Tetanus Etiology, Pathogenesis, Clinical features, Diagnosis, Management

1. TETANUS
DR SHAHNAWAZ F SHAH
MD, FPM, FIAPM,FCPM (MUHS)
Interventional Spine & Pain Physician
Surat

2. Tetanus
• derived from the greek word "to stretch“
• It is an acute disease caused by the anaerobic
(without oxygen) Clostridium tetani bacteria
• Tetanus is a rare and often fatal neurological
disease that causes increased tone and muscle
spasms due to the bacteria.

3. Clostridium tetani
• Gram positive,
• Non-capsulated
• Spore forming
bacteria.
• Can resist very high
temperatures
• Doesn’t spread from
person to person

4. Etiology
• The most common way the bacterium enters
the body is through wounds which are
susceptible to infection if they are:
• Contaminated with soil, feces, or saliva,
• Puncture wounds including unsterile injection
sites,
• Devitalized tissue including burns, avulsions
and de-gloving injuries

5. PATHOGENESIS
• Once the bacteria C. tetani enters the body
the spores multiply and germinate due to the
anaerobic environment.
• In the body, two toxins are released:
tetanospamin and tetenolysin.

6. T
etanolysin
Hemolytic toxin
Potentiates infection but
does not cause
disease process
Tetanospasmin
Binds to NM junctionat the site of injury and
undergoes retrograde axonal transport to
reach presynaptic nerve terminal where it
prevents the inhibitory neurotransmitters
GLYCINEANDGABA.
In normal states these neurotransmitters
prevent release ofAchfrom excitatory neurons
thus prevent muscle contraction.in the
presence of toxins these inhibitory impulsesare
prevented leading to uncontrolled contraction
of muscles,
PATHOGENESIS

8. • Tetanospamin reaches the peripheral nerves by retrograde
neuronal transport through the blood or lymphatic system.
• The length of the peripheral nerves determines how long it
takes for the neurotoxins to reach the CNS and cause
symptoms.
• The toxin tetanospamin disrupts the release of the
inhibitory neurotransmitters glycine and GABA throughout
the CNS but most commonly at the motor end plates,
spinal cord, brain, and sympathetic nervous system.
• The disinhibition allows for unopposed muscular
contraction followed by muscular rigidity and spasms.

9. INCUBATION PERIOD
• Once the bacteria has entered the body the
incubation period may range from days to
months.
• The average incubation period is around 4-14
days.
• The incubation period is shorter the closer the
injury site is to the CNS.
• A shorter incubation period usually correlates
with poor prognosis due to a more severe
disease.

10. Characteristics/Clinical Presentation
• There are four different forms of tetanus:
 Generalized tetanus
 Local tetanus
 Cephalic tetanus
 Neonatal tetanus.

11. Generalized tetanus
• Generalized tetanus attacks muscles throughout
the entire body
• the most common form of tetanus (about 80% of
the cases)
• Generalized Muscular rigidity and spasms
• Tetanospamin attacks and inhibits mostly the
motor neurons of the CNS and later the neurons
of the ANS as well.
• As a result a person experiences uncontrollable
intense muscle contractions

12. • The first muscles affected are the facial and
jaw muscles because of their short nerve
pathways.
• This condition is commonly referred to as lock
jaw or trismus.

13. • As the disease progresses the person will
experience stiffness of the neck, difficulty
swallowing, and stiffness of the abdominal
muscles. Followed by Generalized Muscular
spasm

14. OPISTHOTONOS
Spasm of the muscles causing backward arching of the head, neck, and spine, as in
severe tetanus, some kinds of meningitis, and strychnine poisoning.

15. RISUS SARDONICUS
Uninhibited muscle contractions cause trismus (“lockjaw”), facial grimacing, an
odd but characteristic smile (“RISUS SARDONICUS”)

16. • Spasms can be produced by a stimulus such as
light, noise, touch, or happen unexpectedly
with no specific cause.
• Spasms are extremely painful and can occur
frequently and can last for several minutes.

