Rosen & Barkin's 5-Minute Emergency Medicine Consult (110 page)

CT/MRI of brain:

• Normal
  

• CSF testing:
  
  • Normal
    
  • Helps differentiate from Guillain–Barré syndrome (which as markedly elevated CSF protein)
    
• Electrophysiologic studies:
  
  • Normal nerve conduction with diminished evoked muscle action potential
    
• Edrophonium testing may be positive, but not to the degree seen in myasthenia gravis.
  

• Myasthenia gravis (less acute)
  
• Lambert–Eaton myasthenic syndrome (less acute)
  
• Polio (fever and asymmetric)
  
• Guillain–Barré (simultaneous sensory findings and elevated spinal fluid protein)
  
• Tick paralysis
  
• Magnesium intoxication
  
• Hypokalemic periodic paralysis
  
• Diphtheritic neuropathy
  
• Rare basilar stroke syndromes with bulbar palsy
  

• Often misdiagnosed as dehydration, sepsis, or Reye syndrome
  
• Other diagnoses include inborn errors of metabolism, Guillain–Barré syndrome, and spinal muscle atrophy.
  

TREATMENT

• Intubate as soon as respiratory insufficiency noted, clinically and/or in conjunction with ABG.
  
• May require several weeks of ventilatory support
  

• Transcutaneous pacing for unstable type II 2nd- or 3rd-degree block
  
• Atropine:
  
  • Avoid with type II 2nd-degree block because it may precipitate complete heart block
    
  • Contraindicated in 3rd-degree heart block with a widened QRS complex
    
• Attempts should be made at preventing increases in vagal tone.
  

• Early intubation and ventilatory support is the key to survival.
  
• Respiratory difficulties occur rapidly.
  

• Bivalent AB antitoxin:
  
  • IV administration as soon as the diagnosis is made and initial samples are collected, without waiting for lab confirmation
    
  • Before use assess hypersensitivity with skin test using horse serum or antitoxin
    
  • Using recommended dose <1% will have hypersensitivity reaction
    
• With wound botulism perform wound débridement even if it appears to be healing.
  
• Antibiotics for specific infectious complications
  
• Standard precautions only; no evidence of person-to-person transmission
  
• If environmental exposure, wash clothing and skin with soap and water
  

• ABE antitoxin formulations no longer used because of declines in titer to type E toxin
  
• 1st-line treatment:
  
  • Baby BIG human-derived antitoxin to types A and B licensed by USFDA for treatment of infant botulism and distributed by CA Dept. of Public Health (510-231-7600).
    www.infantbotulism.org/
    
  • Heptavalent antitoxin (H-Bat) available from CDC as an investigational use drug protocol and emergency therapeutic use. Not for infant botulism.
    

• Baby BIG halves average hospital stay from 6–3 wk:
  
  • Adult equine antitoxin should not be used on pediatric patients
    
• Antibiotics:
  
  • Ineffective in eradicating organism from the intestine
    
  • Release of toxin in the gut through bacterial cell lysis may worsen neurologic symptoms.
    

Pentavalent toxoid for lab workers

FOLLOW-UP

Admit patients with suspected botulism poisoning to monitored bed:

• ICU admission for any respiratory deficiency
  

Clinical course of botulism poisoning is unpredictable; it can become rapidly progressive and fatal:

• Discharge patients only after a prolonged period of progressive recovery from symptoms.
  

• Physical medicine and rehabilitation:
  
  • Residual weakness can last for up to 1 yr
    
• Mental health:
  
  • Patients and their families often experience stress and depression with the prolonged recovery.
    

• Botulism is a public health emergency; early consultation with state and federal health departments is required.
  
• Suspect botulism if there are more than 2 cases; other conditions in the differential do not produce outbreaks.
  
• Antitoxin does not reverse paralysis but only halts its progression. Therefore, administer antitoxin once diagnosis is suspected. Do not wait until signs of respiratory compromise are present.
  
• Initial signs of respiratory distress may not be clinically apparent secondary to paralysis.
  
• Bulbar palsy at presentation may be mistaken for altered mental status.
  

• CDC. Botulism. Emergency Preparedness and Response. Accessed on 11/02/09 from
  http://emergency.cdc.gov/agent/botulism
  .
  
• Dembek ZF, Smith LA, Rusnak JM. Botulism: Cause, effects, diagnosis, clinical and laboratory identification, and treatment modalities.
  Disaster Med Public Health Prep
  . 2007;1:122–134.
  
• Domingo RM, Haller JS, Gruenthal M. Infant botulism: Two recent cases and literature review.
  J Child Neurol
  . 2008;23:1336–1346.
  
• Ho RY. Chapter 170. Botulinum antitoxin. In: Olson KR, ed.
  Poisoning & Drug Overdose
  . 6th ed. New York, NY: McGraw-Hill; 2012.
  http://www.accessmedicine.com/content.aspx?aID=55987003
  . Accessed January 10, 2013.
  
• Gouveia C, Mookherjee S, Russell MS. Wound botulism presenting as deep space neck infection.
  Laryngoscope.
  2012;122:2688–2689.
  
• Thurston D. Botulism from drinking prison-made illicit alcohol.
  MMWR Morb Mortal Wkly Rep.
  2012;61:782--784.
  
• Khakshoor H, Moghaddam AA, Vejdani AH, et al. Diplopia as the primary presentation of foodborne botulism.
  Oman J Opthalmol.
  2012;5:109–111.
  

CODES

• 005.1 Botulism food poisoning
  
• 040.41 Infant botulism
  
• 040.42 Wound botulism
  

BASICS

• Obstruction of normal intestinal flow from mechanical or nonmechanical causes
  
• Small-bowel obstruction (SBO):
  
  • 20% of acute surgical admissions
    
  • Adhesions: Most common cause (60%)
    
  • Neoplasms
    
  • Hernias
    
  • Strictures: Inflammatory bowel disease
    
  • Trauma: Bowel wall hematoma
    
  • Miscellaneous (e.g., ascaris infection)
    
• Large-bowel obstruction (LBO):
  
  • Disease primarily of the elderly
    
  • Carcinoma (60%)
    
  • Diverticular disease (20%)
    
  • Volvulus (5%)
    
  • Colitis (e.g., ischemic, radiation)
    
  • Crohn's disease
    
  • Foreign bodies
    
• Functional, nonmechanical:
  
  • Paralytic ileus (e.g., electrolyte abnormalities, injury)
    
  • Pseudo-obstruction (i.e., Ogilvie syndrome [e.g., operative and nonoperative trauma] 11%)
    

• Obstruction leads to proximal dilatation of intestines due to swallowed air and accumulated GI secretions, leading to increased intraluminal pressures.
  
• Retrograde peristalsis causes vomiting.
  
• Distended bowel becomes progressively edematous, and additional intestinal secretions cause further distention and 3rd spacing of fluid into the intestinal lumen.
  
• Obstruction may lead to intestinal wall ischemia (strangulated obstruction), resulting in increased aerobic and anaerobic bacteria, and methane and hydrogen production. Peritonitis, sepsis, and death may follow.
  
• Mortality is 100% in untreated strangulated obstruction, 8% if treated surgically within 36 hr, but 25% if surgery delayed after 36 hr.
  

DIAGNOSIS