Gas gangrene is a life-threatening bacterial infection caused by clostridium bacteria. It begins as pain and swelling around an injury that can quickly progress to soft tissue damage. The bacteria produce toxins and gas, causing tissues to die and air pockets to form, seen as crepitus. Aggressive surgical debridement of dead tissue and antibiotics such as penicillin are the primary treatments. Left untreated, gas gangrene can cause sepsis, organ failure and lead to amputation or death.

1. GAS GANGRENE
Dr Mohammed Akbar KhanDr Mohammed Akbar Khan

2. DEFINITIONDEFINITION
 Gangrene - Massive necrosis of tissue, superadded
by putrefaction
 Gas gangrene - Clostridial myonecrosis
 Myonecrosis - Bacterial infection - Necrotic damage
specific to muscle tissue - Gas tissues in gangrene.
 Deadly form of gangrene - Clostridium perfringens.
 Medical emergency

4.  Microorganisms - opportunistic - Skin breakage - Body
 Myonecrosis - Bacteria - Specific exotoxins.
 Envenomation by snakes of the Bothrops genus
(family Viperidae),
 Ischemic necrosis - vascular blockage (II Diabetes)
 Tumours that block or hoard blood supply
 Disseminated intravascular coagulation (DIC) or other
thromboses

6. ORGANISMSORGANISMS
 Anaerobic - Gram-positive - Spore-forming bacillus
 Genus Clostridium
 C. perfringens - Most common etiologic agent
 Other common clostridial species –
– Clostridium bifermentans
– Clostridium septicum
– Clostridium sporogenes
– Clostridium novyi
– Clostridium fallax
– Clostridium histolyticum
– Clostridium tertium

8. Gram stain of cysts with large rod-shaped bacteriaGram stain of cysts with large rod-shaped bacteria

11.  True saprophytes - soil and dust.True saprophytes - soil and dust.
 Mucous membranes GI tract & Female genital tract.Mucous membranes GI tract & Female genital tract.
 Clostridia - Colonize in skin- mainly around perineum.Clostridia - Colonize in skin- mainly around perineum.
 Obligate anaerobes- some species - Aerotolerant.Obligate anaerobes- some species - Aerotolerant.
 Bacterial multiplication & production of solubleBacterial multiplication & production of soluble
proteins called exotoxins require a low oxygenproteins called exotoxins require a low oxygen
tension.tension.

12.  Non-clostridial organisms - 60-85% cases
 Recent clinical series -gas gangrene in wound cultures
-83.3% of aerobic gram-negative bacilli
-4.5% anaerobic gram-positive bacilli- Clostridium sp
 Aerobic gram-negative bacteria
– Escherichia coli
– Proteus species
– Pseudomonas aeruginosa
– Klebsiella pneumoniae

13.  C perfringens - 20 exotoxins.
– Alpha toxin-lecithinase,necrotizing,hemolytic,cardiotoxic
– Beta toxin - necrotizing
– Epsilon toxin - permease
– Iota toxin - necrotizing
– Delta toxin - hemolysin
– Phi toxin - Hemolysin, cytolysin
– Kappa toxin - collagenase, gelatinase, necrotizing
– Lambda toxin - Protease
– Mu toxin - Hyaluronidase
– Nu toxin - Deoxyribonuclease, hemolytic necrotizing

15. ALPHA-TOXINALPHA-TOXIN
 Zinc metalloenzyme - Phospholipase-c activity
(lecithinase)
 Cell destruction - hydrolysis of key cell membrane
 Lysis of erythrocytes- leukocytes- platelets- fibroblasts
& muscle cells.
 Strains that do not produce alpha-toxin are less
virulent
 Purified alpha-toxin has a myocardial suppressant
effect - shock

16. PREDISPOSING FACTORSPREDISPOSING FACTORS
 Contamination - clostridial spores - posttraumatic or
postoperative lesions
 Local wound conditions > degree of clostridial
contamination
 Disrupted or necrotic tissue provides the necessary
enzymes and a low oxidation/reduction potential,
allowing for spore germination.
 Foreign bodies, premature wound closure& devitalized
muscle reduce the spore inoculum necessary to cause
infection
 Local effects - necrosis of muscle, subcutaneous fat
&thrombosis of blood vessels.
 Marked edema - compromise blood supply

17.  Incubation period - short (<24 h) -1 hour to 6 weeks
 Self-perpetuating destruction of tissue - locally &
systemically acting exotoxins.
 Fermentation of glucose - gas production
 C septicum spontaneous gas gangrene
 Nitrogen is the predominant gas component (74.5%), -
oxygen (16.1%), H2 (5.9%), & CO2 (3.4%).
 Production of hydrogen sulfide and CO2 gas begins
late and dissects along muscle bellies & fascial
planes.
 Local effects - rapid spread of the infection.
 Systemic effects - exotoxins - severe hemolysis.
 Hemoglobin levels - very low levels
 Hypotension- acute tubular necrosis and renal failure

18.  Very high mortality rate - 25%
 spontaneous gas gangrene/ Delay treatment -100%

19. Injury
Dead tissue, blood clots, foreign matter aerobic organisms
Develop Anaerobic Condition
(Exogenous infection) Germination of spores
Gas gangrene
Oedema, Necrosis, Gas production,
Toxaemia, Myositis
Crepitus

20. CLASSIFICATIONCLASSIFICATION
 POST-TRAUMATICPOST-TRAUMATIC
 POST-OPERATIVEPOST-OPERATIVE
 SPONTANEOUSSPONTANEOUS

21. POSTTRAUMATICPOSTTRAUMATIC
 60% of all gas gangrene60% of all gas gangrene
 automobile collisions.automobile collisions.
 Other complications of traumaOther complications of trauma
– Crush injuries,Crush injuries,
– Compound fractures,Compound fractures,
– Gunshot wounds,Gunshot wounds,
– ThermalThermal
– Electrical burns,Electrical burns,
– Frostbite.Frostbite.
 Farm or industrial injuries contaminated with soilFarm or industrial injuries contaminated with soil
 Rare causes- IM or SC injections with insulin,Rare causes- IM or SC injections with insulin,
epinephrine, quinine, or cocaineepinephrine, quinine, or cocaine

22. POSTOPERATIVEPOSTOPERATIVE
 clostridial infections –clostridial infections –
– colon resectioncolon resection
– ruptured appendixruptured appendix
– bowel perforationbowel perforation
– biliary or other GI surgery, including laparoscopicbiliary or other GI surgery, including laparoscopic
cholecystectomy and colonoscopy.cholecystectomy and colonoscopy.
Septic back-street abortions - uterine gas gangrene.Septic back-street abortions - uterine gas gangrene.

