- Tetanus is caused by Clostridium tetani bacteria and is characterized by painful muscle spasms and contractions. - It is more common in wounds, the elderly, and in areas without adequate vaccination programs. Symptoms vary depending on the infected area but often include lockjaw. - Treatment involves antibiotics to kill the bacteria, tetanus immunoglobulin to neutralize toxins, and managing symptoms such as spasms, while prognosis depends on patient age and health. Preventive measures focus on proper vaccination.

1. T E T A N U S
OBJECTIVES:
At the end of this session each student should be able to:
1. Define tetanus.
2. Describe epidemiology of tetanus.
3. Mention cause of tetanus.
4. Describe pathophysiology of tetanus.
5. Describe clinical features of tetanus.
6. Mention differential diagnoses of tetanus.
7. Mention complications of tetanus.
8. Diagnose tetanus.
9. Investigate patients with tetanus.
10. Treat patients with tetanus.
11. Describe prognosis in tetanus patients.
12. Describe preventive measure for tetanus.
J.J. Kambona (M.B.Ch.B; M.Med)
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2. Definition:
Tetanus is an illness characterized by an acute onset of hypertonia, painful muscular
contractions (usually of the muscles of the jaw and neck) and generalized muscle spasms
without other apparent medical causes.
The word tetanus comes from the Greek term teinein, meaning to stretch.
Epidemiology:
• Race:
From 1998-2000, the incidence of tetanus in the USA was highest among Hispanics
(0.38 cases per million population), followed by whites (0.13 cases per million
population) and then African Americans (0.12 cases per million population).
• Age:
Tetanus is more serious at the extremes of ages i.e. neonates and elderly patients.
• Gender:
o In developed countries:
Men are believed to be better protected than women, perhaps because of
additional vaccinations administered during military service or professional
activities.
o In developing countries:
Women are believed to be better protected than men. Women have an increased
immunity where tetanus toxoid is administered to women of childbearing age to
prevent neonatal tetanus. Male to female ratio is 4:1 (KCMC medical record data,
1984-2003).
• Site of the lesions:
Lesions that lead to tetanus are commonly found on lower limbs (41%, KCMC
medical record data, 1984-2003).
• Risk factors:
In adults:
o A penetrating injury.
o A localized ischaemia.
o A foreign body in the wound.
o Devitalized tissue in the wound.
o Lack of tetanus vaccination. o Co-infection with other bacteria.
o Completion of the primary tetanus vaccination without a booster dose in the
preceding 10 years.
In neonate:
o Home delivery. o Unvaccinated mother.
o Unhygienic cutting of the umbilical cord.
o History of neonatal tetanus in a previous child.
o Potentially infectious substances applied to the umbilical stump e.g. animal dung,
mud or clarified butter.
Cause:
Tetanus is caused by Clostridium tetani. The organism is an obligate anaerobic gram-
positive bacillus bacterium, non-encapsulated, slender, motile and spore-forming.
The spores are resistant to heat, drying and to disinfectants. The spores have a
characteristic drumstick appearance and can survive for years in a contaminated soil.
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3. Clostridium tetani are found in the soil, house dust, animal and human faeces.
Pathophysiology:
When the wound gets contaminated with spores of Clostridium tetani, they quickly
undergo autolysis releasing exotoxin called tetanospasmin. Once released, tetanospamin
is taken up by peripheral nerve terminals of lower motor neurons and transported to the
central nervous system intra-axonally, through lymphatics and blood stream.
Tetanospasmin at presynaptic nerve terminal blocks the release of neurotransmitter. The
neurons, which release gamma-aminobutyric acid (GABA) and glycine, the major
inhibitory neurotransmitters, are particularly sensitive to tetanospasmin, leading to failure
of inhibition of motor reflex responses to sensory stimulation. This results in generalized
contractions of the agonist and antagonist musculature characteristic of a tetanic spasm.
Autonomic nervous system may also be activated and either produce sympathetic
hyperactivity that results in higher levels of circulating catecholamines, which may cause
tachycardia, arrhythmias and excessive sweating or produce parasympathetic
hyperactivity with over-salivation, tearing and gastric acid secretion.
Clinical features:
Approximately 30% of individuals with tetanus have either no obvious wound or have
wounds that they are considered to be trivial.
The median incubation period is 7 days and for most cases (73%), incubation ranges from
4-14 days. The incubation period depends on:
• Site of injury, i.e. the shorter the distance of site of injury from the central nervous
system the shorter the incubation period.
• Nature of the wound i.e. toxigenic conditions. The more toxic the wound is, the
shorter incubation period.
There are four clinical forms of tetanus:
• Cephalic tetanus.
• Neonatal tetanus.
• Localized tetanus.
• Generalized tetanus.
Neonatal tetanus:
Non-specific symptoms:
• Irritability.
• Weak sucking. • Refusal to breastfeed.
