Tetanus is caused by Clostridium tetani bacteria and results in painful muscle spasms. It is characterized by three main types: generalized, localized, and neonatal. The bacteria forms spores that can survive in soil for years and enter the body through wounds. The toxin it produces is transported to the central nervous system where it blocks neurotransmitter release, causing spasms. Treatment involves wound cleansing, antitoxin administration to neutralize toxin, antibiotics, and medications or paralysis to control spasms while providing respiratory support. Prevention centers on active immunization with tetanus toxoid vaccine. Prognosis depends on factors like age, incubation period, and vaccination history.

2. Update 2013

3. DEFINITION
Tetanus is a neurologic disorder,
characterized by increased muscle tone and
spasms, that is caused by tetanospasmin, a
powerful protein toxin elaborated by
Clostridium tetani.
*Types
( generalized, neonatal, and localized).

4. Tetanus
(from Ancient Greek: τέτανος tetanos “taut”,
and τείνειν teinein "to stretch")
is a medical condition characterized by a
prolonged contraction of skeletal muscle fibers.

5. History
Tetanus was well known to ancient people who recognized the
relationship between wounds and fatal muscle spasms.
In 1884, Arthur Nicolaier isolated the strychnine-like toxin
of tetanus from free-living, anaerobic soil bacteria.
The etiology of the disease was further elucidated in 1884
by Antonio Carle and Giorgio Rattone, two pathologists of
the University of Turin, who demonstrated the
transmissibility of tetanus for the first time.
They produced tetanus in rabbits by injecting pus from
patient with fatal tetanus into their sciatic nerves

6. In 1891, C. tetani was isolated from a human victim by
Kitasato Shibasaburō , who later showed that the
organism could produce disease when injected into
animals, and that the toxin could be neutralized by
specific antibodies.
In 1897, Edmond Nocard showed that tetanus antitoxin
induced passive immunity in humans, and could be
used for prophylaxis and treatment.
Tetanus toxoid vaccine was developed by P. Descombey
in 1924, and was widely used to prevent tetanus
induced by battle wounds during World War II.

7. ETIOLOGIC AGENT
C. tetani is an anaerobic,
motile, gram-positive rod
that forms an oval, colorless,
terminal spore and thus
assumes a shape resembling
a tennis racket or
drumstick.
The organism is found
worldwide in soil, in animal
feces, and occasionally in
human feces.

8. Spores may survive for years in some environments
and are resistant to various disinfectants and to boil
in for 20 min
Vegetative cells, however, are easily inactivated and
are susceptible to several antibiotics, including
metronidazole and penicillin.
The most powerful toxins known, botulinum toxin and
tetanus toxin

9. EPIDEMIOLOGY
Occurs sporadically and
almost always affect
1-unimmunized persons;
2-partially immunized persons
3- fully immunized individuals who fail to
maintain adequate immunity with booster doses of
vaccine ).

10. *Although tetanus is entirely preventable by
immunization, the burden of disease worldwide
is great.
*Tetanus is a notifiable disease in many countries
*The incubation period :(time from first injury to
first symptom) averages 7-10 days (range 1-60
days), whilst the clinical onset time:(time from
first symptom to first spasm) varies between 1-7

11. EPIDEMIOLOGY
Tetanus is common in
*areas where soil is cultivated, in rural areas,
*in warm climates, during summer months,
*and among males.
*In countries without a comprehensive immunization
program, tetanus occurs predominantly in neonates
and other young children.