23. SPONTANEOUSSPONTANEOUS
 without external wound or injury - serious underlying
conditions.
 Colorectal adenocarcinoma
 Hematologic malignancy
 Children - Neutropenia
chemotherapy
spontaneous C septicum infections.
 Diabetes or neutropenic colitis.
 Many cases - no predisposing condition
 C perfringens
 C septicum

24. SYMPTOMSSYMPTOMS
 Posttraumatic gas gangrene - serious injury - skin or
soft tissues or have experienced open fractures.
 Postoperative gas gangrene - undergone recent
surgery of the GI or biliary tract.
 History is usually unremarkable - occult malignancy–
associated spontaneous gas gangrene.
 Sudden onset of pain is usually the first symptom
 Pain gradually worsens but spreads only as the
underlying infection spreads.
 Feeling of heaviness in the affected extremity.
 Low-grade fever and apathetic mental status

25. SIGNSSIGNS
 Local swelling & serosanguineous exudate - onset of
pain.
 skin - bronze color - blue-black color with skin blebs
and hemorrhagic bullae.
 Within hours, entire region - markedly edematous.
 Nonodorous or may have a sweet mousy odor.
 Crepitus follows gas production
 crepitus may not be detected with palpation owing to
brawny edema.
 Pain and tenderness to palpation disproportionate to
wound appearance
 Tachycardia disproportionate to body temperature is
common, - feeling of impending doom.
 Late signs - include hypotension, renal failure, and a
paradoxical heightening of mental acuity.

29. SUMMARY C/PSUMMARY C/P
 Air under the skin (subcutaneous emphysema)Air under the skin (subcutaneous emphysema)
 Blisters filled with brown-red fluidBlisters filled with brown-red fluid
 Drainage from the tissues, foul-smelling brown-Drainage from the tissues, foul-smelling brown-
red or bloody fluid (serosanguineous discharge)red or bloody fluid (serosanguineous discharge)
 Increased heart rate (tachycardia)Increased heart rate (tachycardia)
 Moderate to high feverModerate to high fever
 Moderate to severe pain around a skin injuryModerate to severe pain around a skin injury
 Pale skin color, later becoming dusky andPale skin color, later becoming dusky and
changing to dark red or purplechanging to dark red or purple
 Progressive swelling around a skin injuryProgressive swelling around a skin injury
 SweatingSweating
 Vesicle formation, combining into large blistersVesicle formation, combining into large blisters
 Yellow color to the skin (jaundice)Yellow color to the skin (jaundice)

30. Laboratory StudiesLaboratory Studies
 Hemolytic anemia
 Increased lactate dehydrogenase (LDH)
 White blood cell – No leukocytosis.
 Toxic shock syndrome - C sordellii or C septicum
Hemoconcentration & leukocytosis.
 Gram stain - exudate or infected tissues
– Box-car & large gram-positive bacilli without neutrophils
 < 1% of blood cultures - grow clostridial species.
 Metabolic abnormalities
– metabolic acidosis & renal failure
– with tissue injuries and hypotension.

31. Gasgangrene C. perfringenstypeA(Principal),
Capsulated,non-motile
LecithinaseC-toxaemia
Naglerreaction
Colonieswithhaloes
Colonieswithout
haloes
Incorporatedwith
Antitoxins

32. C Perfringens
C histolyticum
C septicum
C novyii
C Perfringens Alpha toxin
(lecithinase)

33. IMAGING STUDIES
Radiograph –
 Delineate the typical feathering pattern of gas in
soft tissue
 Gas may not be present in patients
 Gas in soft tissue does not confirm diagnosis

34. Gas feathering in the arm soft tissue

35. Extension of gas gangrene to the chest wall after initial debridementExtension of gas gangrene to the chest wall after initial debridement

36. CT SCANCT SCAN
 Abdominal casesAbdominal cases

37. OTHER TESTS
 Rapid detection of alpha-toxin or sialidases - ELISA
 In vitro amplification of alpha-toxin or DNA - PCR

38. PROCEDURES
 Surgical exploration confirms diagnosis
– muscle appears pale
– No contractile function -incised or electrically stimulated
 Bedside biopsy with immediate frozen section under LA
 Develop massive hemolysis, shock, ARDS &R F
Require invasive procedures
– Right-sided heart catheterization
– Mechanical ventilation
– Hemodialysis.

39. HISTOLOGIC FINDING
 Destruction of other connective tissues and a paucity
of neutrophils - infected area
 Leukocyte aggregates - border regions

40. ANTIBIOTIC THERAPY
 DOC - penicillin G - 10-24 million U/d
 Combination of penicillin and clindamycin
 Protein synthesis inhibitors
– clindamycin, chloramphenicol, rifampin, tetracycline
– Inhibit synthesis of clostridial exotoxins
 Allergic to penicillin - Clindamycin & Metronidazole
 Combination of penicillin and metronidazole
– antagonistic and is not recommended.
 Daptomycin, linezolid, and tigecycline not be used as
primary antibiotics

41. INTENSIVE CAREINTENSIVE CARE
 End-organ failure
 Other concomitant serious medical conditions that
require intensive supportive care.

