ICU · neurocritical-care
Tetanus and Botulism in the ICU — Comprehensive Management
Also known as Tetanus · Botulism · Lockjaw · Trismus · Opisthotonos · Tetanospasmin · Botulinum toxin · Descending flaccid paralysis · HTIG · Botulinum antitoxin
Tetanus and botulism — two clostridial neurotoxin diseases requiring ICU care. TETANUS: tetanus neurotoxin (TeNT) is transported retrogradely to the CNS and blocks GABA and glycine release from inhibitory interneurons → muscle spasms, rigidity, autonomic dysfunction. Management: wound debridement, antibiotics 7–10 days (metronidazole marginally favoured), antitoxin (human or equine IM — no outcome difference), benzodiazepines for spasms, magnesium sulfate targeting serum Mg 2–4 mmol/L, airway protection (about half of adults with generalised tetanus need ventilation), and full immunisation — natural infection does not confer immunity. BOTULISM: botulinum neurotoxin acts at peripheral cholinergic terminals → symmetrical cranial nerve palsies then descending flaccid paralysis with preserved consciousness. Management: botulinum antitoxin (BAT) immediately on clinical suspicion, intensive supportive care with ventilation when needed, recovery over weeks to months as new nerve terminals sprout. Infant botulism: BIG-IV (BabyBIG) shortens hospital stay.
Checked against its sources on 1 Oct 2026
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Target exams
Red flags
- Trismus + generalised rigidity + stimulus-triggered spasms + wound history = TETANUS — a purely clinical diagnosis; start the bundle (debridement, antibiotics, antitoxin, benzodiazepines) without waiting for any test
- Descending flaccid paralysis (cranial nerves first) + dry mouth + no sensory loss + afebrile + alert = BOTULISM — give BAT immediately on clinical suspicion; do not await laboratory confirmation
- In ventilated severe tetanus, autonomic dysfunction (arrhythmias, labile BP) — not spasms — is the leading cause of death; magnesium reduces the need for verapamil 4.7-fold
- Tetanus spasms are triggered by minor stimuli (light, sound, touch) — nurse in a quiet, dark environment; avoid intermittent pneumatic compression (it triggers spasms)
- Aminoglycosides aggravate the neuromuscular blockade of botulism (anecdotal human infant cases, in-vitro NMBA action) — avoid; no routine skin testing before BAT
Meet the patient
A previously well man arrives unable to open his mouth, days after a contaminated wound that has since healed — in up to 30% of tetanus cases no wound is found at all. His masseters are clenched, a fixed grimace furrows his face, and the slightest touch or sound fires a whole-body spasm. He is fully lucid — unlike many neurological infections, lucidity is preserved in tetanus. Trismus and dysphagia are almost always present at admission (93–98% and 83% in retrospective series); dyspnoea at admission is uncommon (5–10%) but signals impending airway compromise.[14]
Across the unit, a person who injects drugs is descending the other way: ptosis, slurred speech, failing swallow — yet alert and oriented, with no sensory deficit. An abscess sits at a skin-popping site. California's wound botulism series documented exactly this epidemic among people who inject black tar heroin subcutaneously, with misdiagnosis and diagnostic delays of up to 64 days.[10][12]
The organising question for both patients: is the toxin blocking inhibition (rigid — tetanus) or blocking excitation (flaccid — botulism)? Same toxin superfamily; the whole clinical difference lives in where the toxin acts.[14]
References22ShowHide
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