Tetanus
Last updated 13th November 2018 - Tom Heaton
This is quite a nice summary video:
https://www.youtube.com/watch?v=XVUFGCzmpbQ
Tetanus is a clinical condition caused by the bacteria clostridium tetani.
This is a gram-positive, drumstick shaped bacteria that is an obligate anaerobe and spore forming.
It is found widespread in the environment in soil, especially related to manure.
The spores are particularly hardy.
https://www.youtube.com/watch?v=XVUFGCzmpbQ
Tetanus is a clinical condition caused by the bacteria clostridium tetani.
This is a gram-positive, drumstick shaped bacteria that is an obligate anaerobe and spore forming.
It is found widespread in the environment in soil, especially related to manure.
The spores are particularly hardy.
Pathophysiology
The clinical effects of tetanus arise from the very potent neurotoxin tetanospasmin.
This is produced by the bacteria after entry to the body.
It acts by entering neurons at the neuromuscular junction and being transported up the neuron to the spinal cord/CNS where there is further spread.
It primarily has its effect by inhibiting inhibitory interneurons (mainly with the neurotransmitter GABA).
The effect of this is uncontrolled activation of motor and autonomic nerves.
The mechanism of action of this is by the inhibition of neurotransmitter release.
This is due to the cleaving of synaptobrevin by the toxin, which is essential for neurotransmitter release.
Infection usually arises from a contaminated wound.
This can be a wound of any size, but requires the anaerobic condition found in necrotic tissue.
The incubation period of the disease is between 3 and 21 days.
The clinical effects usually start to manifest between 1 and 2 weeks.
As the nerves of the face are shorter, it is often these muscle groups that develop symptoms first.
The autonomic nerves are generally affected later.
The binding is permanent, requiring new neuron growth for recovery.
This is produced by the bacteria after entry to the body.
It acts by entering neurons at the neuromuscular junction and being transported up the neuron to the spinal cord/CNS where there is further spread.
It primarily has its effect by inhibiting inhibitory interneurons (mainly with the neurotransmitter GABA).
The effect of this is uncontrolled activation of motor and autonomic nerves.
The mechanism of action of this is by the inhibition of neurotransmitter release.
This is due to the cleaving of synaptobrevin by the toxin, which is essential for neurotransmitter release.
Infection usually arises from a contaminated wound.
This can be a wound of any size, but requires the anaerobic condition found in necrotic tissue.
The incubation period of the disease is between 3 and 21 days.
The clinical effects usually start to manifest between 1 and 2 weeks.
As the nerves of the face are shorter, it is often these muscle groups that develop symptoms first.
The autonomic nerves are generally affected later.
The binding is permanent, requiring new neuron growth for recovery.
Epidemiology
Tetanus has been greatly reduced by the introduction of an effective vaccine (synthesised in 1924 and routine in the UK from 1961).
However, immunity may not be lifelong.
In addition, it can be a significant problem in parts of the world where routine vaccination is not prevalent.
The mortality is around 50% outside the developed world, primarily due to acute respiratory failure.
With critical care support, mortality is around 10% (although higher in certain groups).
Recovery with appropriate supportive care is slow but often complete.
However, immunity may not be lifelong.
In addition, it can be a significant problem in parts of the world where routine vaccination is not prevalent.
The mortality is around 50% outside the developed world, primarily due to acute respiratory failure.
With critical care support, mortality is around 10% (although higher in certain groups).
Recovery with appropriate supportive care is slow but often complete.
Presentation
It is a clinical diagnosis.
The presentation is a triad of:
Muscle spasms are very painful, and can occur spontaneously or be triggered by a stimulus (touch, visual, auditory).
They may be strong enough to cause dislocations, fractures or tendon rupture.
In the face they may manifest as trismus or risus sardonicus.
In the trunk muscle it may result in opisthotonus (arching back) and respiratory failure.
Laryngeal spasm may lead to airway loss.
Dysphagia may also occur.
Autonomic instability usually starts after the muscular effects and lasts 1-2 weeks.
This can be both sympathetic and vagal in nature, with rapid fluctuations.
In may include:
Other types of tetanus have been described but are rarer.
Localised tetanus is just confined to the area of infection/injury.
Cephalic tetanus occurs from a head wound, resulting in cranial nerve involvement and paralysis.
Neonatal tetanus is related to poor umbilical hygiene.
The presentation is a triad of:
- Muscle rigidity
- Muscle spasm
- Autonomic instability
Muscle spasms are very painful, and can occur spontaneously or be triggered by a stimulus (touch, visual, auditory).
They may be strong enough to cause dislocations, fractures or tendon rupture.
In the face they may manifest as trismus or risus sardonicus.
In the trunk muscle it may result in opisthotonus (arching back) and respiratory failure.
Laryngeal spasm may lead to airway loss.
Dysphagia may also occur.
Autonomic instability usually starts after the muscular effects and lasts 1-2 weeks.
This can be both sympathetic and vagal in nature, with rapid fluctuations.
In may include:
- Tachycardia
- Hypertension
- Hypotension
- Asystole
- Bradycardia
- Sweating
- Salivation/bronchial secretions.
- Hyperpyrexia
- Ileus
Other types of tetanus have been described but are rarer.
Localised tetanus is just confined to the area of infection/injury.