42. ADJUVANT THERAPY
 Recombinant human activated protein C
– Drotrecogin alfa activated
– Adjuvant therapy for patients with severe sepsis
 Serious bleeding
– Drotrecogin alfa activated &repeated surgical
debridement
– Frequent interruption of the continuous infusion
– Not recommend this adjuvant therapy

43. Hyperbaric oxygen (HBO) therapy
important adjunct to surgery and antimicrobial therapy
increased survival - treatment with surgery & antibiotics
Direct bactericidal effect on most clostridial species
 inhibits alpha-toxin production
 enhance the demarcation of viable & nonviable tissue
prior to surgery.
100% oxygen at 2.5-3 absolute atmospheres for 90-120
minutes 3 times
Potential risks
 Pressure-related trauma-barotraumatic otitis pneumothorax
 Oxygen toxicity (myopia, seizures).
 Claustrophobia.
 Most adverse effects - self-limiting & resolve after
termination therapy

44. SURGICAL CARE
 Fasciotomy for compartment syndrome - not beFasciotomy for compartment syndrome - not be
delayed in patients with extremity involvement.delayed in patients with extremity involvement.
 Perform daily debridement - necrotic tissue.Perform daily debridement - necrotic tissue.
 Amputation of the extremity may be necessary andAmputation of the extremity may be necessary and
life-saving.life-saving.
 Abdominal involvement requires excision of the bodyAbdominal involvement requires excision of the body
wall musculature.wall musculature.
 Uterine gas gangrene following septic abortionUterine gas gangrene following septic abortion
usually necessitates hysterectomy.usually necessitates hysterectomy.

45. Hemipelvectomy

46. SUMMARYSUMMARY
 Most devastating infections.
 extremity amputation or massive loss of muscles, skin, and soft
tissues, requiring extensive reconstructive surgery and physical
rehabilitation.
 spontaneous gas gangrene may have occult malignancies of
the GI tract.
 Aggressive surgical debridement and intensive medical therapy
are the mainstays of treatment
 HBO therapy has become an important adjunctive therapy
 compartment syndrome - do not delay fasciotomy
 Deterrence/Prevention
 Avoid suturing wounds due to a crush injury or open fractures
with devitalized muscle and soil contamination.
 Provide warnings and instructions of wound care to rescuers
and health care workers - clostridial infections, -tetanus and gas
gangrene, in injured victims of natural disasters such as
earthquake or tsunami.

47. COMPLICATIONS
 Massive hemolysis - repeated blood transfusion
 DIC- Severe bleeding – Complicate aggressive surgical
debridement
 Acute renal failure
 Acute respiratory distress syndrome
 Shock
 Prognosis -
– Failure to provide an early diagnose and inadequate surgical
intervention
– dictate the outcome.
– better if the incubation period is shorter than 30 hours,
– Spontaneous gas gangrene worse prognosis than other
forms of gas gangrene.

48. TETANUSTETANUS

49. EPIDEMOLOGYEPIDEMOLOGY
 International health problem, asInternational health problem, as C. tetaniC. tetani spores are ubiquitous.spores are ubiquitous.
 Persons who are unvaccinated or inadequately immunized.Persons who are unvaccinated or inadequately immunized.
 More common in hot, damp climates with soil rich in organicMore common in hot, damp climates with soil rich in organic
matter.matter.
 Spores introduced into the body through puncture wounds.Spores introduced into the body through puncture wounds.
 Agricultural areas, a significant number of human adults mayAgricultural areas, a significant number of human adults may
harbor the organism.harbor the organism.
 Spores can also be found on skin surfaces and in contaminatedSpores can also be found on skin surfaces and in contaminated
heroin.heroin.
 Tetanus – particularly the neonatal form – remains a significantTetanus – particularly the neonatal form – remains a significant
public health problem in non-industrialized countries.public health problem in non-industrialized countries.
 WHO estimated59,000 newborns worldwide died in 2008WHO estimated59,000 newborns worldwide died in 2008
neonatal tetanus.neonatal tetanus.
 Tetanus is the only vaccine-preventable disease that isTetanus is the only vaccine-preventable disease that is
infectious but is not contagiousinfectious but is not contagious..

50. HistoryHistory
 Ancient people -relationship between wounds and fatalAncient people -relationship between wounds and fatal
muscle spasms.muscle spasms.
 Greek - τέτανο(tetanos) – taut & τείνειν(teinein) - StretchGreek - τέτανο(tetanos) – taut & τείνειν(teinein) - Stretch
 18841884
– Isolated strychnine-like toxin of tetanus from free-living,Isolated strychnine-like toxin of tetanus from free-living,
anaerobic soil bacteria.anaerobic soil bacteria.
– Etiology of the disease - demonstrated transmissibilityEtiology of the disease - demonstrated transmissibility
of tetanus for first time.of tetanus for first time.
– produced tetanus in rabbits by injecting pus from aproduced tetanus in rabbits by injecting pus from a
patient with fatal tetanus into their sciatic nerves.patient with fatal tetanus into their sciatic nerves.
 1889,1889,
– Kitasato ShibasaburōKitasato Shibasaburō -C. tetani -C. tetani was isolated from awas isolated from a
human victimhuman victim
– organism could produce disease when injected intoorganism could produce disease when injected into
animalsanimals
– toxin could be neutralized by specific antibodiestoxin could be neutralized by specific antibodies

51. HistoryHistory
 1897,1897,
– Edmond Nocard - tetanus antitoxin inducedEdmond Nocard - tetanus antitoxin induced
passive immunity in humanspassive immunity in humans
– could be used for prophylaxis and treatment.could be used for prophylaxis and treatment.
 19241924
– P. Descombey - Tetanus toxoid vaccine wasP. Descombey - Tetanus toxoid vaccine was
developeddeveloped
– used to prevent tetanus induced by battleused to prevent tetanus induced by battle
wounds during World War IIwounds during World War II

