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Tetanus

Tetanus is a serious neurological disease caused by the neurotoxin produced by Clostridium tetani. The bacterium forms resistant spores that commonly enter the body through contaminated wounds

Also called

Clostridium tetani infection

ICD-10

A33

Specialty

Infectious

Onset

Acute

Reviewed

August 2026
On This Page

Overview

–Tetanus spores are widely present in soil and can contaminate wounds, particularly deep puncture wounds or wounds containing devitalized tissue.

The disease does not spread from person to person.

 

-The classic presentation is:

Trismus → neck stiffness → generalized muscle rigidity → painful spasms

 

Severe disease can cause respiratory failure and autonomic instability.

Etiology & Risk Factors

–Tetanus is caused by Clostridium tetani, an anaerobic, Gram-positive, spore-forming bacillus.

 

-The organism enters damaged tissue as spores and produces tetanospasmin under anaerobic conditions.

 

Common wound types include:

  • Deep puncture wounds
  • Contaminated wounds
  • Crush injuries
  • Burns
  • Wounds containing foreign bodies

 

-Risk Factors

  • Incomplete or absent vaccination
  • Dirty or contaminated wounds
  • Deep puncture wounds
  • Devitalized tissue
  • Retained foreign bodies
  • Intravenous drug use

Pathophysiology

C. tetani spores enter wound → germination in anaerobic tissue → tetanospasmin production → retrograde transport to the nervous system → toxin binds presynaptic nerve terminals → inhibition of GABA and glycine release → uncontrolled motor neuron activity → muscle rigidity and spasms

The toxin also affects autonomic nervous system regulation, which can produce severe cardiovascular instability.

Clinical Presentation

-Symptoms:

Tetanus typically develops after an incubation period of several days to weeks.

Common symptoms include:

  • Trismus (lockjaw)
  • Neck stiffness
  • Difficulty swallowing
  • Muscle rigidity
  • Painful muscle spasms
  • Abdominal muscle rigidity

 

-Signs:

Characteristic findings include:

  • Trismus
  • Risus sardonicus
  • Generalized muscle rigidity
  • Reflex muscle spasms
  • Opisthotonus in severe disease

 

Spasms may be triggered by:

  • Loud noises
  • Touch
  • Light
  • Minor sensory stimulation
Tetanus Overview
Tetanus Overview

History Taking

-Ask about:

  • Recent wounds
  • Type and depth of wound
  • Soil or fecal contamination
  • Foreign bodies
  • Previous tetanus vaccination
  • Number of previous vaccine doses
  • Time since the last booster
  • Onset of trismus
  • Difficulty swallowing
  • Muscle spasms

Physical Examination

-General Examination

  • Assess airway
  • Respiratory rate and oxygen saturation
  • Heart rate and blood pressure
  • Temperature
  • Level of consciousness

 

-System-Specific Examination:

  • Assess trismus
  • Examine neck stiffness
  • Assess generalized rigidity
  • Observe muscle spasms
  • Examine the wound carefully
  • Assess for respiratory muscle involvement
  • Monitor for autonomic instability

Investigations

Biochemistry / Specific Tests

  • Electrolytes

  • Renal function

  • Creatine kinase (CK) when significant muscle spasms or muscle injury are present

  • Arterial Blood Gas in severe respiratory disease

 

-Imaging

Not routinely required to diagnose Tetanus.

Imaging may be performed to evaluate suspected complications or alternative diagnoses.

 

-Special / Confirmatory Tests

There is no reliable laboratory test that confirms or excludes clinical Tetanus.

 

Diagnosis of Tetanus is primarily clinical.

Wound cultures may identify C. tetani, but a negative culture does not exclude the disease.

 

-Important Investigation Note

Tetanus is a clinical diagnosis; treatment should not be delayed while waiting for laboratory confirmation.

Diagnosis

-Tetanus is diagnosed clinically based on:

Trismus + generalized muscle rigidity/spasms ± autonomic dysfunction + compatible wound history and inadequate immunization.

Laboratory testing is not required for diagnosis.

