Tetanos : Greek word: to stretch • First described by Hippocrates & Susruta • Neurological disease characterized by: 􏰀 Acute onset of hypertonia 􏰀 Painful muscular contractions (usually of the muscles of the jaw and neck) 􏰀 Generalized muscle spasms without other apparent medical causes • Only vaccine preventable disease that is infectious but not contagious 3 CAUSATIVE AGENT • Caused by CLOSTRIDIUM TETANI • Anaerobic • Motile • Gram positive bacilli • Oval, colourless, terminal spores: tennis racket or drumstick shape • It is found worldwide in soil, in inanimate environment, in animal faeces & occasionally human faeces. 4 Clostridium tetani Gram Stain Round terminal spores give cells a “drumstick” or “tennis racket” appearance 5 EPIDEMIOLOGY • Tetanus is an international health problem, as spores are ubiquitous. The disease occurs almost exclusively in persons who are unvaccinated or inadequately immunized • Entirely preventable disease by immunization • Tetanus occurs worldwide but is more common in hot, damp climates with soil rich in organic matter 6 EPIDEMIOLOGY IN NEPAL • Tetanus is the major cause of morbidity and mortality in Nepal • To control tetanus government of Nepal has introduced EPI in 1979 which significantly reduced the burden of VPDs including tetanus • Different programs like maternal and neonatal tetanus elimination program, safe motherhood program, tetanus toxoid (TT) campaign, training to birth attendants, health education etc. are being conducted by GON • NT has been eliminated in Nepal since 2005. Now Nepal is aiming at controlling tetanus and sustaining NT elimination status • According to the latest WHO data published in 2018 Tetanus Deaths in Nepal reached 251 or 0.15% of total deaths. The age adjusted Death Rate is 1.06 per 100,000 of population ranks Nepal #36 in the world. 7 STUDY CONDUCTED AT BPKIHS • Over 22 months period from 2003 to 2005, there were 19 cases of pediatric tetanus and 5 cases of NT • During the fiscal year 2006/2007, Morbidity at age 20-49= 43.2% of cases, Pediatric tetanus= 26.3% cases 8 TRANSMISSION • Tetanus is not transmitted from person to person. • Spores are introduced into wounds through trauma, surgeries and injections, or chronic skin lesions and infections: • Incubation period: 3 days to 3 weeks (median 7 days) ( Depends upon the site of injury) 9 • Shorter incubation periods (<7 days) along with delays in seeking treatment are associated with fatal outcomes. • Outbreaks of tetanus related to injuries associated with natural disasters such as earthquakes and tsunamis have been documented 10 HOST FACTORS • Age: active age (5-40 years), New born baby, Female during delivery or abortion • Sex: Higher incidence in males than females • Occupation: Agricultural workers are at higher risk • Rural-Urban difference: Incidence in urban areas is much lower than in rural areas • Immunity: Herd immunity does not protect the individual • Environmenta

1. TETANUS
DR. PRATIK SILWAL, JUNIOR RESIDENT
MODERATOR: DR. YAM BDR. GURUNG
DEPARTMENT OF ORTHOPAEDICS, BPKIHS
AUGUST 17 , 2021
1

2. • INTRODUCTION
• CAUSATIVE AGENT
• EPIDEMIOLOGY
• TRANSMISSION, HOST FACTORS, ROUTE OF ENTRY
• MECHANISM OF ACTION OF TOXIN
• CLINICAL FEATURES
• TYPES OF TETANUS
• DIAGNOSIS
• TREATMENT
• PREVENTION: ACTIVE & PASSIVE IMMUNIZATION
2

3. INTRODUCTION
• Tetanos : Greek word: to stretch
• First described by Hippocrates & Susruta
• Neurological disease characterized by:
Acute onset of hypertonia
Painful muscular contractions (usually of
the muscles of the jaw and neck)
Generalized muscle spasms without other apparent medical causes
• Only vaccine preventable disease that is infectious but not
contagious
3

4. CAUSATIVE AGENT
• Caused by CLOSTRIDIUM TETANI
• Anaerobic
• Motile
• Gram positive bacilli
• Oval, colourless, terminal spores: tennis
racket or drumstick shape
• It is found worldwide in soil, in inanimate environment, in animal
faeces & occasionally human faeces.
4

5. 5
Clostridium tetani Gram Stain
Round terminal spores give cells a
“drumstick” or “tennis racket” appearance

