updater material for tetanus 2023 for all pediatrician and infectious disease doctors

1. Tetanus
BY:
Dr, WALAA SALAH MANAA
Consultant of pediatric and infectious disease
‫الشـيخ‬ ‫كـفر‬ ‫حمـيات‬ ‫مـستشفى‬

4. Definition
 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)

5. 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.

6.  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 Carleand 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

7.  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.

8. Etiologic agent
C. tetani
-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.

9. 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

13. 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 ).

14.  Although tetanus is entire 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)
 clinical onset time:(time from first symptom to first spasm)
varies between 1-7days

15. 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.

16. 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)

17.  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
Epidemiology

18. 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.

19. pathophysiology of tetanus

21. 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

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

23. Why flexion not extension

24. 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.

25.  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.

27. 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).
Generalized tetanus

28.  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.
Generalized tetanus

29. 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 provoked by even the
slightest stimulation.
A constant threat during generalized spasms is
reduced ventilation or apnea or
laryngospasm..

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

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

34. complication
Autonomic dysfunction
in severe cases:
 Labile or sustained hypertension,
 Tachycardia,
 Dysrhythmia,
 Hyperpyrexia,
 Profuse sweating,
 Peripheral vasoconstriction,
 Increased plasma and urinary
catecholamine levels.
 Periods of bradycardia and
hypotension may also be
documented.
 Sudden cardiac arrest sometimes
occurs.
Other complications
 Aspirationpneumonia,
 Fractures,
 Muscle rupture,
 Deep-vein thrombophlebitis,
 Pulmonary emboli,
 Decubitus ulcer,
 Rhabdomyolysis

36. 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

38. Local tetanus
 Is an uncommon form
 In which manifestations
are restricted to muscles near
the wound.
The prognosis is excellent.

39.  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.

41. 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)

42. CBC WBCs may 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 by ELISA) are considered protective
and make tetanus unlikely, although cases in
patients with protective antitoxin levels have been
reported

43. differential diagnosis
1-trismus *Alveolar abscess,
*Strychnine poisoning,
*Dystonic drug reactions
(e.g.phenothiazines and metoclopramide),
*Hypocalcemic tetany.
2-meningitis/encephalitis, rabies,
3-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

46. PROPHYLAXIS

47.  Immunization of women who are pregnant or of
childbearing age reduces neonatal tetanus mortality by
approximately 94 %.
 Improving hygiene during home births in resource-
limited settings is also likely to play an important role
in preventing neonatal tetanus.
PROPHYLAXIS

48. PROPHYLAXIS

49. 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.

50. 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.

51. 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.

52. 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.

53. 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.

54. 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.

55. 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

56.  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 second line agents.

57. 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;
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.

58. 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.

59. 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.

60. 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.

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

63. ADDITIONAL MEASURES
Like all patients receiving ventilatory support,
patients with tetanus require attention to
1) Hydration
2) Nutrition ;physiotherapy
3) prophylactic anticoagulation
4) bowel, bladder, and renal function
5) Decubitus ulcer prevention
6) Treatment of intercurrent infection.

64. 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

65. 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.

66. 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).

67. *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.

68. 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