Akreditasi PP IAI–2 SKP

Penatalaksanaan Tetanus
Ni Komang Saraswita Laksmi
Puskesmas Mendoyo I, Bali, Indonesia

ABSTRACK

Tetanus is still an important health issue in developing countries because of poor immunization
programme and the poor availability of intensive care unit (ICU) facility. Three goals of tetanus
management are: (1) eradication of tetanospasmin source; (2) unbound toxin
neutralization; (3) supportive care until tissue-bound tetanospasmin has completely been metabolized.
Most cases take 4-6 weeks of supportive care in ICU. The quality of supportive care determine the
outcome, in addition the severity of disease. Ni Komang Saraswita
Laksmi. Management of Tetanus.

Keywords: Intensive care unit, management, tetanus

Background anaerobes. These bacteria are everywhere, able

Until now tetanus is stilla significant
public health problem at developing countries
because of program access poor immunization,
as well as management. Modern tetanus
requires facilities intensive care units (ICU) are
rarely available in most tetanus patients
weight.1 In developing countries, mortality
tetanus exceeds 50% by estimate the number
of deaths from 800,000 to 1 million
people/year, mostly in neonates.2,3 Neonatal
tetanus death is estimated
amounting to 248,000 deaths per year. 1
part of Neurology RS Hasan Sadikin Bandung,
reported 156 cases of tetanus in the year 1999-
2000 with mortality of 35.2%. On a
retrospective study of 2003-October 2004 at
RS Sanglah got 54
tetanus case with 47% mortality .4
Tetanus is a preventable disease.
Implementation of global tetanus
immunization has been the target of WHO
since 1974. Unfortunately, immunity against
tetanus is not lasts a lifetime and is needed
booster injection if one is experiencing
vulnerable wounds infected with tetanus.
Access poor immunization programs reported
causing a high prevalence of disease this is in
developing countries.3
Definition
Tetanus is an acute infection caused
illness exotoxins produced by Clostridium
tetani, characterized by increased general
stiffness and seizures skeletal muscle.4
PATHOPHYSIOLOGY
Tetanus caused by exotoxins
Clostridium tetani, bacteria are obligate
1
to survive in various environments extreme in
the long period due to the spores very strong.
Clostridium tetani has been isolated from soil,
road dust, human feces and animals. Bacteria
are usually insert body after contamination on
skin abrasion, minor puncture wounds, or tip
umbilicus cuts in neonates; on 20% of cases,
may not be found entry. Bacteria can also enter
through skin ulcers, abscesses, gangrene,
burns, infections teeth, ear piercing, injection
or after abdominal pelvic surgery, labor and
abortion. If this organism is on an anaerobic
environment suitable for growth spores, will
flourish breed and produce tetanospasmin
toxin and tetanolysin. Tetanospasmin is Potent
neurotoxin responsible for clinical
manifestations of tetanus, whereas tetanolysin
has little clinical effect.1-3
There are two mechanisms that can
explain the spread of toxins to the arrangement
central nerves: (1) Toxin is absorbed in
neuromuscular junction, then migrate through
the perineural tissue to the nervous system
central, (2) toxins through the lymph vessels
and blood to the central nervous system. Still
not yet clear which is more important, maybe
both are involved.4
In the first mechanism, the toxin
binds to the neuromuscular junction preferring
to spread through nerves motor, then
transinaptically to motor nerves and
autonomous ones adjacent, then transported
retrograde to the central nervous system.1,3
Tetanospasmin which is a
zincdependent endopeptidase splitting
vesicleassociated membrane protein II (VAMP
II or synaptobrevin) on a peptide bond
single. This molecule is important for release
neurotransmitters in synapses, resulting in a
breakdown this disrupts the synapse
transmission.