12. In the United States
and other nations with
successful
immunization
programs,
neonatal tetanus is rare
(only 3 cases were
reported
in the United States
during 1990–2004)

13. EPIDEMIOLOGY
most cases of tetanus follow an acute injury
(puncture wound, laceration, abrasion, or other
trauma).
Tetanus may be acquired indoors or during outdoor
activities (e.g., farming, gardening).
The implicated injury may be major, but can be so trivial
that medical attention is not sought.
In some cases, no injury or portal of entry can be
identified.
The disease may complicate chronic conditions such as
skin ulcers, abscesses, and gangrene.
Tetanus has also been associated with burns, frostbite,
middle-ear infection, surgery, abortion, childbirth, body
piercing, and drug abuse.
Recurrent tetanus has been reported

14. Contamination of wounds with
spores of C. tetani is probably a
frequent occurrence. Germination
and toxin production, however,
take place only in wounds with low
oxidation-reduction potential,
such as those with devitalized
tissue, foreign bodies, or active
infection.
C. tetani does not itself evoke
inflammation, and the portal of
entry retains a benign appearance
unless coinfection with other
organisms is present.

15. pathophysiology of tetanus

16. Toxin released in the wound binds to
peripheral motor neuron terminals, enters
the axon, and is transported to the nerve-
cell body in the brainstem and spinal cord
by retrograde intraneuronal transport.
The toxin then migrates across the synapse
to presynaptic terminals,
where it blocks release of the inhibitory
neurotransmitters glycine and γ-
aminobutyric acid (GABA) from vesicles

17. Loss of inhibition of preganglionic sympathetic neurons
may produce sympathetic hyperactivity and high
circulating catecholamine levels

19. In local tetanus, only the nerves supplying the affected
muscles are involved.
Generalized tetanus occurs when toxin released in the wound
enters the lymphatics and bloodstream and is spread widely to
distant nerve terminals;
BBB blocks direct entry into the CNS.
If it is assumed that intraneuronal transport times are equal for
all nerves, short nerves are affected before long nerves: this
fact explains the sequential involvement of nerves of the
head, trunk, and extremities in generalized tetanus.

20. Tetanospasmin, like botulinum
toxin, may block
neurotransmitter release at
the neuromuscular junction
and produce weakness or
paralysis, but this effect is
clinically evident only in
cephalic tetanus.

22. Generalized tetanus,
the most common form of the disease 80%,
is characterized by increased muscle tone and generalized spasms.
The I.P.is (7 days; 15% of cases occur within 3 days and 10% after 14 days).
Typically, the patient first notices increased tone in
the masseter muscles (trismus, or lockjaw).
Dysphagia or stiffness or pain in the neck, shoulder, and back muscles
appears concurrently or soon thereafter.
The subsequent involvement of other muscles produces a rigid abdomen
and stiff proximal limb muscles; the hands and feet are relatively spared.

23. Sustained contraction of the facial muscles
results in a grimace or sneer (risus sardonicus),and
contraction of the back muscles produces an arched
back (opisthotonos).
Some patients develop paroxysmal,
violent, painful, generalized muscle spasms that
may
cause cyanosis and threaten ventilation.
These spasms occur repetitively and may be
spontaneous or provokedn by even the slightest
stimulation. A constant threat during generalized
spasms is reduced ventilation or apnea or
laryngospasm.

24. Degree of tetanus
Mild:
trismus ,distance between upper & lower incisors >2cm.
Moderate:
trismus + mild fits+ D.I <2cm.
Severe :
trismus +frequent fits +(D.I)<1cm

25. The patient may be febrile,although many patients have no
fever.
Deep tendon reflexes may be increased.
Dysphagia or ileus may prevent oral feeding.

26. complication
Autonomic dysfunction in severe cases:
( labile or sustained hypertension,tachycardia, dysrhythmia,
hyperpyrexia, profuse sweating,peripheral vasoconstriction,
and increased plasma and urinary catecholamine levels.
Periods of bradycardia and hypotension may also be documented.
Sudden cardiac arrest sometimes occurs, but its basis is
unknown.
Othercomplications include aspiration pneumonia, fractures,
muscle rupture, deep-vein thrombophlebitis, pulmonary
emboli, decubitus ulcer, and rhabdomyolysis

27. Neonatal tetanus
usually occurs as the generalized form and
is usually fatal if left untreated.
It develops in
children born to inadequately immunized mothers,
frequently after unsterile treatment of the umbilical cord
stump. Its onset generally comes during the first 2 weeks

28. Local tetanus
is an uncommon form in which manifestations
are restricted to muscles near the wound.
The prognosis is excellent.

