This document provides information about tetanus including: 1. Tetanus is caused by Clostridium tetani bacteria entering the body through a wound and releasing a neurotoxin. 2. Symptoms include painful muscle spasms and stiffness, initially affecting the jaw and face before spreading. 3. Treatment focuses on wound care, antitoxin administration, and controlling spasms with medications while providing supportive care. Immunization is the best preventive strategy.

1. D R M A L L U M C . B
S E N I O R R E G I S T R A R
N E U R O L O G Y U N I T
L U T H
TETANUS

2. HISTORICAL NOTE
 Earliest record dates back to Egyptian civilization.
 In 1890,tetanospasmin was extracted from anaerobic
soil bacteria and found to be responsible for clinical
tetanus.

3. EPIDEMIOLOGY
 Occurs worldwide but more prevalent in developing
countries.
 About 1 million cases (18 per 100,000) are said to
occur annually.
 Case fatality ratio ranges between 20 to over 50
percent.
 Neonatal tetanus is the second leading cause of
death from vaccine preventable disease in children
worldwide.
 Half of the deaths from tetanus occur in children.

4.  Tetanus is rare in developed countries as a result of
immunization.(36 cases of tetanus reported in the
US in 1994)

5. PATHOPHYSIOLOGY
 Clostridium enters the body through a wound.
 Spores germinate in anaerobic conditions.
 Toxins are produced and disseminated through
blood and lymphatics.
 Toxins act at various sites in the nervous system
including the peripheral end plate,spinal cord,brain,
and sympathetic nervous system.

6. PATHOPHYSIOLOGY
 Toxins gain access to the CNS via retrograde axonal
transport in motor nerves.
 Toxins move into the presynaptic inhibitory
interneurons with resulting inhibition of release of
inhibitory neurotransmitters (GABA in the brain,
glycine in the spinal cord).
 This results in heightened muscular activity.
 Loss of glycine inhibition occurs in the
intermediolateral grey matter of the spinal cord
results in increased sympathetic activity.

7. PATHOPHYSIOLOGY
 Reduction of release of acetylcholine from motor
neurons may result in paralysis of cranial nerves in
cephalic tetanus.

8. Clostridium Tetani
 Found primarily in the soil and intestinal tracts of
animals and humans.
 Clostridium tetani is a slender, motile,gram positive,
anaerobic rod that may develop a terminal spore
giving it a drumstick appearance.
 The organism is sensitive to heat and cannot survive
in the presence of oxygen.

9. Clostridium Tetani
 The spores,however, are very resistant to heat and
usual antiseptics.
 Spores may survive several years and are resistant to
various disinfectants and to boiling for 20minutes.
They are relatively resistant to phenol. Spores may
survive autoclaving at 121 degrees C for 10-15 mins.

10.  Spores are found in soil, intestines of animals and on
skin surfaces and contaminated heroin.
 Manure treated soil may contain large numbers of
spores.
 Under anaerobic conditions, spores begin to
germinate and proliferate.
 Spores produce two exotoxins: Tetanolysin and
Tetanospasmin.

11.  The clinical significance of Tetanolysin is still
uncertain.
 Tetanospasmin is a neurotoxin and is responsible for
the clinical manifestations of tetanus.
 The estimated human lethal dose of tetanospasmin is
2.5 ng per kg body weight.

12. MODE OF TRANSMISSION
 Primarily from contaminated wounds.
 May follow elective surgery,burns,deep puncture
wounds, crush wounds,otitis media,dental
infection,animal bites, abortion.
 Tetanus is infectious but not contagious(no person to
person transmission)

13. CLASSIFICATION
 Localized tetanus
 Generalized tetanus
 Neonatal tetanus
 Cephalic tetanus

14. CLINICAL FEATURES
 The hall marks of tetanus are sustained muscular
rigidity, and in severe cases, reflex spasms.
 The interval of time between spore innoculation and
development of the first symptom is the incubation
period .usu 3 and 21 days,range 0-60days
 The time from the first symptom to reflex spasms is
the period of onset.
 Incubation period less than 10-14 days and period of
onset less than 3-6 days is indicative of severe
disease.