Toxins initially affect the pathway
of inhibition, prevent the release of glycine and
γ-amino
butyric acid (GABA). At the time of
interneuron inhibits alpha motor neurons as
well affected its impact, failure occurred
inhibiting the motor ex motor reflections
appeared uncontrolled motor neuron activity,
resulting in increased tone and muscle rigidity
of muscle spasms sudden and potentially
destructive. This matter is a characteristic of
tetanus. Facial muscles exposed early because
of the axonal path short, while the sympathetic
neurons exposed to the most recent, possibly
due to action toxins in the brainstem. In severe
tetanus, failure to inhibit autonomous activity
causing loss of autonomous control, excessive
sympathetic activity and elevated levels of
catecholamines. A neuronal bond toxins are
irreversible, recovery requires the growth of
nerve terminals new, thus lengthening the
duration this disease.
CLINICAL SYMPTOMS
The tetanus incubation period is between 3-21
days (average 7 days). In 80-90% of patients,
symptoms appear 1-2 weeks after infection.3
The time lapse since its appearance the first
symptom to spasm first called the period of
onset. Period onset or incubation period
Significantly determine prognosis. More short
(period of onset <48 hours and period
incubation <7 days) showed more weight
his illness 1 have a clinical picture with
characteristic of the triad of muscle rigidity,
muscle spasm, and autonomous instability. The
initial symptoms include muscle stiffness, first
on muscle groups with short neuronal
pathways, therefore it is visible on more than
90% cases when admitted to hospital is
trismus, stiff neck, and back pain. Involvement
facial and pharyngeal muscles cause
characteristic of risus sardonicus, sore throat,
and dysphagia. Increased muscle tone muscle
trunkal causes opistotonus.
Muscle groups adjacent to where infection is
often involved, produces sight is not
symmetrical.1,3,6,7
Spasm of the muscle appears spontaneous, also
can provoked by physical, visual, auditory, or
2
emotional. Muscle spasms give rise pain and
can cause tendon rupture, joint dislocation and
fractures. Spasm larynx may occur
immediately, resulting acute and respiratory
respiratory tract obstruction arrest. Breathing
can also be affected due to spasm involving the
muscles chest; during an elongated spasm,
severe hypoventilation and apnea may occur
life-threatening.3,6 Without facilities
mechanical ventilation, respiratory failure due
to spasm muscle is the most common cause of
death. Hypoxia usually occurs in tetanus as a
result spasm or difficulty clearing secretions
excessive bronchial and aspiration. Spasm
the heaviest muscle occurs during the week
first and second, and can take place for 3 to 4
weeks, after which rigidity still going on for a
few more weeks Severe tetanus is associated
with hyperkinesia circulation, especially when
muscle spasms do not well controlled.
Autonomic disorder usually starting a few days
after spasm and lasts 1-2 weeks. Increased tone
sympathetic usually dominant cause periods of
vasoconstriction, tachycardia and
hypertension. Autonomic storm is concerned
with elevated levels of catecholamines.
Circumstances this one after another with
episodes of hypotension, bradycardia and
sudden asistole. Other autonomic disruption
features include salivation, sweating, increased
secretions bronchi, hyperpireksia, stasis and
stomach ileus.1,3
In severe conditions various can arise
complications. The intensity of paroxysmal
spasm sometimes enough to cause rupture
spontaneous muscles and intramuscular
hematoma. Compression fracture or vertebral
subluxation can occur, usually in the
vertebrathoracalis.5 Acute kidney failure is a
recognizable tetanus complication due to
dehydration, rhabdomyolysis due to spasms,
and autonomous disorders. Complications
others include atelectasis, aspiration
pneumonia, peptic ulcer, urinary retention,
tract infections urinary, decubitus ulcer,
venous thrombosis, and thromboemboli.1
DIAGNOSIS
The diagnosis of tetanus is purely a
diagnosis clinical history of disease and
findings during examination. On inspection
Physical properties of spatula testing may be
performed by touching the posterior wall
pharynx using the tool with the tip which is
soft and sterile. The test results are positive if
involuntary jaw contraction occurs (biting
spatula) and negative results of ex reflection
gag. The American's brief report Journal of
Tropical Medicine and Hygiene states that the
spatula test has high specificity (no false-
positive results) and high sensitivity (94% of
patients were infected show positive results).
