Tetanus
Summary
Tetanus is caused by the toxin tetanospasmin from Clostridium tetani, a spore-forming anaerobic bacterium found in soil, dust, and faeces. Spores enter through wounds and germinate under anaerobic conditions. The toxin blocks inhibitory neurotransmitter release, causing severe muscle rigidity and spasms. Trismus (lockjaw) is the classic presenting sign. Mortality remains 10-20% even with treatment. Prevention through vaccination is highly effective.
Key Facts
- Cause: Tetanospasmin toxin from Clostridium tetani
- Entry: Contaminated wounds, punctures, burns, IV drug use, unsterile circumcision/delivery
- Incubation: 3-21 days (shorter incubation = worse prognosis)
- Classic signs: Trismus, risus sardonicus, opisthotonus, generalised spasms
- Treatment: TIG, metronidazole, wound debridement, ICU support
- Prevention: DTP vaccine, Td boosters every 10 years
Clinical Pearls
Trismus + recent wound = tetanus until proven otherwise
Shorter incubation period (<7 days) predicts more severe disease
Spasms can be triggered by minimal stimuli — keep environment quiet and dark
Why This Matters Clinically
Tetanus is rare in developed countries due to vaccination but still occurs in unvaccinated/under-vaccinated individuals, elderly, and IVDU. It is a clinical diagnosis — there is no confirmatory test. Early recognition saves lives. Every wound should prompt tetanus immunisation assessment.
Visual assets to be added:
- Opisthotonus photograph (historical)
- Risus sardonicus illustration
- Tetanus prophylaxis algorithm flowchart
- Clostridium tetani microscopy image
Incidence & Prevalence
- UK incidence: ~5-10 cases/year (extremely rare due to vaccination)
- Global burden: ~35,000 deaths/year (mostly neonatal tetanus in developing countries)
- Case fatality: 10-20% in high-income countries; up to 50% in resource-limited settings
- Neonatal tetanus: Major cause of neonatal mortality in developing countries
Demographics
- Age: Bimodal — elderly (waning immunity) + unvaccinated children
- Sex: Slight male predominance (occupational exposure)
- UK cases: Mainly elderly, IVDU, migrants from non-vaccinated countries
- IVDU: Muscle-popping, contaminated heroin ("black tar")
Risk Factors
| Risk Factor | Mechanism |
|---|---|
| Unvaccinated/under-vaccinated | No protective antibodies |
| Elderly | Waning immunity (last booster >0 years) |
| Contaminated wounds | Soil, faeces, rust (not the rust itself!) |
| Puncture wounds | Anaerobic environment for germination |
| IVDU | Subcutaneous injection ("skin popping") |
| Burns | Devitalised tissue |
| Chronic wounds | Ulcers, gangrene |
| Unsterile delivery/circumcision | Neonatal tetanus |
Toxin Mechanism
1. Inoculation & Germination
- C. tetani spores enter through wound
- Germinate in anaerobic environment (devitalised tissue)
2. Toxin Production
- Vegetative bacteria produce tetanospasmin (and tetanolysin)
- Tetanospasmin is one of the most potent toxins known (lethal dose ~1ng/kg)
3. Retrograde Axonal Transport
- Toxin binds to peripheral motor neuron terminals
- Transported retrogradely via axons to CNS
4. Synaptic Blockade
- Toxin irreversibly blocks release of GABA and glycine (inhibitory neurotransmitters)
- Location: Spinal cord interneurons and brainstem
- Result: Unopposed excitatory signals → muscle rigidity and spasms
Clinical Consequence
- Rigidity: Continuous muscle contraction (trismus, opisthotonos)
- Spasms: Paroxysmal, triggered by stimuli
- Autonomic dysfunction: Catecholamine storms → HTN, tachycardia, arrhythmias
Recovery
- Toxin binding is irreversible
- Recovery requires regeneration of nerve terminals (weeks to months)
Clinical Forms
| Form | Features | Frequency |
|---|---|---|
| Generalised | Trismus → descending rigidity → spasms | 80% |
| Localised | Rigidity confined to wound area | 10-15% |
| Cephalic | Cranial nerve involvement (wound on head/neck) | Rare |
| Neonatal | Generalised in newborns (umbilical infection) | Rare in UK |
Generalised Tetanus Progression
Stage 1: Prodrome (1-7 days)
Stage 2: Onset of Rigidity
Stage 3: Generalised Rigidity & Spasms
Stage 4: Autonomic Instability (Severe)
Key Examination Findings
| Sign | Description |
|---|---|
| Trismus | Inability to open mouth (masseter spasm) |
| Risus sardonicus | Fixed smile from facial muscle rigidity |
| Opisthotonus | Arched back from paravertebral spasm |
| Board-like abdomen | Rigid abdominal wall |
| Limb rigidity | Generalised hypertonicity |
| Reflex spasms | Triggered by minimal stimuli |
Wound Assessment
- Look for entry point (may be minor/healed)
- Puncture wounds, burns, chronic ulcers
- Injection sites in IVDU
Differential Diagnosis
| Condition | Distinguishing Features |
|---|---|
| Strychnine poisoning | No trismus, history of ingestion |
| Dystonic drug reaction | History of antipsychotics, responds to anticholinergics |
| Rabies | Hydrophobia, animal bite history |
| Hypocalcaemia | Chvostek's sign, Trousseau's sign, low calcium |
| Meningitis | Neck stiffness but jaw opens, fever, CSF changes |
Clinical Diagnosis
- There is no confirmatory laboratory test
