Tetanus Presentation 77 slides Including drip rates of muscle relaxants PDF : http://www.mediafire.com/download/k00ciibf73d7y6p/ For more, visit www.medicalgeek.com

1. TETANUSTETANUS
Dr. Ankita Patel
Second year resident,
Medical Unit - 1
G.M.C , Surat.
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2. TETANUS
 INTRODUCTION
 CAUSATIVE AGENT
 EPIDEMIOLOGY
 TRANSMISSION, HOST FACTORS, ROUTE OF
ENTRY
 MECHANISM OF ACTION OF TOXIN
 CLINICAL FEATURES
 TYPES OF TETANUS
 DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
 TREATMENT
 PREVENTION – ACTIVE & PASSIVE IMMUNIZATION
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3. INTRODUCTION
 Tetanos – a greek word – to strech
 First described by Hippocrates & Susruta
 Tetanus an neurological disease characterized by
an acute onset of hypertonia, painful muscular
contractions (usually of the muscles of the jaw
and neck), and generalized muscle spasms
without other apparent medical causes.
 Only vaccine preventable disease that is
infectious but not contagious
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4. CAUSATIVE AGENT
 Caused by CLOSTRIDIUM TETANI
 Anaerobic
 Motile
 Gram positive bacilli
 Oval, colourless, terminal spores – tennis racket
or drumstick shape.
 It is found worldwide in soil, in inanimate
environment, in animal faeces & occasionally
human faeces.
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6. Clostridium tetani Gram Stain
NOTE: Round terminal spores give cells a
“drumstick” or “tennis racket” appearance.
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7. EPIDEMIOLOGY
 Tetanus is an international health problem, as spores
are ubiquitous. The disease occurs almost exclusively
in persons who are unvaccinated or inadequately
immunized.
 Entirely preventable disease by immunization
 Tetanus occurs worldwide but is more common in hot,
damp climates with soil rich in organic matter.
 More common in developing and under developing
countries.
 More prevalent in industrial establishment, where
agricultural workers are employed.
 Tetanus neonatorum is common due to lack of MCH
care.
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8. India
Tetanus is important endemic infection in India.
Causative factors
Hand washing
Delivery practices
Traditional birth customs
Interest in immunization
Prior to the national immunization programme estimated
3.5 lakh children were dying annually. 70,000 cases
continue to occur largely in the states – Orissa, Bihar,
MP, Aasam, Rajasthan, UP ,where TT immunization
coverage is less than national coverage(70%) .
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9. TRANSMISSION :
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10. Host Factors
 Age : It is the disease of active age (5-40 years),
New born baby, female during delivery or
abortion
 Sex : Higher incidence in males than females
 Occupation : Agricultural workers are at higher
risk
 Rural –Urban difference: Incidence of tetanus in
urban areas is much lower than in rural areas
 Immunity : Herd immunity does not protect the
individual
 Environmental and social factors: Unhygienic
custom habits,Unhygienic delivery practices
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11. ROUTE OF ENTRY
 Apparently trivial injuries
 Animal bites/human bites
 Open fractures
 Burns
 Gangrene
 In neonates usually via infected umbilical stumps
 Abscess
 Parenteral drug abuse
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12. TETANUS PRONE WOUND
 A wound sustained more than 6 hr before
surgical treatment.
 A wound sustained at any interval after injury
which is puncture type or shows much
devitalised tissue or is septic or is contaminated
with soil or manure.
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13. Sporulated Vegetative
• Spores that gain entry can persist in normal tissue for months to
years under anaerobic conditions.
• When the oxygen levels in the surrounding tissue is sufficiently
low, the implanted C. tetani spore then germinates into a new, active
vegetative cell that grows and multiplies and most importantly
produces tetanus toxin - tetanospasmin and tetanolysin.
• Tetanolysin is not believed to be of any significance in the clinical
course of tetanus.
•Tetanospasmin is a neurotoxin and causes the clinical
manifestations of tetanus.
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14. • The toxin migrates across the synapse (small space
between nerve cells critical for transmission of signals
among nerve cells) where it binds to presynaptic nerve
terminals and inhibits or stops the release of certain
inhibitory neurotransmitters (glycine and gamma-amino
butyric acid).
