PENDUKUNG TETANUS

TETANUS

 nervous system disorder

 characterized by muscle spasm
 caused by toxin producing anaerobe Clostridium tetani

Epidemiology
Most of patients :
- lack a history of receipt of a full series of tetanus toxoid immunization
- receive inadequate prophylaxis following a wound
 PATHOGENESIS
Spores of Clostridium tetani gain access to damaged human tissue  inoculation  transform
into a vegetative rod-shape bacterium  produce metalloprotease tetanospasmin (tetanus
toxin)
Reaching spinal cord and brainstem (retrograde axonal transport)  within motor neuron,
enters adjacent inhibitory interneurons  block neurotransmission

Inactivation inhibitory neurotransmission (normally modulates anterior horn cells and muscle
contraction)  loss of inhibition anterior horn cells and autonomic neurons

 increased muscle tone, painful spasms, autonomic instability

 PATHOGENESIS
Death of Clostridium  toxin released  activated by bacterial / tissue proteases

For binding and entry into neurons

Heavy
 Cleaved by pepsin into specific fragments
chain
 mediated binding into specific types of neural cells
Activated form
Toxic properties
Light chain
 Presynaptic inhibition neurotransmitter

Tetanolysin
 toxin in early growth phase
 haemolytic properties (cause membrane damage)
 role in tetanus in uncertain
PREDISPOSISING FACTORS
Combination of absence of antibodies (ie, from inadequate vaccination) plus two or more following
:
1. penetrating injury resulting in the inoculation of C.spores
2. co infection with other bacteria
3. devitalized tissue
4. a foreign body
5. localized ischemia

Tetanus prone injuries  splinters and other puncture wounds, gunshot wounds, compound fractures,
burn, unsterile IM/IV injection
Unknown cause
 no cause can be identified in a small percentage patients with sign and symptoms
 cryptogenic cases  unnoticed abrasion / skin injuries
CLINICAL PRESENTATION
 CLINICAL FEATURES
Incubation period
 8 days ( 3 – 21 days)
 inoculation of spores in body locations distant from the CNS (ex hands or feet) results in a longer
incubation period
Generalized tetanus
 most common and severe clinical form
 >50% is trismus (lockjaw)
 develop reflex spasm of masseter muscle rather than normal gag response (in spatula test)
(sensitivity 94%, specificity 100%)
 tonic contraction of skeletal muscles and intermittent intense muscular spasms
1. intensely painful ec no impairment in consciousness
2. triggered by loud noises or other sensory stimuli (physical/light contact
 CONT..
Tonic and periodic spastic muscular contraction :
1. stiff neck
2. opisthotonos
3. ricus sardonicus (sardonic smile)
4. board like rigid abdomen
5. periods of apnea / upper airway due to vise-like contraction of respiratory muscle
6. dysphagia
During generalized tetanic spasm  clench their fists, arch their back, flex and abduct their
arms while extending their legs, often becoming apneic during there dramatic posture
 autonomic overactivity : irritability, restlessness, sweating, tachycardia
 Later Stage : profuse sweating, cardiac arrhytmia, labile
hypertension/hypotension, fever
 CLINICAL FEATURES
Local tetanus
 Rarely
 tonic and spastic muscle contractions in one extremity/ body region
 invariably evolves into generalized tetanus
Cephalic tetanus
 involving only crania nerve
 injuries in head or neck
 subsequently develop generalized tetanus
 mostly cranial nerves VI, III, IV, and XII
 CLINICAL FEATURES
Duration of illness
 long lasting – recovery requires the growth of the new axonal nerve terminals\
 4-6 weeks
Severity of illness
Depending upon the amount of tetanus toxin reaches CNS
Sign and symptoms progress for up to two weeks after onset
 milder clinical features : Longer the interval (onset – appearance of spasms)
preexisting but nonprotective levels of antitetanus antibodies
 DIFFERENTIAL DIAGNOSIS
1. Drug induced dystonias ( ex phenotiazines)
Pronounced deviation of the eyes, writhing movement of head and neck, absence tonic
muscular contraction between spasms
 tx – benztropine mesylate
2. Trismus due to dental infection
Presence of dental abscess
 Lack progression or superimposed spasm
3. Malignant neuroleptic syndrome
Presence of fever, altered mental status, recent receipt of an agent
TREATMENT

