Resident Report 4/7 – NM diseases

Teaching Points:

  • Wound Botulism is due to a bacterial toxin that disturbs the transmission of acetylcholine to bind to nicotinic/muscarinic receptors.
  • Majority of patients get botulism primary from foodborne illnesses, only a small percentage get botulism from wounds.
  • Wound botulism can also be commonly seen in patients who use black tar heroin (skin poppers). Injection of material into subcutaneous and/or muscle tissue provides the ideal environment for anaerobic bacteria – Clostridium botulinum.
  • Clostridium botulinim can produce 8 different strains of toxin – A – H
  • Clinical Manifestations
    • Patients present initially with bulbar symptoms and occasionally ocular abnormalities (diplopia, disconjugate eye movement, pupillary defects)
    • Also present as a symmetric descending paralysis complicated respiratory drive
    • Check history for evidence of skin popping
    • Wound botulism is more likely to cause fever and leukocytosis compared to other forms of botulism.
    • Patients with foodborne botulism typically present first with GI symptoms prior to onset of neurologic abnormalities
  • Diagnosis
    • Important to suspect this in a patient with evolving neurologic deficits
    • Important to obtain wound culture for those who perform skin popping.
    • Diagnosis made by injecting mice and observing clinical manifestation. Then you reinject a second mouse with patient’s serum and antitoxin. If second mouse lives, that’s the diagnosis.
  • Treatment
    • Supportive care including close airway monitoring (intubation if needed)
    • Botulinum heptavalent antitoxin
    • Monitor clinical status – typically a prolonged course of recovery as new axons grow from neurons to develop new neuromuscular junctions for function.
  • Differential Diagnosis
    • Myasthenia Gravis
      • fluctuating weakness worse with repetition/activity
      • Initially involves the bulbar muscles, ptosis
      • Classically associated with thymomas (~80%)
    • Lambert Eaton Syndrome
      • No bulbar involvement. Proximal muscle involvement, ptosis.
      • Improves with repetition
      • Classically associated with small cell lung CA
    • Guillan Barre Syndrome
      • ascending paralysis, sensation intact although patients complain of vague symptoms.
      • Preceding viral URI or GI symptoms
      • Presence of autonomic symptoms such as hyper/hypotension, fluctuating temperatures, urinary incontinence/retention, brady/tachycardia, etc
    • Tick paralysis
      • Very similar presentation to GBS except no autonomic symptoms
      • Often times a tick can be found on the patient’s skin.

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