Tetanus is a nervous system disorder caused by Clostridium tetani bacteria that produces a toxin. It causes muscle spasms and there are four clinical patterns: generalized, local, cephalic, and neonatal. Treatment involves halting toxin production, neutralizing unbound toxin with immunoglobulin, controlling muscle spasms and autonomic dysfunction, and providing supportive care. Prognosis depends on availability of supportive care, with neonatal tetanus having higher mortality than other forms.

1. Tetanus
Muhammad Asim Rana
MBBS, MRCP, SF-CCM, EDIC, FCCP
Department of Critical Care Medicine
King Saud Medical City
Riyadh, KSA

2. INTRODUCTION
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Nervous system disorder characterized by
muscle spasms
Caused by the toxin-producing anaerobe,
Clostridium tetani.
Four clinical patterns
Generalized
 Local
 Cephalic
 Neonatal
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3. EPIDEMIOLOGY
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Developed countries
0.16 cases/million population
Developing countries
approximately 1,000,000 cases of tetanus are
estimated to occur worldwide each year with
200,000 to 300,000 deaths
Neonatal tetanus, accounted for 180,000
deaths in the year 2002

4. PATHOGENESIS
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Spores of Clostridium tetani, an obligate
anaerobe
After inoculation, C. tetani transforms into a
vegetative rod-shaped bacterium and produce
the metalloprotease, tetanospasmin (also known
as tetanus toxin).

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After reaching the spinal cord and brain stem via
retrograde axonal transport and binding tightly and
irreversibly to receptors at these sites
tetanus toxin blocks neurotransmission by its
cleaving action on membrane proteins involved in
neuroexocytosis.
The net effect is disinhibition of neurons that
modulate excitatory impulses from the motor
cortex.
Disinhibition of anterior horn cells and autonomic
neurons result in
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increased muscle tone,
painful spasms, and
widespread autonomic instability

6. 
Adrenal malfunction
Lack of neural control of adrenal release of
catecholamines induced by tetanus toxin
produces a hypersympathetic state that manifests
as
 sweating, tachycardia andhypertension.
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Muscular rigidity
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increase in the resting firing rate of disinhibited
motor neurons and lack of inhibition of reflex
motor responses to afferent sensory stimuli

7. Remember
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Tetanus toxin-induced effects on anterior horns
cells, the brain stem, and autonomic neurons last
are long-lasting because recovery requires the
growth of new axonal nerve terminals.
Tetanolysin is another toxin produced by C.
tetani during its early growth phase. It has
hemolytic properties and causes membrane
damage in other cells, but its role in clinical
tetanus is uncertain.

8. Predisposing factors
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(C. tetani will not grow in healthy tissues, a
convergence of factors must be present in order for
tetanus toxin to be elaborated in the human host.)
A penetrating injury resulting in the inoculation of C.
tetani spores
Co-infection with other bacteria
Devitalized tissue
A foreign body
Localized ischemia

9. These predisposing factors can also explain
why tetanus can develop in unusual clinical
settings such as in:
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Neonates (due to infection of the umbilical stump)
Obstetric patients (after septic abortions)
Postsurgical patients (with necrotic infections involving
bowel flora)
Patients with dental infections
Diabetic patients with infected extremity ulcers
Patients who inject illicit and/or contaminated drugs

10. CLINICAL FEATURES
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Incubation period
The incubation period of tetanus can be as short
as one to three days or as long as several
months, with a median of 7 to 8 days (range 0 to
112 days in one report)
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Inoculation of spores in body locations distant from
the central nervous system (eg, the hands or feet)
results in a longer incubation period than inoculation
close to the central nervous system (eg, the head or
neck).

