2.
A 60 yrs old houeswife ,uanabai thakur r/o katedhara M.P.
admitted on 24/9/13 in micu with c/o
1.difficulty in swallowing since 5 days
2. difficulty in opening mouth since 5 days
3.
H/o pain in both ears since 15 days
No h/o injury
No h/o fever / convulsion
No h/o consumption of any substance
Not taking any medication
No h/o similar complaints in past
No HT/DM/IHD in past
Non tobacco chewer
15. Historical perspective
The word tetanus comes from the Greek tetanos, which is derived from the
term teinein, meaning to stretch.
During World War I, tetanus occurred in 1.47 per 1000 British wounded and
in 12.5 per 1000 persons involved in the Peninsular campaign.
Nicolaier discovered Clostridium tetani in 1885 .
In 1889, Koch's pupil, Kitasato, obtained the bacillus of tetanus in pure
culture .
introduction of tetanus toxoid vaccination by Behring and Knorr in 1886.
16. Problem
Although it is an entirely preventable disease by immunization , the burden
of disease worldwide is great.
W.H.O considers reporting is inaccurate & incomplete, particularly in
devoleping countries,
In 2008 16628 cases 0f tetanus other than neonatal and 6658 cases reported
to who worldwide !
in 2009 Govt. of India reported (other than NT) 2051 cases and 160
death.there were 889 NT cases and 31 deaths!!
In 2009 maharastra reported 392 (other than NT) cases and 1 death.while 57
NT cases and 0 death !!! (park 21)
17. The Organism
Clostridium tetani is a gram positive, obligately anerobe, spore forming
bacillus, which give it a characteristic drumstick or a tennis racket
appearance.
distributed in soil and in intestine of
horses, sheep, cattle, dogs, cats, rats, chickens and nearly 10% of humans.
Hot and damp climate with soil rich in organic matter
Spores are especially resistant to heat, usual antiseptics and chemical agents
but are destroyed by autoclaving at 1200C for 15 minutes or boiling for
atleast 4 hours.
18.
19. Pathogenesis
Disease Occurs sporadically ,Affects unimmunized, partially immunized & fully
immunized who fail to maintain adequate immunity with booster doses of
vaccine
The incubation period ranges from 3-14 days, Although can as short as one day
to as long as several months have been reported
IP have prognostication and correlates with the severity of disease,
Tetanus usually follows a recognized injury.
It can complicate burns, ulcers, gangrene, necrotic snakebites, middle ear
infections, septic abortions, childbirth, intramuscular injections, and surgery.
Up to 50% of cases the injury not considered serious enough to seek medical
treatment.
In 15-25% of patients, there is no evidence of a recent wound
20. Pathogenesis
Contamination of wounds with spores of C.tetani.
Germination & toxin production – in wounds with low oxidation –
reduction potential ( devitalized tissues, F.B, active infection )
Tetanospasmin ( neurotoxin )
Tetanolysin ( hemolysin
Tetanospasmin ( exotoxin ) produced locally , released into bloodstream .
Binds to peripheral motor neuron terminals & nerve cells of ant.horn of
spinal cord
The toxin after entering axon , transported to nerve cell body in brain stem
& spinal cord – retrograde intraneuronal transport
Toxin – migrates across synapse – presynaptic terminals- blocks the release
of Glycine & GABA from vesicles.
21. Pathogenesis
The blocking of neurotransmitter
release
by
Tetanospasmin
involves
cleavage
of
Synaptobrevin – essential for
proper fn of synaptic vesicle
release apparatus
With diminished inhibition –
resting firing rate of alpha motor
neurons increases – rigidity
Lessened activity of reflexes
which limit polysynaptic spread
of
impulses,
agonists
&
antagonists recruited - spasms
22. Clinical presentation
Four clinical forms of this disease are recognized depending upon the extent
and location of neurons involved.
Generalized
Neonatal
Cephalic
local.
23. Clinical presentation
Generalized tetanus
Commonest form and is characterized by increased muscle tone and generalized spasms.