• Loss of inhibition of preganglionic sym neurons –
sympathetic hyperactivity
• These neurons become incapable to release
neurotransmitter. The neurons, which release gamma-
aminobutyric acid (GABA) and glycine, the major
inhibitory neurotransmitters, are particularly
sensitive to tetanospasmin, leading to failure of
inhibition of motor reflex responses to sensory
stimulation.
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15.  This results in generalized contractions of the agonist and
antagonist musculature characteristic of a tetanic spasm.
 The shortest peripheral nerves are the first to deliver
the toxin to the CNS, which leads to the early symptoms of
facial distortion and back and neck stiffness.
 Once the toxin becomes fixed to neurons, it cannot be
neutralized with antitoxin. Recovery of nerve function from
tetanus toxins requires sprouting of new nerve terminals and
formation of new synapses.
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16. Mechanism of Action of Tetanus Toxin
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17. 1. C. tetani enters
body from through
wound.
3. Germinates under
anaerobic conditions and
begins to multiply and
produce tetnospasmin.
2. Stays in sporulated
form until anaerobic
conditions are
presented.
4. Tetnospasmin spreads
using blood and lymphatic
system, and binds to motor
neurons.
5. Travels along the
axons to the spinal cord.
6. Binds to sites responsible
for inhibiting skeletal
muscle contraction.
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19.  Spores are extremely stable,although
immersion in boiling water for 15 minutes
kills most spores. Exposure to saturated steam
under 15 lbs.of pressure for 15-20 minutes at
121°c is highly effective against spores .
 Sterilization by dry heat is slower than by
moist heat (1 -3 hrs at 160 °C),but it is also
effective against spores.
 Ethylene oxide sterilization is also sporocidal.
 Autoclaving at 121°C for 15min kills the spores
readily.
 Iodine(1% aqueous soon) and H2O2 (10 volume)
kills spores within few hours.
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20. CLINICAL FEATURES:
 IP : Time from injury to the first symptom.The median
incubation period is 7 days, and, for most cases (73%),
incubation ranges from 3-21 days.
 Period of onset : It is the time from first symptoms to
the reflex spasm.
 In general the further the injury site is from the
central nervous system, the longer the incubation
period.
 The shorter the incubation period, the higher the
chance of death.
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21.  Triad of muscle rigidity, spasms &
autonomic dysfunction
 Early symptoms are neck stiffness, sore throat
and poor mouth opening.
 Patients with generalized tetanus present with
trismus (ie, lockjaw) in 75% of cases.
 Other presenting complaints include stiffness,
neck rigidity, dysphagia, restlessness, and reflex
spasms. Spasms usually continue for 3-4
weeks.
 Subsequently, muscle rigidity becomes the major
manifestation. Rigid Abdomen.
 Muscle rigidity spreads in a descending
pattern from the jaw and facial muscles over the
next 24-48 hours to the extensor muscles of the
limbs – stiff proximal limb muscles & relatively
sparing hand & feet.
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22. TRISMUS
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23.  Risus sardonicus: Sustained contraction of
facial musculature produces a sneering grin
expression known as risus sardonicus.
 Contraction of the muscles at the angle of mouth
and frontalis
 Trismus (Lock Jaw): Spasm of Masseter
muscles.
 Opisthotonus: Spasm of extensor of the neck,
back and legs to form a backward curvature.
 Muscle spasticity
 Poor cough, inability to swallow, gastric stasis
all increase the risk of aspiration. Respiratory
failure continues to be a major cause of
mortality in developing countries, whereas
severe autonomic dysfunction causes most
deaths in the developed world.
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24. RISUS SARDONICUS
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25. Opisthotonos in Tetanus Patient
The contractions by the muscles of the back and extremities may become
so violent and strong that bone fractures may occur
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27.  Dysphagia occurs in moderately severe tetanus due to
pharyngeal muscle spasms, and onset is usually
insidious over several days.
 Reflex spasms develop in most patients and can be
triggered by minimal external stimuli such as noise,
light, or touch. The spasms last seconds to minutes;
become more intense; increase in frequency with disease
progression; and can cause apnea, fractures,
dislocations, and rhabdomyolysis.
 Laryngeal spasms can occur at any time and can
result in asphyxia.