These non-specific symptoms progress quickly to tetanus specific symptoms.
Specific symptoms:
• Trismus. • Spasticity.
• Facial grimacing (risus sardonicus).
Localized tetanus:
Localized tetanus progresses to generalized tetanus in a matter of days or weeks in most
cases. It is a very rare form of tetanus and reflects partial immunity to tetanospasmin.
Clinical features:
• Weakness and loss of tone of the affected muscles.
• Painful spasms of the group of muscles in close proximity to the site of injury.
These symptoms usually resolve spontaneously but may persist occasionally for months.
Cephalic tetanus:
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4. Rare form of tetanus; commonly associated with head injury or Clostridium tetani
infection of the middle ear.
Clinical features:
• Trismus (lockjaw).
• Ophthalmoplegic tetanus is a variant that develops after penetrating eye injuries and
results in cranial nerve-III palsies and ptosis.
• Dysfunction of many cranial nerves. Facial nerve being commonly affected leading to
difficulties with feeding, swallowing and oral hygiene.
Patients with cephalic tetanus who are untreated progress to generalized tetanus.
Generalized tetanus:
It is the most common form of tetanus. The muscles innervated by nerves with shortest
neural pathways are usually the first to be affected, e.g. facial, cervical and masticatory
muscles.
Clinical features:
• Stiffness.
• Restlessness.
• Neck rigidity.
• Trismus (lockjaw).
• Difficulty swallowing or chewing.
• Localized or generalized weakness.
• Patients are conscious throughout the illness.
• Abdominal tenderness and guarding, mimicking an acute abdomen.
• Intense pain associated with each spasm, which may occur spontaneously or
precipitated by aural, visual or tactile stimuli.
• Involvement of the autonomic nervous system may cause:
o Arrhythmia.
o Diaphoresis.
o Urinary retention.
o Hyperthermia or hypothermia.
o Extreme fluctuation in blood pressure.
Only 60% of patients with uncomplicated tetanus presents with fever of more than 38o
C
due to aspiration pneumonia or septicaemia.
Differential diagnosis:
• Acute abdominal emergencies.
• Generalized muscle rigidity and/or spasms:
o Rabies.
o Meningitis.
o Encephalitis.
o Hypocalcaemia.
o Seizure disorder.
o Cerebral malaria.
o Serotonin syndrome. o Conversion disorder.
o Stiff-man syndrome. o Strychnine poisoning.
o Cerebrovascular accident. o Neuroleptic malignant syndrome.
o Drug-induced dystonic reactions:
 Narcotics and alcohol withdrawal.
 Phenothiazines side effect e.g. tardive dystonia or overdose.
• Lockjaw and dysphagia:
o Mumps.
o Oral abscess.
o Dental infection.
o Peritonsillar abscess.
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5. o Mandibular dislocations.
Complications:
• Bed sores.
• Septicaemia.
• Stress ulcers.
• Arrhythmias.
• Malnutrition.
• Dehydration.
• Paralytic ileus.
• Cardiac arrest.
• Respiratory failure.
• Flexion contractures.
• Pulmonary embolism.
• Aspiration pneumonia.
• Deep venous thrombosis.
• Long bone fractures from sustained muscle contractions.
• Glenohumeral joint and temporomandibular joint dislocations.
• Coma, nerve palsies, neuropathies and psychological after-effects.
Long-term complications: (after discharge)
• Seizures. • Irritability. • Sleep disturbance.
• Osteoarthritis as a consequence of bone damage.
Diagnosis:
• The diagnosis is clinically based on the presence of trismus, dysphagia, generalized
muscular rigidity and/or spasm.
• Spatula test: (Sensitivity: 94% and specificity: 100%)
This simple test involves touching the oropharynx with a spatula or tongue blade.
o This test typically elicits a gag reflex and the patient tries to expel the spatula i.e.
a negative test result.
o If tetanus is present, patients develop a reflex spasm of the masseters and bite the
spatula i.e. a positive test result.
Investigations:
Laboratory studies:
No specific laboratory tests exist for determining the diagnosis of tetanus.
• Serum electrolytes. • Random blood glucose.
• Blood slide for malaria. • Liver and renal functions tests.
• Full blood picture: It may demonstrate a moderate peripheral leukocytosis.
• Serum antitoxin levels:
Serum antitoxin levels of ≥ 0.01 IU/ml are protective, making the diagnosis of tetanus
less likely.
• Swab culture from the wound:
It is usually not helpful because Clostridium tetani is usually isolated from wounds in
only 30% of patients with clinical tetanus.
Imaging studies:
• Erect plain abdominal x-ray and ultrasound scans of the abdomen in patients with
acute abdomen.
• Computed tomography-scans of the brain.
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6. Procedure:
Lumbar puncture:
It is necessary after funduscopy to exclude central nervous system infections, although
cerebral spinal fluid is normal (except for the increased opening pressure especially
during spasms).
