TETANUS

Audry Devisanty Wuysang

Department of Neurology Hasanuddin University

DEFINITION
Tetanus

is an illness characterized by an
acute onset of persistent tonic spasm of the
muscles, painful muscular contractions
(usually of the muscles of the jaw and neck),
and can lead to generalized muscle spasms,
caused by exotoxins of Clostridium tetani.

Epidemiology

Tetanus affects all age groups, with the highest

prevalence found in newborns and young people.
In South Africa approximately 300 cases occur each
year, approximately 1215 cases are reported each
year in Britain and between 50 and 70 in the USA.
The overall mortality rate is approximately 45%. The
mortality rate is highest for people older than 60
years (40%) compared with those aged 20 - 59
years (8%). From 1998-2000, 75% of the deaths in
the United States were in patients older than 60
years.

Microbiology
Caused

by a bacillus, Clostridium tetani.

Clostridium tetani obligate anaerobic
gram-positive bacillus, is nonencapsulated
and forms spores,
Spores resistant to heat, desiccation, and
disinfectants.
Natural habitat of soil, can also be found in
house dust, animal intestines, stools of
domestic animals and humans.

Microbiology
The

spore is incompletely destroyed by

boiling but eliminated by autoclaving at 1
atmosphere pressure and 120C for 15 min.
The incubation period: averages 5 14 days,
The onset time/onset period (time from first
symptom to first spasm) varies between 17
days.
Shorter incubation and onset times are
associated with more severe disease.

Patophysiology
Spores

of C.tetani, under anaerobic

conditions spores geminate and elaborate
tetanospasmin and tetanolysin.
Tetanolysin locally damaging otherwise
viable tissue surrounding the infection and
optimizing the conditions for bacterial
multiplication.
Tetanospasmin is a neurotoxin and causes
the clinical manifestations of tetanus.

Patophysiology

Tetanospasmin (released by the maturing bacilli)

distributed via the lymphatic and vascular
circulations to the end plates of all nerves enters
the nervous system peripherally at the
neuromuscular junction and transported
centripetally into neurons of the central nervous
system (CNS) these neurons become incapable
of neurotransmitter release.
The neurons (which release GABA and glycine, the
major inhibitory neurotransmitters) sensitive to
tetanospasmin failure of inhibition of motor reflex
responses to sensory stimulation generalized
contractions of the agonist and antagonist
musculature characteristic of a tetanic spasm.

Patophysiology
The

shortest peripheral nerves (shorter

axonal pathways) are the first to deliver the
toxin to the CNS, which leads to the early
symptoms of facial distortion and back and
neck stiffness (trismus, risus sardonicus,
neck rigidity).
The trunk and limbs follow but peripheral
muscles in the hands and feet are relatively
spared

Patophysiology
Neuronal

binding of toxin is thought to be

irreversible. Recovery requires the growth of
new nerve terminals which explains the
prolonged duration of tetanus.

Clinical features
Clinical

triad: rigidity, muscle spasms and, if

severe, autonomic dysfunction.
Neck stiffness, sore throat, and difficulty
opening the mouth (trismus/lockjaw) due to
masseter spasm early symptoms.
Facial muscles causing the typical facial
expression risus sardonicus
Dysphagia.

Clinical features

Rigidity of the neck muscles leads to retraction of

the head.
Truncal rigidity may lead to opisthotonus
Respiratory difficulty with decreased chest wall
compliance.
Tonic contractions convulsion-like appearance
Spasms may be almost continual, leading to
respiratory failure.
Pharyngeal spasms are often followed by laryngeal
spasms and are associated with aspiration and lifethreatening acute airway obstruction.

Diagnostic Criteria

Local muscle spasms around the wound. (local

tetanus)
Hypertonicity and muscle spasm (trismus, risus
sardonicus, neck rigidity, abdominal wall muscles
spasm, opisthotonus, etc).
Tonic spasm with conscious preserved.
History of wound (port dentree)
Urinary retention and hyperpyrexia may occur
Cranial nerves may be involved.

Differential diagnosis
The

differential diagnosis includes orofacial

infection (retropharyngeal abscess, dental
abscess, mandibular subluxation), dystonic
drug reactions, hypocalcaemia, strychnine
poisoning, hysteria, meningitis, rabies, and
tetani.