52. INTRODUCTIONINTRODUCTION
 TetanusTetanus - Prolonged contraction of skeletal muscle- Prolonged contraction of skeletal muscle
fibers.fibers.
 Primary symptoms – tetanospasminPrimary symptoms – tetanospasmin
– neurotoxin - Gram-positive, obligate anaerobicneurotoxin - Gram-positive, obligate anaerobic
bacteriumbacterium Clostridium tetaniClostridium tetani..
 Infection - wound contaminationInfection - wound contamination
 Cut or deep puncture wound.Cut or deep puncture wound.
 muscle spasms - jaw (lockjaw) and elsewhere in themuscle spasms - jaw (lockjaw) and elsewhere in the
bodybody
 Infection can be prevented by proper immunizationInfection can be prevented by proper immunization
and by post-exposure prophalysisand by post-exposure prophalysis

53. INTRODUCTIONINTRODUCTION
 Skeletal muscleSkeletal muscle
 Cardiac or heart muscle cannot be tetanized - IntrinsicCardiac or heart muscle cannot be tetanized - Intrinsic
electrical properties.electrical properties.
 Mortality rates - 48% to 73%.Mortality rates - 48% to 73%.
 Highest mortality rates - Unvaccinated & > 60 yearsHighest mortality rates - Unvaccinated & > 60 years
 Shorter the incubation period -More severe symptomsShorter the incubation period -More severe symptoms
 Neonatal tetanus,Neonatal tetanus,
– symptoms usually appear from 4 to 14 days aftersymptoms usually appear from 4 to 14 days after
birthbirth
– averaging about 7 daysaveraging about 7 days

54. TypesTypes
Basis of clinical findings, four different forms of tetanusBasis of clinical findings, four different forms of tetanus
 Generalized tetanusGeneralized tetanus
 Neonatal tetanusNeonatal tetanus
 Local tetanusLocal tetanus
 Cephalic tetanusCephalic tetanus

55. GENERALIZED TETANUSGENERALIZED TETANUS
 Most common type of tetanus - 80% of cases.Most common type of tetanus - 80% of cases.
 Descending pattern.Descending pattern.
 First sign - trismus or lockjaw & facial spasms called risusFirst sign - trismus or lockjaw & facial spasms called risus
sardonicus,sardonicus,
 Stiffness of the neck,Stiffness of the neck,
 Difficulty in swallowing,Difficulty in swallowing,
 Rigidity of pectoral and calf muscles.Rigidity of pectoral and calf muscles.
 Other symptoms - elevated temperature, sweating,Other symptoms - elevated temperature, sweating,
elevatedelevated blood pressure, and episodic rapid heart rate.blood pressure, and episodic rapid heart rate.
 Spasms may occur frequently and last for several minutesSpasms may occur frequently and last for several minutes
with the body shaped into a characteristic form calledwith the body shaped into a characteristic form called
opisthotonos.opisthotonos.
 Spasms continue for up to 4 weeks, and completeSpasms continue for up to 4 weeks, and complete
recovery may take monthsrecovery may take months

57. NEONATAL TETANUSNEONATAL TETANUS
 Generalized tetanus that occurs in newborns.Generalized tetanus that occurs in newborns.
 Infants - Not acquired passive immunity -Infants - Not acquired passive immunity -
mother has never been immunized - risk.mother has never been immunized - risk.
 Infection of the unhealed umbilical stump -Infection of the unhealed umbilical stump -
stump is cut with a non-sterile instrument.stump is cut with a non-sterile instrument.
 Neonatal tetanus - developing countriesNeonatal tetanus - developing countries
-Responsible for about 14% neonatal deaths,-Responsible for about 14% neonatal deaths,
-Very rare in developed countries-Very rare in developed countries

58. LOCAL TETANUSLOCAL TETANUS
 UncommonUncommon
 Persistent contraction of muscles - same anatomicPersistent contraction of muscles - same anatomic
area as the injury.area as the injury.
 Contractions may persist for many weeks beforeContractions may persist for many weeks before
gradually subsiding.gradually subsiding.
 Local tetanus is generally milder- 1% fatalLocal tetanus is generally milder- 1% fatal
 Generalized tetanus.Generalized tetanus.

59. CEPHALIC TETANUSCEPHALIC TETANUS
 Rare formRare form
 Otitis media (ear infections) in whichOtitis media (ear infections) in which C. C. tetani istetani is
present in the flora of the middle ear,present in the flora of the middle ear,
 Injuries to the head.Injuries to the head.
 Cranial nerves -FacialCranial nerves -Facial area.area.

60. ETIOLOGYETIOLOGY
 Tetanus – Rust- rusty nails,Tetanus – Rust- rusty nails,
 Objects with rust –outdoors or harbor anaerobicObjects with rust –outdoors or harbor anaerobic
bacteriabacteria
 Rust - not cause tetanus /contain moreRust - not cause tetanus /contain more C. C. tetanitetani
bacteria.bacteria.
 Rough surface of rusty metal merely provides a primeRough surface of rusty metal merely provides a prime
habitat for a C. tetani endospore to reside, & nail -habitat for a C. tetani endospore to reside, & nail -
puncture skin & deliver endospore into the wound.puncture skin & deliver endospore into the wound.
 Endospore is a non-metabolizing survival structure -Endospore is a non-metabolizing survival structure -
metabolize and cause infection once in an adequatemetabolize and cause infection once in an adequate
environment - Anaerobicenvironment - Anaerobic
 Stepping on a nail (rusty or not) - tetanus infection –Stepping on a nail (rusty or not) - tetanus infection –
– puncture wound, delivering endospores to apuncture wound, delivering endospores to a
suitable environment for growth.suitable environment for growth.

