Ensure adequate urine output via IV fluids.
    
  • Sodium bicarbonate therapy for acidemia with pH < 7.1:
    
    • The goal is to maintain a serum pH in the normal range.
      
• Monitor/replace calcium:
  
  • Deposition of calcium into tissues can result in hypocalcemia.