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TETANUS
TETANUS
 INTRODUCTION
 CAUSATIVE AGENT
 EPIDEMIOLOGY

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 TRANSMISSION, HOST FACTORS, ROUTE OF
ENTRY
 MECHANISM OF ACTION OF TOXIN
 CLINICAL FEATURES
 TYPES OF TETANUS
 DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
 TREATMENT
 PREVENTION – ACTIVE & PASSIVE
IMMUNIZATION
INTRODUCTION

 Tetanos – a greek word – to strech

 First described by Hippocrates & Susruta
 Tetanus an neurological disease characterized by an

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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
CAUSATIVE AGENT
 Caused by CLOSTRIDIUM TETANI
 Anaerobic

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 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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Clostridium tetani Gram Stain

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NOTE: Round terminal spores give cells a
“drumstick” or “tennis racket” appearance.
EPIDEMIOLOGY
 Tetanus is an international health problem, as spores
are ubiquitous. The disease occurs almost exclusively
in persons who are unvaccinated or inadequately

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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.
India
Tetanus is important endemic infection in India.
Causative factors
Hand washing

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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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TRANSMISSION :
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

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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
ROUTE OF ENTRY
 Apparently trivial injuries
 Animal bites/human bites
 Open fractures
Burns

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

 Gangrene
 In neonates usually via infected umbilical stumps
 Abscess
 Parenteral drug abuse
TETANUS PRONE WOUND
 A wound sustained more than 6 hr before
surgical treatment.

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 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.
 Sporulated Vegetative

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•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.
• 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).

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• 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.
 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

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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.
Mechanism of Action of Tetanus Toxin

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 1. C. tetani enters 2. Stays in sporulated
body from through form until anaerobic
conditions are
wound. presented.

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3. Germinates under 4. Tetnospasmin spreads
using blood and lymphatic
anaerobic conditions and system, and binds to motor
begins to multiply and neurons.
produce tetnospasmin.

6. Binds to sites responsible for

5. Travels along the
inhibiting skeletal muscle
axons to the spinal cord. contraction.
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 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

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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)
 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

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

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.
 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.

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 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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TRISMUS
 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

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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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RISUS SARDONICUS
 Opisthotonos in Tetanus Patient

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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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 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

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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.
AUTONOMIC DYSFUNCTION
 Tetanospasmin has a disinhibitory effect on the
autonomic nervous system (ANS) due to increased
release of catecholamines it causes :

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 Hyperpyrexia
 Sweating
 Peripheral vasoconstriction
 Labile/Sustained Hypertension
 Episodic tachycardia, dysrhythmias and cardiac arrest
 Occasionally period of bradycardia & hypotension
Other symptoms include:
 Drooling
 Fever usually absent
 Mentation unimpaired

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 Hand or foot spasms
 Irritability
 Uncontrolled
 urination orof illness — Tetanus toxin- induced
Duration
defecation
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.
SEQUENCE OF EVENTS

Lock Jaw

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Stiff Neck

Difficulty Swallowing

Muscle Rigidity Spasms

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TYPES OF TETANUS
 Generalied vs Local
 Cephalic

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 Traumatic
 Otogenic
 Idiopathic
 Puerperal
 Tetanus neonatorum
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.

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•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
NEONATAL TETANUS
 Tetanus neonatorum (8thday disease)
 Usually fatal if untreated

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 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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LOCAL TETANUS
 Uncommon form
 Manifestations are restricted to muscles near the

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wound.
 Cramping and twisting in skeletal muscles
surrounding the wound – local rigidity
 Prognosis – excellent
CEPHALIC TETANUS
 A rare form of local tetanus
 Follows head injury / ear infection

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 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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Ophthalmoplegic tetanus is a variant that develops after
penetrating eye injuries and results in CN III palsies and
ptosis.

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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.

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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.

DIRECT SMEAR

 Show Gram-positive
bacilli with drum-stick
appearance.
 Morphologically

indistinguishable from
similar nonpathogenic
bacilli.

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CULTURE
 Done in blood agar under anaerobic
condition or in Robertson’s cooked meat

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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.
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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 Procedures:
 The spatula test is one diagnostic bedside test.

 This simple test involves touching the

oropharynx with a spatula or tongue blade.

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 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
DIFFERENTIAL DIAGNOSIS
 Drug induced Dystonic Reactions e.g. Phenothiazines
 Strychnine poisoning
 Neuroleptic Malignant Syndrome, Serotonin syndrome
 Trismus d/t Peritonsillar Abscess/Dental infection

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 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)
PRINCIPLE OF TREATMENT
1. Neutralization of unbound toxin
-HTIG/ATS
2. Prevention of further toxin production

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-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…
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.

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 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.
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

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• (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.
•
2. PREVENTION OF FURTHER TOXIN
PRODUCTION
• Debridement of Wound to remove organisms and to
create an aerobic environment.

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• 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.
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

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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.
 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.

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- 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.
 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

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-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
 Skeletal muscle relaxants:

 These agents can inhibit both monosynaptic and

polysynaptic reflexes at spinal level, possibly by
hyperpolarization of afferent terminals.

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 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.
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.

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 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
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.

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 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
 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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 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

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 Maintainance dose : 0.8 – 1.2 µg/kg/min
METHOCARBAMOL (ROBINAX)
 May be used as adjunct but not much useful in
tetanus.
 Skeletal muscle relaxant

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 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
 5. MANAGEMENT OF AUTONOMIC
DYSFUNCTION:
Fluid loading is a useful in minimizing autonomic
instability.
Magnesium Sulphte:
 It is an effective adjunct in relaxation , sedation &

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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.
 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.

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 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


6. SUPPORTIVE CARE:

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PREVENTION

 Tetanus is completely preventable

by active tetanus immunization.

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 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.
ACT I V E
IMMUNIZATION
 1stdose - 6thweek (DPT)
 2nddose - 10th week (DPT)

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 3rddose - 14th week (DPT)
 1stbooster - 18thmonth (DPT)
 2ndbooster - 6thyear (DT)
 3rdbooster - 10thyear (TT)
MONOVALENT VACCINES
 Purified tetanus toxoid ( adsorbed )
supplanted the plain toxoid – higher & long
lasting immunity response

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 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
 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.

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 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.
POSTEXPOSURE PROPHYLAXIS:
 All wound receive surgical toilet

Wounds less then 6 hours Old , other wounds

clean, non-penetrating,
& with negligible tissue damage

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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
 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 ora

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booster dose more then 10 year ago
 D - has not had a complete course of toxoid or
immunity status unknown
PASSIVE IMMUNIZATION
 Temp protection – human tetanus
immunoglobulin /ATS

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 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 )
PASSIVE IMMUNIZATION
 ATS ( EQUINE ) :
• 1500 IU s/c after sensitivity testing

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• 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.
ACTIVE & PASSIVE
IMMUNIZATION
 In non immunized persons
 1500 IU of ATS / 250-500 units of Human Ig in one

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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
PREVENTION OF NEONATAL
TETANUS
 Clean delivery practices
 3 cleans : clean hands, clean delivery surface,
clean cord care
 Tetanus toxoid protects both mother & child

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 Unimmunized pregnant women : 2 doses tetanus
toxoid (16th-36th week)
• 1stdose as early as possible during pregnancy
• 2nddose – 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.
REFERECES:
 Harrison’s PRINCIPLES OF INTERNAL MEDICINE :
Eighteenth Edition
 Textbook of preventive & social medicine – Park – 19th

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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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