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TETANUS AND GG

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Title: TETANUS AND GG


1
  • TETENUS AND GAS GANGRENE
  • DR MZIRAY

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), a11d generalized
muscle spasms .
4
Etiology
5
Etiology
  • 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, 111ud,
    or clarified b11tter) are risk factors for
    neonates

8
Pathophysiology
9
Pathophysiology
  • Clostridium tetani is an obligate anaerobic,
    motile, grain-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 gtEntry of SporesgtAnerobic
    conditions.gtMultiplication of bacteriagt Toxin -
    TetanospasmingtEntry into motor nerve
    endingsgtTravel to spinal cord gtEntry into Central
    Inhibitory neurongtLoss of inhibitory action on
  • motor and autonomic neuronsgtPotentiating of
    muscle response to rnild stimulus autonomic
    overactvity.

11
Pathophysiology
  • Once the toxin becomes fixed to neurons, it cant
    be neutralized with antitoxin. Recovery of nerve
    function from tetan1.1s toxins requires sprouting
    of new nerve te1minals and formation of new
    synapses.
  • Localized tetanus develops when only the nerves
    supplying the affected 1n11scle are involved.
  • Generalized tetanus develops when the toxin
    released at the wound spreads through the
    lymphatics and blood to mttltiple nerve
    terminals.
  • The blood-brain barrier prevents direct entry of
    toxin to the CNS.

12
Pathophysiology
  • Mortality t1sually 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 predo1ninantly 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
    im1nunization 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 gtWorse 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,
  • Rbabdon1yolysis.
  • Laryngeal spasms gtasphyxia.

25
Other Menifestations
26
Other Menifestations
  • Dysphagia/Hydrophobia
  • Drooling
  • Sweating
  • Fever
  • Hypertension
  • Tachycardia
  • 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 coutries.
  • Infection results from umbilical cord
    contamination during unsanitary delivery, coupled
    with a lack of matemal 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 inteneurons 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 unconunon 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
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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 gt 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,
    compot1nd fractures, septic abortion, umbilical
    stun1p, or intramuscular injection
  • Narcotic addiction
  • Generalized tetanus
  • Temperature l1igher than 104F (40C)
  • 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 1nortality 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
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41
Prognosis
  • Mortality is higher for people older than 60
    years.
  • Mortality is higher in who require 1nechanical
    ventilation.
  • Less severe among patients wl10 have received a
    primary series of teta11us toxoid sometime dm-ing
    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 gennination
  • Stopping the production of toxin within the wound
  • Neutralizing unbound toxin
  • Controlling disease manifestations
  • Ma.naging complications

48
Initial Supportive Therapy
49
Initial Supportive Therapy
  • ICU care dark quiet avoid unnecessary touch
  • Intubation/Tracheosto1ny-
  • Prophylactic intubation sl1ould be seriously
    considered in all patients with moderate-to
    severe clinical manifestations
  • Tracbeostomy should be perfonned in patients
    reqt1iring intt1bation for 111ore tl1an 10 days.
  • Tracheostomy bas also been reco1nmended 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 wo11nds.
  • Inadequate vaccination status
  • Immunocomproised host.

59
TIGTetanits imniunoglobitlin (hitman
60
TIGTetanits immunoglobitlin (hitman
  • 250 units by intramusc11lar injection
  • 500 units if
  • wound older than 12 hottrs
  • 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 hot1rs
    before s11rgical treatn1ent 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 prod11cing
    clostridia.

65
Etiology
66
Etiology
  • In 1861, Louis Pasteur identified the first
    clostridial species, Clostridiitni bittyricum.
  • Bacillits aerogenes capsulatus, was later
    rena1ned Bacillus perfringens, and
  • then Clostridiitni welchii. The organism is now
    na1ned Clostridiuni perfringens.

67
Etiology
  • Anaerobic, gram-positive, spore-forming bacillus
    of tl1e genus Clostridium.
  • C pe,frin.gen.s is tl1e most common
  • Clostridiuni bifernien.tans,
  • Clostl'idi'un1septicum, Clostridiu1n sporogenes,
    Clostridiitni 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
PathophysiologyExotoxins
  • Alpha toxin - Lethal, lecithinase, necrotizing,
    hemolytic, cardiotoxic
  • Beta toxin - Lethal, necrotizing
  • Epsilon toxin - Lethal, pennease
  • Iota toxin - Lethal, necrotizing
  • Delta toxin - Lethal, hemolysin
  • Phi toxin - Hemolysin, cytolysin
  • Kappa toxin - Letl1al, collagenase, gelatinase,
    necrotizing

72
PathophysiologyExotoxins
  • Lambda toxin - Protease
  • Mu toxin - Hyaluronidase
  • Nu toxin - Lethal, deoxyribonuclease, hemolytic,
    necrotizing
  • Lethal as tested by injection in mice

73
Clinical FeaturesDemography
74
Clinical FeaturesDemography
  • Less co1nmon in developed countries.

75
Clinical FeaturesHistory
  • Trauma Crush injuries,open fractures.
  • Cornmomn in war injuries.
  • Abortion
  • Post op GI Biliary, liposuction
  • Occult malignancy

76
Symptoms
77
Symptoms
  • A sudden onset of pain .
  • Feeling ofl1eaviness in the affected extremity.
  • A low-grade fever
  • Apathetic mental status

78
Examination
79
Examination
  • Local swelling to 1nassive edema
  • Skin discoloration with hen1orrhagic blebs and
    bullae
  • Serosanguineot1s 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 he1nolytic anemia witl1 an
    increased lactate dehydrogenase (LDH) level.
  • The chemistry profile may show significant
    metabolic abnormalities (metabolic acidosis and
    renal failure) .
  • Operative exploration

84
Diagnostic StudiesImaging
85
Histologic Findings

86
Histologic Findings
  • Widespread myonecrosis, destruction of otl1er
    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
  • Hysterecto1ny.

95
  • The END
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