Tetanus

Tetanus is an acute, often life threatening illness caused by the neurotoxin tetanospasmin. The toxin is produced by Clostridium tetani, an anaerobic, spore forming, Gram positive bacillus found ubiquitously in soil, dust and animal faeces.

Disease results from toxin production at the site of a contaminated wound, not from bacterial invasion itself. It is entirely preventable through effective vaccination. Unvaccinated or inadequately vaccinated status is the single most important risk factor.

Pathophysiology

Spores introduced into a wound produce tetanospasmin. Devitalised tissue and a low oxygen environment favour anaerobic germination.

The toxin travels retrogradely along peripheral motor neurons to the spinal cord and brainstem. There it blocks release of the inhibitory neurotransmitters glycine and gamma aminobutyric acid. This produces unopposed motor neuron activity and the characteristic sustained muscle rigidity and spasms.

Trismus (lockjaw) is the commonest presenting feature. It occurs together with risus sardonicus (a sustained grimace from facial muscle spasm) and neck stiffness. These typically develop within the first week after the inciting injury. The incubation period ranges from days to several weeks, depending on the distance of the wound from the central nervous system.

Progressive generalised muscle rigidity and painful, often violent, spasms follow. Minimal external stimuli (light, sound, touch) trigger them. Opisthotonus (severe back arching from paraspinal spasm) occurs in severe disease.

Autonomic instability (labile blood pressure, tachycardia, hyperthermia) characterises the most severe cases and contributes significantly to mortality.

Laryngospasm and respiratory muscle involvement can cause life threatening airway obstruction and respiratory failure. They require intensive monitoring and, frequently, ventilatory support in moderate to severe disease.

Neonatal tetanus occurs through umbilical stump contamination in inadequately immunised populations. It presents with poor feeding, rigidity and spasms in the first weeks of life. Mortality is very high without intensive supportive care.

Diagnosis is entirely clinical. It rests on the characteristic combination of trismus, rigidity and spasms in a patient with a compatible wound history and inadequate immunisation status. No reliable laboratory test confirms the diagnosis, and wound culture is frequently negative even in confirmed clinical disease.

Serum tetanus antitoxin level can support the diagnosis if measured before administration of any immunoglobulin. A protective level effectively excludes tetanus. A low or absent level does not confirm the diagnosis, given overlap with unvaccinated but unaffected individuals.

Assess wound characteristics, which support the clinical suspicion:

• Puncture wounds
• Devitalised or necrotic tissue
• Contamination with soil or foreign material
• Delayed presentation for wound care

Obtain a thorough vaccination history. Inadequate documentation is common, and a pragmatic approach to prophylaxis is generally taken where vaccination status is uncertain.

Give human tetanus immunoglobulin as soon as the diagnosis is suspected, at a dose of 3000 to 6000 units intramuscularly. Infiltrate part of the dose around the wound where identifiable. It neutralises circulating and unbound toxin before it can reach the central nervous system. It cannot reverse toxin already bound within neural tissue.

Metronidazole 500 mg intravenously every 8 hours (or 400 mg orally every 8 hours if intravenous access is not required for other reasons) for 7 to 10 days is the preferred antibiotic. It eliminates the ongoing source of toxin production.

Penicillin is an alternative, though theoretically less favoured. It has a proposed, though not definitively established, gamma aminobutyric acid antagonist effect that could theoretically worsen spasms.

Wound debridement of any devitalised or necrotic tissue is essential. It eliminates the anaerobic environment favouring ongoing toxin production. Perform it after immunoglobulin and antibiotic administration have been initiated.

Manage muscle rigidity and spasms with benzodiazepines as first line therapy. Typically diazepam is titrated to effect, given in repeated intravenous doses or as a continuous infusion in severe disease. Doses are individualised and often substantially higher than for other indications, given the severity of spasm control required.

Magnesium sulphate infusion is an effective adjunct for controlling both spasms and autonomic instability in moderate to severe disease.

Severe disease with significant rigidity, spasms or autonomic instability requires management in an intensive care setting. Minimise external stimulation (a darkened, quiet environment).

Neuromuscular blockade and mechanical ventilation are required for the most severe cases. These are cases where spasms cannot be adequately controlled with sedation alone, or where laryngospasm threatens the airway.

Manage autonomic instability with short acting agents (labetalol, esmolol infusion, or magnesium sulphate) titrated to effect, given the labile and unpredictable nature of the dysfunction. Morphine infusion is also used, both for analgesia and for its beneficial effect on autonomic stability.

Give active immunisation with tetanus toxoid containing vaccine during convalescence, and complete it according to standard schedule. Natural infection with tetanus does not confer reliable lasting immunity. The quantity of toxin required to produce clinical disease is extremely small relative to that needed to stimulate an adequate immune response.

Wound management and tetanus prophylaxis in the acute injury setting, for any patient presenting with a wound, is guided by both wound characteristics and vaccination history. Wounds are either clean minor wounds or tetanus prone wounds. Tetanus prone wounds include any wound with significant contamination, devitalised tissue, puncture mechanism or delayed presentation.

• A fully vaccinated patient with a clean wound requires no additional prophylaxis.
• An incompletely vaccinated or unknown status patient with a tetanus prone wound requires both a dose of tetanus toxoid containing vaccine and human tetanus immunoglobulin 250 units intramuscularly. Increase this to 500 units for heavily contaminated wounds or where treatment has been delayed beyond 24 hours.
• Complete the vaccination course subsequently according to standard schedule.