Usually, the first symptom is trismus or lock jaw. Dysphagia, stiffness and pain in
neck, shoulder and back muscles appears.
Rigidity of abdomen and facial grimacing, popularly known as
„Risus sardonicus‟ ,opsthotonus.
Appearance of generalized muscle spasms, occurring spontaneously or due to minor
stimuli
Spasms may lead to respiratory compromise necessitating respiratory support.
Spasms can cause compressive fractures of the spine, rupture of muscles, rhabdomyolysis
and renal failure.
These are maximum during the first two weeks of illness and decrease thereafter in
frequency and intensity.
24. Clinical presentation
Autonomic Disturbances Seen in Tetanus
Sustained or labile hypertension
Progressive and refractory hypotension
Peripheral vasoconstriction
Tachycardia (episodic commonly)
Bradycardia and asystole
Arrythmias
Fever
Profuse diaphoresis, salivation
Increased bronchial secretions
Gastric stasis and ileus
Urinary retention
25. Clinical presentation
Localised tetanus
This is a relatively uncommon and benign form of the
Disease process in which patients have persistent contraction of muscles in
same anatomic area as the injury preceding the tetanus.
Local tetanus might generalize over time but overall mortality is about 1%.
The most important indicator for poor prognosis was the progression to
secondary generalization (27%).
26. Clinical presentation
Cephalic tetanus :
This involves cranial nerves and has an overall incidence of 6%.
It commonly results from middle ear infections and head injuries.
Facial muscles are most commonly affected, followed by 6th, 3rd, 4th and
12th cranial nerves in the order of frequency.
Trismus may be present but usually follows other cranial nerve deficits in
42% of patients.
Although, overall mortality described is high (15-30%), many cases with a
milder disease have been reported from India.
27. Clinical presentation
Neonatal tetanus
This form of tetanus still has a high incidence and mortality in the
developing countries
The common age of onset is between 5 and 15 days following birth.
Common presenting complaints are rigidity, spasms, failure to
suck, trismus, fever and seizures.
Due to lack of inhibiting influences from higher centers in newborns, the
anterior horn cells react more violently, resulting in more spasms.
Overall mortality is around 70% and most patients with severe disease die.
30. Ablett Classification of the Severity of Tetanus
I Mild- Mild to moderate trismus; general spasticity; no respiratory
embarrass - ment; no spasms; little or no dysphagia
II Moderate -Moderate trismus; well-marked rigidity; mild to moderate but
short spasms; moderate respiratory embarrassment with an increased
respiratory rate greater than 30, mild dysphagia
III Severe -Severe trismus; generalized spasticity; reflex prolonged spasms;
respiratory rate greater than 40; apnoeic spells, severe dysphagia;
tachycardia > 120.
IV Very severe- Grade III and violent autonomic disturbances involving the
cardiovascular system. Severe hypertension and tachycardia alternating with
relative hypotension and bradycardia, either of which may be persistent
31. Diagnosis
Tetanus is diagnosed by clinical observation.
Electromyographic studies are occasionally useful in questionable cases.
Antitetanus antibodies are undetectable in most tetanus
patients, “protective” concentration of 0.01 IU/L.
Rare patients apparently develop antibodies that are not protective.
Attempts to culture C. tetani from wounds are not useful in diagnosis
„Spatula test‟ to aid in diagnosis with a sensitivity of 94% and specificity of
100%. (Apte and Karnad )`
32. Differential diagnosis
Strychnine poisoning,
Dystonic reactions to neuroleptic drugs or other central dopamine.
Treatment with anticholinergic agents (benztropine or diphenhydramine) is
rapidly effective against dystonic reactions.
Dental infections can produce trismus, and should be sought, but they do
not cause the other manifestations of tetanus.
33. Management
Management of tetanus patients involves a team approach.