- Diagnosis is entirely clinical
Supportive Investigations
| Investigation | Purpose |
|---|---|
| Wound culture | May isolate C. tetani but insensitive |
| Serum anti-tetanus antibody | May be protective if >.01 IU/ml (but doesn't exclude diagnosis) |
| CK | Elevated from muscle spasm |
| ABG | Respiratory acidosis if hypoventilation |
| ECG | Arrhythmias from autonomic instability |
| CT head/LP | Rule out meningitis/encephalitis if uncertain |
Spatula Test
- Touch posterior pharynx with spatula
- Positive: Jaw closes (spasm) — suggests tetanus
- Negative: Gag reflex as normal
Ablett Severity Classification
| Grade | Features | Mortality |
|---|---|---|
| I (Mild) | Mild trismus, no dysphagia, no spasms, no respiratory compromise | <10% |
| II (Moderate) | Moderate trismus, dysphagia, mild spasms | 10-20% |
| III (Severe) | Severe trismus, generalised spasms, respiratory compromise | 20-40% |
| IV (Very Severe) | Grade III + autonomic instability | >0% |
Prognosis Score
- Shorter incubation (<7 days) = worse
- Shorter period of onset (time from first symptom to first spasm) = worse
Immediate Management
1. Neutralise Unbound Toxin
- Human Tetanus Immunoglobulin (TIG): 3000-6000 units IM
- Give as soon as diagnosis suspected
- Does NOT neutralise already-bound toxin
2. Eliminate Source
- Wound debridement: Surgical if needed
- Antibiotics: Metronidazole 500mg IV TDS × 7-10 days (first-line)
- Alternative: Penicillin (but may enhance spasms via GABA antagonism)
3. Control Spasms
| Drug | Regimen | Notes |
|---|---|---|
| Benzodiazepines | Diazepam 10-30mg IV PRN or midazolam infusion | First-line |
| Magnesium sulphate | 4g IV loading then 1-2g/hr | Adjunct for spasms and autonomic dysfunction |
| Baclofen | Intrathecal (specialist) | Refractory cases |
| Neuromuscular blockade | + intubation | If spasms uncontrolled |
4. Supportive Care
- Quiet, dark environment — minimise triggers
- Airway management — intubation if respiratory compromise
- Nutrition — NG or TPN
- DVT prophylaxis
- ICU admission for moderate-severe cases
Management of Autonomic Instability
- Magnesium sulphate
- Morphine/fentanyl
- Avoid beta-blockers (mixed reports; may cause rebound)
- Clonidine, dexmedetomidine (specialist)
Vaccination
- Give Td vaccine to establish active immunity
- TIG only provides passive short-term protection
- Complete primary course if incomplete
Acute Complications
- Respiratory failure: Laryngospasm, diaphragm spasm
- Aspiration pneumonia
- Rhabdomyolysis: From prolonged spasms
- Fractures: Vertebral, long bone from violent spasms
- Arrhythmias and sudden death: Autonomic storms
- Hyponatraemia: SIADH
- Thromboembolic disease: Prolonged immobility
Long-Term Complications
- Prolonged ICU stay (weeks to months)
- Critical illness myopathy/neuropathy
- Persistent rigidity during recovery
- Psychological trauma
Mortality
- Overall: 10-20% with modern ICU care
- Severe (Grade III/IV): 30-50%
- Neonatal tetanus: Up to 90% in resource-limited settings
Recovery Timeline
- ICU stay: 3-6 weeks (range: 2-12 weeks)
- Full recovery: 2-6 months
- No immunity: Having tetanus does NOT confer immunity — vaccinate!
Prognostic Factors
| Factor | Impact |
|---|---|
| Incubation period | <7 days = worse |
| Period of onset | <48 hours = worse |
| Age | Extremes of age = worse |
| Grade | Grade III/IV = worse |
| Autonomic instability | Present = worse |
| Access to ICU | Critical |
Key Guidelines
- PHE Tetanus: Guidance on Management and Prevention (2019)
- WHO Position Paper on Tetanus Vaccines (2017)
- Green Book Chapter 30: Tetanus (UKHSA)
Key Evidence
- Metronidazole superior to penicillin for antibiotic treatment
- Magnesium sulphate reduces spasm frequency and autonomic dysfunction
- Human TIG preferred over equine (fewer adverse reactions)
What is Tetanus?
Tetanus is a serious infection caused by bacteria (Clostridium tetani) that can get into your body through cuts or wounds. It causes severe muscle stiffness and spasms, including "lockjaw" where you can't open your mouth.
Warning Signs
- Stiff jaw (can't open mouth)
- Stiff neck and back
- Painful muscle spasms
- Difficulty swallowing
Prevention
- Keep your tetanus vaccination up to date
- Td booster every 10 years
- Booster if you have a dirty wound and it's been >5 years since last vaccine
- Clean all wounds promptly
When to Seek Help
- If you have a deep, dirty wound and aren't sure about your vaccination status
- If you develop jaw stiffness or muscle spasms after a wound
Resources
Primary Guidelines
- Public Health England. Tetanus: Guidance on the management of suspected cases and on the assessment of tetanus-prone wounds. 2019. gov.uk
- WHO. Tetanus vaccines: WHO position paper—February 2017. Wkly Epidemiol Rec. 2017;92(6):53-76. PMID: 28185446
Key Studies
- Ahmadsyah I, Salim A. Treatment of tetanus: an open study to compare the efficacy of procaine penicillin and metronidazole. Br Med J. 1985;291(6496):648-650. PMID: 3929900
- Thwaites CL, et al. Magnesium sulphate for treatment of severe tetanus: a randomised controlled trial. Lancet. 2006;368(9545):1436-1443. PMID: 17055945