Epidemiology
Tetanus is an entirely preventable disease; the
first vaccine was produced in 1924. Routine
vaccination began in the UK in 1961. It is
given as a combined vaccine along with diphtheria and pertussis (DPT). Unfortunately,
immunity to tetanus may not be life-long
and booster injections may be required after
individuals sustain tetanus-prone wounds.
Tetanus immunization guidelines are available in the British National Formulary.1
Poor access to a programme of immunization
accounts for the high prevalence of the disease
in the developing world. Implementation
of global tetanus immunization has been a
target of the World Health Organization
since 1974.
Recently there has been a cluster of tetanus
cases amongst injecting drug-users in the UK.
Twenty-four cases were reported between 2003
and 2004. The majority of these had no record
of (or, at best, incomplete) immunization.
This outbreak is thought to be a result of
a batch of contaminated heroin.2 I.M or s.c.
drug-use is a particularly high risk activity for
developing tetanus.
Pathophysiology
C. tetani spores are widespread in the environment residing in soil, faeces and dust.3 Tetanus
spores are extremely hardy and can survive
extreme conditions for prolonged periods.
They usually enter the body after contamination of an abrasion or minor puncture wound,
although, in 20% of cases, no entry site can
be found. Spores also gain entry through skin
ulcers, abscesses, gangrene, burns or after
abdominal/pelvic surgery, childbirth and
abortion.4 The incubation period of the disease is between 3 and 21 days (average 7 days).
The manifestations of tetanus are caused by
tetanospasmin, which is released by the tetanus bacillus on entry into the body. Symptoms
arise 12 weeks after infection. Tetanospasmin
is an extremely potent neurotoxin; it is estimated that as little as 240 g is enough to kill the
entire world population. The toxin spreads
into the nervous system by binding to the
neuromuscular junction. Once bound, it is
transported retrogradely to the cell body.
Further spread occurs trans-synaptically to
adjacent motor and autonomic nerves.4
Tetanospasmin exerts its effect by cleaving
synaptobrevin, a vesicle-associated membrane
protein which is essential for the release of
neurotransmitter. The toxin primarily affects
inhibitory pathways, preventing the release of
glycine and g-amino butyric acid (GABA).
When interneurones inhibiting alpha motor
neurones are affected, there is failure to inhibit
motor reflexes. This causes increased muscle
tone and rigidity, interposed by sudden
and potentially devastating muscle spasms.
Muscles of the face are affected early because
of their short axonal pathways. Sympathetic
neurones become affected later in the disease.
Disinhibited autonomic discharge leads to loss
of autonomic control, resulting in sympathetic
overactivity and increased catecholamine
levels.
Neuronal binding of the toxin is irreversible. Recovery requires the growth of new
nerve terminals, which explains the prolonged
duration of the disease.
doi:10.1093/bjaceaccp/mkl014
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Key points
Tetanus is a preventable
disease; it is a significant cause
of mortality worldwide
causing one million deaths
annually.
At least 20 cases of tetanus
occur in the UK each year.
Management of tetanus is
essentially supportive using
antibiotics, surgery,
immunization, sedation and,
when necessary, ventilation.
The mortality from tetanus
remains high despite modern
intensive care.
101
Tetanus
Mortality
Grade 1 (mild)
Mild trismus, general spasticity, no respiratory compromise, no spasms,
no dysphagia
Grade 2 (moderate)
Moderate trismus, rigidity, short spasms, mild dysphagia, moderate respiratory
involvement, ventilatory frequency >30
Grade 3 (severe)
Severe trismus, generalized rigidity, prolonged spasms, severe dysphagia,
apnoeic spells, pulse >120, ventilatory frequency >40
Grade 4 (very severe)
Grade 3 with severe autonomic instability
Clinical features
Table 2 Differential diagnosis of tetanus
Hypocalcaemic tetany
Epilepsy
Chorea
Meningitis
Encephalitis
Subarachnoid haemorrhage
Strychnine poisoning
Rabies
Sepsis
Drug withdrawal
Grading severity
There are several grading systems; the scale proposed by Ablett5
is the most widely used (Table 1). This categorizes patients
into four grades depending upon the intensity of spasms, and
respiratory and autonomic involvement.
Differential diagnosis
Tetanus is a purely clinical diagnosis. The differential diagnosis
is listed in Table 2.
Management
Classification of tetanus
Four different forms of tetanus are described; local, cephalic,
generalized and neonatal. In local tetanus, spasm and rigidity
are confined to the site of injury. It is an uncommon and relatively
mild form of tetanus with a low mortality (1%). Cephalic tetanus
occurs after a wound to the head and neck or otitis media. It is
characterized by cranial nerve palsies (especially the seventh)
and leads to paralysis; it is associated with a high mortality.
The most common type is generalized tetanus which is
responsible for 80% of cases. It results from the haematogenous
spread of the toxin. The muscles of the head and neck are affected
first with progressive distal spread of spasm and rigidity throughout the body. Neonatal tetanus is responsible for over 50% of
deaths associated with tetanus. It is caused by poor umbilical
hygiene and is entirely preventable by maternal vaccination. It
carries a poor prognosis. Neonatal tetanus has been completely
eliminated from the UK.
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Tetanus
Supportive treatment
Successful management of tetanus requires the entire armamentarium of the modern intensive care unit. A multidisciplinary
approach is essential. Most cases require 46 weeks of supportive
treatment. Poor nutrition and weight loss occur rapidly because
of dysphagia, altered gastrointestinal function and increased
metabolic rate. Enteral nutrition should be established as early
as possible. Nosocomial infections are common because of the
prolonged course of tetanus and remain an important cause of
mortality. Prevention of respiratory complications involves
meticulous mouth care, chest physiotherapy and tracheal suction.
Adequate sedation during invasive procedures is mandatory to
prevent provoking spasm or autonomic instability. Pulmonary
embolism is a particular problem and thromboprophylaxis is
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Tetanus
References
1. British National Formulary Number 49. British Medical Association and
Royal Pharmaceutical Society of Great Britain: Pharmaceutical Press, 2005
2. Health Protection Agency. Ongoing national outbreak of tetanus in
injecting drug users. Commun Dis Rep CDR Wkly [serial online] 2004;
14(a): news. Available at http://www.hpa.org.uk/cdr/ PDFfiles/2004/
cdr0904.pdf
3. Thwaites CL. Tetanus. Curr Anaesth Crit Care 2005; 16: 5057
4. Cook TM, Protheroe RT, Handel JM. Tetanus: a review of the literature.
Br J Anaesth 2001; 87: 47787
5. Ablett JJL. Analysis and main experiences in 82 patients treated
in the Leeds Tetanus Unit. In: Ellis M. ed. Symposium on tetanus
in Great Britain. Boston Spa, UK: Leeds General Infirmary, 1967;
110
6. Ahmadsyah I, Salim A. Treatment of tetanus: an open study to compare
the efficacy of procaine penicillin and metronidazole. Br Med J (Clin Res Ed)
1985; 291: 64850
7. Attygalle D, Rodrigo N. Magnesium as first line therapy in the
management of tetanus: a prospective study of 40 patients. Anaesthesia
2002; 57: 81117
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