TETANUS

EU MBCHB 3

DR D M KILLINGO
 INTRODUCTION
 Tetanus is a nervous system disorder
characterised by increased muscle tone and
spasm
 A.k.a lock jaw
 Caused by tetanospasmin ( a powerful
protein elaborated by Clostridium tetani)
 EPIDEMIOLOGY
 Incidence has greatly reduced worldwide (more so
in the developed countries) since the advent of
universal vaccination
 Developing countries still have significantly large
no.s of tetanus with ~ 1m cases per year. E.g.
among pts. admitted for neurological conditions in
a nigerian hospital: 50% stroke, 14% tetanus, 12%
meningitis
 Etiologic Agent– Clostridium
tetani
 Anaerobic, motile, gram positive rod
 Has a terminal oval spore giving appearance
of a tennis raquet or a drumstick
 Found in soil, animal faeces and even human
faeces
 Spores survive for years and show resistance
to disinfectants and boiling for 20 minutes
 Clostridium tetani ….cont’d
 The vegetative cells are however easily
inactivated and are susceptible to various
antibiotics (flagyl, penicillin)
 The toxin - tetanospasmin
 Formed in vegetative cells
 Is a single polypeptide chain that undergoes
autolysis to form a hetero dimer consisting of:
 a heavy chain (100kda) that moderates
binding to nerve cell receptors and entry into
these cells
 A light chain (50kda) which acts to block NT
release
 Pre-requisites for tetanospasmin
elaboration
2 or more of the following needed for tetanospasmin
elaboration in the human host:
 Penetrating injury with inoculation of cl. tetani
spores
 Co-infection with other bacteria
 Devitalized tissue
 Foreign body
 Localised ischaemia
 PATHOGENESIS
 Cl. tetani does not in itself evoke
inflammation
 Toxin released in the wound binds to
peripheral motor neuron terminals, enters
axon and is transported to the nerve cell
body in the brain stem and spinal cord by
retrograde intraneural transport
 Pathogenesis cont’d
 Toxin migrates across synapse to pre
synaptic terminals where it blocks release
of inhibitory neurotransmitters GLYCINE
and GABA
 Blockage of release achieved by its
cleaving action on membrane proteins
(synaptobrevin 2) involved in
neuroexoscytosis
 Pathogenesis cont’d
 Net effect = disinhibition of neurons that
modulate excitatory impulses from motor
cortex.
 Disinhibition of ant horn cells & autonomic
neurons result in increased muscle tone,
painful spasms and widespread autonomic
instability (sweating, tachycardia,
hypertension).
 Pathogenesis cont’d
 Tetanospasmin may also block NT release
at NMJ and produce weakness and paralysis
 Note: tetanospasmin effects last for a
remarkably longtime, recovery requires the
growth of new axonal terminals. The usual
duration of clinical tetanus is thus 4-6
weeks.
 CLINICAL PRESENTATION
 Incubation period: range 1-112 days.
Usually 7 days
4 clinical patterns:
 Generalised
 Local
 Cephalic
 Neonatal
 1. GENERALISED
TETANUS
 Characterised by Increased muscle tone and
generalised spasms
Typical progression:
 Increased masseter muscle tone (trismus)
 Dysphasia +/- stiffness in neck, shoulder and
back muscles
 Rigid abdomen, stiff proximal limb muscles
 Hands and feet relatively spared
 Generalised tetanus cont’d
 Sustained contraction of facial muscles –
grimace/sneer (risus sardonicus)
 Contraction of back muscles – opisthortonus
 Some pts. dev paroxysmal, violent, painful and
genealised muscle spasms.
 Threat to life due to reduced ventilation following
apnea or laryngospasm. May be spontaneous or
provoked by even the slightest stimuli.
 Dysphagia & ileus may preclude oral feeding
 Generalised tetanus cont’d

Autonomic dysfunction:
 Sustained elevated BPs.
 Tachycardia
 Dysrrythmias
 Hyperpyrexia
 Xs diaphoresis
 Peripheral vasoconstriction
 Sudden cardiac arrest s.t.s occurs – basis unknown
 Generalised tetanus cont’d

Grading of severity:
 Mild – muscle rigidity + few/no spasms
 Moderate – trismus, dysphagia, rigidity,
spasms
 Severe – frequent explosive paroxysms
 Generalised tetanus cont’d

Complications:
 Aspiration pneumonia
 Fractures
 Muscle rupture
 Decubitus ulcer
 rhabdomyolysis
 LOCAL TETANUS
 uncommon
 Good prognosis
 Manifestations ltd to muscles around the
wound
 CEPHALIC TETANUS
 Form of local tetanus
 Trismus and dysfunction of 1 or more
cranial nerves (mostly vii)
 Follows head injury or ear infection
 High mortality
 NEONATAL TETANUS
 Occurs within 14 days of birth
 Rigidity, trismus, inability to suck, seizures
 Follows deliveries lacking in aseptic
techniques esp in umbilical stump
management.
 Mostly seen in offspring of mothers who
are poorly immunised
 DIAGNOSIS
 Largely clinical
 Wound culture (cl. tetani may be isolated from
wounds of pts without tetanus and frequently cant
be isolated from wounds of patients with tetanus)
 Csf – usually normal
 Elevated muscle enzymes
 Emg – continuous discharge of motor units and
shortening or absence of silent interval normally
seen after an action potential
 DIAGNOSIS ……cont’d
 Serum antitoxin levels >0.15 u/ml are
considered protective and make tetanus
unlikely
 DIFFERENTIAL
DIAGNOSIS
Include
 Alveolar abcess
 Strychnine poisoning
 Dystonic drug reactions
 Hypocalcemic tetany
 Malignant neuroleptic syndrome
 Meningitis/encephalitis
 Acute intra – abdominal process (rigid abd)
 DIFFERENTIALS

