Rosen & Barkin's 5-Minute Emergency Medicine Consult (109 page)

FOLLOW-UP

All cases of Boerhaave syndrome must be admitted to surgical ICU:

• Cervical esophageal perforations may be treated by drainage alone.
  
• All thoracic and abdominal perforations require surgical intervention.
  

None

Thoracic or general surgeon must be consulted for admission and possible operative intervention.

As per surgeon recommendations

• Chest radiographs done immediately after injury may be normal.
  
• Left pleural space involvement is usually associated with a distal esophageal perforation.
  
• Right pleural space involvement is usually associated with proximal esophageal perforations.
  
• If esophagram is negative and there is high suspicion, repeat with patient in left and right decubitus positions.
  
• Immediate surgical consultation is the keystone of management.
  
• Significant increases in mortality are seen with delay in diagnosis and management.
  

• Brinster CJ, Singhal S, Lee L, et al. Evolving options in the management of esophageal perforation.
  Ann Thoracic Surg
  . 2004;77:1475–1483.
  
• Katabathina VS, Restrepo CS, Martinez-Jimenez S, et al. Nonvascular, nontraumatic mediastinal emergencies in adults: A comprehensive review of imaging findings.
  Radiographics
  . 2011;31:1150–1153.
  
• Onat S, Ulku R, Cigdem KM, et al. Factors affecting the outcome of surgically treated non-iatrogenic traumatic cervical esophageal perforation: 28 years experience at a single center.
  J Cardiothorac Surg
  . 2010;5:46.
  
• Vogel SB, Rout WR, Martin TD, et al. Esophageal peforation in adults: Aggressive, conservative treatment lowers morbidity and mortality.
  Ann Surg
  . 2005;241:1016–1023.
  
• Wu JT, Mattox KL, Wall MJ Jr. Esophageal perforations: New perspectives and treatment paradigms.
  J Trauma
  . 2007;63:1173–1184.
  

CODES

530.4 Perforation of esophagus

BASICS

• Rare in US, causing <200 cases/yr; however, has significant bioterrorism potential.
  
• Caused by a polypeptide, heat-labile exotoxin produced by
  Clostridium botulinum:
  
  • Most potent poison known
    
• Toxin blocks neuromuscular transmission in cholinergic nerve fibers.
  
• Symptoms occur by inhibition of acetylcholine release from presynaptic nerve membranes:
  
  • Damage is permanent.
    
  • Recovery is by formation of new synapses through sprouting from the axon.
    
• Onset: 12–72 hr after exposure; may be up to 1 wk after exposure:
  
  • Death can occur 24 hr after onset of symptoms.
    
• Slow recovery; symptoms often persist for months
  
• Mortality:
  
  • Untreated: 60–70%
    
  • With supportive care: 3–10%
    
• 3 major types: Food-borne botulism, wound botulism, and infantile botulism (see “Pediatric Considerations”). Absorbed through mucosal surfaces or nonintact skin
  
• Food-borne botulism:
  
  • Occurs by ingestion of preformed toxin; from improperly canned food, improper refrigeration
    
  • Conditions required for exposure:
    
    • Food product contaminated with
      C. botulinum
      bacilli or spores
      
    • Proper conditions for germination of spores exist.
      
    • Time and conditions permit production of toxin before eating.
      
    • Food not heated sufficiently to destroy botulism toxin
      
    • Toxin-containing food ingested by susceptible host
      
• Wound botulism:
  
  • Clinical evidence of botulism after trauma with a resultant infected wound and no history suggestive of food-borne illness
    
  • Botulinum isolated in about 50%
    
  • Wounds usually contaminated with soil
    
  • Majority of US cases from IV drug use
    
• Other types:
  
  • Adult intestinal toxemia botulism:
    
    • Seen in adults with functional or structural GI abnormalities, are immunocompromised or with prolonged antibiotic use
      
    • Predisposes to
      Clostridial
      colonization
      
    • May have sporadic or recurrent botulism with no known source and even after immunoglobulin treatment
      
  • Iatrogenic botulism:
    
    • Doses found in cosmetic applications are insufficient to cause systemic symptoms.
      