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28. AUTONOMIC DYSFUNCTION
 Tetanospasmin has a disinhibitory effect on the
autonomic nervous system (ANS) due to
increased release of catecholamines it causes :
 Hyperpyrexia
 Sweating
 Peripheral vasoconstriction
 Labile/Sustained Hypertension
 Episodic tachycardia, dysrhythmias and cardiac
arrest
 Occasionally period of bradycardia & hypotension
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29. Other symptoms include:
 Drooling
 Fever usually absent
 Mentation unimpaired
 Hand or foot spasms
 Irritability
 Uncontrolled urination or defecation
 Duration of illness — Tetanus toxin-
induced effects are long-lasting because
recovery requires the growth of new axonal
nerve terminals. The usual duration of clinical
tetanus is four to six weeks.
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30. SEQUENCE OF EVENTS
Lock Jaw
Stiff Neck
Difficulty Swallowing
Muscle Rigidity
Spasms
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31. THANK YOU
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33. TYPES OF TETANUS
 Generalied vs Local
 Cephalic
 Traumatic
 Otogenic
 Idiopathic
 Puerperal
 Tetanus neonatorum
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34. Maternal tetanus
•Tetanus occurring during pregnancy or within 6 weeks
after any type of pregnancy termination, is one of the
most easily preventable causes of maternal mortality.
•It includes postpartum or puerperal tetanus
(i) postpartum or puerperal tetanus, usually resulting
from septic procedures during delivery,
(ii) postabortal tetanus, following septic maneuvers
during induced abortion
(iii) Tetanus during pregnancy, generally resulting from
inoculation through a nongenital portal of entry
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35. NEONATAL TETANUS
 Tetanus neonatorum (8th
day disease)
 Usually fatal if untreated
 Children born to inadequately immunized
mothers, after unsterile treatment of umbilical
stump
 During first 2 weeks of life.
 Poor feeding ,rigidity and spasms
 It is easily preventable by 2 tetanus toxoid
injections and ‘5 cleans’ while conducting
deliveries.
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38. LOCAL TETANUS
 Uncommon form
 Manifestations are restricted to muscles near the
wound.
 Cramping and twisting in skeletal muscles
surrounding the wound – local rigidity
 Prognosis – excellent
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39. CEPHALIC TETANUS
 A rare form of local tetanus
 Follows head injury / ear infection
 Involves one / more facial cranial nerves
 Trismus and localised paralysis ,usually
facial nerve, often unilateral.
 Involvement of cranial nerves VI,III, IV, and XII
may also occur either alone or in combination
with others
 Incubation period : few days
 Mortality : high
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41. Ophthalmoplegic tetanus is a variant that
develops after penetrating eye injuries and results
in CN III palsies and ptosis.
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42. DIAGNOSIS
 There are currently no blood tests that can be
used to diagnose tetanus. Diagnosis is done
clinically based on the presence of trismus,
dysphagia, generalized muscular rigidity, and/or
spasm.
 Laboratory studies may demonstrate a moderate
peripheral leukocytosis.
 An assay for antitoxin levels is not readily
available. However, a level of 0.01 IU/mL or
greater in serum is generally considered
protective, making the diagnosis of tetanus less
likely.
 Cerebrospinal fluid (CSF) study findings are
usually within normal limits.
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43. DIRECT SMEAR
 Show Gram-positive
bacilli with drum-stick
appearance.
 Morphologically
indistinguishable from
similar nonpathogenic
bacilli.
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44. CULTURE
 Done in blood agar under anaerobic
condition or in Robertson’s cooked meat
medium.
 Produces swarming growth after 1-2 days
of incubation.
 In contaminated specimen heat at 80°C
for 10mins before culture to destroy non-
sporing organisms.
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45. ANIMAL INOCULATION
 To demonstrate
toxigenicity.
 Positive case : test animal
develops stiffness & spasm
of tail & inoculated hind
limb within 12-24hrs
which spreads to rest of
the body. Death occurs in
1-2 days.
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46.  Procedures:
 The spatula test is one diagnostic bedside
test.
 This simple test involves touching the
oropharynx with a spatula or tongue blade.
 This test typically elicits a gag reflex, and the
patient tries to expel the spatula (ie, a negative
test result).
 If tetanus is present, patients develop a reflex
spasm of the masseters and bite the spatula (ie, a
positive test result).