61. PATHOPHYSIOLOGYPATHOPHYSIOLOGY
 Clostridium tetani,Clostridium tetani,
– obligate nonencapsulated anaerobic gram-positive bacillusobligate nonencapsulated anaerobic gram-positive bacillus
– Rod-shaped bacteriaRod-shaped bacteria
 sporesspores
– resistant to heat, desiccation, and disinfectants.resistant to heat, desiccation, and disinfectants.
– soil, house dust, animal intestines, and human feces.soil, house dust, animal intestines, and human feces.
– gain entry can persist in normal tissue for months to years.gain entry can persist in normal tissue for months to years.
– anaerobic conditions, geminate & elaborate tetanospasminanaerobic conditions, geminate & elaborate tetanospasmin
and tetanolysin.and tetanolysin.
 Tetanolysin - no role - clinical course of tetanusTetanolysin - no role - clinical course of tetanus
 TetanospasminTetanospasmin
– neurotoxinneurotoxin
– causes the clinical manifestations of tetanuscauses the clinical manifestations of tetanus..

64. TetanospasminTetanospasmin
 Toxin is inactive inside the bacteria, - Bacteria dies -Toxin is inactive inside the bacteria, - Bacteria dies -
Released and activated by proteasesReleased and activated by proteases
 Active tetanospasmin - Retrograde axonal transport toActive tetanospasmin - Retrograde axonal transport to
the spinal cord and brain stemthe spinal cord and brain stem
– Lymphatic & vascular circulations - End plates of all nerves.Lymphatic & vascular circulations - End plates of all nerves.
– Enters nervous system peripherally - Myoneural jn.Enters nervous system peripherally - Myoneural jn.
– Transported centripetally into neurons of the CNSTransported centripetally into neurons of the CNS
 Most potent toxinsMost potent toxins
 Minimum lethal dose - 2.5 nanograms per kilogram ofMinimum lethal dose - 2.5 nanograms per kilogram of
body weight or 175 nanograms for a 70-kgbody weight or 175 nanograms for a 70-kg
 Neurons - incapable of neurotransmitter release -Neurons - incapable of neurotransmitter release -
GABA and Glycine - Major inhibitory neurotransmittersGABA and Glycine - Major inhibitory neurotransmitters

65. TetanospasminTetanospasmin
 Failure of inhibition of motor reflex responses to sensoryFailure of inhibition of motor reflex responses to sensory
stimulation.stimulation.
 Generalized contractions of the agonist and antagonistGeneralized contractions of the agonist and antagonist
musculature characteristic of a tetanic spasm.musculature characteristic of a tetanic spasm.
 Shortest peripheral nerves - first to deliver the toxin to the CNS,Shortest peripheral nerves - first to deliver the toxin to the CNS,
- early symptoms of facial distortion & back & neck stiffness- early symptoms of facial distortion & back & neck stiffness
 Damaged UMNDamaged UMN
– cannot inhibit LMN ( Renshaw cells),cannot inhibit LMN ( Renshaw cells),
– cannot control reflex responses to afferent sensory stimuli.cannot control reflex responses to afferent sensory stimuli.
 Both mechanisms – hallmark - muscle rigidity and spasms.Both mechanisms – hallmark - muscle rigidity and spasms.
 Toxin becomes fixed to neurons, it cannot be neutralized withToxin becomes fixed to neurons, it cannot be neutralized with
antitoxin.antitoxin.
 Recovery of nerve function from tetanus toxins requiresRecovery of nerve function from tetanus toxins requires
sprouting of new nerve terminals and formation of newsprouting of new nerve terminals and formation of new
synapses.synapses.

66. SYMPTOMSSYMPTOMS Tetanus are seen inTetanus are seen in
– either never vaccinated oreither never vaccinated or
– completed primary series but no booster in preceding 10 yrscompleted primary series but no booster in preceding 10 yrs..
 Patients with clinical manifestations occurring within 1Patients with clinical manifestations occurring within 1
week of an injury have more severe clinical courses.week of an injury have more severe clinical courses.
 Patients with generalized tetanus present with trismusPatients with generalized tetanus present with trismus
(lockjaw)(lockjaw)
 Stiffness,Stiffness,
 Neck rigidity- Muscle rigidity - Major manifestationNeck rigidity- Muscle rigidity - Major manifestation
 Descending pattern - jaw & facial muscles over theDescending pattern - jaw & facial muscles over the
next 24-48 hours to extensor muscles of the limbsnext 24-48 hours to extensor muscles of the limbs
 Dysphagia - pharyngeal muscle spasmsDysphagia - pharyngeal muscle spasms

67. SYMPTOMSSYMPTOMS
 Restlessness,Restlessness,
 Reflex spasmsReflex spasms
– Triggered by minimal external stimuli - Noise, light, or touch.Triggered by minimal external stimuli - Noise, light, or touch.
– Last seconds to minutesLast seconds to minutes
– More intenseMore intense
– Increase in frequency with disease progressionIncrease in frequency with disease progression
– Cause apnea, fractures, dislocations, and rhabdomyolysis.Cause apnea, fractures, dislocations, and rhabdomyolysis.
– Laryngeal spasms can occur - Asphyxia.Laryngeal spasms can occur - Asphyxia.
 Other symptomsOther symptoms
– Elevated temperature, sweating, elevated blood pressure,Elevated temperature, sweating, elevated blood pressure,
and episodic rapid heart rate.and episodic rapid heart rate.
 Sustained contraction of facial musculature producesSustained contraction of facial musculature produces
a sneering grin expression known as risus sardonicus.a sneering grin expression known as risus sardonicus.

