Related Subjects:
|Pasteurella Multocida
|Capnocytophaga canimorsus
|Snake Bites
|Dog Bites
|Tetanus
|Clostridium perfringens
|Clostridioides difficile Infection
|Clostridium botulinum Infection
When tetanus spores enter a suitable low-oxygen environment (soil-contaminated wounds, devitalised tissue), Clostridium tetani germinates and releases tetanospasmin β a lethal neurotoxin causing spastic paralysis. π¦ Recovery does not confer immunity, so vaccination is always required after infection.
| π¨ Initial Tetanus Management Summary |
- Assess Airway, Breathing, Circulation (ABC) β laryngeal spasm may require intubation/ventilation (ITU support).
- Sedation & Neuromuscular Blockade: IV benzodiazepines are first-line for spasm control.
- Tetanus Immune Globulin (TIG): Give before wound debridement to neutralise circulating toxin.
- Antibiotics: IV metronidazole (preferred over penicillin). π§ͺ
- Ensure vaccination status is updated (active immunisation needed even post-infection).
|
π About
- Clostridium tetani is a Gram-positive, spore-forming anaerobe found in soil, dust, and animal waste.
- Disease results from tetanospasmin toxin β blocks inhibitory neurotransmitters (GABA, glycine) β sustained muscle contraction.
- Fatality rate: 20β60% (highest in neonates and elderly, often due to respiratory failure or autonomic instability).
- High-risk in areas with poor wound hygiene or inadequate immunisation programmes.
- No natural immunity: Even survivors must complete full tetanus toxoid vaccination. π
π¬ Microscopy
π§« Characteristics
- Gram-positive, motile, obligate anaerobe.
- Spore-forming bacillus with a "drumstick" appearance (terminal spores).
- Produces:
- Tetanospasmin β neurotoxin (clinical tetanus).
- Tetanylisin β haemolysin, minor role in disease.
βοΈ Aetiology & Pathophysiology
- Transmission: Spores enter via puncture wounds, deep lacerations, burns, animal bites, or contaminated surgical wounds. Neonatal tetanus: via infected umbilical stump.
- Toxin action: Retrograde axonal transport β spinal cord β blocks inhibitory neurotransmitters (GABA, glycine) β unchecked motor neuron activity β spasms/rigidity.
- Incubation: 3β21 days (shorter = worse prognosis).
π©Ί Clinical Presentation
- Trismus (lockjaw) π¬ β often first sign.
- Risus sardonicus β characteristic βsardonic smile.β
- Opisthotonus β severe arching of the back from spasm.
- Generalised rigidity, painful spasms triggered by minor stimuli (light, touch, noise).
- Autonomic features: tachycardia, labile hypertension, sweating, salivation, fever.
- Respiratory muscle involvement β hypoxia, arrest.
- Forms: Generalised, localised, cephalic, neonatal.
π Grading of Severity
- I (Mild): Trismus + rigidity, no spasms or respiratory compromise.
- II (Moderate): Rigidity + spasms, mild respiratory distress.
- IIIβIV (Severe): Frequent prolonged spasms, airway compromise, autonomic dysfunction.
π§Ύ Differential Diagnosis
- Strychnine poisoning: Glycine antagonist; mimics tetanus.
- Acute dystonia: Can cause trismus; resolves with anticholinergics (benztropine).
π Investigations
- Primarily clinical diagnosis β lab confirmation is rare.
- Blood agar culture: poor, indistinct growth.
- Toxin assays confirm but not widely available.
- Check wound cultures β but often negative.
π Prevention
- Vaccination: Tetanus toxoid (part of UK DTaP schedule: 2, 3, 4 months + boosters at 3 yrs, 14 yrs).
- Wound prophylaxis: TIG for contaminated wounds if vaccination incomplete/uncertain.
- Neonatal tetanus: Prevented via maternal immunisation + clean delivery practices.
π Management
- Supportive Care: ABC support, ITU, tracheostomy/ventilation if needed.
- Sedation/Spasm control: Diazepam or midazolam IV; may require neuromuscular blockade + ventilation.
- Antitoxin: Human TIG 150 U/kg IM across multiple sites. (Equine TIG possible where human unavailable, but risk of anaphylaxis.)
- Antibiotics: IV metronidazole preferred. (Older studies showed penicillin may worsen spasms.)
- Wound Care: Debridement after TIG to remove necrotic tissue/spores.
- VTE prophylaxis in immobilised patients.
- Autonomic dysfunction: Morphine (sympathetic overdrive), labetalol (hypertension), inotropes (hypotension).
β οΈ Complications
- Respiratory failure from spasm.
- Autonomic dysregulation β labile BP, arrhythmias.
- Secondary infections (VAP, sepsis) in ITU.
- Fractures/dislocations from violent spasms.