 Sensitivity of 94% and a specificity of 100%.[2]
 No adverse sequelae (eg, laryngeal spasm) from
this procedure were reported
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47.  Drug induced Dystonic Reactions e.g. Phenothiazines
 Strychnine poisoning
 Neuroleptic Malignant Syndrome, Serotonin syndrome
 Trismus d/t Peritonsillar Abscess/Dental infection
 Stiff person syndrome
 Acute abdominal emergencies
 Dislocations, Mandible
 Encephalitis, Meningitis
 Hysteria
 Hypocalcemia
 Rabies
 Seizure disorder (partial or generalized)
 Spider Envenomations, Widow
 Stroke, Hemorrhagic
 Stroke, ischemic (cephalic tetanus)
 Subarachnoid Hemorrhage
DIFFERENTIAL DIAGNOSIS
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48. PRINCIPLE OF TREATMENT
1. Neutralization of unbound toxin
-HTIG/ATS
2. Prevention of further toxin production
-Wound debridement & antibiotics
3. Antibiotics
4. Control of spasm
-Anticonvulsants, Sedatives, Muscle relaxants etc.
5. Management of autonomic dysfunction
-MGSO4, Betablockers etc.
6. Supportive care
-Physiotherapy, Nutrition, Thromboembolism
prophylaxis ABC etc…
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49. PRINCIPLE OF TREATMENT
 Admit patients to the intensive care unit (ICU).
 Because of the risk of reflex spasms, maintain a
dark and quiet environment for the patient.
Avoid unnecessary procedures and
manipulations.
 Attempting endotracheal intubation may induce
severe reflex laryngospasm; prepare for
emergency tracheostomy.
 Seriously consider prophylactic tracheostomy
in all patients with moderate-to-severe clinical
manifestations. Intubation and ventilation are
required in 67% of patients.
 Tracheostomy has also been recommended after
onset of the first generalized seizure.
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50. TOXIN
• A single intramuscular dose of 3000-5000 units
(100U/kg-half in each buttocks) is generally
recommended for children and adults, with part of
the dose infiltrated around the wound if it can be
identified.
• The WHO recommends TIG 500 units by IM/IV
(depending on the available preparation) as soon as
possible; in addition, administer age-appropriate
TT-containing vaccine (Td, Tdap, DT, DPT, DTaP, or
TT depending on age or allergies), 0.5 cc by
intramuscular injection at separate site with HTIG.
• TIG can only help remove unbound tetanus
toxin, but it cannot affect toxin bound to nerve
endings.
• 250 U/vial available in our hospital, so 10 vial in
each buttock is usual dose.
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51. 2. PREVENTION OF FURTHER TOXIN
PRODUCTION
• Debridement of Wound to remove organisms and
to create an aerobic environment.
• The current recommendation is to excise at least
2 cm of normal viable-appearing tissue around
the wound margins.
• Incise and drain abscesses.
• Delay any wound manipulation until several
hours after administration of antitoxin due to
risk of releasing tetanospasmin into the
bloodstream.
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52. 3. ANTIBIOTICS
 Theoretically, antibiotics may prevent
multiplication of C tetani, thus halting
production of toxin. Penicillin G was the drug of
choice initially but now Metronidazole is
preffered drug.
 Penicillin G aqueous : (10-12 MU IV in 2-4
divided doses- 2-4 MU IV every 4 to 6 hrs)
 A 10- to 14-d course of treatment is recommended
 Metronidazole: (5oomg 6 hrly or 1gm 12
hrly)
 A 10- to 14-d course of treatment is recommended. Some
consider this the DOC since penicillin G is also a GABA
agonist, which may enhance effects of the toxin.
 Doxycycline, Clindamycin and Erythromycin are
alternative for penicillin allergic patients who can not
tolerate metronidazole.
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53.  4. Control of spasm
- Nursing in quiet environment, avoid unnecessary
stimuli, Protecting the airway.
- Drugs used to treat muscle spasm, rigidity, and
tetanic seizures include sedative-hypnotic agents,
general anesthetics, centrally acting muscle
relaxants, and neuromuscular blocking agents.
- Anticonvulsants
- Sedative-hypnotic agents are the mainstays of tetanus
treatment. Benzodiazepines are the most effective primary
agents for muscle spasm prevention and work by enhancing
GABA inhibition.
 Diazepam :
 Mainstay of treatment of tetanic spasms and tetanic
seizures. Depresses all levels of CNS, including limbic and
reticular formation, possibly by increasing activity of
GABA, a major inhibitory neurotransmitter.
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54.  Diazepam reduces anxiety, produces sedation, and
relaxes muscles. Lorazepam is an effective alternative.
Large amounts of either may be required (up to 600
mg/d).