17. • In generalized tetanus “spasms continue for 3-
4 weeks and complete recovery may take
months.”
• After several days, the ANS will be affected
showing others signs such as fever, sweating,
elevated blood pressure, and increased or
rapid heart rate.

18. Local tetanus
• Local tetanus can occur before generalized
tetanus but this is a much milder form with a
decreased amount of associated toxin release.
• Local tetanus, for the most part, just attacks
muscles in a specific (local) area of the body

19. Local tetanus
• Localized tetanus is rare, but there is a better
prognosis with only about 1% of the cases
resulting in death.
• The presentation of local tetanus is muscle
rigidity and continuous contractions close to
the injury site.

20. Cephalic tetanus
• Cehalic tetanus is also rare
• Shows a combination of
both generalized and local
tetanus.
• The characteristics are
facial spasms and paralysis
as a result of involvement
of the cranial nerves.

21. Cephalic tetanus
• Head wounds are the main cause with
occasional occurrence found with ear
infections (otitis media) associated with a
head wound.
• Cephalic tetanus can progress to generalized
tetanus and can be associated with a high
fatality rate.

22. Neonatal tetanus
• Neonatal tetanus (which is found in newborn
babies) is a form of generalized tetanus which
also has a high fatality rate.
• The diagnosis is determined from the
symptoms that present.
• When the baby is born they are able to suck
and swallow normally for 2-3 days and then
they lose that ability.

23. • The symptoms of neonatal tetanus are muscle
rigidity and spasms which appear around "4-14
days after birth”.

24. Neonatal tetanus
• The most common way neonatal tetanus
occurs is due to non- immune mothers and
poor hygiene during the delivery process.
• Most of the cases of infected infants is a result
of infection of the unhealed stump of the
umbilical cord especially if the cord has been
cut with unsterile instruments.
• Neonatal tetanus is very common in third
world countries.

25. Systemic Involvement
Cardiovascular:
• Hyperkinetic circulation is a result of elevated
basal sympathetic and muscle activity.
• Tachycardia with hypertension
• Increased stroke volume
• Thromboembolus

26. Systemic Involvement
Respiratory:
• Muscular spasms: chest wall, diaphragm,
abdomen, pharyngeal, and laryngeal tract (can
lead to an obstructed airway which can be life
threatening)
• Atelectasis, pneumonia, and aspiration: inability
to cough secondary to muscular rigidity, spasms,
and being sedated.
• Hyperventilation: common because of fear and
autonomic disturbances.

27. Systemic Involvement
Renal
Renal involvement is only found in severe cases
of tetanus.
• Dehydration
• Urinary stasis and infection
• Renal failure
• Altered renal blood flow secondary to
catecholamine surges

28. Systemic Involvement
Gasto-intestinal:
• Gastric statis
• Illeus
• Diarrhea
• Hemorrhage
• Weight loss: As a result of the inability to
swallow

29. Systemic Involvement
Neuromuscular:
• Autonomic dysfunction: Leads to excess sympathetic
activation and catecholamine levels
Musculoskeletal:
• Muscle rigidity and spasms
• Lock-jaw (trismus)
• Risus sardonicus
• Opisthotonos (reactions of the head)
• Tendon avulsions: a result of spasms
• Fractures: a result of spasms

30. Differential Diagnosis
• Infections of the head, neck, and central nervous
system
• Orofacial infection
• Dystonic drug reactions:
– HALOPERIDOL,
– METOCLOPROMIDE (PERINORM),
– Anti-depressants, Anti-Epileptics, Midazolam.
• Hypocalcaemia
• Strychnine poisoning
• Seizures

32. Diagnosis
• The diagnosis is made based on clinical signs
and symptoms and not on the confirmation of
the bacteria C. tetani in the body.
• There are no specific laboratory or diagnostic
tests used to diagnosis tetanus.