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Management

Tetanus · Management

Immediate Priorities — On Admission
Airway
Early intubation — do not wait for respiratory failure; laryngospasm is sudden
Grade III–IV: tracheostomy preferred over prolonged intubation
Dark, quiet room — minimise sensory stimuli triggering spasms
Mechanical ventilation if Grade III–IV
Neutralise toxin
Human tetanus immunoglobulin (HTIG) 3,000–6,000 IU IM — immediately; neutralises unbound toxin only
Give at different site from toxoid vaccine
Equine ATS 1,500 IU — if HTIG unavailable; test for allergy first
Give HTIG before wound débridement — débridement releases more toxin
Wound management
Débride thoroughly — remove necrotic tissue, foreign bodies; eliminates toxin source
Irrigate with H₂O₂ — disrupts anaerobic environment
Tetanus toxoid vaccine — give simultaneously at different site
Disease does NOT confer immunity — always vaccinate
Antibiotics
AgentDoseRoleDuration
Metronidazole
1st line		 500 mg IV/PO q8h Kills vegetative C. tetani at wound — stops ongoing toxin production. Preferred: does NOT antagonise GABA unlike penicillin. 7–10 days
Benzylpenicillin
Alternative		 1.2g IV q6h Effective against C. tetani but may worsen spasms — penicillin is a GABA antagonist. Use only if metronidazole unavailable. 7–10 days
Doxycycline
Alternative		 100 mg BD PO Oral alternative — resource-limited settings or PO step-down. 7–10 days
Key rule: Antibiotics kill bacteria but do NOT neutralise already-bound toxin. HTIG is the only agent that neutralises unbound circulating toxin. Antibiotics prevent further toxin production only.
Spasm Control
AgentDoseRolePriority
Diazepam 5–10 mg IV q1–4h PRN or 50–100 mg/day continuous infusion GABA-A agonist — muscle relaxation + sedation. Large doses often needed. 1st line in most settings. 1st line
Midazolam 0.05–0.1 mg/kg/h IV infusion Preferred for ICU continuous infusion — shorter acting, less propylene glycol toxicity than diazepam. 1st line (ICU)
Magnesium sulphate Loading: 5g IV over 20 min → 2–3g/h infusion. Titrate to loss of patellar reflex. Reduces spasm frequency + autonomic instability. Blocks NMJ, inhibits catecholamine release. Monitor: patellar reflex, RR, UO. 2nd line / adjunct
Vecuronium / Pancuronium Vecuronium 0.1 mg/kg IV bolus or infusion Neuromuscular blockade — refractory spasms uncontrolled by benzodiazepines. Requires mechanical ventilation. Refractory only
Intrathecal baclofen Specialist use only GABA-B agonist — reduces spinal spasm directly. Severe refractory tetanus only. Specialist / refractory
Autonomic Control & Supportive Care
Autonomic dysfunction
Labetalol IV — 1st choice; combined α+β blocker for sympathetic surges
Magnesium sulphate infusion — blunts catecholamine release
Clonidine — central α₂ agonist; reduces sympathetic outflow
Morphine IV infusion — reduces catecholamine surges + pain
Atropine — for vagal episodes and bradycardia
Avoid pure β-blockers (propranolol) — unopposed α → severe hypertension
Supportive care
Dark, quiet room — minimise all sensory triggers
NG feeding — high caloric need (massive energy expenditure from spasms)
DVT prophylaxis — LMWH + compression stockings
Pressure ulcer prevention — regular repositioning
Monitor: patellar reflex (Mg toxicity), SpO₂, ECG, UO
Vaccinate before discharge — disease confers no immunity

Tetanus · Prevention & Wound Management

Wound Management Algorithm
Wound typeVaccination statusAction
Clean wound Fully vaccinated (≥3 doses) + last dose <10 years Nothing required
Clean wound Fully vaccinated + last dose >10 years Toxoid booster only
Dirty / tetanus-prone wound
Soil, manure, puncture, devitalised tissue, burns, animal bites		 Fully vaccinated + last dose <5 years Nothing required (adequate protection)
Dirty / tetanus-prone wound Fully vaccinated + last dose >5 years Toxoid booster only
Dirty / tetanus-prone wound Unvaccinated or unknown or incomplete (<3 doses) HTIG 250 IU IM (different site) + Full toxoid course (3 doses)
Primary vaccination: 3 doses DTP (childhood) + booster at 10 years. Disease does NOT confer immunity — always complete vaccination during recovery. Neonatal tetanus prevention: maternal TT vaccination during pregnancy (2 doses) + sterile cord cutting.