Examination blood and cerebrospinal fluid
usually normal. C. tetani culture of the wound
is very difficult (only 30% positive), and
positive culture results supports diagnosis, not
confidentiality Some circumstances that can be
removed with a careful examination is
meningitis, subarachnoid hemorrhage,
infection orofacial and temporomandibular
arthralgia which causes trismus, poisoning
strychnine, tetany hypocalcemia, hysteria,
encefalitis, phenotiazine therapy, serum
sickness, epilepsy and rabies.4
MANAGEMENT
There are three goals of tetanus management,
namely:
(1) removing the source of tetanospasmin;
(2) neutralizing unbound toxins;
(3) supportive care (suportive) up
tetanospasmin that binds to
the network has been metabolized.4,5,7-14
Disposing of Tetanospasmin Source
The wound should be thoroughly cleaned and
didebridement to reduce bacterial load and
prevent release Further toxin.1,3,5
Antibiotics are given
to eradicate the bacteria, whereas effects for
the purpose of prevention of tetanus Clinically
it is minimal. In the study in Indonesia,
metronidazole has to be the treatment of choice
in some services health. Metronidazole is
given iv with the initial dose of 15 mg / kgBB
continued dose of 30 mg / kg / day every 6
hours 7-10 days. Metronidazole effectively
reduces number of C. tetani vegetative form.
As a second line can be given penicillin
procain 50.000-100.000 U / kgBB / day for 7-
10 days, if hypersensitive to penicillin can be
given tetracycline 50 mg / kgBW / day (for
children older than 8 years). Penicillin kills
vegetative form C. tetani. To date, the
provision of penicillin G 100,000 U / kgBB /
day iv, every 6 hours during 10 days is
recommended in all cases tetanus. A study
3
states that penicillin may act as a agonist
against tetanospasmin with inhibits the release
of aminobutyric acid gama (GABA) .3-5,12
Neutralization of unrestricted toxins Antitoxin
should be given to neutralize toxins that have
not been binding. After the initial evaluation,
human tetanus immunoglobulin (HTIG)
immediately injected intramuscularly with a
total dose of 3,000- 10,000 units, divided into
three equal doses and injected in three different
places. There is no consensus of HTIG proper
dosage. Recommendation The British National
Formulary is a 5,000- 10,000 units of
intravenous. For the baby, the dose is 500 IU
intramuscular single dose.
Most doses are given infi ltration at
place around the wound; only needed once
treatment because the half-life of 25-30 day.
The sooner the treatment is given, the more
effective. HTIG contraindication is history
hypersensitivity to immunoglobulin or human
immunoglobulin component previous; severe
thrombocytopenia or other coagulation states
that can is contraindicated administration intra
muscular. If not available then used ATS with
a dose of 100,000- 200,000 units were given
50,000 intramuscular units and 50,000 units
intravenously on the day first, then 60,000
units and 40,000 each intramuscular unit on
second and third days.1,4,5 After the patient
healed, before leaving the hospital should be
given active immunization with toxoid,
someone who has recovered from
tetanus has no immunity.1,3,5
Supportive treatment
Further management consists of
supportive therapy to the effects of toxins that
have been tied up. All patients suspected
tetanus should be treated in ICU agar can be
observed continuously. For minimizing the risk
of paroxysmal spasm which precipitated
extrinsic stimuli, the patient should be treated
in a dark room and calm.3-5,12
Patient is positioned to prevent
aspiration pneumonia. Intravenous fluids
should be given, electrolyte examination as
well an important blood gas analysis as a guide
therapy.5
Handling of the airway is priority. Muscle
spasms, laryngospasm, aspiration, or a large
dose of sedatives may interfere with
respiration. Bronchial secretion excessive
action requires suctioning often.1
Tracheostomy is addressed to keep the airway
especially if there is opistotonus and muscle
involvement back, chest, or respiratory
distress.6 Death from sudden spasms of the
larynx, paralysis of the diaphragm, and muscle
contraction Inadequate respiration often occurs
