DEFINITION

• Tetanus is an acute disease manifested by

skeletal muscle spasm & ANS disturbance.

• CDC defines probable tetanus as acute illness

with muscle spasms/hypertonia in e absence o
a more likely dx.
ODONG LAMECK YR 3
LIWA LAWRENCE YR 5
 DEFINITION cont

• WHO defines Neonatal tetanus as illness

occurrin in a child who has e normal ability 2
suck & cry in e 1st 2 days o life bt who loses
this ability btn days 3 and 28 of life and
becomes rigid and has spasms.”
• WHO defines Maternal Tetanus as tetanus
occurrin durin preg or within 6 wks afta e
conclusion o preg(whether with birth,
miscarriage, or abortion)
 ETIOLOGY
• C. tetani ,an anaerobic, gram+ve, spore-formin
rod whose spores r highly resilient,Spores
resist boiling and many disinfectants.
• spores and bacilli survive in the intestinal
systems of many animals, and fecal carriage is
common
• The spores/bacteria enter e body thru
abrasions, wounds, or umbilical stump.
 ETIOLOGY cont
• Superficial abrasions to the limbs,open fracture,
abortion,or drug injection.
• In neonates, infxn o e umbilical stump can result 4rm
inadequate umbilicalcord care; in some cultures eg
cord is cut with grass or animal dung is applied to the
stump. Circumcision or earpiercin also can result in
neonatal tetanus
• Once in suitabo anaerobic env’t, orgs grow or spore
germinates , multiply, & release tetanus toxin;enters
NS & causes dz.
 EPIDEMIOLOGY
• rare dz in e developed world. 2 cases o neonatal
tetanus have occurred in the US since 1989. In
2013, 26 cases were reported to the U.S & most
cases occur in incompletely vaccinated or
unvaccinated individuals.
• >60 yrs o age r at greater risk o tetanus.
• Pipo who inject drugs,heroin subcutaneously r
increasingly recognized as a HRG (15% o all
cases in 2001–2008).
 EPIDEMIOLOGY cont
• In developing countries, mortality rate can be
nearly 100% and around 40% in others.
• In Ug in a study conducted at Masafa hosp,
tetanus entry wounds were mostly due to
RTAs,& among young males. Tetanus case
fatality was 47.4%
• In Ug, burden is increasin, esp among females
aged 5+ yrs.
• In northern Ug( St Mary’s Lacor),overall
mortality was 51.5-72.4% in neonatal dz,25%
in children,57.8% in adults. More males than
females.
 PATHOGENESIS
• Tetanospasmin is intra-axonally transpted 2
motor nuclei o e CNs or ventral horns o e spinal
cord; binds 2 specific membrane components in
presynaptic α-motor nerve terminals.
• This binding results in toxin internalizatn &
uptake in 2 e nerves. Once inside the neuron, the
toxin enters a retrograde tp pathway, whereby t
is carried proximally 2 e motor neuron body.
 PATHOGENESIS cont
• undergoes translocation across e synapse 2 e
GABAergic presynaptic inhibitory interneuron
terminals.
• The clinical manifestations o tetanus occur
only afta tetanus toxin has reached
presynaptic inhibitory nerves.
 PATHOGENESIS cont
• cleaves VAMP2(synaptobrevin); molecule
necessary 4 presynaptic binding & release o
NT,thus tetanus toxin prevents NT release &
effectively blocks inhibitory interneuron dx.