 Diazepam or Midazolam can be used as 5-10mg iv/im
every 1-4 hrly.
 Midazolam can be given as an intravenous infusion (5
-15 mg/hr).
 Phenobarbitone (up to 200 mg IV or PO/NG 12-hourly),
and phenothiazines (usually chlorpromazine-25mg/ml,
100mg IM f/b 50-100mg 12hrly) may be added as an
adjunctive sedative.
 Propofol, dantrolene, intrathecal baclofen,
succinylcholine & magnesium sulfate can be tried
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55. Skeletal muscle relaxants:
 These agents can inhibit both monosynaptic and
polysynaptic reflexes at spinal level, possibly by
hyperpolarization of afferent terminals.
 Muscle relaxation is indicated where sedation alone
is inadequate. Vecuronium (0.1 mg/kg IV as needed)
or atracurium (0.5 mg/kg IV) are appropriate.
 Pancuronium may worsen autonomic instability by
inhibiting catecholamine reuptake.
 Prolonged usage of aminosteroid muscle relaxants has
been associated with critical illness neuropathy and
myopathy.
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56. BACLOFEN
 Intrathecal (IT) baclofen, a centrally acting
muscle relaxant, has been used experimentally
to wean patients off the ventilator and to stop
diazepam infusion. IT baclofen is more potent
than PO baclofen.
 May induce hyperpolarization of afferent
terminals and inhibit both monosynaptic and
polysynaptic reflexes at spinal level.
 Entire dose of baclofen is administered as a bolus
injection. Dose may be repeated after 12 h or
more if spontaneous paroxysms return.
 It can also be given as T. Baclofen 5mg tds,
increase 5mg/day every 3 days,maximum
dose 80mg
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57. DRIP RATE OF COMMON DRUGS
 Diazepam 1 Amp. = 2 ml = 10 mg ( 5 mg / ml )
 5Amp in 50cc (40+10) NS – 50mg/50ml = 1mg/ml
 Usually needed 5-10ml/hr (10ml/hr=240mg/hr),
may need even more than that.
 Ideally not given by continuous infusion because
of precipitation in IV fluids & absorption of drug
into infusion bags & tubing. Usually 10-40mg
every 1-8 hours needed.
 Midazolam 1 vial = 5 ml = 5 mg ( 1 mg / ml)
 10 vial = 50cc @ 5ml/hr (=5mg/hr)
 Usually 5-15mg/hr (5-15ml/hr) needed
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58.  Atracurium 1 Amp. = 2.5 ml = 25 mg ( 10 mg / ml)
 8Amp in 500cc NS/5%DW = 0.4mg/ml = 200mg
 1 Amp (0.5mg/kg=25mg) IV stat f/b 5-10 µg/kg/min=
0.25-0.5 mg/min = 15-30 mg/hr = 37.5-75ml/hr
 Maintainance dose : 11-13 µg/kg/min
 For infusion pump in 50cc, divide drip rate by 10.
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59.  Vecuronium 1 Vial = 4 mg to be reconstituted
with 2 ml of sterile water = (2 mg / ml)
 5 vial in 50 cc NS/5%DW = 20mg = 0.4mg/ml
 0.1mg/kg bolus = 5mg = 2.5 ml f/b 0.8 -1.7
µg/kg/min (1 µg/kg/min = 50µg/min = 3mg/hr =
7.5 ml/hr
 Maintainance dose : 0.8 – 1.2 µg/kg/min
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60. METHOCARBAMOL (ROBINAX)
 May be used as adjunct but not much useful in
tetanus.
 Skeletal muscle relaxant
 100mg/ml , 10ml/vial – total 1gm/vial
 Tablet : 500/750mg
 IV : 1-2gm direct IV injection (at 3ml/min =
300mg/min). Additional 1-2gm IV infusion for
total dose of 3gm initially.May repeat 1-2 gm IV
every 6 hourly untill can give TRT/PO. Injection
should not be used for more than 3 consecutive
days. Total oral daily dose upto 24gm may be
neded.
 Oral : 1.5-2.0 gm QID for 48-72 hrs, then
decrease to 1 gm every 6 hr, <8gm/day
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61. 5. MANAGEMENT OF AUTONOMIC
DYSFUNCTION:
Fluid loading is a useful in minimizing autonomic
instability.
Magnesium Sulphte:
It is an effective adjunct in relaxation , sedation &
controlling the autonomic disturbance in tetanus.
