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- DR. RITESH DHANBHAR
TETANUS
Predisposing Factors for Tetanus
1) Absence tetanus toxoid immunisation.
2) Trauma wounds, presence of foreign body, wounds with anaerobic
environment in the tissues.
3) Chronic suppurative otitis media with perforation, caries teeth.
4) Improper sterilisation.
5) Tattooing
6) ear lobe price
7) colloquial perianal therapies
Casative Organism
Clostridium tetani
 It is a Gram-positive, anaerobic, motile, noncapsulated, organism with
peritrichous fl agella, and terminal spores (Drum stick appearance).
 Toxines : tetanospasmin and tetanolysin
PathogenesisSpore
↓
Enters the wound
↓
It germinates in anaerobic media releasing bacteria, which multiply
↓
Release of Exotoxins Tetanospasmin + Tetanolysin
↓ ↓
Through lymphatics, perineural sheath & Circulation Haemolysis
↓ ↓
Enters the central nervous system Toxaemia
↓ ↓
Tonic, clonic convulsions Aggravates the muscle Spasm
↓ .
Once toxin is fi xed in nerve tissue,
it can no longer be neutralised by antitoxin
Opisthotonus
Symptoms
1) Trismus is the most common symptom
2) Jaw stiffness, pain and stiffness in the neck and back muscles
3) Anxiousness, sweating
4) Headache, delirium, sleeplessness
5) Dysphagia
6) Dyspnoea
Signs
1) Trismus, due to spasm of masseter and pterygoids.
2) Risus sardonicus (smiling facies), due to spasm of the facial muscle—zygomaticus
major.
3) Neck rigidity.
4) Spasm and rigidity of all muscles.
5) Hyperrefl exia.
6) Respiratory changes—due to laryngeal muscle spasm, infection,aspiration.
7) Tonic clonic convulsions.
8) Abdominal wall rigidity often with haematoma formation.
9) Severe convulsion may often lead to fractures, joint dislocationsand tendon ruptures.
10) Fever and tachycardia.
11) Retention of urine , constipation.
12) Symptoms will be aggravated by stimuli like light, noise.
Different Postures in Tetanus
 Opisthotonus: Posterior muscles are acting more, so
backward bending.
 Orthotonus: Straight posture. Both front and back muscles
are acting equally.
 Emprosthotonus: Forward bending as front muscles are
acting more.
 Pleurosthotonus: Lateral bending as lateral muscles act
more.
Complications
a. Fracture bones
b. Haematoma
c. Aspiration pneumonia, respiratory failure, ARDS
d. Carditis, arrhythmias—life-threatening
e. DVT, pulmonary embolism
f. Toxaemia
g. Secondary infection—septicaemia
Treatment
General measures:
1) Isolation
2) Avoid noise and light
3) ATG 3,000 units IM
4) ATS-50,000 IM and 50,000 IV—after test dose
5) Antibiotics like inj penicillin 20 lacs 6th hourly
6) Inj tetanus toxoid 0.5 ml IM—to deltoid muscle
7) IV fl uids with TPN
8) Urinary catheterisation
9) Nasogastric tube is passed to prevent aspiration initially, later for feeding Regular
suction of throat
10) Nasal oxygen when required
11) Prevention of bedsore formation
12) Prevention of DVT by low molecular weight heparin
Treatment
Specific measures:
1) IV diazepam 20 mg 6th hourly
2) IV phenobarbitone 30 mg 6th hourly
3) IV chorpromazine 25 mg 6th hourly
4) Endotracheal intubation and ventilator support
5) Tracheostomy if there is severe respiratory secretions
6) Steroids
7) Bronchodilators like deriphylline
8) Wound care—debridement, drainage, and local injection of ATG
GAS GANGRENE
Definition
It is an infective gangrene caused by clostridial
organisms involving mainly skeletal muscle as oedematous
myonecrosis.
Organisms
a. Clostridium welchii (perfringens): Gram-positive, central
spore bearing, nonmotile, capsulated organisms, most
common.
b. Clostridium oedematiens.
c. Clostridium septicum.
d. Clostridium histolyticum.
Pathogenesis
 Lecithinase is important toxin which is haemolytic, membranolytic
and necrotic causing extensive myositis. It splits lecithin into
phosphocholine.
 Haemolysin causes extensive haemolysis.