Severity grading
Ablett classification of severity of tetanus
I. Mild mild to moderate trismus; general
spasticity; no respiratory embarrassment; no
spasms; little or no dysphagia.
II. Moderate moderate trismus; well-marked
rigidity; mild to moderate but short spasms;
moderate respiratory embarrassment with an
increased respiratory rate greater than 30;
mild dysphagia.

Severity grading
Ablett classification of severity of tetanus
III. Severe severe trismus; generalized spasticity;
reflex prolonged spasms; increased respiratory rate
greater than 40; apnoeic spells; severe dysphagia;
tachycardia greater than 120.
IV. Very severe grade III and violent autonomic
disturbances involving the cardiovascular system.
Severe hypertension and tachycardia alternating
with relative hypotension and bradycardia, either of
which may be persistent.

Management
Treatment strategies involve three management
principles:
1. Organisms present in the body should be
destroyed to prevent further toxin release
2. Toxin present in the body, outside the CNS
should be neutralized
3. Minimizing th effects of toxin already in the
CNS.

Management
Anti tetanus toxin (for neutralization of unbound
toxins):
Anti tetanus serum (ATS) 20.000IU/day/IM, for 3
5 days. Perform skin test before administration, for
allergic reaction.
Human Tetanus Immunoglobulin (HTIG), 30005000 units/IM, with part of the dose infiltrated around
the wound if it can be identified.

Management
Antibiotics

Penicillin Procain (PP) 1,5 million IU, 6 hourly or 3

million, 12 hourly, combined with Metronidazole
500mg, 8 hourly by IVFD; or
Ampicillin 1 grams/8 hours/iv, combined with
Metronidazole; or
Erythromycin, tetracycline, chloramphenicol, and
clindamycin are all accepted as alternatives

Debridement of wounds

Where present, obvious wounds should be

surgically debrided.

Diazepam

On admission, Diazepam can be given 10-20mg/slow iv,

and continued for maintanance dose 10 mg/kg/day with
continuous infusion (syringe pump). Can be increased until
tetanic spasm ceased, with the maximum dose of 12 mg/
kg/day.
If tetanic spasm (tetanic convulsion) occur, administer
Diazepam 10mg/slow iv (3 5 minutes), can be repeated
every 15 minutes, with the maximum administration of 3
times.
If the patient is seizure free for 48 hours, maintanance dose
of Diazepam can be tapered 10% every 1 3 days. As
soon as oral intake is possible, diazepam should be given
orally with frequent dose (every 3 hours).

Nutrition

Nutrition should be high calory and protein. The

maintenance of nutrition is extremely important
and should be carried out in seriously ill patients
via nasoduodenal tubes, gastrostomy tube
feedings, or parenteral hyperalimentation.

Further Inpatient Care

Limitiation of actions that can give stimulation

effect to patient (avoid overstimulation). Institute
prevention measures for deep venous thrombosis,
gastrointestinal ulcer, and decubitus ulcer.

Complications
Sudden

cardiac death
Nosocomial infections (include sepsis from
decubitus ulcers, hospital-acquired
pneumonias, and indwelling catheters,
pulmonary embolism is particularly a problem
in drug users and elderly patients)
Further complications include the following:

Complications

Further complications include the following:

Long bone fractures

Glenohumeral joint and temporomandibular joint
dislocations
Hypoxic injury and aspiration pneumonia.
Adverse effects of autonomic instability, including
hypertension and cardiac dysrhythmias
Paralytic ileus, pressure sores, and urinary retention
Malnutrition and stress ulcers
Coma, nerve palsies, neuropathies, psychological after
effects, and flexion contractures

Prognosis

Poorer prognosis if trismus < 1cm, incubation period

< 7 days, onset period < 48hours, elderly and
hyperpirexia.
Recovery is slow and usually occurs over 2-4
months.
Some patients remain hypotonic.
Clinical tetanus does not produce a state of
immunity; therefore, patients who survive the
disease require active immunization with tetanus
toxoid to prevent a recurrence.

Risus sardonicus

N. VII paresis