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Tetanus
Tetanus
• Tetanos – a greek word – to strech
• First described by Hippocrates & Susruta
• A Neurological disease characterised by increased muscle tone & spasms.
• Caused by CLOSTRIDIUM TETANI
• An anaerobic, motile, gram positive rod that forms oval, colourless, terminal spores –tennis racket or drumstick shape.
• It is found worldwide in soil, in inanimate environment, in animal faeces & occasionally human faeces.
Epidemiology
• Occurs sporadically
• Affects unimmunized, partially immunized & fully immunized who fail to maintain adequate immunity with booster doses of vaccine.
• Although it is an entirely preventable disease by immunization , the burden of disease worldwide is great.
• As reporting is inaccurate & incomplete, particularly in devoleping countries, W.H.O considers reported cases to be an underestimate & takes case/death estimates to assess the burden of disease.
• In 2002, the estimated deaths in all age groups 2,13,000of which 1,80,000 were attributable to neonatal tetanus.
• More common in areas where soil is cultivated, in rural areas, in warm climates, during summer, among males.
Pathogenesis
• Contamination of wounds with spores of C.tetani.
• Germination & toxin production – in wounds with low oxidation – reduction potential ( devitalized tissues, F.B, active infection )
• Tetanospasmin ( neurotoxin )
• Tetanolysin ( hemolysin )
• Tetanospasmin ( exotoxin ) produced locally , released into bloodstream .
• Binds to peripheral motor neuron terminals & nerve cells of ant.horn of spinal cord
• The toxin after entering axon , transported to nerve cell body in brain stem & spinal cord – retrograde intraneuronal transport
• Toxin – migrates across synapse – presynaptic terminals- blocks the release of Glycine & GABA from vesicles.
• The blocking of neurotransmitter release by Tetanospasmin involves cleavage ofSynaptobrevin – essential for proper fn of synaptic vesicle release apparatus
• With diminished inhibition – resting firing rate of alpha motor neurons increases – rigidity
• Lessened activity of reflexes which limit polysynaptic spread of impulses, agonists & antagonists recruited - spasms
• Loss of inhibition of preganglionic sym neurons – sympathetic hyperactivity
Mode of transmission
• Infection is acquired by contamination of wounds with tetanus spores.
• Range of injuries & accidents – trivial pin prick, skin abrasion, puncture wounds, burns, human bites, animal bites & stings, unsterile surgery, IUD, bowel surgery, dental extractions, injections, unsterile division of umbilical cord, compound #, otitis media, chr.skin ulcers, eye infections, gangrene
• NOT TRANSMITTED FROM PERSON TO PERSON
Types
• Traumatic
• Puerperal
• Otogenic
• Idiopathic
• Tetanus neonatorum
PARK 19th
• Generalized
• Neonatal
• local
HARRISON 17th
Clinical features
• May begin from 2 days to several weeks after the
injury – USUALLY 1 WEEK
• Remember
Shorter the incubation period
More severe the attack
Worse the prognosis
Clinical features
• GENERALIZED TETANUS• Most common• Increased muscle tone & generalized spasms• Median time of onset after injury – 7 days• Pt 1st notices increased tone in masseter
( Trismus, lock jaw )• Dysphagia • Stiffness / pain in neck, shoulder, back muscles
appear concurrently / or soon thereafter• Rigid abd & stiff prox.limb muscles . Hands, feet
spared.
trismus
• Risus Sardonicus : Spasm of facial muscles ( frontalis & angle of mouth muscles ) producing grinning facies
• Opisthotonus : Painful spasms of neck, trunk and extremity. producing characteristic bowing and arching of back
• Some pts devolep paroxysmal, violent, painful, generalized muscle spasms – cyanosis . Spasms occur repetitively & may be spontaneous / provoked by slightest stimulation.
• Constant threat during gen.spasm is reduced ventilation, apnea / laryngospasm.
Risus sardonicus
• Mild ds ( muscle rigidity , no / few spasms )
• Moderate ds (trismus, dysphagia, rigidity, spasm)
• Severe ds ( freq explosive paroxysms )
• Autonomic dysfn complicates severe cases -labile htn, hyperpyrexia, profuse sweating, peripheral vasoconstriction, raised catecholamines.