    • No known recent cases from medical use.
      
    • Symptoms would be expected to be classic.
      
  • Inhalation botulism:
    
    • Aerosolization of toxin may have bioterrorism applications. Last reported naturally occurring case in 1962 from the disposal of animal remains.
      

• Infantile botulism occurs from the ingestion of
  C. botulinum
  spores, which germinate in the gut and produce the toxin.
  
• Accounts for 50–76% of botulism cases
  
• 90% occur in children <6 mo:
  
  • Associated with patient or family exposure to soil, dust, or agricultural industry.
    
  • May also be associated with weaning from breast milk, which may alter intestinal flora and increase susceptibility to
    Clostridia
    infection.
    
• Usually presents with change in stool pattern or constipation, progressing over several days to symptoms of bulbar weakness, then descending flaccid paralysis.
  
• Slower onset is attributed to the toxin being produced locally as opposed to being ingested in 1 dose.
  
• C. botulinum
  spores found in honey:
  
  • Honey not recommended for children <1 yr.
    

• C. botulinum
  is a large spore-forming, usually gram-positive, strictly anaerobic bacilli ubiquitous in nature.
  
• Each strain produces antigenically distinct toxins, designated types A to G:
  
  • Types A, B, E, and rarely F are responsible for most human cases.
    

DIAGNOSIS

• Ingestions/food history for previous 4–5 days:
  
  • Exposures traditionally from home-processed fruit or vegetable products
    
  • In prison populations ingestion of “pruno” (alcohol product created by prisoners using leftover food products)
    
• Immune status (AIDS, cancer, chronic illness)
  
• IV drug use
  

• Food-borne botulism (classic botulism):
  
  • Bulbar weakness is invariably the initial presentation: Diplopia, dysphagia, dysarthria, and dysphonia
    
  • Subsequent symmetric, descending weakness or paralysis of the extremities (hallmark of the disease)
    
  • No sensory deficit
    
  • May have progressively diminishing deep tendon reflexes
    
  • Patient remains awake/alert; mentation unaffected.
    
  • Ventilatory insufficiency from weakness of respiratory muscles
    
  • Autonomic dysfunction (sympathetic and parasympathetic):
    
    • Dry mouth
      
    • Blurred vision
      
    • Orthostatic hypotension
      
    • Constipation
      
    • Urinary retention
      
  • Nausea and vomiting with food-borne botulism only
    
  • Afebrile
    
• Wound botulism:
  
  • Finding similar to food-borne botulism
    
  • May be febrile as a result of soft-tissue infection
    
• Infantile botulism:
  
  • Constipation
    
  • Weakness
    
  • Poor suck
    
  • Weak cry
    
  • Lethargy
    
  • Hypotonia
    
  • Flaccid facial expression
    
  • Respiratory difficulty
    
• Inhalation botulism:
  
  • Similar to food-borne botulism with absence of GI symptoms
    

• Diagnosis is entirely clinical.
  
• Workup focuses on differentiation from other conditions causing general paralysis.
  
• If diagnosis is suspected, immediately notify state health department or CDC (770-488-7100 for adults or 1-510-231-7600 for infant cases).
  

• CBC
  
• Electrolytes, BUN/creatinine, and glucose:
  
  • Check for hypokalemia.
    
• Arterial blood gas (ABG):
  
  • For signs of respiratory insufficiency
    
• Confirmatory testing via mouse assay performed by select state and federal labs, using samples from:
  
  • Blood
    
  • Feces
    
  • Gastric contents
    
  • Suspected food and containers
    
  • Takes between 6–96 hr for results
    
• Anaerobic blood cultures:
  
  • May detect bacterium
    
• Nasal swab for ELISA test:
  
  • For inhalation botulism, as less reliably detected in sera and stool than other forms
    
  • Sample needs to be collected within 24 hr of exposure