68. RISUS SARDONICUS.RISUS SARDONICUS.

69. SIGNSSIGNS
 Site of antecedent acute injurySite of antecedent acute injury
– Lower Extremity 52%Lower Extremity 52%
– Upper Extremity 34%,Upper Extremity 34%,
– Head or Trunk 5%Head or Trunk 5%
 Autonomic dysfunctionAutonomic dysfunction
– extremes in blood pressure, dysrhythmias, and cardiacextremes in blood pressure, dysrhythmias, and cardiac
arrest.arrest.
 Neonatal tetanusNeonatal tetanus
– Inability to suck 3-10 days after birth.Inability to suck 3-10 days after birth.
– Presenting symptoms include irritability, excessive crying,Presenting symptoms include irritability, excessive crying,
grimaces, intense rigidity, and opisthotonus.grimaces, intense rigidity, and opisthotonus.
– Tetanic seizures may occur and portend a poor prognosis.Tetanic seizures may occur and portend a poor prognosis.
 Frequency and severity of seizures are related to severity of theFrequency and severity of seizures are related to severity of the
disease.disease.
 Seizures resemble epileptic seizures with the presence of aSeizures resemble epileptic seizures with the presence of a
sudden burst of tonic contractionssudden burst of tonic contractions..

70. SIGNSSIGNS No LOC & experiences severe pain.No LOC & experiences severe pain.
 Seizures - muscle groupsSeizures - muscle groups
– Opisthotonos, flexion and abduction of the armsOpisthotonos, flexion and abduction of the arms
– Clenching of the fists against the thoraxClenching of the fists against the thorax
– Extension of the lower extremitiesExtension of the lower extremities
 Localized tetanusLocalized tetanus
– Painful spasms muscles in close proximity to the site ofPainful spasms muscles in close proximity to the site of
injury.injury.
– Disorder may persist for several weeks but is usually self-Disorder may persist for several weeks but is usually self-
limiting.limiting.
 Cephalic tetanusCephalic tetanus
– Characterized by variable cranial nerve (CN) palsiesCharacterized by variable cranial nerve (CN) palsies
– CN VII is most frequently involvedCN VII is most frequently involved
– Untreated progress to generalized tetanusUntreated progress to generalized tetanus
 Ophthalmoplegic tetanus - variantOphthalmoplegic tetanus - variant
– Develops after penetrating eye injuriesDevelops after penetrating eye injuries
– Results in CN III palsies and ptosisResults in CN III palsies and ptosis

71. SIGNSSIGNS
 Abdominal tenderness and guarding,Abdominal tenderness and guarding,
– Mimicking an acute abdomen.Mimicking an acute abdomen.
– Exploratory laparotomies have been performed .Exploratory laparotomies have been performed .
 Tetanospasmin –Tetanospasmin –
– Disinhibitory effect on the ANSDisinhibitory effect on the ANS
– level of toxin in the CNS increases.level of toxin in the CNS increases.
 ANS disturbances,ANS disturbances,
– Sweating, fluctuating blood pressure,Sweating, fluctuating blood pressure,
– Episodic tachydysrhythmia,Episodic tachydysrhythmia,
– Increased release of catecholaminesIncreased release of catecholamines
 Drugs with beta-blocker effectsDrugs with beta-blocker effects
– Cardiovascular manifestations of ANS instability,Cardiovascular manifestations of ANS instability,
– Associated with increased risk of sudden death.Associated with increased risk of sudden death.

74. TESTSTESTS
 No blood tests that can be used to diagnose tetanus.No blood tests that can be used to diagnose tetanus.
 Diagnosis - presentation of tetanus symptomsDiagnosis - presentation of tetanus symptoms
 Laboratory identification ofLaboratory identification of C. tetaniC. tetani can only becan only be
demonstrated by production of tetanospasmin in mice.demonstrated by production of tetanospasmin in mice.
 Spatula testSpatula test
– Touching the posterior pharyngeal wall with a sterile, soft-Touching the posterior pharyngeal wall with a sterile, soft-
tipped instrument,tipped instrument,
– Positive test -involuntary contraction of the jaw (biting downPositive test -involuntary contraction of the jaw (biting down
on the "spatula"),on the "spatula"),
– Negative test - gag reflex attempting to expel the foreignNegative test - gag reflex attempting to expel the foreign
object.object.
– High specificity and a high sensitivityHigh specificity and a high sensitivity

75. PREVENTIONPREVENTION
 Recovery from naturally acquired tetanus does notRecovery from naturally acquired tetanus does not
result in immunity to tetanus.result in immunity to tetanus.
 Extreme potency of the tetanospasmin toxin; even aExtreme potency of the tetanospasmin toxin; even a
lethal dose of tetanospasmin is insufficient to provokelethal dose of tetanospasmin is insufficient to provoke
an immune response.an immune response.
 Tetanus can be prevented by vaccination with tetanusTetanus can be prevented by vaccination with tetanus
toxoidtoxoid
 The CDC recommends that adults receive a boosterThe CDC recommends that adults receive a booster
vaccine every ten yearsvaccine every ten years

76. PREVENTIONPREVENTION
 Standard care practiceStandard care practice
– booster to any patient with a puncture wound who isbooster to any patient with a puncture wound who is
uncertain last vaccinated,uncertain last vaccinated,
– he or she has had fewer than 3 lifetime doses of the vaccinehe or she has had fewer than 3 lifetime doses of the vaccine
 BoosterBooster
– not prevent a potentially fatal case of tetanus from thenot prevent a potentially fatal case of tetanus from the
current woundcurrent wound
– It take up to two weeks for tetanus antibodies to formIt take up to two weeks for tetanus antibodies to form
 children under the age of seven,children under the age of seven,
– tetanus vaccine is often administered as a combinedtetanus vaccine is often administered as a combined
vaccine,-DPT/DTaP diphtheria and pertussis.vaccine,-DPT/DTaP diphtheria and pertussis.
 Adults and children >7,Adults and children >7,
– Td vaccine (tetanus and diphtheria)Td vaccine (tetanus and diphtheria)
– Tdap (tetanus, diphtheria, and acellular pertussis)Tdap (tetanus, diphtheria, and acellular pertussis)