29. Cephalic tetanus
a rare form of local tetanus,
follows head injury or ear
infection and involves one or
more facial cranial nerves.
The I.P. is a few days.
. M.R is high.

31. The diagnosis of tetanus is based entirely on clinical
findings.
Tetanus is unlikely if a reliable history indicates
the completion of a primary vaccination series and the
receipt of appropriate booster doses.
Wounds should be cultured in suspected cases.
(However, C. tetani can be isolated from wounds of patients
without tetanus and frequently cannot be recovered from
wounds of those with tetanus)

32. CBC,,,,,,,WBCsmay be elevated.
CSF ,,,,,,normal results.
EMG ,,,,,,may show continuous discharge of motor units and
shortening or absence of the silent interval normally seen after an
action potential.
ECG ,,,,,,,non specific changes may be evident .
Muscle enzyme ,,,,,levels may be raised.
Serum antitoxin levels of ≥0.1 IU/mL (as measured byELISA) are
considered protective and make tetanus unlikely, although cases in
patients with protective antitoxin levels have been reported

33. differential diagnosis
trismus, *alveolar abscess,
*strychnine poisoning,
dystonic drug reactions (e.g., phenothiazines and
metoclopramide),
*hypocalcemic tetany.
meningitis/encephalitis, rabies,
acute abdomen (because of the rigid abdomen).
Markedly increased tone in central
muscles (face, neck, chest, back, and abdomen), with
superimposed generalized spasms and relative sparing of
the hands and feet, strongly suggests tetanus

35. GENERAL MEASURES
The goals of therapy are
*(to eliminate the source of toxin +neutralize unbound toxin+
prevent muscle spasms while monitoring the patient’s condition
and providing support—especially respiratory support—until
recovery).
*Patients should be admitted to a quiet room in an intensive care
unit, where observation and cardiopulmonary monitoring can be
maintained continuously, but stimulation can be minimized.
*Protection of the airway is vital.
*Wounds should be explored, carefully cleansed, and debrided.

36. ANTIBIOTIC THERAPY
Although of unproven value, antibiotic therapy is administered to eradicate vegetative
cells.
The use of penicillin
(10–12 million units IV, given daily for 10 days) has been recommended,
but metronidazole (500 mg every 6 h or 1 g every 12 h) is preferred by some
experts on the basis of this drug’s excellent antimicrobial activity and the absence of
the GABA-antagonistic activity seen with penicillin.
(The drug of choice remains unclear)
one nonrandomized clinical trial found a survival benefit with metronidazole, but
another study failed to find a difference among benzathine penicillin, benzyl
penicillin, and metronidazole.

37. Clindamycin and erythromycin
are alternatives for the treatment of penicillin allergic pt.
Additional specific antimicrobial therapy should be given
for co-infection with other organisms.

38. ANTITOXIN
Given to neutralize circulating toxin and unbound toxin in the
wound, antitoxin effectively lowers mortality; toxin already
bound to neural tissue is unaffected.
Human tetanus immune globulin (TIG)
is the preparation of choice and should be given
promptly. The dose is 3000–6000 units IM, usually in
divided doses because the volume is large.
The optimal dose is not known, however, and results from one
study indicated that a 500-unit dose was as effective as
higher doses.

39. A.T.S
Neutralise toxin is an alternative when human Ig is unavailable
10,000-100,000U
Then 750 U/24hr …to the cut of the 3 days.
The value of administering antitoxin before wound manipulation or
of injecting a dose proximal to the wound or infiltrating the
wound is unclear.
Additional doses are unnecessary because the half-life of
antitoxin is long.
Antibody does not penetrate the blood-brain barrier.

40. Equine tetanus antitoxin
(TAT) is not available in the
United States but is used
elsewhere.
It is cheaper than human antitoxin,
but the half-life is shorter, and its
administration commonly elicits a
hypersensitivity reaction and
serum sickness.