Neonatal Tetanus
• 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
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
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.
• Incubation period : few days
• Mortality : high
Diagnosis
• Based entirely on clinical findings• Examine all cases with wound infection & muscle
stiffness• Wound cultures – in suspected cases
C.tetani can be isolated from wounds of pts without tetanus & freq cannot be isolated from wounds of those with tetanus
• Electromyograms – continous discharge of motor units, shortening / absence of silent interval seen after AP.
• Muscle enzymes – raised
• Serum Anti toxin levels >= 0.1 IU/ml –protective & makes tetanus unlikely .
Differential diagnosis
• Cond producing trismus : alveolar abscess, strychnine poisoning, dystonic drug reactions, hypocalemic tetany
• Meningitis/encephalitis
• Marked increased tone in central muscles , with superimposed generalized spasms & relative sparing of hands & feet – sugg tetanus
Treatment – general measures
• Goal is to eliminate the source of toxin, neutralize the unbound toxin & prevent muscle spasm & providing support - resp support
• Admit in a quiet room in ICU • Continuous careful observation &
cardiopulmonary monitoring• Minimize stimulation• Protect airway• Explore wounds – debridement
• NEUTRALIZE TOXIN :
• Inj.Human Tetanus Immunoglobulin 3000 – 6000 units IM, usually in divided doses as volume is large.
ANTIBIOTIC THERAPY :
• Although of unproven value , antibiotics adm to eradicate vegetative cells – the source of toxin
• IV Penicillin 10 -12 million units daily for 10 days
• IV Metronidazole 500mg Q 6 hrly / 1gm Q 12 hrly
• Allergic to Penicillin : consider Clindamycin & Erythromycin
Control of Spasms
• Nurse in a quiet dark room
• Avoid noise & other stimuli
• IV Diazepam / Lorazepam / Midazolam
• Barbiturates & Chlorpromazine –2nd line drugs
• Continued spasms : intubate & ventilate
• Propofol, dantrolene, intrathecal baclofen, succinylcholine & magnesium sulfate can be tried
Management of autonomic dysfn
• Labetalol
• Continuous infusion of esmolol
• Clonidine / verapamil
Additional measures
• Pts recovering from tetanus should be actively immunized
• Hydration
• Nutrition
• Physiotherapy
• Prophylactic anticoagulation
• Bowel, bladder, back care
• Treatment of intercurrent infection
Prevention – Active Immunization
• For partially immunized, unimmunized and
recovering from tetanus
• It stimulates production of protective antitoxin
• 2 prep : combined vaccine : DPT
monovalent vaccine : plain / formol
toxoid
tetanus vaccine , adsorbed
Combined vaccine
• According to National Immunization, 3 doses of DPT – at intervals of 4-8 wks, starting at 6 wks age, followed by
• booster at 18 months age
• 2nd booster (only DT) at 5-6 yrs
• 3rd booster ( only TT) after 10 yrs age
Monovalent vaccines
• Purified tetanus toxoid ( adsorbed ) supplanted the palin toxoid – higher & long lasting immunity response
• Primary course of immunization – 2 doses • Each 0.5 ml , injected into arm given at intervals of 1-
2 months• The longer the interval b/w two doses, better is the
immune response• 1st booster – 1 yr after the initial 2 doses• 2nd Booster : 5 yrs after the 1st booster ( optional )• Freq boosters to be avoided
Passive immunization
• Temp protection – human tetanus immunoglobulin /ATS
• Human Tetanus Hyperimmunoglobulin :
• 250-500 IU
• 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
• 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 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• Unimmunized pregnant women : 2 doses
tetanus toxoid• 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
Prevention of tetanus after injury
• All wounds should be thoroughly cleaned soon after injury
• Remove all foreign bodies, soil, dust, necrotic tissue
A – completed course of toxoid/booster < 5 yrs ago
B- completed course of toxoid / booster >5 yrs ago & < 10 yrs ago
C- completed course of toxoid / booster >10 yrs ago
D- not completed course of toxoid / immunity status unknown
Thank You