6. EPIDEMIOLOGY
• Tetanus is an international health problem, as spores are ubiquitous.
The disease occurs almost exclusively in persons who are
unvaccinated or inadequately immunized
• Entirely preventable disease by immunization
• Tetanus occurs worldwide but is more common in hot, damp climates
with soil rich in organic matter
6

7. EPIDEMIOLOGY IN NEPAL
• Tetanus is the major cause of morbidity and mortality in Nepal
• To control tetanus government of Nepal has introduced EPI in 1979 which
significantly reduced the burden of VPDs including tetanus
• Different programs like maternal and neonatal tetanus elimination
program, safe motherhood program, tetanus toxoid (TT) campaign, training
to birth attendants, health education etc. are being conducted by GON
• NT has been eliminated in Nepal since 2005. Now Nepal is aiming at
controlling tetanus and sustaining NT elimination status
• According to the latest WHO data published in 2018 Tetanus Deaths in
Nepal reached 251 or 0.15% of total deaths. The age adjusted Death Rate is
1.06 per 100,000 of population ranks Nepal #36 in the world.
7

8. STUDY CONDUCTED AT BPKIHS
• Over 22 months period from 2003 to 2005, there were 19 cases of
pediatric tetanus and 5 cases of NT
• During the fiscal year 2006/2007, Morbidity at age 20-49= 43.2% of
cases, Pediatric tetanus= 26.3% cases
8

9. TRANSMISSION
• Tetanus is not transmitted from person to person.
• Spores are introduced into wounds through trauma, surgeries and
injections, or chronic skin lesions and infections:
• Incubation period: 3 days to 3 weeks (median 7 days)
( Depends upon the site of injury)
9

10. • Shorter incubation periods (<7 days) along with delays in seeking
treatment are associated with fatal outcomes.
• Outbreaks of tetanus related to injuries associated with natural
disasters such as earthquakes and tsunamis have been documented
10

11. HOST FACTORS
• Age: active age (5-40 years), New born baby, Female during delivery
or abortion
• Sex: Higher incidence in males than females
• Occupation: Agricultural workers are at higher risk
• Rural-Urban difference: Incidence in urban areas is much lower than
in rural areas
• Immunity: Herd immunity does not protect the individual
• Environmental and social factors: Unhygienic custom habits,
Unhygienic delivery practices
11

12. ROUTE OF ENTRY
• Apparently trivial injuries
• Animal bites/human bites
• Open fractures
• Lacerated wounds and war time injuries
• Burns
• Gangrene
• In neonates usually via infected umbilical stumps
• Abscess
• Ear and Dental infections
• Post surgical infections
• Parenteral drug abuse
12

13. 13

14. TETANUS PRONE WOUND
• Wound > 6 hours old
• Wound sustained at any interval after injury which is puncture type or
shows much devitalized tissue or is septic or is contaminated with soil
or manure.
• Injury mechanism: missile, crush, burn or frostbite
14

15. PATHOPHYSIOLOGY
15
• Spores that gain entry can persist in
normal tissue in sporulated form for
months to years under anaerobic
conditions
• When the oxygen levels in the surrounding
tissue is sufficiently low, the implanted C.
tetani spore then germinates into a new,
active vegetative cell that grows and
multiplies
• Produces tetanus toxin:
tetanospasmin and
tetanolysin
• Tetanolysin is not believed to be of
any significance in the clinical
course of tetanus.
• Tetanospasmin is a neurotoxin and
causes the clinical manifestations of
tetanus.

16. 16
• Tetanospasmin spreads via blood
and perineural lymphatic system
from infected region
• Travels along the axons to the spinal
cord
• Motor neuron of spinal cord
(anterior horn) and of brainstem
become hyperactive because toxin
specifically attacks inhibitory
(Renshaw) neurons
• Generalized contractions of the
agonist and antagonist musculature

17. MOLECULAR MECHANISM OF TETANOSPASMIN
• Is a proteases that cleaves SNARE
(Soluble NSF Attachment Protein
Receptor), a set of proteins
required for neurotransmitter
release via vesicular fusion.
• Prevents release of inhibitory
(GABA and Glycine)
neurotransmitters from Renshaw
Cells in spinal cord.
17

18. STERILIZATION OF CLOSTRIDIUM TETANI SPORES
• Spores are extremely stable, although immersion in boiling water for
15 minutes kills most spores
• Autoclaving: Exposure to saturated steam under 15 lbs. of pressure
for 15-20 minutes at 121°c is highly effective against spores .
• Sterilization by dry heat is slower than by moist heat (1 -3 hrs at 160
°C), but it is also effective against spores.
• Ethylene oxide
• Iodine(1% aqueous soon) and H2O2 kills spores within few hours.
18