if not available ventilator access.3
Muscle spasms and rigidity are
overcome effective with sedation. Patients get
more slightly affected by peripheral stimuli
and less likely to experience muscle spasms.5
Diazepam is effectively overcome spasm and
hypertonicity without suppressing cortical
center. Recommended dose of diazepam is 0.1-
0.3 mg / kgBW / times at 2-4 hour intervals as
symptomatic clinical, recommended dosage for
age <2 years is 8 mg / kgBB / day orally in
doses of 2-3 mg every 3 hours. Spasm should
be stopped immediately with diazepam 5 mg
per rectal for weight <10 kg and 10 mg per
rectal for children with weight ≥10 kg, or
intravenous diazepam for children 0.3 mg /
kgBB / times. After spasm stop, giving
diazepam continued with maintenance dose
according to circumstances clinical. Another
alternative, for babies (tetanus neonatorum) is
given an onset dose of 0.1-0.2mg / kgBB iv to
eliminate spasm acute, followed by constant
drip infusion 15-40 mg / kgBB / day. After 5-7
days dose of diazepam gradually lowered 5-10
mg / day and can be given through an
orogastric tube. Dose The maximum is 40 mg /
kg / day. Sign Clinically improved when no
spasm is present spontaneous, body still stiff,
awareness improved (not comatose), not found
respiratory disorders.1,10,13,14
Additional effects sedation can be
obtained from barbiturate in particular
phenobarbital and phenotiazine like
chlorpromazine, its use can b benefit patients
with disorders autonom.1,3
Phenobarbital administered with
doses of 120-200 mg intravenously, and
diazepam can be added apart with the dose
up to 120 mg / day. Chlorpromazine is given
every 4-8 hours with dose of 4-12 mg for
infants up to 50-150 mg for adult.5,10
Morphine can have the same effect and is
usually used in addition benzodiazepine
sedation.
If the spasm is not adequately
controlled with benzodiazepine, can be
selected paralysis muscle nondepolarisasi with
4
intermittent positive-pressure ventilation
(IPPV). There is no comparison data on drugs
muscle paralysis in tetanus, recommendations
obtained from case reports. Pancuronium
should be avoided because of
sympathomimetic side effects.1 Atracurium
may be an option. Vecuronium has also been
used because stable in the heart.3,10,14
Tetanus patient weight often
requires IPPV over 2 to 3 weeks until the
spasme subsides. Incidence of ventilator-
associated pneumonia in patients of tetanus of
52.6% .1 Nosocomial infections are common
due to the long course of tetanus disease and
still an important cause Dead. Prevention of
respiratory complications including careful
oral care, fi therotherapy chest and suction
trachea.
Sedation Adequate during
preventive invasive procedures provocation of
spasm or instability autonom.3,6,7,10
Autonomous instability occurs several days
following the onset of common spasms and
fatality the rate is 11-28%. Manifestations of
hypertensionlabile, tachycardia, and fever.
Various cardiovascular disorders such as
dysrhythmias and myocardial infarction and
circulatory collapse often leads to death.6,7,11
Signs Sympathetic overactivity is
tachycardia uktuatif, hypertension that is
sometimes followed hypotension, pale and
frequent sweating seen several days after
spasm onset muscle.5,10 Sudden cardiac arrest is
common occurs and is said to be precipitated
by a combination of catecholamine levels high
and direct work of tetanus toxin on
myocardium. The sympathetic activity that
elongate may end with hypotension and
bradycardia. Excessive parasympathetic
activity can cause sinus arrest, it is said
because of direct damage to the nucleus vagus
by tetanus toxin.3,6,7
Instability autonomic difficult to
treat. Blood pressure fluctuations needing
drugs with time short bill. Conventional
therapy consists from deep sedation as first-
line therapy, using large doses of
benzodiazepines, morphine, and / or
chlorpromazine.1 This, intravenous magnesium
sulphate is tried to control spasm and
dysfunction autonomous; dose loading 5 g (or
75 mg / kg) IV is continued from 1 to 3 g / hr
until controlled spasm has been used for get
serum concentration 2 to 4 mmol / L. To avoid
overdose,
monitored refl ek patella.7,13