15. CLINICAL FEATURES
 The earliest manifestations of generalized tetanus
are rigidity of the masseter muscle (lockjaw or
trismus ) and facial muscles , with straightening of
the upper lip(Grimace or Risus Sardonicus).
 This is soon followed by rigidity of axial muscles with
prominent involvement of the neck and back
muscles(Opisthotonus).
 Rigidity of axial muscles may precede or accompany
trismus.
 Stiffness of the limb muscles may be evident with
sparing of distal muscles.

16. CLINICAL FEATURES
 Reflex spasms are violent, paroxysmal contractions
of the muscles in response to attempts at voluntary
movement and to external and internal(fear,hunger)
stimuli.
 Spasms of the deglutition muscles in severe cases
may result in difficulties in swallowing and verbal
expression.
 Laryngospasm may also occur leading to
asphyxiation.

17. CLINICAL FEATURES
 Disease severity continues for 10-14 days and is
usually followed by recovery.
 Autonomic instability may manifest by fluctuations
of heart rate and blood pressure,arrhythmias,profuse
sweating, hyper salivation,extreme hyperpyrexia.
They reflect a hypersympathetic state and complicate
severe cases.

18. CLINICAL FEATURES(Localized tetanus )
 Localized stiffness near the injury
 Fixed muscular rigidity confined to wound-bearing
extremity may persist for months.
 Localized tetanus usually precedes generalized
tetanus.

19. Cephalic tetanus:
 Usually associated with infections of paracranial
structures eg chronic otitis media and dental
infection.
 Presents as trismus and paralysis of one or more
cranial nerves.
 Facial paresis and dysphagia.
 Abnormal ocular movements – bilateral trochlear
nerve palsy(ophthalmoplegic tetanus) and downbeat
nystagmus.

20. INVESTIGATIONS
 Diagnosis is entirely clinical.
 Clostridium tetani is isolated from the wound in only
30% of patients and may be present in individuals
without tetanus.
 Serum antitoxin levels >0.01u/ml make the
diagnosis unlikely.
 Ancillary investigations like FBC,U&E,CR

21. DIFFERENTIAL DIAGNOSIS
 Strychnine intoxication- trismus is absent,abdominal
muscle is less rigid.
 Neuroleptic Malignant syndrome- lack of reflex
spasms
 Acute dystonic reactions(extrapyramidal side effects
of dopamine blocking agents)- lack of reflex spasms.
 Stiff-person syndrome- insidious onset, less
involvement of face,jaw muscles;muscle rigidity
reduced by sleep.

22. DIFFERENTIAL DIAGNOSIS
 Hypocalcemic tetany- involves extremities more than
trunk;chvostek and trousseau’s sign.
 Meningoencephalitis- also has abnormal tone and
nuchal rigidity but this does not have normal
sensorium as in tetanus.
 Dental abscess- may mimic trismus
 Subarachnoid haemorrhage,
 Hysteria

23. COMPLICATIONS OF TETANUS
 Laryngospasm and/or spasms of muscles of
respiration.
 Fractures of spine and /or long bones from sustained
contraction.
 Hypertension and/or abnormal heart rhythm- due to
hyperactivity of autonomic nervous system.
 Nosocomial infections- sepsis from indwelling
catheters,decubitus ulcers,hospital-aquired
pneumonia.

24. COMPLICATIONS OF TETANUS
 Pulmonary embolism especially in elderly and IV
drug users.
 Aspiration pneumonia-
 Death in 11% of reported cases more common in
persons older 60yrs,unvaccinated persons.
Causes include larygnospasm,cardiac arrest.
 Renal insufficiency

25. MANAGEMENT
 The principles of management are:
1.Elimination of source of toxin
2.Toxin neutralization
3.Control of muscular rigidity and spasms.
4.Supportive care

26. ElIMINATION OF THE SOURCE OF TOXIN
 Wound exploration, cleansing and debridement are
important to reduce the bacterial load.
 Antibiotic therapy is given. Iv metronidazole 500mg
8hrly,
 IV penicillin is usually given but may worsen the
spasm because it has a central GABA antagonistic
effect.