33. Medical Management
Categorized into three steps.
1) First the organism in the body needs to be
destroyed to prevent further release of the
toxin.
2) Next the toxin in the body outside of the CNS
needs to be neutralized and
3) finally the effects of the toxin in the CNS
need to be minimized

34. Surgical Management
• WOUND DEBRIDEMENT, if possible, should be
done to help remove the toxin from the body

35. HUMAN TETANUS
IMMUNOGLOBULIN
• Neutralization of
free toxin
• TIg cannot dislodge
toxins in the nerve
root.
• Theroute of
administrationis
intra muscular or
intra-thecal.
• Dose:500 –1000IU

36. General Medical Management
• AIRWAY MANAGEMENT & Respiratory support:
Maintenance of oxygen is essential
• Supportive care:
– Control fluid and electrolyte balance
– Maintain adequate hydration,
– Early detection of myoglobinuria
– Prevention of renal shutdown.
• Oropharyngeal secretions should be sucked
periodically.
• Prevent other infections

37. General Medical Management
• Oral feeding should be stopped and IV line
should be established for providing adequate
fluids , calories , electrolytes and for
administration of various drugs.
• After 3 – 4 days of treatment milk feeding
through nasogastric tube may be started.

38. Controlling the spasms
• Spasmsareprecipitated by minimal stimuli
therefore efforts should be made to avoid
noxious stimuli including bright lights, pain ,
loud noises.
• So,Patientshould bekept in dark quiet and
isolated rooms.
• I.M injectionsshould beavoided.
• Temperatureshould bemaintainedwithin
normal limits.

39. Controlling the spasms
• Relief of Spasm is by using sedation and
muscle relaxants like benzodiapenes
• DIAZEPAM
–prevents spasms by causing GABA mediated
central inhibition.
–it promotes muscle relaxation.

40. Medications
Antibiotic therapy is needed to abolish bacteria from the
wound site.
Most commonly used
• Penicillin and Cephalosporins
• Metronidazole: for treating and preventing anaerobic
bacterial diseases
• Erythromycin,
• Tetracycline,
• Chloramphenicol, and
• Clindamycin.

41. • ANS Instability treated by: alpha and beta
blockers, IV magnesium.
• The prognosis of individuals with tetanus
depends on the supportive care and
ventilatory access.

42. ROLE OF PHYSIOTHERAPIST
• Currently research is limited on the Physical
therapy management of individuals with
tetanus.
• Cardiopulmonary physical therapy can be used
to help in the prevention of respiratory
complications.
• Physical therapy can also be used to help with
muscle rigidity and spasms.

43. Vaccinations
Tetanus can be prevented through vaccinations.
The vaccination consists of being injected with
the tetanus toxoid.
The toxoid is available in two different forms:
1. Absorbed toxoid and
2. Fluid toxoid.

44. TETANUS TOXOIDS
The toxoids work by producing specific
antitoxins that will neutralize the bacteria
The toxoid is inactivated and does not contain
any live organisms.
Therefore, the toxoids can not replicate
themselves once injected

46. DPT VACCINE
• The tetanus vaccine has
been combined with
pertussis and diptheria to
make the DPT vaccine for
infants.
• The vaccination is started
in infants at 6 weeks of age
& repeated twice at 4
weeks intervals.

47. Age National Rural Heath Mission
Birth
BCG,
OPV(0),
Hep B Birth dose
(To be given at the place of delivery)
6 Weeks OPV1, Penta1(DPT+HepB+HiB)
10 Weeks OPV2, Penta2(DPT+HepB+HiB)
14 Weeks OPV3, Penta3(DPT+HepB+HiB),
IPV
9 Months
MMR-1, /MR/Measels,
JE Vaccine-1
16-24 Months
MMR-1,
OPV Booster,
DPT 1st Booster,
JE Vaccine-2
5-6 Years DPT 2nd Booster
10 Years TT1
16 Years TT2
Vaccination as per the National Immunization schedule by
Government of India

48. For adolescents and adults :
• the Tdap vaccine
• combination of tetanus and diphtheria toxin
with acellular pertussis
• It is recommended to get a booster shot every
10 years.

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