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2. Tetanus: Introduction

3. Tetanus: Introduction
Tetanus is a non communicable infectious
disease characterized by an acute onset of
hypertonia, painful muscular contractions
(usually of the muscles of the jaw and
neck), and generalized muscle spasms .

4. Etiology

5. Etiology
• The source of infection usually is a wound which
often is minor eg, from wood or metal splinters or
thorns
• Chronic skin ulcers .
• no obvious source
• abscesses and gangrene
• burns,
• frostbite,
• middle ear infections, dental or surgical
procedures, abortion, childbirth, and intravenous
(IV) or subcutaneous drug use.

6. Etiology
• dental or surgical procedures,
• abortion,
• childbirth,
• and intravenous (IV) or subcutaneous drug
use.
• tooth extractions,
• root canal therapy,
• intraoral soft tissue trauma

7. Etiology
• Unvaccinated mother, home delivery, and
unhygienic cutting of the umbilical cord
increase susceptibility to tetanus
• A history of neonatal tetanus in a previous
child is a risk factor for subsequent neonatal
tetanus
• Potentially infectious substances applied to
the umbilical stump (eg, animal dung, mud,
or clarified butter) are risk factors for
neonates

8. Pathophysiology

9. Pathophysiology
• Clostridium tetani is an obligate anaerobic,
motile, gram-positive bacillus.
• They are found in soil, house dust, animal
intestines, and human feces. Spores can
persist in normal tissue for months to years.
• To germinate, the spores require specific
anaerobic conditions, such as wounds with
low oxidation-reduction potential (eg, dead
or devitalized tissue, foreign body, active
infection).

10. Pathophysiology
• Infection by C tetani results in a benign
appearance at the portal of entry because of the
inability of the organism to evoke an
inflammatory reaction
• Trauma >Entry of Spores>Anerobic
conditions.>Multiplication of bacteria> Toxin –
Tetanospasmin>Entry into motor nerve
endings>Travel to spinal cord >Entry into Central
Inhibitory neuron>Loss of inhibitory action on
motor and autonomic neuurons>Potentiating of
muscle response to minor stimuli + autonomic
overactvity.

11. Pathophysiology
• Once the toxin becomes fixed to neurons, it cannot
be neutralized with antitoxin. Recovery of nerve
function from tetanus toxins requires sprouting of
new nerve terminals and formation of new
synapses.
• Localized tetanus develops when only the nerves
supplying the affected muscle are involved.
• Generalized tetanus develops when the toxin
released at the wound spreads through the
lymphatics and blood to multiple nerve terminals.
• The blood-brain barrier prevents direct entry of
toxin to the CNS.

12. Pathophysiology
• Mortality usually results from autonomic
dysfunction
– extremes in blood pressure
– Dysrhythmias
– cardiac arrest.

13. Clinical Features

14. Clinical Features
• Demography
• Symptoms
• Signs
• Complications
• Prognosis

15. Demography

16. Demography
• Less in developed countries.but still occurs.
• In developing countries neonatal tetanus is a
public health problem approx.200,000 cases
per year.
• Young adults are next.
• Tetanus is predominantly a disease of
underdeveloped countries.

17. Demography
It is common in areas where-
• soil is cultivated
• in rural areas
• in warm climates
• during summer months,
• among males.
• In countries without a comprehensive
immunization program, tetanus
predominantly develops in neonates and
young children.

18. Clinical Types
• Localised Tetanus.
• Generalised Tetanus
• Neonatal Tetanus
• Cephalic Tetanus

19. History

20. History
• Underimmunization.
• Incubation Period –Average 7 days.
• 4-14 days
• Short >Worse prognosis.

21. Presenting complaints

22. Presenting complaints
• Sore Throat
• Dysphagia
• Lockjaw(Trismus)
• Localised stiffness,
• Neck rigidity
• Restlessness
• Reflex spasms.
• Abdominal rigidity

23. Chief Menifestations

24. Chief Menifestations
• Muscle rigidity
• Muscle Spasms Leading to
– Opisthotonus
– Risus Sardonicus
– Apnea,
– Fractures, dislocations,
– Rhabdomyolysis.
– Laryngeal spasms >asphyxia.

25. Other Menifestations

26. Other Menifestations
• Dysphagia/Hydrophobia
• Drooling
• Sweating
• Fever
• Hypertension
• Tachycardia
• Spatula Test
• During these episodes, patients have an
intact sensorium and feel severe pain

27. Neonatal Tetanus

28. Neonatal Tetanus
• Aka tetanus neonatorum is a major cause of
infant mortality in underdeveloped
countries
• Rare in the developed countries.
• Infection results from umbilical cord
contamination during unsanitary delivery,
coupled with a lack of maternal
immunization.