The defined goals of treatment include the following :
a) halting production of toxin within the wound,
b) neutralization of unbound toxin,
c) control of muscle spasms,
d) management of autonomic instability,
e) supportive therapy,
f) management of complications,
g) prevention
34. Management
Halting the production of toxin
Wound management eradicate spores and change conditions for germination, thereby preventing
further elaboration and absorption of the neurotoxin.
Antibiotic therapy :
Penicillin still remains a standard therapy in many parts of the
world, although metronidazole seems to be replacing it and is being
considered as a drug of choice by.
The usual dose of penicillin is 100,000 – 200,000 IU/kg/day given
intravenously or intramuscularly. Metronidazole is used at a dose of 500 mg
every 6 hours intravenously or per orally and 400 mg rectally every 6
hours, for 7-10 days.
35. Management
Neutralization of the unbound toxin
This is achieved through passive immunization with either human or equine
tetanus immunoglobulin. should be undertaken as early as possible since the
toxin becomes inaccessible once it is bound to the nerve terminus.
The usual dose of equine preparation is 500- 1000 IU/kg given
intravenously or intramuscularly.
The dose of HTIG is 5000-8000 IU intramuscularly.
Usual dose for prophylaxis is1500-3000 IU of equine and 250-500 IU of
human preparation.
37. Supportive Management
Secure airway/tracheostomy/ventilatory support
Pts recovering from tetanus should be actively immunized
Hydration
Nutrition
Physiotherapy
Prophylactic anticoagulation
Bowel, bladder, back care
Treatment of intercurrent infection
38. Prevention – Active Immunization
For partially immunized, unimmunized and recovering from tetanus
It stimulates production of protective antitoxin
2 prep :
combined vaccine : DPT
monovalent vaccine : plain / formol toxoid tetanus vaccine , adsorbed
39. Combined vaccine
According to National Immunization, 3 doses of DPT – at intervals of 4-8
wks, starting at 6 wks age, followed by
booster at 18 months age
2nd booster (only DT) at 5-6 yrs
3rd booster ( only TT) after 10 yrs age
40. Monovalent vaccines
Purified tetanus toxoid ( adsorbed ) supplanted the palin toxoid – higher &
long lasting immunity response
Primary course of immunization – 2 doses
Each 0.5 ml , injected into arm given at intervals of 1-2 months
The longer the interval b/w two doses, better is the immune response
1st booster – 1 yr after the initial 2 doses
2nd Booster : 5 yrs after the 1st booster ( optional )
Freq boosters to be avoided
41. Passive immunization
•
•
•
•
•
•
•
Human Tetanus Hyperimmunoglobulin :
250-500 IU
Does not cause serum sickness
Longer passive protection compared to horse ATS( 30 days / 7 -10 days
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.
42. Active & Passive Immunization
In non immunized persons
1500 IU of ATS / 250-500 units of Human Ig in one arm & 0.5 ml of
adsorbed tetanus toxoid into other arm /gluteal region
6 wks later, 0.5 ml of tetanus toxoid
1 yr later , 0.5 ml of tetanus toxoid
43. Prevention of neonatal tetanus
Clean delivery practices
3 cleans : clean hands, clean delivery surface, clean cord care
Tetanus toxoid protects both mother & child
Unimmunized pregnant women : 2 doses tetanus toxoid
1st dose as early as possible during pregnancy
2nd dose – at least a month later / 3 wks before delivery
Immunized pregnant women : a booster is sufficient
No need of booster in every consecutive pregnancy
44. Prevention of tetanus after injury
All wounds should be thoroughly cleaned soon after injury
Remove all foreign bodies, soil, dust, necrotic tissue
A – completed course of toxoid/booster < 5 yrs ago
B- completed course of toxoid / booster >5 yrs ago & < 10 yrs ago
C- completed course of toxoid / booster >10 yrs ago
D- not completed course of toxoid / immunity status unknown
45. Wounds < 6hrs, clean, non penetrating & negligible tissue
damage
Immunity Category
Treatment
•
A
B
C
D
•
Nothing more required
Toxoid 1 dose
Toxoid 1 dose
Toxoid complete course
•
•
•
•
•
•