It is a pre-syneptic neuromuscular blocker, reduces
catecholemine release from nerves & adrenal medulla;
and reduces responciveness to released catechlemines.
A loading dose of 5gm should be given over 20
minutes, followed by intravenous infusion of 2gm/hr. the
dose can be incresed by upto 0.5g/hr until spasms are
relieved or the patellar reflex disappears.
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62.  If infusion devices are unavailable , give 2.5gm i.v.
every 2 hours , titrating the frequency of
administration to spasms.
 To avoid overdose, monitor patellar reflex as
areflexia(absence of patellar reflex) occurs at the upper
end of the therapeutic range (4mmol/L). If areflexia
develops, dose should be decreased.
 By antagonizing the calcium metabolism MgSO4
causes weakness & paralysis in overdose. Monitoring of
serum magnesium level is important to prevent this:
the normal serum magnesium level is 0.7- 1.0 mmol/l &
acceptable therapeutic level is 2-3.5 mmol/l.
 Another drugs:
 Labetalol
 Continuous infusion of esmolol
 Clonidine / verapamil
 Morphine
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63. 6. SUPPORTIVE CARE:
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65. PREVENTION
 Tetanus is completely preventable
by active tetanus immunization.
 Immunization is thought to provide
protection for 10 years.
 Begins in infancy with the DTP
series of shots. The DTP vaccine is
a "3-in-1" vaccine that protects
against diphtheria, pertussis, and
tetanus.
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66.  1st
dose - 6th
week (DPT)
 2nd
dose - 10th
week (DPT)
 3rd
dose - 14th
week (DPT)
 1st
booster - 18th
month (DPT)
 2nd
booster - 6th
year (DT)
 3rd
booster - 10th
year (TT)
ACTIVE
IMMUNIZATION
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67. MONOVALENT VACCINES
 Purified tetanus toxoid ( adsorbed )
supplanted the plain toxoid – higher &
long lasting immunity response
 Primary course of immunization – 3 doses
 Each 0.5 ml , injected into arm given at
intervals of 0,1,6 months
 The longer the interval b/w two doses,
better is the immune response
 Booster doses : After 1 yr f/b Every 10 yrs
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68.  Older teenagers and adults who have
sustained injuries, especially puncture-type
wounds, should receive booster
immunization for tetanus if more than 10
years have passed since the last booster.
 Recovered clinical tetanus does not
produce immunity to further attacks
because very small amount of tetanus toxin
produced can not elicit strong protective
immune response.Therefore, even after
recovery patients must receive a full course
of tetanus toxoid.
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69. POSTEXPOSURE PROPHYLAXIS:
 All wound receive surgical toilet
Wounds less then 6 hours other wounds
Old , clean, non-penetrating,
& with negligible tissue damage
immunity treatment immunity treatment
category category
A nothing more required A nothing more
required
B toxoid 1 dose B toxoid 1 dose
C toxoid 1 dose C toxoid 1 dose +
D toxoid complete course human tetanus Ig.
D toxoid complete
course +
human tetanus Ig
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70.  A - has had a complete course of toxoid or
booster dose with in the past 5 year
 B - has had a complete course of toxoid or booster
dose more then 5 years ago & less then 10 years
ago
 C - has had a complete course of toxoid or a
booster dose more then 10 year ago
 D - has not had a complete course of toxoid or
immunity status unknown
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71. PASSIVE IMMUNIZATION
 Temp protection – human tetanus
immunoglobulin /ATS
 Human Tetanus Hyperimmunoglobulin :
• 250-500 IU
• Produces protective antibody level for atleast 4-6
weeks.
• Does not cause serum sickness
• Longer passive protection compared to horse
ATS( 30 days / 7 -10 days )
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72. PASSIVE IMMUNIZATION
 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.
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73. 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
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74. 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 (16th
-36th
week)
• 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
 To newborn of unimmunized mother, 500U HTIG
within 6 hours of birth.
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75. REFERECES:
 Harrison’s PRINCIPLES OF INTERNAL MEDICINE :
Eighteenth Edition
 Textbook of preventive & social medicine – Park – 19th
Edition
 UpToDate (http://www.uptodate.com)
 eMedicine (http://www.emedicine.com)
 Current recommendations for treatment of tetanus
during humanitarian emergencies : WHO Technical
Note
 World Federation of Societies of Anaesthesiologists -
WFSA
 CDC Article - Tetanus
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