29. Neonatal Tetanus
• At the end of the first week of life,
• Irritability
• Poor feeding
• Rigidity, Opisthotonus
• Facial grimacing
• Severe spasms with touch.
• Poor prognosis.

30. localized Tetanus

31. localized Tetanus
• Persistent rigidity in the muscle group close
to the injury site.
• The muscular rigidity is caused by a
dysfunction in the interneurons that inhibit
the alpha motor neurons of the affected
muscles.
• No further central nervous system (CNS)
involvement occurs in this form, and
mortality is very low.

32. Cephalic tetanus

33. Cephalic tetanus
• is uncommon and usually occurs after head
trauma or otitis media.
• Patients with this form present with cranial
nerve (CN) palsies.
• The infection may be localized or may
become generalized.

34. Prognosis

35. Prognosis
• Dependent on-
– incubation period
– the time from spore inoculation to first
symptom
– time from first symptom to first tetanic spasm.
• In general, shorter intervals indicate more
severe .
• Delay in treatment
• Contaminated lesions of the head and the
face

36. Prognosis
• Patients who survive tetanus and return to
their predisease state of health
• Recovery is slow and usually occurs over 2-
4 months
• Some patients remain hypotonic
• Clinical tetanus does not produce a state of
immunity > vaccinate.

37. Prognosis: rating scale

38. Prognosis: rating scale
1 point is given for each of the following:
• Incubation period shorter than 7 days
• Period of onset shorter than 48 hours
• Tetanus acquired from burns, surgical wounds,
compound fractures, septic abortion, umbilical
stump, or intramuscular injection
• Narcotic addiction
• Generalized tetanus
• Temperature higher than 104°F (40°C)
• Tachycardia exceeding 120 beats/min (150
beats/min in neonates)

39. Prognosis: rating scale
The total score :
• 0 or 1 – Mild tetanus; mortality below 10%
• 2 or 3 – Moderate tetanus; mortality of 10-
20%
• 4 – Severe tetanus; mortality of 20-40%
• 5 or 6 – Very severe tetanus; mortality
above 50%
• Cephalic tetanus is always severe or very
severe.
• Neonatal tetanus is always very severe.

40. Prognosis

41. Prognosis
• Mortality is higher for people older than 60
years.
• Mortality is higher in who require
mechanical ventilation.
• Less severe among patients who have
received a primary series of tetanus toxoid
sometime during their life.

42. Diagnostic Studies

43. Diagnostic Studies
Spatula Test
• Touch the oropharynx with a spatula or
tongue blade. In normal circumstances, it
elicits a gag reflex, and the patient tries to
expel the spatula (ie, a negative test result).
If tetanus is present, patients develop a
reflex spasm of the masseters and bite the
spatula (ie, a positive test result).

44. Differential Diagnosis

45. Differential Diagnosis
• Strychnine poisoning (Rat poison):the
onset of symptoms is fast and the duration
much lesser
• Epilepsy
• Rabies
• Hysteria
• Malignant hyperthermia.
• Dystonic drug reactions

46. Management

47. Management
• Initiating supportive therapy
• Debriding the wound to eradicate spores
and alter conditions for germination
• Stopping the production of toxin within the
wound
• Neutralizing unbound toxin
• Controlling disease manifestations
• Managing complications

48. Initial Supportive Therapy

49. Initial Supportive Therapy
• ICU care dark quiet avoid unnecessary
touch
• Intubation/Tracheostomy-
– Prophylactic intubation should be seriously
considered in all patients with moderate-to-
severe clinical manifestations
– Tracheostomy should be performed in patients
requiring intubation for more than 10 days.
Tracheostomy has also been recommended
after onset of the first generalized seizure.

50. Wound Care

51. Wound Care
• Wounds should be explored, carefully
cleansed, and properly debrided.
• Excise at least 2 cm of normal viable-
appearing tissue around the wound margins.
• Abscesses should be incised and drained.
• After the patient has been stabilized.
• Several hours after administration of
antitoxin.

52. Pharmacological Therapy

53. Pharmacological Therapy
• Benzodiazepine
• Barbiturates
• Propofol
• Midazolam
• Intrathecal Baclofen
• Magnesium sulphate
• Esomolol

54. Antotoxin

55. Antotoxin
• TIG: Tetanus Immunoglobin.
• A single intramuscular (IM) dose of 3000-
5000 units is generally recommended for
children and adults, with part of the dose
infiltrated around the wound if it can be
identified.