19. CLINICAL FEATURES
• In general the farther the injury site is from the central nervous
system, the longer the incubation period.
• The shorter the incubation period, the higher the chance of death.
• Triad of muscle rigidity, spasms & autonomic dysfunction
19

20. • Early symptoms are neck stiffness, sore throat and poor mouth
opening.
• Patients with generalized tetanus present with trismus (i.e. lockjaw)
in 75% of cases.
20

21. MUSCLE RIGIDITY
• Muscle rigidity spreads in a descending pattern from the jaw and
facial muscles
• Over the next 24-48 hours to the extensor muscles of the limbs: stiff
proximal limb muscles & relatively sparing hand & feet.
21

22. SPASM
• Risus Sardonicus:
Sustained contraction
of facial musculature
produces a sneering
grin expression
• Contraction of the
muscles at the angle
of mouth and frontalis
22

23. • Trismus: Spasm of Masseter muscles (Lock Jaw)
23

24. • Opisthotonos: Spasm of extensor of the neck, back and legs to form a
backward curvature
24

25. AUTONOMIC DYSFUNCTION
• Tetanospasmin has a disinhibitory effect on the autonomic nervous system
(ANS)
• Due to increased release of catecholamines it causes:
Hyperpyrexia
Sweating
Peripheral vasoconstriction
Labile/Sustained Hypertension
Episodic tachycardia, dysrhythmias and cardiac arrest
Occasionally period of bradycardia & hypotension.
25

26. OTHER CLINICAL MANIFESTATIONS
• Dysphagia: due to pharyngeal muscle spasms and onset is usually insidious
over several days
• Reflex spasms: triggered by minimal external stimuli such as noise, light or
touch. The spasms last seconds to minutes.
Increases in frequency with disease progression and can cause apnea,
fractures, dislocations and rhabdomyolysis.
• Laryngeal spasms can occur at any time and can result in asphyxia.
26

27. SEQUENCE OF EVENTS
LOCK JAW
STIFF NECK
DIFFICULTY
SWALLOWING
MUSCLE RIGIDITY
SPASMS

28. Duration of illness
28
• Tetanus toxin-
induced effects are
long-lasting
because recovery
requires the growth
of new axonal
nerve terminals.
The usual duration
of clinical tetanus is
four to six weeks

29. Ablett Classification of severity
29

30. TYPES OF TETANUS
• Generalized vs local tetanus
• Maternal and neonatal tetanus
• Cephalic tetanus
• Ophthalmoplegic Tetanus
30

31. LOCAL TETANUS
• Uncommon form
• Manifestations are
restricted to muscles
near the wound.
• Cramping and twisting in
skeletal muscles
surrounding the wound:
local rigidity
• Prognosis: Excellent
31

32. NEONATAL TETANUS
• Tetanus Neonatorum (8th day
disease)
• Usually fatal if untreated
• Children born to inadequately
immunized mothers, after unsterile
treatment of umbilical stump
• During first 2 weeks of life
• Poor feeding, rigidity and spasms
• It is easily preventable by proper
tetanus toxoid immunization
32

33. MATERNAL TETANUS
• Tetanus occurring during pregnancy or within 6
weeks after any type of pregnancy termination
• One of the most easily preventable causes of
maternal mortality
• It includes :
1. Postpartum or Puerperal tetanus usually
resulting from septic procedures during delivery
2. Post abortal tetanus: following septic
manoeuvres during induced abortion
3. Tetanus during pregnancy: generally resulting
from inoculation through a non genital portal of
entry
33

34. CEPHALIC TETANUS
• A rare form of local tetanus
• Follows head injury / ear infection
• Involves one / more facial cranial nerves
• Trismus and localized paralysis ,usually
facial nerve, often unilateral.
• Involvement of cranial nerves III, IV, VI
and XII may also occur either alone or in
combination with others
• Incubation period : few days
• Mortality : high
34

35. OPHTHALMOPLEGIC TETANUS
• is a variant that develops
after penetrating eye
injuries and results in CN III
palsies and ptosis
35

36. DIAGNOSIS
• There are currently no blood tests that can be used to diagnose
tetanus. Diagnosis is done clinically based on the presence of trismus,
dysphagia, generalized muscular rigidity, and/or spasm
• Laboratory studies may demonstrate a moderate peripheral
leucocytosis
• An assay for antitoxin levels is not readily available. However, a level
of 0.01 IU/mL or greater in serum is generally considered protective,
making the diagnosis of tetanus less likely
• Cerebrospinal fluid (CSF) study findings are usually within normal
limits
36