27. TOXIN NEUTRALIZATION
 Neutralization of circulating toxin is done by giving
Sc ATS anti tetanus serum(ATS) at 10,000 IU stat
after a negative test dose
 An alternative is IM Human tetanus Immunoglobin
500 IU stat where available.

28. CONTROL OF SPASMS
 Benzodiazepines such as
diazepam,lorazepam,midazolam
 IV diazepam is given in infusion IV 5% dextrose
water in 0.9%normal saline .
 Dose of diazepam to titrated in response to spasm
frequency and to be reduced in event of any
drowsiness.
 IV diazepam 20mg every 2hours via intravenous
push can be given for breakthrough spasms.

29. CONTROL OF SPASMS
 Barbiturates such as IV phenobarbital are second
line drugs.
 Neuromuscular blockade with
atracurium,vecuronium or pancuronium is required
in severe cases with violent spasms and respiratory
depression.
 Other alternatives are morphine,fentanyl,clonidine,
atropine, continuous spinal anaesthesia.

30. Supportive care
 Autonomic instability has been treated with combined
alpha and beta blockers eg labetalol with varying success
 Patient is to be nursed in a dark, quiet room.
 NPO
 A spasm chart is to be kept.
 DVT prophylaxis with SC clexane or heparin.
 Feeding can be recommenced once patient is spasm free
 Physiotherapy may assist in mobilization once patient is
spasm free.
 ICU admission + tracheostomy may be required in
severe cases

31. IMMUNIZATION SCHEDULE ON DISCHARGE
 IM TT 0.5mls stat is given on presentation
 A Repeat dose is given 6 weeks after the first
 The 3rd dose is given 6 months afterwards.

32. PROGNOSIS
 Poor prognostic factors:
-short incubation period
-short period of onset
-cephalic tetanus
-neonatal tetanus
-poor prior vaccination
-dysautonomia

33. PREVENTION
 Appropriate wound care and immunization
 Especially for wounds with severe tissue
necrosis,suppuration,retained foreign bodies.
 Eg burns,umbilical stumps,compound
fractures,septic abortion,intramuscular injections.
 Antibiotic prophylaxis has no place in the
management of tetanus

34. PREVENTION
 Prophylaxis is antibody dependent and can be either
passive(Tetanus-specific immunoglobulin) or
active(tetanus toxoid)

35.  Patients should receive antitetanus globulin as well
as tetanus toxoid.
 Wounds that are neither clean nor minor
 0-2 prior doses of tetanus toxoid
 Uncertain history of prior doses.

36. IMMUNIZATION
 The only reliable immunity against tetanus is
achieved by vaccination with tetanus toxoid.
 Tetanus toxoid can safely be given in pregnancy and
in immunocompromised individuals.
 1st dose=IgM + small IgG) insufficient protection
2nd dose = 90% protection but after 1 yr drops to 80%
3rd dose = 98% protection and lasts several years

37. IMMUNIZATION
 Length of protection after 5-6 doses = 20-25 yrs.
 WHO recommends that 5 doses of tetanus toxoid be
given over 12-15 yrs , starting at infancy, with a sixth
dose often given in adulthood to ensure long lasting
protection.

38. MCQS
 Regarding spores of causative organism of tetanus ,
which is true?
 - Highly susceptible to heat and disinfectants
 Survive for less than 24 hours
 Require high oxygen tension to grow
 Aquired from contamination of deep wounds by
rusty implements or dust
 Susceptible to autoclaving when present on surgical
instruments

39. MCQS
 Complications of tetanus include the following
 - Acute renal failure
 -fractures
 -Respiratory failure
 Sympathetic overactivity
 Sudden cardiac death

40. MCQS
 In the diagnosis of tetanus, which of the following is
confirmatory?
 ESR
 Serum antitoxin levels
 Serum tetanus toxin levels
 CSF tetanolysin antibody test
 No laboratory test is required

41. MCQS
 The following are poor prognostic features in
tetanus:
-Presence of autonomic features
-short incubation period
-short period of onset
- More cephalic presentation of culprit wound
- Presence of difficulty opening mouth as the first
symptom