Treatment:
1. Elimination of the source of toxins:
Metronidazole 500 mg IV 6 hourly alone or in combination with crystalline penicillin
2.5 MU 6 hourly IV for 10-14 days.
• Metronidazole IV may be changed to oral 400 mg TDS after 24 hours.
• Crystalline penicillin may be changed to ampiclox/Amoxycillin 500 mg TDS
orally after 24 hours or doxycycline 100 mg BD to those allergic to penicillin.
Crystalline penicillin should not be given alone as it is a GABA antagonist and hence
may enhance effects of the tetanospasmin.
2. Neutralization of unbound toxin:
• Anti-tetanus serum (ATS) 500-15,000 I.M/IV 5-7 days (after test dose).
• Anti-tetanus serum (ATS) infiltration around the wound.
3. Anti-spasms:
• A cock-tail combination:
o Diazepam 2-20 mg 2-8 hourly orally. Diazepam reduces anxiety, produces
sedation and relaxes muscles.
o Chlorpromazine 50-150 mg 4-8 hourly orally.
o Phenobarbitone 60-180 mg 4-12 hourly orally. Phenobarbitone prolongs effects
of diazepam.
• Magnesium sulphate:
It can be used alone or in combination with benzodiazepines to control spasm and
autonomic dysfunction:
o Dose:
Magnesium sulphate 5 g or 75 mg/kg IV loading dose, then 2-3 g/hour until
spasm control is achieved.
o Monitor patellar reflex, as areflexia occurs at the upper end of the therapeutic
range (4 mmol/L). If areflexia develops, dose should be decreased to avoid
overdose.
An infusion of magnesium sulfate reduces the requirement for other drugs to
control muscle spasms and cardiovascular instability.
When giving these medications do not compete with the spasms, start with loading
dose and then reduce it as the spasms improves.
4. Supportive:
• Nursing care:
o Catheterization. o 2-hourly turning.
o Nasogastric tube for feeding.
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7. o Reduce stimuli precipitating spasms (nurse in dark and quite environment).
• Pulmonary care: (PRN)
o Suction.
o Intubation.
o Tracheostomy.
o Mechanical ventilation.
• Water, electrolytes and nutrition balance.
• +/- H2 receptor blockers, antacids or sucralfate to prevent stress ulcers.
• Heparinization in patients with prolonged hospital admission.
• Wound debridement, cleaning with hydrogen peroxide and removal of foreign
body and then leave the wound open.
• To prevent dysautonomia only Esmolol is currently recommended. Beta-blockers
such as propranolol were used in the past but can cause hypotension and sudden
death.
• Consider physiotherapy when spasms stop.
Prognosis:
• Prognosis of the patient with tetanus depends on:
o Incubation period: The shorter the incubation period the worse the prognosis.
o Site of the lesion: The shorter the distance from CNS the worse the prognosis.
o Age: The prognosis is usually poor in neonates and elderly patients.
o Forms of tetanus: Cephalic and neonatal tetanus have poor prognosis.
• The common causes of death are:
o Asphyxia.
o Exhaustion. o Aspiration pneumonia.
Prevention:
• Give tetanus toxoid 0.5 ml IM on discharge.
• Contaminated injuries should be treated by debridement.
• DPT is administered to children at ages: 2-months, 4-months, 6-months, 12-15
months and between 4-6 years. Then a tetanus booster shot every 10 years is
recommended.
• If the patient has not had a tetanus toxoid booster in the previous 10 years, administer
a single dose booster injection on the day of injury. For severe wounds, consider
administer a booster injection if more than 5 years have elapsed since the last dose.
• Non-immunized pregnant women should receive at least 2 doses of tetanus toxoid
according to the following schedule:
o The first dose at initial contact or as early as possible during pregnancy.
o The 2nd
dose 4 weeks after the first or preferably at least 2 weeks before delivery.
o The 3rd
dose could be given 6-12 months after the 2nd
dose or during her next
pregnancy.
o Additional 2 doses should be given at annual intervals.
• Consider vaccinating males on routine basis just as females do.
Follow-up:
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8. These patients should be given an appointment to attend MOPD for follow-up after
discharge for long-term complications and booster doses of tetanus toxoid.
References:
1. Daniel J. sexton, Eric L. westerman. Tetanus. UpToDate volume 12 number 1. Last
updated: September 07, 2004.
2. Dire D.J. Tetanus in emergency medicine. www.emedicine.medscape.com Last
updated: September 16, 2010.
3. Allen C.M.C. and Lueck C.J. Infections of the nervous system (tetanus); Davidson’s
principles and practice of medicine. 19th
edition, chapter 22, page 1200-1201.
4. Kilimanjaro Christian Medical Center (KCMC) medical records data, 1984-2003.
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