- Less than 100 cases per year reported each year in the UK
- Seen following deep or penetrating wound in relatively avascular areas
- More prevalent in developing countries
- Seen in neonate (tetanus neonaturum) following the use of cow dung on the umbilicus
Microbiology
- Due to Clostridium tetani
- Gram-positive spore forming rod
- Typical 'drum-stick' appearance with terminal spore
- Widely found in the environment and soil
- A strict anaerobe that produces a powerful exotoxins
- Exotoxin is resistant to autoclaving
- Exotoxin is not antigenic and repeat infection can occur
- Infection produces few signs of local inflammation
Pathogenesis
- Germination of spores releases the exotoxin
- Toxin affects nervous system and reaches CNS via the peripheral nerves
- Acts on presynaptic terminals of inhibitor nerves
- Reduces the release of inhibitory neurotransmitters (e.g. glycine)
- Excess activity of motor neurones produces muscle spasm
Clinical features
- Facial muscle spasm produces trismus
- Typical facial appearance = 'risus sardonicus'
- Back muscle spasm produces opisthotomous
- Eventually exhaustion and respiratory failure leads to death
- The diagnosis is essentially clinical
- Differentiating between contamination and infection on wound swabs is difficult
Treatment
Prevention
- Tetanus can be prevented by:
- Active immunisation with tetanus toxoid with booster every 5-10 years
- Adequate wound toilet of contaminated wounds
- Consider passive immunisation with hyperimmune immunoglobulin
Treatment
- In suspected cases:
- Passive immunisation with anti-tetanus immunoglobulin
- Adequate wound debridement
- Intravenous benzylpenicillin
- Intensive care support
- Despite
the use of ITU mortality is about 50%
Bibliography
Cook T M, Protheroe R T, Handel J M. Tetanus: a review of the literature. Br
J Anaesth 2001; 87: 477-487.
Hollander J E, Singer A J.
Laceration management. Ann Emerg Med 1999;
34: 356-367.
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