56. Antibiotic
• Metronidazole

57. Prevention

58. Prevention
• Adequate lifelong active immunization.
• TIG
– Tetanus prone wounds.
– Inadequate vaccination status
– Immunocomproised host.

59. TIG:Tetanus immunoglobulin (human)

60. TIG:Tetanus immunoglobulin (human)
• 250 units by intramuscular injection
• 500 units if
– wound older than 12 hours
– presence, or risk of, heavy contamination
– if patient weights more than 90 kg.

61. Tetanus-prone wounds

62. Tetanus-prone wounds
• If they are sustained either more than 6 hours
before surgical treatment of the wound .
• Puncture-type wound, a significant degree of
devitalized tissue
• Clinical evidence of sepsis
• Contamination with soil/manure
• Burns
• Frostbite
• High velocity missile injuries
• Bites

63. Gas Gangrene

64. Gas Gangrene
• Gas gangrene//clostridial myonecrosis -an
infection of muscle tissue by toxin-
producing clostridia.

65. Etiology

66. Etiology
• In 1861, Louis Pasteur identified the first
clostridial species, Clostridium butyricum.
• Bacillus aerogenes capsulatus, was later
renamed Bacillus perfringens, and
then Clostridium welchii. The organism is
now named Clostridium perfringens.

67. Etiology
• Anaerobic, gram-positive, spore-forming
bacillus of the genus Clostridium.
– C perfringens is the most common
– Clostridium bifermentans,
– Clostridium septicum, Clostridium sporogenes,
Clostridium novyi, Clostridium fallax,
Clostridium histolyticum, and Clostridium
tertium.

68. Etiology
• Posttraumatic
• Postoperative
• Spontaneous.

69. Pathophysiology

70. Pathophysiology
• Anerobic conditions of wound-
– Dead tissue
– Foreign bodies
– infection

71. Pathophysiology:Exotoxins
• Alpha toxin - Lethal,* lecithinase,
necrotizing, hemolytic, cardiotoxic
• Beta toxin - Lethal,* necrotizing
• Epsilon toxin - Lethal,* permease
• Iota toxin - Lethal,* necrotizing
• Delta toxin - Lethal,* hemolysin
• Phi toxin - Hemolysin, cytolysin
• Kappa toxin - Lethal,* collagenase,
gelatinase, necrotizing

72. Pathophysiology:Exotoxins
• Lambda toxin - Protease
• Mu toxin - Hyaluronidase
• Nu toxin - Lethal,* deoxyribonuclease,
hemolytic, necrotizing
• *Lethal as tested by injection in mice

73. Clinical Features:Demography

74. Clinical Features:Demography
• Less common in developed countries.

75. Clinical Features:History
• Trauma Crush injuries,open fractures.
• Commomn in war injuries.
• Abortion
• Post op GI Biliary, liposuction
• Occult malignancy

76. Symptoms

77. Symptoms
• A sudden onset of pain .
• Feeling of heaviness in the affected
extremity.
• A low-grade fever
• Apathetic mental status

78. Examination

79. Examination
• Local swelling to massive edema
• Skin discoloration with hemorrhagic blebs
and bullae
• Serosanguineous exudate
• Sweet odor
• Crepitus
• Fever
• Relative tachycardia,

80. Differential Diagnosis

81. Differential Diagnosis
• Abscess
• Cellulitis
• Toxic Shock Syndrome

82. Diagnostic Studies

83. Diagnostic Studies
• Gram’s Stain-"box-car," large gram-positive
bacilli without neutrophils.
• Rapidly developing hemolytic anemia with
an increased lactate dehydrogenase (LDH)
level.
• The chemistry profile may show significant
metabolic abnormalities (metabolic acidosis
and renal failure) .
• Operative exploration

84. Diagnostic Studies:Imaging

85. Histologic Findings
•

86. Histologic Findings
• Widespread myonecrosis, destruction of
other connective tissues
• Paucity of neutrophils in the infected area.

87. Management

88. Management
• The combination of aggressive surgical
debridement and effective antibiotic
therapy .

89. Antibiotics

90. Antibiotics
• Penicillin and clindamycin combination.
• Combination of clindamycin and
metronidazole is a good choice for patients
allergic to penicillin.

91. HBO

92. HBO
• Hyperbaric oxygen (HBO) therapy

93. Operative Therapy

94. Operative Therapy
• Debridement
• Fasciotomy
• Excision of abd.wall
• Hysterectomy.

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