• unregulated activity in e motor NS,similarly in

ANS. X-tic fxs of skeletal muscle spasm and
autonomic system disturbance.
 CLINICAL MANIFESTATIONS
• most important early symptom is trismus –
spasm o e masseter muscles, wic causes
difficulty in opening e mouth & in masticatin
(lockjaw),difficulty swallowing.
• tonic rigidity spreads 2 involve e muscles o e
face,neck & trunk. Contraction of the frontalis
& e muscles at e angles o e mouth leads 2
(risus sardonicus).
OPisthotonus
Trismus
RIsus Sadonicus
 CLINICAL MANIFESTATIONS cont
• The back is usually slightly arched (opisthotonus)
& there is a board-like abdominal wall.
• In more severe cases,violent spasms lastin 4 a
few secs to 3–4 mins occur spontaneously, or
may be induced by stimuli such as mov’t or
noise;these episodes r painful & exhaustin,&
suggest a grave outluk.
• Pt may die 4rm exhaustion, asphyxia(main cause
of death) or aspiration pneumonia.
 CLINICAL MANIFESTATIONS cont
• Spasms strong enough 2 produce tendon
avulsions & crush fractures have been reported.
• ANS involvement may cause CVS complicatns,
such as hypertension,tachycardia,bradycardia,GI
stasis,tracheal secretions,sweating,RF.
• Rarely, e only manifestation o e dz mayb ‘local
tetanus’ – stiffness or spasm o e muscles near e
infected wound
 DIAGNOSIS
• based on clinical findings
• treatment shud nt b delayed while laboratory
tests r conductd.
• Culture of C. tetani from a wound
• Serum anti-tetanus IgG levels >0.1 IU/mL do
not support the dx of tetanus
• PCR 4 detection o tetanus toxin
 Differential Dx
• dental abscess
• septic throat
• Conversion
• Strychnine poisonin
• dystonic rxns to antidopaminergic drugs.
• Hypocalcemia
• meningoencephalitis
 TREATMENT
• General measures
• Nurse pt intensively in a quiet isolated area
• Maintain close observatn & attentn 2 airway, temp, spasms
• Insert NGT 4 nutrition, hydratn,& medicine administratn
• O2 therapy if needed
• Prevent aspiration of fluid into the lungs
• Avoid IM injections as much as possibo; use alternative routes
(e.g. NGT, rectal) wea possibo
• Maintain adequate nutritn as spasms result in high metabolic
demands
• Treat respiratory failure in ICU with ventilation
 TREATMENT cont
• Neutralise toxin
• Giv TIG 150 IU/kg (adults & children). Give
the dose in at least 2 different sites IM
• In addition, administer full course of age
appropriate TT vaccine (TT or DPT) – starting
immediately
 TREATMENT cont
• importnt 2 establish a secure airway early in
severe tetanus(tracheostomy).
• Ideally, pts shud b nursed in calm, quiet env’ts
coz light & noise can trigger spasms.
• CVS stability is improvd by increasin sedatn with
IV magnesium sulfate or morphine,fentanyl. In
addition, drugs acting specifically on e
cardiovascular system (e.g., esmolol, calcium
antagonists,and inotropes) mayb requird.
 TREATMENT cont
• Treatment to eliminate source of toxin
• Clean wounds and remove necrotic tissue.
• First line antibiotics-Metronidazole 500 mg
every 8 hours IV or by mouth for 7 days
• Second line antibiotics-Benzylpenicillin 2.5
MU every 6 hours for 10days
 TREATMENT cont
• Control muscle spasms
• First line-Diazepam 10 mg (IV or rectal) every
1 to 4 hours
• Other agents-Magnesium sulphate (alone or
with diazepam): 5g IV loading dose then 2
g/hour til spasm control is achieved- Monitor
knee-jerk reflex, stop infusion if absent
 TREATMENT cont
• Control pain-Morphine 2.5-10 mg IV every 4-6
hours (monitor 4 resp depression)
• Paracetamol 1 g every 8 hours
 Prevention

• Immunise all children against tetanus durin

routine childhood immunisation
• Proper wound care & immunisation : Full
course if patient not immunised or not fully
immunised,Booster if fully immunised but
last dose >10 yrs ago
• Prophylaxis in pts at risk as a result o
contaminated wounds: give TIG IM
 PROGNOSIS
• Recovery from tetanus may take 4–6 weeks
• Rapid devt o tetanus is associatd with more
severe disease & poorer outcome.
• Ts generally acceptd that recovery is typically
complte unless periods o hypoventilatn hav been
prolongd or other complicatns hav ensued.
(ischaemic brain injury)
• Neonates mayb at increasd risk o learnin
disabilities, behavioral problms, CP,&deafness