Clostridium tetani causes tetanus through the release of neurotoxins that block inhibitory neurotransmitters in the central nervous system. It enters the body through puncture wounds and causes symptoms like muscle spasms and rigidity. Treatment involves wound debridement, antitoxin administration, active immunization, and controlling muscle spasms and autonomic dysfunction through various medications. Prognosis depends on severity but case fatality rates in developing countries range from 8-50%.

1. Clostridium tetani
• Gram positive spore forming anaerobic rod
• Reservoir – soil
• Transmission – puncture wounds, trauma, human bites
• The incubation period of tetanus is approximately 8 days but ranges from 3 to 21 days
• Pathogenesis
Spores germinate in tissues with low oxygen and produce tetanus toxins
C. tetani produces two exotoxins
Tetanospasmin – neurotoxic and causes the clinical manifestations of tetanus
Tetanolysin – haemolytic , tissue lysis
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2. • Although tetanus is now rare in the developed world, the disease remains a threat
to all unvaccinated people, particularly in developing countries.
• Persons >60 years of age are at greater risk of tetanus because antibody levels
decrease over time.
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3. Predisposing factors
• Absence of antibodies (ie, from inadequate vaccination) + plus ≥2 of the following
A penetrating injury resulting in the inoculation of C. tetani spores
Coinfection with other bacteria
Devitalized tissue
A foreign body
Localized ischemia
• Cryptogenic(unknown cause)-10% = may be due to unnoticed skin abrasions
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4. pathogenesis
•  Release of tetanospasmin from vegetative C. Tetani  the toxin binds to
peripheral motor neuron terminals
• Retrograde intra-axonal transport of toxin to the spinal cord and brain stem
• Blockade of inhibitory neurotransmitters (glycine and GABA) release in
presynaptic terminalsresting firing rate of motor neurons  rigidity 
Simultaneous recruitment of agonist and antagonistic muscles 20 to limited
glycinegic activity Spasm
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5. • Preganglionic sympathetic activity Sympathetic hyperactivity and 
circulating catecholamine level
• Blockade of neurotransmitter release at the NMJ paralysis
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6. • Toxins are produced and disseminated via blood and lymphatics.
• Toxins act at several sites within the central nervous system, including peripheral
motor end plates, spinal cord, and brain, and in the sympathetic nervous system
• Seizures may occur
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7. Tetanus
• Forms: generalized, localized, cephalic, neonatal
• Defn of terms:
IP – time gap b/n injury and first symptom (trismus)
Onset time – time b/n trismus and first spasm
Risus sardonicus – recession of the lips backward and a grinning like grimace
Opisthotonus – backward arched posture
Trismus (lockjaw) 20 to masseter muscle hypertonicity
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8. Generalized tetanus(80%)
• Most common presentation of tetanus
• Trismus (lockjaw) 20 to masseter muscle hypertonicity
• Neck shoulder and back muscle stiffness and pain
• Rigid abdomen and stiff proximal limb muscles
• Risus sardonicus, Arched back (Opisthotonus)
• paroxysmal generalized muscle spasm apnea /Cyanosis /laryngospasm
(spontaneous or provoked)
• Hyperpyrexia with clear mentation
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9. • The disease usually presents with a descending pattern.
• The first sign is trismus or lockjaw, followed by stiffness of the neck, difficulty in
swallowing, and rigidity of abdominal muscles.
• Other symptoms include elevated temperature, sweating, elevated blood pressure,
and episodic rapid heart rate.
• Spasms may occur frequently and last for several minutes. Spasms continue for
3–4 weeks.
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10. Severity of generalized tetanus
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11. Complications
• Aspiration pneumonia
• Vertebral fracture
• Muscle rupture
• DVT+PE (VTE)
• Decubitus ulcer
• Rhabdomyolysis (pigment-induced nephropathy)
• Autonomic dysfunction - Labile or sustained HTN, Tachycardia, Hyperpyrexia,
Profuse sweating, Bradycardia and hypotension episodes, Sudden cardiac arrest
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12. Neonatal tetanus
• Generalized form of tetanus
• Develops in neonates born in unimmunized mothers after unsterile treatment of
the umbilical cord stump
• Occurs within 2 weeks of neonatal life(typically occurs 5 to 7 days following
birth)
• Manifests with poor feeding, rigidity and spasm
• High rate of mortality
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13. Local tetanus
• Uncommon form of tetanus
• Manifests with localized muscle contraction near the wound
• good prognosis
Cephalic tetanus : Rare form of local tetanus
• Follows head injury or ear infection
• Manifests with trismus and CN palsy (often CN VII), but involvement of cranial nerves
VI, III, IV, and XII may also occur
• High mortality
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14. Clinical and pathologic progression of tetanus
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15. Diagnosis
• Entirely on clinical findings
• Spatula test – gag stimulation causes masseter muscle spasm
• The WHO definition of adult tetanus requires at least one of the following signs:
Trismus (inability to open the mouth) or
Risus sardonicus (sustained spasm of the facial muscles); or
Painful muscular contractions.
