TETANUS

DR OSEMWEGIE N
 OUTLINE

 INTRODUCTION
 EPIDEMIOLOGY
 AETIOLOGY
 PATHOGENESIS
 CLINICAL TYPES/FEATURES
 DIAGNOSIS
 COMPLICATIONS
 INTRODUCTION

 Tetanus is a disease of the nervous system characterised by episodic

painful muscle contractions.
 It is caused by a toxin, elaborated by a bacteria. Apart from the skeletal
muscle, it also involves disturbance of the autonomic nervous system.
 Tetanus is defined by the Centre for Disease Control and Prevention as
an acute onset of hypertonia and painful muscular contraction, usually
of the muscles of the jaw and neck and generalised muscle spasms
without other apparent medical causes.
 EPIDEMIOLOGY

 It is largely preventable, though still common with high mortality in

developing countries due to poor immunization coverage.
 In developed nations, it is common amongst patients that abuse
intravenous drugs.
 The reported annual incidence is 0.5 –1 million and of the 215, 000
deaths due to tetanus reported in 1998, 50% occurred in Africa
 It occurs in all ages but with higher prevalence in the elderly and
neonates. It is also more severe in these age groups. No gender
predilection
 AETIOLOGY

 It is caused by a neurotoxin called Tetanospasmin, a 150 KDa protein. It

is an exotoxin elaborated by an obligate anaerobic gram positive
Baccilus Clostridium tetani.
 The spores of these bacteria which is ubiquitous in soils can survive for
months to years. It is also resistant to boiling and chemical
disinfectants.
 The spores or bacteria often enter the body through any epithelial
breakage such as abrasions, burns and puncture wounds. It can also be
through the umbilical cord stump, ear or body piercing and otitis media.
In about a third of cases, no obvious portal of entry is found. The
incubation period which is the duration between onset of wound and
onset of first symptom, usually trismus (lock jaw) is from one day to 2
months.
 PATHOGENESIS

 If the condition is favourable, the bacteria multiply and the dormant

spores become vegetative elaborating the neurotoxin.
 The toxin binds to surface membrane proteins of peripheral nerves and
it is then internalized. It is transported within the axon in a retrograde
direction to the anterior horn cells of the spinal cord and motor nuclei of
cranial nerves in the brainstem and to the inhibitory interneurons.
 Tetanospasmin inhibits these inhibitory interneurons by preventing
release of GABA. This causes unregulated activity of the motor nerves
resulting in muscle rigidity and episodic muscle contraction either
spontaneously or in response to external stimuli (touch or light).
 A similar activity in autonomic nervous system also occurs
 CLINICAL TYPES/FEATURES

 These include:
1.Local
2.Cephalic
3.Generalised
4.Neonatal
5.Maternal
 CLINICAL TYPES/FEATURES

 Localised Tetanus: This is characterised by muscle pain, stiffness and

superimposed episodic clonic muscle spasm. It is restricted to an isolated part of
the body. It is usually mild.
 Cephalic: There is stiffness and episodic spasm of facial muscles. The
incubation period is in days (1-2 days) .it is a severe form with poor outcome.
 Generalised: This may begin locally and then generalise or it is generalised
form the beginning. It usually begins with jaw stiffness (trismus), neck pain and
stiffness. This then spreads to involve limb, trunk, respiratory, laryngeal and
pharyngeal muscles. Later, spontaneous or provoked muscle spasm then occurs.
There is also autonomic dysfunction presenting as labile blood pressure, labile
pulse rate, excessive sweating and increased tracheal secretions. There is no
alteration in consciousness.
 CLINICAL TYPES/FEATURES

 Neonatal Tetanus: This is an illness occurring in a child who has the

normal ability to suck and cry in the first 2 days of life, but loses this
ability between day 3 and 28 of life and becomes rigid and has spasm.
This is as defined by the World Health Organization. It is a generalised
form of tetanus. Mortality rate is very high.
 Maternal Tetanus: This is defined by the World Health Organisation as
tetanus occurring during pregnancy or within 6 weeks after the
conclusion of pregnancy (birth, miscarriage or abortion
 DIAGNOSIS

 This is largely clinical. Tests that can be done include:

1.Word swab culture to isolate Clostridium tetani and other organisms.
2.Serum level of anti-tetanus immunoglobulin G.
3.Serum tetanus toxin level
4.Electromyography – shows absence of silent period.
5.Serum creatine kinase which is moderately elevated in generalised
tetanus.
6.Renal function, in cases complicated by acute kidney injury.
 COMPLICATIONS

 Asphyxia and respiratory failure

 Aspiration pneumonia
 Acute kidney injury
 Crush fracture
 Tendon avulsion
 Venous thromboembolism
 Dehydration and malnutrition
 Pressure ulcers
 DIFFERENTIAL DIAGNOSIS

 Strychnine poisoning
 Hypocalcaemic tetany
 Stiff person syndrome
 Neuroleptic induced Dystonia
 Temporomandibular joint disorder
 Black widow spider envenomation
 TREATMENT

 The principles of treatment include:

A.Wound Care: Includes debridement and cleaning to reduce the growth
and multiplication of the bacteria. This also stops toxin production.
B.Use of Antibiotics: Metronidazole IV 500mg 6-hourly for 7-10-days or
metronidazole suppository 400mg 6-hourly is the preferred antibiotics.
Penicillin and Tetracycline can also be used.
C.Neutralise Circulating Toxin – with the use of antitoxin.Human
tetanus immune globulin: 3000-5000 units intramuscularly or equine
antitoxin 10,000-20,000 units intramuscularly
 TREATMENT

D.Control of Spasm: This involves the use of benzodiazepine, chlorpromazine,

phenobarbital, magnesium sulphate, or propofol. If spasms are not controlled with
above medications, the short acting non-depolarizing neuromuscular blockers such
as pancuronium are used.
E.Autonomic Dysfunction Management: This is treated with beta blockers,
calcium channel blocker or morphine
F.Supporting Care
 Adequate hydration and nutrition
 Ventilator support
 Prevention of venous thromboembolism
 Nurse in a quiet area
 PROGNOSIS

 Death from tetanus often range from 30-80% being higher in developing countries. For those
that survive, complete recovery usually occurs within 4-6 weeks.
Factors associated with poor outcome are:
 Persons older than 70 years
 Incubation period shorter than 7 days
 Period of onset less than 48 hours
 Systolic blood pressure greater than 140 mmHg
 Tachycardia with heart rate greater than 140 beats/minute
 Fever with temperature of 38.5 0C or greater
 Intravenous drug abusers, puerperal, post-surgery and burns.
 Cephalic and neonatal tetanus.
 Delayed treatment.
 PREVENTION

These include:
 Immunization (Primary immunisation and booster doses)
 Optimal wound care
 Safe delivery and puerperal practises
 Active immunization is required after an attack because this does not
confer a permanent immunity
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