 Hyaluronidase helps in rapid spread of gas gangrene.
 Proteinase causes breaking down of proteins in an infected tissue
Clinical Features
Incubation period is 1-2 days.
1) Features of toxaemia, fever, tachycardia.
2) Wound is under tension with foul smelling discharge (sickly
sweety/decaying apple odour).
3) Brown coloured skin due to haemolysis.
4) Crepitus can be felt.
5) Jaundice, oliguria.
6) Clostridium welchii can infect limbs, abdominal wall, appendix,
gallbladder, common bile duct, intestine, uterus
Classification
A. Fulminant type causes rapid progress and often death due to toxaemia,
renal failure or liver failure or MODS or ARDS.
B. Massive type involving whole of one limb containing fully dark coloured
gas filled areas.
C. Group type: Infection of one group of muscles, extensorsof thigh, fl exors
of leg.
D. Single muscle type affecting one single muscle.
E. Subcutaneous type of gas gangrene involves only subcutaneous tissue
Complications
1. Septicaemia, toxaemia.
2. Renal failure, liver failure.
3. Circulatory failure
4. DIC
5. secondary infection.
6. Death.
Investigations
1) X-ray shows gas in muscle plane or under the skin.
2) Liver function tests, blood urea, serum creatinine, TLC.
3) CT scan useful in chest or abdominal wounds.
4) Gram’s stain shows Gram-positive bacilli.
5) Robertson’s cooked meat media is used which causes meat to turn
pink with sour smell and acid reaction.
Treatment
a. Injection benzyl penicillin 20 lacs 4th hourly + Injection
metronidazole 500 mg 8th hourly + Injection aminoglycosides
or third generation cephalosporins .
b. Fresh blood transfusion.
c. Polyvalent antiserum 25,000 units
d. Hyperbaric oxygen.
e. All dead tissues are excised and debridement is done.
Treatment
f. Rehydration and maintaining optimum urine output(0.5ml/kg/hour).
g. Electrolyte management.
h. In severe cases amputation has to be done as a life-saving
i. procedure
j. Often ventilator support is required.
k. Hypotension in gas gangrene is treated with whole blood transfusion.
Tetanus & Gas Gangrene

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Tetanus & Gas Gangrene

  • 1. - DR. RITESH DHANBHAR
  • 3. Predisposing Factors for Tetanus 1) Absence tetanus toxoid immunisation. 2) Trauma wounds, presence of foreign body, wounds with anaerobic environment in the tissues. 3) Chronic suppurative otitis media with perforation, caries teeth. 4) Improper sterilisation. 5) Tattooing 6) ear lobe price 7) colloquial perianal therapies
  • 4. Casative Organism Clostridium tetani  It is a Gram-positive, anaerobic, motile, noncapsulated, organism with peritrichous fl agella, and terminal spores (Drum stick appearance).  Toxines : tetanospasmin and tetanolysin
  • 5. PathogenesisSpore ↓ Enters the wound ↓ It germinates in anaerobic media releasing bacteria, which multiply ↓ Release of Exotoxins Tetanospasmin + Tetanolysin ↓ ↓ Through lymphatics, perineural sheath & Circulation Haemolysis ↓ ↓ Enters the central nervous system Toxaemia ↓ ↓ Tonic, clonic convulsions Aggravates the muscle Spasm ↓ . Once toxin is fi xed in nerve tissue, it can no longer be neutralised by antitoxin
  • 7. Symptoms 1) Trismus is the most common symptom 2) Jaw stiffness, pain and stiffness in the neck and back muscles 3) Anxiousness, sweating 4) Headache, delirium, sleeplessness 5) Dysphagia 6) Dyspnoea
  • 8. Signs 1) Trismus, due to spasm of masseter and pterygoids. 2) Risus sardonicus (smiling facies), due to spasm of the facial muscle—zygomaticus major. 3) Neck rigidity. 4) Spasm and rigidity of all muscles. 5) Hyperrefl exia. 6) Respiratory changes—due to laryngeal muscle spasm, infection,aspiration. 7) Tonic clonic convulsions. 8) Abdominal wall rigidity often with haematoma formation. 9) Severe convulsion may often lead to fractures, joint dislocationsand tendon ruptures. 10) Fever and tachycardia. 11) Retention of urine , constipation. 12) Symptoms will be aggravated by stimuli like light, noise.