Complications

Tetanus · Complications

Quick Review — Aetiology & Clinical Forms
Organism & mechanism
Clostridium tetani — gram-positive, anaerobic, spore-forming rod
Toxin: Tetanospasmin — retrograde axonal transport → blocks GABA + glycine → unopposed muscle contraction
Incubation: 3–21 days — shorter = more severe
Clinical signs
Trismus — earliest sign; masseter spasm (lockjaw)
Risus sardonicus — sustained grimace; pathognomonic
Opisthotonus — severe back arching; extensor spasm
Consciousness fully preserved — key DDx feature
Ablett grading
Grade I — mild trismus, no spasms
Grade II — moderate trismus, short spasms, mild dysphagia
Grade III — severe trismus, prolonged spasms, dysautonomia
Grade IV — Grade III + severe autonomic instability → mandatory ICU
Complications
ComplicationDetailsTiming / Notes
Laryngospasm / asphyxia Spasm of laryngeal muscles → sudden airway obstruction → respiratory arrest. Most acute life-threatening complication. Triggered by noise, touch, light. Any time — acute emergency
Respiratory failure Sustained spasm of respiratory muscles → hypoxia, hypercapnia, CO₂ retention. Compounded by diaphragm involvement. Requires mechanical ventilation. Early — leading cause of death
Autonomic dysfunction Catecholamine storm — tachycardia, hypertension, sweating, hypersalivation alternating with bradycardia, hypotension. Appears day 4–8 after spasm onset. Late — leading ICU cause of death
Rhabdomyolysis Sustained violent muscle spasms → massive muscle breakdown → markedly elevated CK → myoglobinuria → acute kidney injury. Proportional to spasm severity
Fractures Intense opisthotonus and spasms → compression fractures of vertebrae, long bone fractures — especially in elderly. Severe / prolonged disease
Aspiration pneumonia Dysphagia + hypersalivation + impaired airway protection → aspiration of secretions → pneumonia. Common in ventilated patients. ICU — ventilated patients
Deep vein thrombosis / PE Prolonged immobility + ICU admission → DVT risk. Pulmonary embolism is a recognised cause of death in tetanus. Prolonged ICU stay
Pressure ulcers / contractures Prolonged rigidity and bed rest → pressure sores over bony prominences. Long-term muscle contractures in survivors. Prolonged disease
Neonatal tetanus Generalised tetanus in neonate — umbilical stump entry. Poor feeding, rigidity, spasms day 3–14 of life. Mortality up to 50% even with treatment. High mortality — preventable
Overall mortality: 10–20% in adults with good ICU care. Up to 50% in neonatal tetanus. Death caused by: respiratory failure (early) → autonomic instability (late) → PE or nosocomial infection (prolonged ICU). Shorter incubation period + shorter period of onset (time from first symptom to first spasm) = worse prognosis.

Prognosis

The prognosis of Tetanus depends on disease severity, incubation period, vaccination status, age, and the presence of respiratory or autonomic complications. Severe generalized disease can be fatal, but early intensive supportive treatment significantly improves survival.

Recovery may take weeks to months because the nervous system requires time to restore normal neuromuscular function.

Key Points / Clinical Pearls

  • Tetanus is caused by Clostridium tetani toxin.
  • The disease is not transmitted person-to-person.
  • Spores commonly enter through contaminated wounds.
  • Deep puncture wounds are an important risk factor.
  • Inadequate vaccination greatly increases risk.
  • Tetanospasmin blocks inhibitory neurotransmission.
  • GABA and glycine release are inhibited.
  • Trismus is a classic early feature.
  • Generalized rigidity and painful spasms are characteristic.
  • Sensory stimulation can trigger spasms.
  • Diagnosis is primarily clinical.
  • There is no reliable test that excludes Tetanus.
  • Human tetanus immune globulin neutralizes unbound toxin.
  • Wound cleaning and debridement are essential.
  • World Health Organization (WHO). Tetanus .
  • Centers for Disease Control and Prevention (CDC). Tetanus .
  • Centers for Disease Control and Prevention (CDC). Tetanus — Pink Book .
  • Thwaites CL, Yen LM, Glover C, et al. Predicting the Clinical Outcome of Tetanus: The Tetanos Severity Score. Trop Med Int Health. 2006;11(2):279-287. PubMed .
  • Yen LM, Thwaites CL. Tetanus. Lancet. 2019;393(10181):1657-1668. PubMed .
  • National Library of Medicine (NIH). Tetanus . StatPearls.