37. DIRECT SMEAR
• Show Gram-positive
bacilli with drum-stick
appearance
37

38. CULTURE
• Done in blood agar under anaerobic
condition or in Robertson’s cooked meat
medium
• Produces swarming growth after 1-2
days of incubation
• In contaminated specimen heat at 80°C
for 10mins before culture to destroy
non-sporing organisms
38

39. ANIMAL INOCULATION
• To demonstrate toxigenicity
• Positive case: test animal develops stiffness & spasm of tail &
inoculated hind limb within 12-24 hours which spreads to rest of the
body. Death occurs in 1-2 days.
39

40. CLINICAL DIAGNOSTIC TEST
• SPATULA TEST:
Diagnostic bedside test
Posterior pharyngeal wall is touched with spatula
and a reflex spasm of the masseters indicates a
positive test
Sensitivity of 94% and a specificity of 100%.
• ALTERED WHISTLE: early effect of increased tone in
facial muscles which causes risus sardonicus.
40

41. DIFFERENTIAL DIAGNOSIS
• Drug induced Dystonic Reactions e.g. typical antipsychotics
• Strychnine poisoning
• Neuroleptic Malignant Syndrome, Serotonin syndrome
• Trismus d/t Peritonsillar Abscess/Dental infection
• Stiff person syndrome
• Acute abdominal emergencies
• Dislocations, Mandible
• Encephalitis, Meningitis
41

42. • Hysteria
• Hypocalcemia
• Rabies
• Seizure disorder (partial or generalized)
• Black Widow Spider Envenomation Stroke, Hemorrhagic
• Stroke, ischemic (cephalic tetanus)
• Subarachnoid Haemorrhage
42

43. PRINCIPLE OF TREATMENT
1. Neutralization of unbound toxin
• HTIG/ATS
2. Prevention of further toxin production
• Wound debridement & antibiotics
3. Antibiotics
4. Control of spasm
• Anticonvulsants, Sedatives, Muscle relaxants etc.
5. Management of autonomic dysfunction
• MGSO4, Betablockers etc.
6. Supportive care
• Physiotherapy, Nutrition, Thromboembolism prophylaxis ABC etc.
43

44. PRIMARY CARE
• Because of the risk of reflex spasms, maintain a dark and quiet
environment for the patient. Avoid unnecessary procedures and
manipulations.
• Attempting for intubation may induce severe reflex laryngospasm;
prepare for emergency tracheostomy.
• Consider prophylactic tracheostomy in all patients with moderate-to-
severe clinical manifestations
44

45. ANTI-TOXIN ADMINISTRATION
• A single intramuscular dose of 3000-5000 units (100U/kg-half in each
buttock), part of the dose infiltrated around the wound
• The WHO recommends TIG 500 units by IM/IV (depending on the
available preparation) as soon as possible
• In addition, administer TT-containing vaccine or TT (0.5 cc) IM
injection at a separate site via separate syringe
• TIG can only help remove unbound tetanus toxin, but it cannot
affect toxin bound to nerve endings
45

46. PREVENTION OF FURTHER TOXIN PRODUCTION
• Debridement of Wound to remove organisms and to create an
aerobic environment.
• The current recommendation is to excise at least 2 cm of normal
viable-appearing tissue around the wound margins.
• Incise and drain abscesses.
• Delay any wound manipulation until several hours after
administration of antitoxin due to risk of releasing tetanospasmin into
the bloodstream.
46

47. ANTIBIOTICS
• Theoretically, antibiotics may prevent multiplication of C. tetani
• Penicillin G was the drug of choice initially but now Metronidazole is
preferred drug
• Penicillin G aqueous (10-12 MU IV in 2-4 divided doses) for 10 to 14
days
• Metronidazole (500 mg 6 hrly or 1gm 12 hrly) for 10 to 14 days
• Doxycycline, Clindamycin and Erythromycin are alternative for
penicillin allergic patients who can not tolerate metronidazole
47

48. CONTROL OF SPASM
• Nursing in quiet environment, avoid unnecessary stimuli, Protecting
the airway.
• Drugs to treat muscle spasm, rigidity, and tetanic seizures include
1. Sedative-hypnotic agents
2. General anesthetics
3. Centrally acting muscle relaxants
4. Neuromuscular blocking agents
48