  • 9. Different Postures in Tetanus  Opisthotonus: Posterior muscles are acting more, so backward bending.  Orthotonus: Straight posture. Both front and back muscles are acting equally.  Emprosthotonus: Forward bending as front muscles are acting more.  Pleurosthotonus: Lateral bending as lateral muscles act more.
  • 10. Complications a. Fracture bones b. Haematoma c. Aspiration pneumonia, respiratory failure, ARDS d. Carditis, arrhythmias—life-threatening e. DVT, pulmonary embolism f. Toxaemia g. Secondary infection—septicaemia
  • 11. Treatment General measures: 1) Isolation 2) Avoid noise and light 3) ATG 3,000 units IM 4) ATS-50,000 IM and 50,000 IV—after test dose 5) Antibiotics like inj penicillin 20 lacs 6th hourly 6) Inj tetanus toxoid 0.5 ml IM—to deltoid muscle 7) IV fl uids with TPN 8) Urinary catheterisation 9) Nasogastric tube is passed to prevent aspiration initially, later for feeding Regular suction of throat 10) Nasal oxygen when required 11) Prevention of bedsore formation 12) Prevention of DVT by low molecular weight heparin
  • 12. Treatment Specific measures: 1) IV diazepam 20 mg 6th hourly 2) IV phenobarbitone 30 mg 6th hourly 3) IV chorpromazine 25 mg 6th hourly 4) Endotracheal intubation and ventilator support 5) Tracheostomy if there is severe respiratory secretions 6) Steroids 7) Bronchodilators like deriphylline 8) Wound care—debridement, drainage, and local injection of ATG
  • 14. Definition It is an infective gangrene caused by clostridial organisms involving mainly skeletal muscle as oedematous myonecrosis.
  • 15.
  • 16. Organisms a. Clostridium welchii (perfringens): Gram-positive, central spore bearing, nonmotile, capsulated organisms, most common. b. Clostridium oedematiens. c. Clostridium septicum. d. Clostridium histolyticum.
  • 17. Pathogenesis  Lecithinase is important toxin which is haemolytic, membranolytic and necrotic causing extensive myositis. It splits lecithin into phosphocholine.  Haemolysin causes extensive haemolysis.  Hyaluronidase helps in rapid spread of gas gangrene.  Proteinase causes breaking down of proteins in an infected tissue
  • 18. Clinical Features Incubation period is 1-2 days. 1) Features of toxaemia, fever, tachycardia. 2) Wound is under tension with foul smelling discharge (sickly sweety/decaying apple odour). 3) Brown coloured skin due to haemolysis. 4) Crepitus can be felt. 5) Jaundice, oliguria. 6) Clostridium welchii can infect limbs, abdominal wall, appendix, gallbladder, common bile duct, intestine, uterus
  • 19. Classification A. Fulminant type causes rapid progress and often death due to toxaemia, renal failure or liver failure or MODS or ARDS. B. Massive type involving whole of one limb containing fully dark coloured gas filled areas. C. Group type: Infection of one group of muscles, extensorsof thigh, fl exors of leg. D. Single muscle type affecting one single muscle. E. Subcutaneous type of gas gangrene involves only subcutaneous tissue
  • 20. Complications 1. Septicaemia, toxaemia. 2. Renal failure, liver failure. 3. Circulatory failure 4. DIC 5. secondary infection. 6. Death.
  • 21. Investigations 1) X-ray shows gas in muscle plane or under the skin. 2) Liver function tests, blood urea, serum creatinine, TLC. 3) CT scan useful in chest or abdominal wounds. 4) Gram’s stain shows Gram-positive bacilli. 5) Robertson’s cooked meat media is used which causes meat to turn pink with sour smell and acid reaction.
  • 22. Treatment a. Injection benzyl penicillin 20 lacs 4th hourly + Injection metronidazole 500 mg 8th hourly + Injection aminoglycosides or third generation cephalosporins . b. Fresh blood transfusion. c. Polyvalent antiserum 25,000 units d. Hyperbaric oxygen. e. All dead tissues are excised and debridement is done.
  • 23.
  • 24. Treatment f. Rehydration and maintaining optimum urine output(0.5ml/kg/hour). g. Electrolyte management. h. In severe cases amputation has to be done as a life-saving i. procedure j. Often ventilator support is required. k. Hypotension in gas gangrene is treated with whole blood transfusion.