DRUG INDUCED DYSTONIAS

 Mostly seen with phenothiazines
 Pronounced deviation of eyes (non in tet)
 Writhing movements of the head and neck
 Absence of tonic muscular contractions between
spasms
 Benztropine mesylate (anticholinergic)
immediately reverses the spasms
 DIFFERENTIALS

ALVEOLAR ABSCESS
 Characterised by trismus
 Presence of dental abscess
 Lack of progression or superimposed
spasms
 DIFFERENTIALS

STRYCHNINE POISONING
 E.g. following ingestion of rat poison
 May mimic tetanus therefore initial
management similar
 Assay of blood, urine and tissue for
strychnine to differentiate
 DIFFERENTIALS

MALIGNANT NEUROLEPTIC SYNDROME

 Mostly seen with haloperidol and fluphenazine
 Idiosynchratic rather than dose dependent
 Usually within first 1-2 weeks of treatment
 Fever (>38 degees), h/o mental illness
 Striking symptoms of autonomic instability
 Muscular rigidity (lead pipe)
 MANAGEMENT OF TETANUS

TREATMENT GOALS
 Eliminate source of infection
 Neutralize unbound toxin
 Prevent muscle spasm
 Monitor patient and provide supportive
management
 Management … cont’d

GENERAL
 Admit to a quiet room in icu
 Explore, clean and debride wounds
 Management … cont’d

ANTIBIOTICS
 Eradicate vegetative cells
 X-pen 10 – 12 mu iv for 10 days
 Flagyl 1gm bd. Studies show higher efficacy
and survival rate than penicillin. Lacks the anti
– GABA activity which is present with
penicillin
 Alternatives: clindamycin, erythromycin
 Management … cont’d

ANTITOXIN
 Neutralize circulating toxin and unbound
toxin in the wound
 Toxin already bound to neural tissue
unaffected
 500 – 1000 iu i/m stat
 Additional dose unnecessary as has long t0.5
 Management … cont’d

CONTROL OF SPASMS
 Diazepam (benzodiazepine and GABA agonist).
Also lorazepam and clonazepam
 2nd line: barbiturates
 3rd line: therapeutic paralysis with mechanical
ventilation
 Intrathecal baclofen (stimulates post synaptic
GABA receptors). Reduces duration of
mechanical ventilation
 Management … cont’d

RESPIRATORY CARE
 In laryngospasm and oversedation, trismus,
swallowing dysfunction
 tracheostomy or intubation with
mechanical ventilation
 Management … cont’d

AUTONOMIC DYSFUNCTION
 Adrenergic blockade and suppression of
autonomic hyperactivity
 Labetalol, morphine sulphate (sedation and
ctrl autonomic dysfunction), magnesium
sulphate (also useful in spasm control),
atropine
 Management … cont’d

VACCINE
 Actively immunize recovering patients
 Immunity not induced by the small amount of
toxin that produces disease
 3 doses of tet/diph (Td) vaccine at t=0, t+1
month and t+1 year
 Immunity maintained by booster Td given
every 10 yrs throughout adulthood
 Management … cont’d

OTHER MEASURES
 Hydrate to ctrl fluid losses
 Tpn/ppn
 Physiotherapy to prevent contractures
 Heparin (prophylactic)
 Monitor bowel, bladder and renal function
 Prevent decubitus ulcers
 PREVENTION

ACTIVE IMMUNIZATION
 For those partially immunised or
unimmunised
 3 doses, first 2 doses 4 – 8 weeks apart, 3 rd
dose 6 – 12 months after the second
 PREVENTION …. Cont’d
WOUND MANAGEMENT

Td status Clean minor other wounds

wounds
h/o Td Td TIG Td TIG
Unknown YES NO YES YES
or <3 dose
3 doses NO unless NO NO NO
> 10 yrs unless > 5
from last yrs since
dose last dose
 PREVENTION

NEONATAL TETANUS
 Maternal vaccination in pregnancy
 Encouraging hospital deliveries
 Train TBAs
 PROGNOSIS
 Course 4 – 6 weeks
 Pts may require prolonged ventilator
support
 Hypertonia and spasms may last months but
recovery usually complete
 PROGNOSIS

POOR OUTCOME PREDICTORS

 Short incubation period
 Short interval from onset of syptoms to
admission
 Short period from onset of symptoms to first
spasm
 Extent of prior vaccine
 Neonates and elderly