41. CONTROL OF MUSCLE SPASMS
(alone and in combination).
In some developing countries, cost, availability, and the
ability to provide ventilatory support are important factors
in the choice of therapy.
The ideal therapeutic regimen would abolish spasmodic
activity without causing oversedation and hypoventilation

42. Diazepam, a benzodiazepine and GABA agonist, is in
wide use.
The dose is titrated, and large doses (≥250 mg/d) may be
required.
and midazolam, with a short half-life, are other options.
Barbiturates and chlorpromazine are considered
secondline agents.

43. Therapeutic paralysis with a nondepolarizing neuromuscular
blocking agent and mechanical ventilation may be used for
spasms unresponsive to medication or spasms that threaten
ventilation. However, prolonged paralysis after discontinuation of
therapy has been described.
Other agents include propofol, which is expensive; dantrolene and
intrathecal baclofen, which may allow shortening of the duration
of therapeutic paralysis;
succinylcholine, which has been associated with hyperkalemia; and
Magnesium sulfate.
clinical trial of magnesium sulfate in severe
tetanus did not find a reduction in the need for ventilation
or in mortality rate; however, use of midazolam and
pipecuronium for treatment of muscle spasms and of
verapamil for treatment of cardiovascular instability was reduced.

44. RESPIRATORY CARE
Intubation or tracheostomy, with or without mechanical
ventilation,may be required
for hypoventilation due to oversedation or laryngospasm
or for the avoidance of aspiration by patients with
trismus, disordered swallowing, or dysphagia.
The need for these procedures should be anticipated,
and they should be undertaken electively and early.

45. AUTONOMIC DYSFUNCTION
The optimal therapy for sympathetic overactivity has not been
defined.
Agents that have been considered include labetalol (an
α- and β-blocker that is recommended
by some experts but that reportedly has caused
sudden death), esmolol administered by continuous
infusion (a beta blocker whose short half-life may be
advantageous in the event of severe hypertension from
unopposed α-adrenergic activity), clonidine (a centralacting
antiadrenergic drug), verapamil, and morphine sulfate.

46. Parenteral magnesium sulfate and continuous spinal or
epidural anesthesia have been used but may be more
difficult to administer and monitor.
The relative efficacy of these modalities has yet to be
determined.
Hypotension or bradycardia may require volume
expansion, use of vasopressors or chronotropic agents,
or pacemaker insertion.

47. VACCINE
Patients recovering from tetanus should be actively
immunized (see below) because immunity is not
induced by the small amount of toxin required to
produce disease

48. ADDITIONAL MEASURES
Like all patients receiving ventilatory support, patients with
tetanus require attention to
Hydration==== nutrition;===physiotherapy===prophylactic
anticoagulation===bowel, bladder, and renal
function====decubitus ulcer prevention===and
treatment of intercurrent infection.

49. PREVENTION
Toxoid------for:1-partilly immune pt.
2-non immune pt.
3-pt recoverd from the disease.
Dose ( 01 m6 m )
Booster every 16 yrs

50. Active Immunization

51. Wound Management

52. Neonatal Tetanus
Preventive measures include
maternal vaccination, even during pregnancy;
proportion of births that take place in the hospital;
and the provision of training for nonmedical birth
attendants.

53. PROGNOSIS
.
Mortality rates ,,,,,,, 48%:73%.
The outcome is poor in
1-neonates and the elderly
2-patients with a short incubation period,
short interval from the onset of symptoms
to admission,
3-a short period from the onset of
symptoms to the first spasm (period of onset).

54. *Outcomenis also related to the extent of prior
vaccination.
*The course of tetanus extends over 4–6 weeks,
and patients may require prolonged ventilator
support.
*Increased tone and minor spasms can last for
months,but recovery is usually complete.

55. Take home massage
Markedly increased tone in central
muscles (face, neck, chest, back, and abdomen), with
superimposed generalized spasms and relative sparing of
the hands and feet, strongly suggests tetanus