Harvey's Garden

Tetanus

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aliases—

3 min read

Epidemiology

Etiology

Pathophysiology

  • Tetanospasmin: reaches the CNS through retrograde axonal transport
    • Toxin binds to receptors of peripheral nerves and is then transported to interneurons (Renshaw cells) in the CNS via vesicles.
    • Acts as protease that cleaves synaptobrevin, a SNARE protein → prevention of inhibitory neurotransmitters (i.e., GABA and glycine) release from Renshaw cells in the spinal cord → uninhibited activation of alpha motor neurons → muscle spasms, rigidity, and autonomic instability
  • Tetanolysin: causes hemolysis and has cardiotoxic effects

Tetanus vs botulism

Both work on SNARE proteins

Clinical features

  • Incubation period: Days to weeks.
  • Presents with a descending pattern of muscle rigidity.
  • Early signs:
    • Trismus (lockjaw): Spasm of masseter muscles. c
    • Risus sardonicus: “Sardonic smile” from facial muscle spasm.
  • Later signs:
    • Opisthotonos: Arching of the back due to severe extensor muscle spasm.
    • Painful, generalized muscle spasms, often triggered by minor stimuli (noise, light).
    • Autonomic instability: Tachycardia, hypertension, sweating.
  • Pt remains conscious throughout.

Diagnostics

  • Clinical Diagnosis: Based on physical examination findings and immunization history; no lab or imaging confirmation needed. c
  • Key Labs:
    • Wound cultures have low sensitivity/specificity (do not wait for culture results to initiate therapy).
    • Serum anti-tetanus antibody levels < 0.1 IU/mL support susceptibility but are not routinely used acutely.
  • Imaging: Not diagnostic; indicated only to rule out foreign bodies or complications (e.g., vertebral compression fractures).

Treatment

  • Initial Stabilization:
    • ICU admission in a dark, quiet room (minimize sensory stimuli).
    • Early airway protection (endotracheal intubation or tracheostomy) for severe spasms or laryngospasm.
  • Targeted Therapy:
    1. Human Tetanus Immune Globulin (HTIG): IM administration to neutralize unbound circulating toxin (give prior to wound debridement).
    2. Vaccination: Active immunization with Tdap or Td IM at a separate anatomical site (infection does NOT confer immunity).
    3. Antibiotic Therapy: Metronidazole IV (1st-line) or Penicillin G IV for 7-10 days to eradicate vegetative bacteria.
    4. Wound Care: Surgical debridement of necrotic tissue after HTIG administration.
  • Symptomatic Control:
    • Muscle spasms: Benzodiazepines (e.g., IV diazepam, midazolam).
    • Severe refractory spasms: Neuromuscular blockade (e.g., vecuronium) + mechanical ventilation.
    • Autonomic dysfunction: IV MgSO4, labetalol, or alpha-2 agonists (clonidine).
  • High-Yield Post-Exposure Prophylaxis (PEP) Algorithm: c
    • Clean, minor wound:
      • Unvaccinated / < 3 doses / Unknown: Tdap/Td (Yes) | HTIG (No).
      • ≥ 3 doses: Tdap/Td (Only if > 10 yrs since last dose) | HTIG (No).
    • Dirty / contaminated / puncture wound:
      • Unvaccinated / < 3 doses / Unknown: Tdap/Td (Yes) | HTIG (Yes).
      • ≥ 3 doses: Tdap/Td (Only if > 5 yrs since last dose) | HTIG (No).
    • Rationale
      • Clean, Minor Wounds: Minimal spore load + well-oxygenated tissue = extremely low risk of rapid toxin production. Incubation period is long enough that vaccine alone suffices; HTIG risk/cost is unnecessary.
      • ≥ 3 doses: Toxin exposure or booster vaccine triggers a rapid secondary IgG surge faster than the typical C. tetani incubation period (3–21 days).

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