Cephalic tetanus occurs from a head wound, resulting in cranial nerve involvement and paralysis.
Neonatal tetanus is related to poor umbilical hygiene.
Grading
The Ablett system is most commonly used for describing severity.
- Mild - mild trismus, generalised spasticity but no spasms, no respiratory compromise
- Moderate - moderate trismus, rigidity, short spasms, moderate respiratory involvement
- Severe - severe trismus, prolonged spasms, severe dysphagia, apnoeic spells, RR > 40
- Very severe - grade 3 with autonomic instability
Management
This can be considered as supportive and specific.
Supportive
Intensive care admission for observation is required in all patients.
Patients may need a month or longer of supportive care.
A low threshold is needed for I&V and respiratory support due to the risk of respiratory arrest from airway or respiratory muscle failure.
Muscle spasms can be treated with sedation.
Benzodiazepines can be effective, but mechanical ventilation may be needed due to the degree of sedation that may be needed.
Drugs that have been used include:
Autonomic instability is also supportive.
Sedation can be helpful with this.
Agents for managing sympathetic overactivity include:
Specific
The treatment of the toxin is human tetanus immunoglobulin.
This binds to and neutralises circulating toxin, but not toxin already bound to neurons.
It has a long half life in the circulation so does not need repeating.
Antibiotics may be needed to treat the infection itself.
Metronidazole is a common choice.
Source control may be needed.
This will involve surgical debridement and removal of any necrotic tissue.
Supportive
Intensive care admission for observation is required in all patients.
Patients may need a month or longer of supportive care.
A low threshold is needed for I&V and respiratory support due to the risk of respiratory arrest from airway or respiratory muscle failure.
Muscle spasms can be treated with sedation.
Benzodiazepines can be effective, but mechanical ventilation may be needed due to the degree of sedation that may be needed.
Drugs that have been used include:
- Benzodiazepines
- Propofol
- Dantrolen
- Opioids
Autonomic instability is also supportive.
Sedation can be helpful with this.
Agents for managing sympathetic overactivity include:
- Opioids
- Beta blockers
- Alpha 2 agonists
- Magnesium
Specific
The treatment of the toxin is human tetanus immunoglobulin.
This binds to and neutralises circulating toxin, but not toxin already bound to neurons.
It has a long half life in the circulation so does not need repeating.
Antibiotics may be needed to treat the infection itself.
Metronidazole is a common choice.
Source control may be needed.
This will involve surgical debridement and removal of any necrotic tissue.
Prevention
Tetanus infection itself does not confer immunity.
A vaccination schedule exists in the UK to provide immunity.
It is felt that a total of 5 doses of the vaccine is sufficient to provide lifelong immunity.
In the UK, this consists of:
A booster is recommended for people travelling to remote areas where immunoglobulin may not be easily and immediately available.
The ‘standard’ vaccine for adults is tetanus/diphtheria/inactivated polio virus (Td/IPV)
Tetanus Prone Wounds
A tetanus prone wound is a wound that is:
Wound contact with manure, soil or musty metal contribute to risk.
In very high risk wound immunoglobulin should be given.
When patients have an up to date immunisation schedule, no further vaccination is needed.
In cases of incomplete vaccination schedules or uncertainty, tetanus vaccination should be given.
A vaccination schedule exists in the UK to provide immunity.
It is felt that a total of 5 doses of the vaccine is sufficient to provide lifelong immunity.
In the UK, this consists of:
- Primary vaccination
- Usually 3 doses, each one at 2, 3 and 4 months of age.
- Can be given at later times, with at least a 1 month gap between doses if it has been missed.
- Usually 3 doses, each one at 2, 3 and 4 months of age.
- Boosters
- 3 years (if under 10) or 5 years (if over 10) after primary course completion
- 10 years after primary vaccination course
- 3 years (if under 10) or 5 years (if over 10) after primary course completion
A booster is recommended for people travelling to remote areas where immunoglobulin may not be easily and immediately available.
The ‘standard’ vaccine for adults is tetanus/diphtheria/inactivated polio virus (Td/IPV)
Tetanus Prone Wounds
A tetanus prone wound is a wound that is:
- Sustained over 6 hours before definitive surgery
- Any wound or burn that has:
- Significant amount of devitalised tissue
- Foreign bodies
- Compound fracture
- Clinical evidence of sepsis
- Significant amount of devitalised tissue
Wound contact with manure, soil or musty metal contribute to risk.
In very high risk wound immunoglobulin should be given.
When patients have an up to date immunisation schedule, no further vaccination is needed.
In cases of incomplete vaccination schedules or uncertainty, tetanus vaccination should be given.
Questions
- Which organism is responsible for causing tetanus?
- What is the clinical triad of tetanus?
- What is the pathophysiology of tetanus?
Links & References
- Taylor, A. Tetanus. CEACCP. 2006. 6(3):101-104. https://academic.oup.com/bjaed/article/6/3/101/375396
- AB MBBS. Tetanus. 2017. https://www.youtube.com/watch?v=XVUFGCzmpbQ
- Newson, L. Tetanus and tetanus vaccination. 2017. Patient.info https://patient.info/doctor/tetanus-and-tetanus-vaccination
- Murray, P. Basic medical microbiology. 2018. Philadelphia, Pennsylvania. Elsevier.