49. • Sedative-hypnotic agents
Sedative-hypnotic agents are the mainstays of tetanus treatment
Benzodiazepines are the most effective primary agents for muscle
spasm prevention
Diazepam: Mainstay of treatment of tetanic spasms and tetanic
seizures. Depresses all levels of CNS, including limbic and reticular
formation
Lorazepam is an effective alternative
Others: Phenobarbitone, Midazolam
49

50. • Skeletal muscle relaxants
Inhibit both monosynaptic and polysynaptic reflexes at spinal level,
possibly by hyperpolarization of afferent terminals
Muscle relaxation is indicated where sedation alone is inadequate
1. General anesthetics
Vecuronium (0.1 mg/kg IV as needed) or atracurium (0.5 mg/kg IV)
are appropriate
50

51. 2. BACLOFEN
Intrathecal (IT) baclofen, a centrally acting muscle relaxant, has been
used experimentally to wean patients off the ventilator
3. METHOCARBAMOL:
May be used as adjunct but not much useful in tetanus
51

52. MANAGEMENT OF AUTONOMIC DYSFUNCTION
• Fluid loading is a useful in minimizing autonomic instability
• Magnesium Sulphate: effective adjunct in relaxation, sedation &
controlling the autonomic disturbance in tetanus
• Another drugs:
Labetalol
Continuous infusion of esmolol
Clonidine / verapamil
Morphine
52

53. SUPPORTIVE CARE
• Since the toxin cannot be displaced from the system once bound to
neurons, supportive treatment is the mainstay for established
tetanus.
• Early tracheostomy is frequently indicated because of the likelihood
of prolonged mechanical ventilation.
• Energy demands in early tetanus may be unreasonably high, so early
and adequate nutritional support is mandatory
53

54. • Prevent ventilator associated pneumonia-nursing in the semi-
recumbant position.
• Chest physiotherapy, mouth care and regular tracheal suctioning may
be necessary due to increased secretions.
• Prophylaxis for thromboembolism with heparin, LMW heparin
54

55. PREVENTION
• Tetanus is completely preventable by active tetanus immunization
• Immunization is thought to provide protection for 10 years
• Immunization begins in infancy with the DPT vaccine
"3-in-1" vaccine that protects against diphtheria, pertussis, and
tetanus
55

56. ACTIVE IMMUNIZATION
• According to EPI of Nepal:
1. For child:
1st dose - 6th week (DPT)
2nd dose - 10th week (DPT)
3rd dose - 14th week (DPT)
2. For pregnant women:
Primi: 2 doses of Td 1 month apart after 12
weeks
Multi: 1 dose of Td
56

57. Post- Exposure prophylaxis
57

58. PASSIVE IMMUNIZATION
• Temporary protection: Human Tetanus Immunoglobulin /Anti-Tetanus
Serum
• Human Tetanus Immunoglobulin:
250-500 IU
Produces protective antibody level for at least 4-6 weeks.
Does not cause serum sickness
Longer passive protection compared to horse ATS (30 days/7 -10
days)
58

59. • ATS (EQUINE):
1500 IU s/c after sensitivity testing
7 – 10 days
High risk of serum sickness
It stimulates formation of antibodies to it , hence a person who has
once received ATS tends to rapidly eliminate subsequent doses
59

60. ORTHOPEDICS PERSPECTIVE OF TETANUS
• We have role to prevent and diagnose tetanus in At-risk patients
1. Prophylactic treatment: Grows only in necrotic tissue under
anaerobic conditions so wounds should be properly treated:
Tetanus toxoid is best preventable treatment and should be given to
all patients with open traumatic wounds
Prompt and thorough wound toilet prevent most of the infection
In established infection, minor debridement of wound may need to
be performed and antibiotic treatment

61. • If wound is contaminated, and particularly with a delay before
operation, antitoxin is advisable
• Old healed open fractures free from drainage for months to years
may still contain viable spores. Hence reconstructive procedures (E.g.
Bone grafting) should not be done until the patient is actively
immunized with TT
2. Diagnosis: At-risk patient should be timely recognized

62. References
• Harrison’s Principles of Internal Medicine: 18th Edition.
• Park’s Textbook of preventive & social medicine: 19th Edition.
• A Textbook Of Microbiology by P. Chakraborty
• Bailey and Love’s Short Practice of Surgery: 26th Edition
• Apley’s System of Orthopedics and Fractures: 10th Edition
• Various Internet Sources

63. THANK YOU
63