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16. DDx: -
Strychnine poisoning, Dystonic drug reaction (phenothiazines, metoclopramide),
Hypocalcemic tetany, Malignant neuroleptic syndrome
Rabies, Stiff-person syndrome (SPS)
Meningitis /encephalitis,
Acute intraabdominal process ,Alveolar abscess, Dental infection
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17. Duration of illness
• Tetanus toxin-induced effects are long lasting because recovery requires the
growth of new axonal nerve terminals.
• The usual duration of clinical tetanus is 4-6 weeks
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18. Treatment
• Principle
Cardiorespiratory support
Eliminate the source of toxin
Neutralize unbound toxin
Prevent muscle spasms
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19. goals of treatment
• The goals of treatment include:
Halting the toxin production
Neutralization of the unbound toxin
Airway management
Control of muscle spasms
Management of dysautonomia
General supportive management
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20. 1. General measures
• Admit in a quiet ICU with a possibility for continuous monitoring but minimal
disturbance
• Hydration
• Nutritional support (IV/PO)
spasms result in high metabolic demands and a catabolic state.
• Physiotherapy to prevent contracture
• psychological support, analgesia
• Treatment of superimposed infection eg aspiration pneumonia
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21. 2. Treatment of source infection
• Wound debridement
• Antibiotic therapy to eradicate vegetative C.Tetani; choice are:
Metronidazole 500mg IV TID or QID , Penicillin 2 -4 million units IV Q4-6hrs
lower dose of penicillin should be used as high dose has a GABA inhibitory effect
Others Clindamycin, vancomycin ,chloramphenicol, Tetracyclines, macrolides,
cephalosporins can be used .
We suggest a treatment duration of 7 to 10 days.
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22. 3. Neutralization of unbound toxin
Antitoxin
• Since tetanus toxin is irreversibly bound to tissues, only unbound toxin is available
for neutralization
• Human tetanus immune globulin (HTIG)
A dose of 3000 to 6000 units IM should be given as soon as the diagnosis of
tetanus is considered, with part of the dose infiltrated around the wound .
HTIG should be administered at different sites than tetanus toxoid
• Pooled IV Ig and equine antitoxin are used as alternative to HTIG
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23. 4. Active immunization
• Since tetanus is one of the few bacterial diseases that 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 (Td) spaced at
least two weeks apart, commencing immediately upon diagnosis.
• Subsequent tetanus doses, in the form of Td, are recommended at 10-year intervals
throughout adulthood
Tetanus toxoid should be administered at a different site than tetanus immune
globulin.
It should be assumed that anyone who is not adequately vaccinated or protected
against tetanus is also inadequately protected against diphtheria (not Tdap)
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25. 2. Control of muscle spasm
• Generalized muscle spasms are life threatening since they can cause respiratory failure,
lead to aspiration, and induce generalized exhaustion
• Benzodiazepines (Diazepam, midazolam), Barbiturates, chlorpromazine, propofol,
dantrolene, baclofen
Diazepam 10 to 30 mg IV and repeated as needed every 1 to 4 hours; total daily
doses as high as 500 mg may be required for an adult
Chlorpromazine 50–150 mg IM injection every 4–8 hours
• Neuromuscular blocking agents- Vecuronium is less likely to cause autonomic problems
than Pancuronium
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26. Respiratory care
• Intubation / Tracheostomy + mechanical ventilation for adequate oxygenation
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27. Management of autonomic dysfunction
• Magnesium sulfate -acts as a presynaptic neuromuscular blocker, blocks catecholamine release
from nerves,
5 gm (75mg/kg) IV loading dose, then 2–3 grams/hour until spasm control is achieved
Can control the autonomic dysfunction and spasm
• Labetalol – both α and β blockers are preferred.
Beta blockade alone with propranolol, for example, should be avoided because of reports of
hypotension and sudden death.
• Esmolol (short acting B blocker), verapamil, clonidine, morphine can be used.
• Continuous spinal anesthesia can also be used- epidural bupivacaine-20 to 50 mL of 0.25%
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28. prognosis
 Case-fatality rates for non-neonatal tetanus in developing countries range from 8
to 50 percent
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29. Reference
• Harrison 20th edition
• Uptodate 2018
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