77. TETANUS IMMUNE GLOBULINTETANUS IMMUNE GLOBULIN
 Recommended for treatment of tetanus.Recommended for treatment of tetanus.
 Remove unbound tetanus toxin, but it cannot affect toxin boundRemove unbound tetanus toxin, but it cannot affect toxin bound
to nerve endings.to nerve endings.
 A single intramuscular dose of 3000-5000 units is generallyA single intramuscular dose of 3000-5000 units is generally
recommended for children and adults, with part of the doserecommended for children and adults, with part of the dose
infiltrated around the wound if it can be identified.infiltrated around the wound if it can be identified.
 WHO recommendsWHO recommends
– TIG 500 units by intramuscular injection or intravenously immediatlyTIG 500 units by intramuscular injection or intravenously immediatly
– administer age-appropriate TT-containing vaccine (Td, Tdap, DT, DPT,administer age-appropriate TT-containing vaccine (Td, Tdap, DT, DPT,
DTaP, or TT depending on age or allergies), 0.5 cc by intramuscularDTaP, or TT depending on age or allergies), 0.5 cc by intramuscular
injection at separate site.injection at separate site.
 Tetanus disease does not induce immunity;Tetanus disease does not induce immunity;
 Patients without a history of primary TT vaccination shouldPatients without a history of primary TT vaccination should
receive a second dose 1–2 months after the first dose and areceive a second dose 1–2 months after the first dose and a
third dose 6-12 months later.third dose 6-12 months later.

78. TREATMENTTREATMENT The wound must be cleaned.The wound must be cleaned.
 Dead and infected tissue should be removed by surgicalDead and infected tissue should be removed by surgical
debridement.debridement.
 Administration of the antibiotic metronidazole decreasesAdministration of the antibiotic metronidazole decreases
the number of bacteria but has no effect on the bacterialthe number of bacteria but has no effect on the bacterial
toxin.toxin.
 Penicillin was once used to treat tetanus, but is no longerPenicillin was once used to treat tetanus, but is no longer
the treatment of choice, owing to a theoretical risk ofthe treatment of choice, owing to a theoretical risk of
increased spasms. - Metronidazole is not available.increased spasms. - Metronidazole is not available.
 Passive immunization with human anti-tetanospasminPassive immunization with human anti-tetanospasmin
immunoglobulin or tetanus immunoglobulin is crucial.immunoglobulin or tetanus immunoglobulin is crucial.
 If specific anti-tetanospasmin immunoglobulin is notIf specific anti-tetanospasmin immunoglobulin is not
available, then normal human immunoglobulin may beavailable, then normal human immunoglobulin may be
given instead.given instead.
 All tetanus victims should be vaccinated against theAll tetanus victims should be vaccinated against the
disease or offered a booster shot.disease or offered a booster shot.

79. MILD TETANUSMILD TETANUS
 Muscle spasms - Diazepam or Other muscle relaxantsMuscle spasms - Diazepam or Other muscle relaxants
 Extreme cases - Paralyze the patient with curare-likeExtreme cases - Paralyze the patient with curare-like
drugs and use a mechanical ventilator.drugs and use a mechanical ventilator.
 Maintenance of an airway and proper nutritionMaintenance of an airway and proper nutrition
 Total parenteral nutritionTotal parenteral nutrition
– Intake of 3500-4000 C & at least 150 g of protein per dayIntake of 3500-4000 C & at least 150 g of protein per day
– liquid form -tube directly into stomach (Percutaneousliquid form -tube directly into stomach (Percutaneous
endoscopic gastrostomy)endoscopic gastrostomy)
– drip into a veindrip into a vein
– high-caloric diet maintenance - increased metabolic strainhigh-caloric diet maintenance - increased metabolic strain
brought on by the increased muscle activity.brought on by the increased muscle activity.
 Full recovery takes 4 to 6 weeks because the bodyFull recovery takes 4 to 6 weeks because the body
must regenerate destroyed nerve axon terminalsmust regenerate destroyed nerve axon terminals

80. SEVERE TETANUSSEVERE TETANUS
 Admission to intensive care.Admission to intensive care.

81. Lockjaw symptoms are caused due to Clostridium tetani infection.Lockjaw symptoms are caused due to Clostridium tetani infection.
Damaged upper motor neurons cause muscular rigidity leading to Lock-jawDamaged upper motor neurons cause muscular rigidity leading to Lock-jaw

82. SURGICAL THERAPYSURGICAL THERAPY
 Debridement of wounds to remove organismsDebridement of wounds to remove organisms
and to create an aerobic environment.and to create an aerobic environment.
 Excise at least 2 cm of normal viable-appearingExcise at least 2 cm of normal viable-appearing
tissue around the wound margins.tissue around the wound margins.
 Incise and drain abscesses.Incise and drain abscesses.
 Delay wound manipulation - several hours afterDelay wound manipulation - several hours after
administration of antitoxin - risk of releasingadministration of antitoxin - risk of releasing
tetanospasmin into the bloodstream.tetanospasmin into the bloodstream.

