The document details the case of a 60-year-old housewife diagnosed with cephalic tetanus presenting with swallowing difficulties and muscle spasms. It outlines the clinical symptoms, historical context of tetanus, its pathogenesis, and treatment protocols, including the administration of tetanus immunoglobulin and antibiotics. Key points include the importance of timely intervention, prevention through vaccination, and management strategies for autonomic disturbances and muscle spasms.

1. TETANUS
DR. ABHAY MANGE

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

4. On examination

Afebrile

Pulse -110/min

Bp -150/90 mmhg

Resp -24/min, intermittent spasms +

Risus sardonicus +

Neck stiffness +

Trismus +

Oral cavity – wnl

No external injury

5. On examination

CNS :-Conscious ,oriented
Power gr 4+ ul/ll
Sensation –wnl
DTR +
Planters – flexor b/l

P/A:- Ant .abdominal wall Rigidity +

RS :- wnl

CVS:-wnl

8. PROVISIONAL DIAGNOSIS

Cephalic Tetanus

9. Investigations

Routines investigations - wnl

Fundus- wnl

ENT opinion:- s/o b/l safe csom

10. Final diagnosis

B/L CSOM (safe) with Cephalic tetanus

11. Treatment


Tetanus human immunoglobulin 2750 U
Antibiotcs –inj C/P 2 MU 4 hrly
inj metronidazole 500 mg tds
inj cefotaxime 1 gm tds
inj robinex tdS
inj pantoprazole 40 mg bd

Day 2 -Tracheostomy done

Day 3- spasms increased,bp 200/100 mmhg , HR- 140/MIN
So put on mechanical ventilation with knock down by inj atracuronium
+midazolam infusion,tab labetolol 200mg bd started


12. Treatment

Day 5- patient febrile so inj meropenam added ,culture sent

Day 10- patient weaned from mechanical ventilation, tracheal culture –
pseudomonas aregionosa s/t imepenam

Day 12 – patient transferred to IDH

13. Treatment

Day 18 –

Put on non-cuffed TT

Antibiotics continued

Nutrition

Physiotherapy

14. DISCUSSION

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.

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.

28. Opisthotonus
Neonatal Tetanus

29. Risus sardonicus
Trismus

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.

36. Management
Control of muscle spasms
 Sedatives : Diazepam-.Midazolam,Propofol,
 Neuromuscular blocking agents :
 Magnesium sulfate
 Baclofen
 Methacarbamol
 Dantrolene
Management of dysautonomia
 Sedatives- benzodiazepenes, Morphine
 Adrenergic blockers Labetolol, Esmolol, Clonidine,
 Magnesium sulfate
 Intrathecal baclofen

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
•
•
•
•
•
•

46. Other Wounds

Immunity Category

Treatment
•
•
•
A
B
C
•
D
•
Nothing more required
Toxoid 1 dose
Toxoid 1 dose + Human
Tetanus Ig
Toxoid complete course +
Human Tetanus Ig
•
•
•

47. Thank You!