Tetanus
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Direct answer
Tetanus is an acute toxigenic infection by Clostridium tetani spores entering through wounds, whose toxin tetanospasmin blocks inhibitory neurotransmitter release in the spinal cord and brainstem, producing muscle rigidity and reflex spasms. Trismus (lockjaw) is usually first, followed by risus sardonicus, neck stiffness, opisthotonus and life-threatening laryngeal or respiratory spasms, with a clear sensorium and no fever throughout. Treatment combines wound debridement, human tetanus immunoglobulin, metronidazole, spasm control with benzodiazepines and early ventilation with tracheostomy.
What you must remember
- Organism: Clostridium tetani, an obligate anaerobic, drumstick-shaped, spore-forming Gram-positive bacillus; tetanospasmin travels retrogradely in peripheral nerves to block glycine and GABA release from inhibitory interneurons (Renshaw cells).
- Diagnosis is clinical; the spatula test (touching the posterior pharynx provokes jaw spasm instead of a gag) is a useful bedside sign; no laboratory test confirms it.
- Clinical features: trismus, risus sardonicus (facial muscle spasm), stiff abdomen, opisthotonus with sustained extensor posturing, and sudden reflex spasms triggered by noise, light or touch; autonomic instability (labile blood pressure, arrhythmia, sweating) dominates in the second week; a short incubation period (under about one week) and short onset time signal severe disease.
- Management pillars: quiet dark room; wound debridement; human tetanus immunoglobulin (3,000 to 6,000 units intramuscularly in standard texts, with some Indian protocols adding 500 units intrathecally) to neutralise unbound toxin; metronidazole as the preferred antibiotic (penicillin is a GABA antagonist and may aggravate spasms); diazepam or midazolam for spasms, magnesium for spasm and autonomic control; early elective tracheostomy or intubation with ventilation in severe disease.
- Neonatal tetanus — from unhygienic cord cutting — presents with poor feeding, rigidity and spasms in the first two weeks of life; prevention is maternal immunisation and clean delivery.
- Recovery confers no immunity: every patient must receive a full primary course of tetanus toxoid, at a different site from immunoglobulin.
- Prevention: tetanus toxoid boosters every ten years; TIG 250 to 500 units for heavily contaminated wounds in the incompletely immunised.
- Complications: respiratory failure, aspiration pneumonia, rhabdomyolysis with acute kidney injury, fractures and autonomic storms; intensive care is decisive.
Managing a case from wound to ward
A 50-year-old farmer presents with jaw stiffness five days after a puncture wound from a rusted nail; he cannot open his mouth, the spatula test is positive, and he is fully conscious with no fever — the clinical diagnosis is made, no laboratory test needed. Move him to a quiet, dark room, because noise, light and touch trigger the reflex spasms that kill. Debride the wound and give human tetanus immunoglobulin 3,000 to 6,000 units intramuscularly (some Indian protocols add 500 units intrathecally) — it neutralises only unbound toxin and reverses nothing already fixed to neurons. Start metronidazole rather than penicillin, whose GABA-antagonism can aggravate spasms. Control spasms with diazepam or midazolam, add magnesium for spasm and autonomic storms, and in severe disease — short incubation, laryngeal or respiratory spasms — secure the airway early with elective intubation or tracheostomy before the first respiratory spasm makes it an emergency. Watch for aspiration pneumonia, rhabdomyolysis with acute kidney injury, and fractures from convulsive contractions. On recovery, start a full primary course of tetanus toxoid at a site away from the immunoglobulin, since the disease-conferring dose of toxin is too small to immunise.
Where students slip
The mimics are the opening trap: strychnine poisoning looks identical but carries a shorter course; dystonic reactions follow metoclopramide or antipsychotics and relax with anticholinergics; peritonsillar abscess causes trismus with fever; and meningitis depresses consciousness, whereas tetanus leaves the sensorium clear. The antibiotic trap is the most reliably planted wrong option: penicillin looks like the natural Clostridium drug and is wrong for tetanus. The immunoglobulin trap follows: candidates expect TIG to reverse established spasms, when all it can do is neutralise what is still circulating.
Frequently asked questions
How does tetanospasmin produce its effects?
It ascends peripheral nerves and blocks the release of inhibitory neurotransmitters glycine and GABA, leaving motor neurons unchecked, causing rigidity and reflex spasms.
Which antibiotic is preferred?
Metronidazole; penicillin is avoided because its GABA-antagonistic action can worsen spasms.
What is the dose of human tetanus immunoglobulin for treatment?
Commonly 3,000 to 6,000 units intramuscularly, with some Indian protocols adding 500 units intrathecal; it neutralises only circulating, unbound toxin.
What is the spatula test?
Touching the pharynx with a spatula provokes jaw clenching in tetanus (a positive test) instead of the normal gag reflex.
Does surviving tetanus give immunity?
No — the amount of toxin causing disease is too small to immunise, so active toxoid vaccination must follow recovery.
How is neonatal tetanus prevented?
By immunising pregnant women (tetanus toxoid), ensuring clean deliveries and cord care with sterile instruments.