11. Generalized tetanus
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Trismus (lockjaw)
symptoms of autonomic overactivity
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irritability
restlessness
sweating
tachycardia
cardiac arrhythmias
labile hypertension
hypotension,
fever

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Stiff neck
Opisthotonus
Risus sardonicus (sardonic smile)
A board-like rigid abdomen
Periods of apnea due to vise-like contraction of
the thoracic muscles and/or glottal or
pharyngeal muscle contraction
Dysphagia

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Cephalic tetanus
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Neonatal tetanus
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injuries to the head or neck
involving initially only cranial nerves
may manifest confusing clinical findings including
dysphagia, trismus and focal cranial neuropathies
facial nerve is most commonly in cephalic tetanus,
but involvement of cranial nerves VI, III, IV, and XII
may also occur either alone or in combination with
others
infants within 14 days following birth
Local tetanus
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tonic and spastic muscle contractions in one extremity or body
region

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Severity of illness
the amount of tetanus toxin that reaches the CNS
 to the incubation period of the illness
 the interval from the onset of symptoms to the
appearance of spasms
 the longer the interval, the milder the clinical
features of tetanus.
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15. DIFFERENTIAL DIAGNOSIS
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Drug-induced dystonias such as those due
to phenothiazines
Trismus due to dental infection
Strychnine poisoning due to ingestion of rat
poison
Malignant neuroleptic syndrome
Stiff-man syndrome

16. TREATMENT
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The goals of treatment include:
Halting the toxin production
 Neutralization of the unbound toxin
 Control of muscle spasms
 Management of dysautonomia
 General supportive management
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17. Halting toxin production
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Wound management
Antimicrobial therapy
Penicillin G
cefazolin, cefuroxime, or ceftriaxone
Metronidazole

18. Neutralization of unbound toxin
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Since tetanus toxin is irreversibly bound to tissues, only
unbound toxin is available for neutralization.
Human tetanus immune globulin (HTIG) should be readily
available and is the preparation of choice. A dose of 3000 to
6000 units intramuscularly should be given as soon as the
diagnosis of tetanus is considered.
Intrathecal administration of tetanus immune globulin is of
unproven benefit.
Where HTIG is not readily available, equine antitoxin is used
in doses of 1500 to 3000 units intramuscularly or
intravenously in order to achieve a serum concentration of
0.1 IU/mL
The use of pooled intravenous immune globulin (IVIG) has
been proposed as a possible alternative to HTIG.

19. 
Active immunization
does not confer immunity following recovery from
acute illness
 ALL patients with tetanus should receive active
immunization with a total of three doses of tetanus
and diphtheria toxoid spaced at least two weeks
apart, commencing immediately upon diagnosis
 Subsequent tetanus doses, in the form of Td, should
be given at 10-year intervals throughout adulthood.
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20. Control of muscle spasms
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Generalized muscle spasms are life-threatening
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respiratory failure
lead to aspiration
induce generalized exhaustion in the patient.
Drugs used to control spasm
 Sedatives
 Neuromuscular blocking agents
 Propofol
 Intrathecal Baclofen

21. Management of autonomic dysfunction
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Beta blockade
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Morphine sulphate
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(0.5 to 1.0 mg/kg per hour by continuous intravenous infusion)
is commonly used to control autonomic dysfunction as well as
to induce sedation
Magnesium sulfate
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Labetalol (0.25 to 1.0 mg/min) has frequently been
administered because of its dual alpha and beta blocking
properties.
acts as a presynaptic neuromuscular blocker, blocks catecholamine
release from nerves, and reduces receptor responsiveness to
catecholamines
Other drugs — Other drugs for the treatment of various
autonomic events, which have been reported to be
useful, are: atropine, clonidine and epidural
bupivacaine.

22. Supportive care
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In patients with severe tetanus, prolonged immobility in
the intensive care unit is common
Such patients are predisposed to
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nosocomial infection
decubitus ulcers
tracheal stenosis
gastrointestinal hemorrhage
thromboembolic disease.

23. PROGNOSIS
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Case-fatality rates for non-neonatal tetanus in
developing countries range from 8 to 50 percent,
while the majority of patients with tetanus
recover when modern supportive care is
available.
Neonatal tetanus, once nearly always fatal, now
has mortality rates of 10 to 60 percent

24. Thank you