Goals of treatment :
●Halting the toxin production
●Neutralization of the unbound toxin
●Airway management
●Control of muscle spasms
●Management of dysautonomia
●General supportive management
TREATMENT CON’T
●Halting the toxin production
1. Wound management : debridement to eradicate spores and necrotic tissue
2. Antimicrobial therapy :
- metronidazole 500mg IV every 6-8 hours
- penicillin G 2-4 millions IU IV every 4-6 hours ( alternative )
- ceftriaxone 1-2gr IV every 24 hours (mixed infection)
GABA antagonist effect of penicillin and 3rd generation od cephalosporin
Metronidazole vs Penicillin G
Low mortality rate
Required fewer muscle relaxants and sedative
Alternative : doxycycline (100mg/12 hours), macrolide, clindamycin, vancomycin
 TREATMENT
●Neutralization of the unbound toxin
The use of passive immunization to neutralize unbound toxin is associated with improved
survival, and it is considered to be standard treatment.
- tetanus immune globulin (HTIG)
 3000 – 6000 units IM as soon as diagnosis of tetanus is considered
 administered at different sites than tetanus toxoid

Active immunization
 bacterial disease that does not confer immunity following recovery from acute illness
 ALL patient with tetanus should receive active immunization with full series ( 3 doses) of
tetanus and diphteria toxoid-containing vaccines
TETANUS TOXOID
TETANUS IMMUNE GLOBULIN
TREATMENT
●Control of muscle spasms
- life threatening  can cause respiratory failure, lead to aspiration, indeuced
generalized exhaustion
- attention to placement
- control light and noise
Treatment
1. Benzodiazepin
Diazepam  10-30mg IV, repeated as needed every 1-4 hours (max 500mg)
 ventilator assistance
Midazolam  recommended for higher doses (min. acute kidney injury, MODS)
 TREATMENT
2. Anesthetic propofol
3. Neuromuscular blocking agents
 when sedation alone inadequate
 Pancuronium : long acting agent, worsen autonomic instability (inhibitor
catecholamine reuptake)
 Vecuronium : short acting, less likely autonomic problem
 Baclofen : stimulates postsynaptic GABA receptor
: bolus 1000mcg / intrathecal initial 40-200mcg followed by continuous
infusion 20mcg/hour
TREATMENT
●Management of autonomic dysfunction
1. Magnesium sulfate
 presynaptic neuromuscular blocker (block catecholamine release from nerves)
 reduces receptor responsiveness to catecholamine
Magnesium infusion significantly reduced the requirement for other drugs to control muscle
spasms, and patients treated with magnesium were 4.7 times (95% CI 1.4-15.9) less likely
to require verapamil to treat cardiovascular instability than those in the placebo group
(Thwaites 2006)
2. Beta blockade
Labetolol 2,5 – 1 mg/min
Morphine sulfate 0,5 – 1 mg/kg/hour
TREATMENT
●Airway management
- early tracheostomy is frequently indicated because of the likelihood of prolonged
mechanical ventilation
- Energy demands in tetanus may be extremely high, so early nutritional support is
mandatory , profilactic treatment with sucralfate/acid blocker
- prophylaxis thromboembolism with heparin, LMWH or other anticoagulants
- Physical therapy should be started as soon as spasms have ceased
PROGNOSIS
Case-fatality rates for non-neonatal tetanus in resource-limited countries range from
8 to 50 percent
Patients with shorter incubation periods (eg, ≤7 days) have increased disease
severity and mortality
AUTONOMIC DISTURBANCE
TETANUS GRADE
CATECHOLAMINE