83. DRUGSDRUGS
 Muscle spasm, rigidity, and tetanic seizuresMuscle spasm, rigidity, and tetanic seizures
– sedative-hypnotic agents,sedative-hypnotic agents,
– general anesthetics,general anesthetics,
– centrally acting muscle relaxants,centrally acting muscle relaxants,
– neuromuscular blocking agents.neuromuscular blocking agents.
– Antibiotics are used to prevent multiplication ofAntibiotics are used to prevent multiplication of CC
tetani,tetani, thus halting production and release of toxins.thus halting production and release of toxins.
 Antibiotics - prevent multiplication ofAntibiotics - prevent multiplication of C tetani,C tetani,
thus halting production and release of toxinsthus halting production and release of toxins

84. ANTICONVULSANTSANTICONVULSANTS
 Sedative-hypnotic agents - mainstays of tetanusSedative-hypnotic agents - mainstays of tetanus
treatment.treatment.
 Benzodiazepines - primary agents for muscle spasmBenzodiazepines - primary agents for muscle spasm
prevention and work by enhancing GABA inhibition.prevention and work by enhancing GABA inhibition.
 Diazepam is the most frequently studied and used drug.Diazepam is the most frequently studied and used drug.
 Diazepam reduces anxiety, produces sedation, andDiazepam reduces anxiety, produces sedation, and
relaxes muscles.relaxes muscles.
 Lorazepam is an effective alternative. Large amounts (upLorazepam is an effective alternative. Large amounts (up
to 600 mg/d).to 600 mg/d).
 Phenobarbital is another anticonvulsant that may be usedPhenobarbital is another anticonvulsant that may be used
to prolong effects of diazepam.to prolong effects of diazepam.
 Phenobarbital is also used to treat severe muscle spasmsPhenobarbital is also used to treat severe muscle spasms
and provide sedation when neuromuscular blockingand provide sedation when neuromuscular blocking
agents are used.agents are used.

85. OTHER AGENTSOTHER AGENTS
 Spasm controlSpasm control
– baclofen,baclofen,
– Dantrolene,Dantrolene,
– Short-acting barbituratesShort-acting barbiturates
– Chlorpromazine.Chlorpromazine.
 Magnesium sulphate can +/- benzodiazepinesMagnesium sulphate can +/- benzodiazepines
– Control spasm and autonomic dysfunctionControl spasm and autonomic dysfunction
– 5 g (or 75 mg/kg) intravenous loading dose, then 2-3 g/h until5 g (or 75 mg/kg) intravenous loading dose, then 2-3 g/h until
spasm controlledspasm controlled
– Monitor patellar reflex, - Areflexia - Upper end of the therapeuticMonitor patellar reflex, - Areflexia - Upper end of the therapeutic
range (4 mmol/L).range (4 mmol/L).
– Areflexia develops, dose should be decreased to avoid overdose.Areflexia develops, dose should be decreased to avoid overdose.
– Does not reduce need for mechanical ventilation in adults withDoes not reduce need for mechanical ventilation in adults with
severe tetanus,severe tetanus,
– Reduce requirement for other drugs to control muscle spasms andReduce requirement for other drugs to control muscle spasms and
cardiovascular instability.cardiovascular instability.

86. COMPLICATIONSCOMPLICATIONS
 Prior to 1954, asphyxia from tetanic spasms was the usualPrior to 1954, asphyxia from tetanic spasms was the usual
cause of death.cause of death.
 Advent of neuromuscular blockers, mechanical ventilation, andAdvent of neuromuscular blockers, mechanical ventilation, and
pharmacologic control of spasms, sudden cardiac death haspharmacologic control of spasms, sudden cardiac death has
become the leading cause of death.become the leading cause of death.
 Sudden cardiac death has been attributed to excessiveSudden cardiac death has been attributed to excessive
catecholamine productions, direct action of tetanospasmin, orcatecholamine productions, direct action of tetanospasmin, or
tetanolysin on the myocardium.tetanolysin on the myocardium.
 Nosocomial infections are common when hospitalization isNosocomial infections are common when hospitalization is
prolonged.prolonged.
 Secondary infections may include sepsis from decubitus ulcers,Secondary infections may include sepsis from decubitus ulcers,
hospital-acquired pneumonias, and indwelling catheters.hospital-acquired pneumonias, and indwelling catheters.
 Pulmonary embolism is particularly a problem in drug users andPulmonary embolism is particularly a problem in drug users and
elderly patients.elderly patients.

87.  Further complications include the following:Further complications include the following:
 Long bone fracturesLong bone fractures
 Glenohumeral joint and temporomandibular jointGlenohumeral joint and temporomandibular joint
dislocationsdislocations
 Hypoxic injury and aspiration pneumonia is a commonHypoxic injury and aspiration pneumonia is a common
late complication of tetanus, found in 50–70% oflate complication of tetanus, found in 50–70% of
autopsied cases.autopsied cases.
 Adverse effects of autonomic instability, includingAdverse effects of autonomic instability, including
hypertension and cardiac dysrhythmiashypertension and cardiac dysrhythmias
 Paralytic ileus, pressure sores, and urinary retentionParalytic ileus, pressure sores, and urinary retention
 Malnutrition and stress ulcersMalnutrition and stress ulcers
 Coma, nerve palsies, neuropathies, psychologicalComa, nerve palsies, neuropathies, psychological
aftereffects, and flexion contracturesaftereffects, and flexion contractures

88. PROGNOSISPROGNOSIS
 Dependent on incubation period, time from sporeDependent on incubation period, time from spore
inoculation to first symptom, and time from firstinoculation to first symptom, and time from first
symptom to first tetanic spasm.symptom to first tetanic spasm.
 shorter intervals indicate more severe tetanus and ashorter intervals indicate more severe tetanus and a
poorer prognosis.poorer prognosis.
 Survive tetanus and return to their predisease state ofSurvive tetanus and return to their predisease state of
health.health.
 Recovery is slow and usually occurs over 2-4 months.Recovery is slow and usually occurs over 2-4 months.
 Some patients remain hypotonic.Some patients remain hypotonic.
 Clinical tetanus does not produce a state of immunity;Clinical tetanus does not produce a state of immunity;
patients who survive the disease require activepatients who survive the disease require active
immunization with tetanus toxoid to prevent aimmunization with tetanus toxoid to prevent a
recurrence.recurrence.

89. Thank you