Beta blockers can be causing severe
hypotension. Episode hypotension that does
not improve with the addition of intravascular
volume requires inotropic.1 Atropine high
doses, more than 100 mg / h, has been
recommended on state of the bradycardia.3 No
regimen therapies that are believed to be
universally effective for autonomous
instability.11
Tetanus is clinically and biochemically proven
causing excessive sympathetic activity and
protein catabolism so that maintenance
nutrition is necessary. Nutrition bad and
weight loss occurs fast due to dysphagia,
malfunction gastrointestinal and increased
metabolism,
lower body resistance thus exacerbating
prognosis. 3.13
Nutrition parenteral total contains
glucose hypertonis and insulin in sufficient
quantities to control blood sugar levels, can
suppress protein catabolism. Formula Amino
acids greatly help limit protein catabolism.5, 12
On the first day need intravenous
administration of fluids as well as giving
medicine, and if until the 3rd day infusion can
not be removed should be considered granting
nutrition parenterally. After spasm
ease can be installed sonde gastric for food and
medicine with special attention to aspiration
risk.5,12
Pulmonary embolus is also one
cause of death, so it is widely used
anticoagulants on a regular basis such as
subcutaneous heparin; the risk of
thromboembolism and bleeding should be
considered. Passive movement must continue
to be provided if used
muscle paralysis.5,12
OUTSIDE
There are several tetanus assessment systems
The scale proposed by Ablett is that most
widely used (Table 1).
In addition to Ablett scoring, there is
a scoring system
to assess the prognosis of tetanus-like
Phillips score and Dakar score. Both systems
This scoring enters the period criterion
incubation and period of onset, as well
neurologic and cardiac manifestations. Phillips
5
The score also includes immunization status
patient. Phillips score <9, mild severity; 9-18,
moderate severity; and> 18, heavy severity.
Dakar score 0-1, mild severity with 10%
mortality; 2-3, medium severity with 10-20%
mortality; 4, heavy severity with 20-40%
mortality; 5-6, severity is very heavy with
mortality> 50% .10
The results of tetanus depend on the
severity of the disease and available treatment
facilities. If untreated, the mortality is over
60% and higher in neonates. In good facilities,
mortality rates
13% to 25%. Just a little researc long lengths
in successful patients congratulations. Portable
tetanus recovery
slow but often cured perfectly, some patients
have an abnormality persistent
electroencephalography and balance disorder,
Speech, and memory.1,2
Table 1 Severity of Tetanus Based on
Ablett3,6-9 Classification
Grade 1 (light)
Light trismus, total spasticity, nothing
which endangers respiration, no spasm,
no dysphagia
Grade 2 (medium)
Medium trismus, rigidity, short spasms,
dysphagia mild, moderate respiratory
involvement, frequency breathing> 30
Grade 3 (heavy)
Heavy trismus, total rigidity, spasm
elongated, severe dysphagia, apneu attack,
pulse pulse> 120, respiratory rate> 40
Grade 4 (very heavy)
Grade 3 with heavy autonomous instability
 Tabel 3 Dakar score10
Tabel 2 Phillips score4,10
Dakar scorekar score
Factor Score Factor
Incubation period prognosis Score 0
Score 1
• <48 hours 5
• 2-5 days 4 ≥7 days or
Incubation
• 5-10 days 3 period
<7 days unknown
• 10-14 days 2
•> 14 days 1 Period of ≥2 days
<2 days
onset
Location of infection Umbilikus,
• Internal organs and umbilicus 5 burns, uterus,
• Head, neck, and body 4 open Apart from
• Proximal periphery 3 Entrance
fractures, those already
• Distal peripheral 2 surgical mentioned,
• Not known 1 wound, or unknown
intramuscular
Status of protection injection
• There is no
• There may be or immunization Spasme Spasme
Nothing
10
in the mother for the patients
8 > 38,4˚C
neonates Fever <38,4˚C
42
• Protected> 10 years
0
• Protected <10 years Adult> 120 Adult <120
• Complete protection times / times /
minute minute
Takikardi
Factors of complications Neonates> Neonates
• Injury or disease 150 times / <150 times /
life threatening min min
• Severe injury or illness
10
which is not immediately
8
threatening
4
lives
2
• Ciedera or disease
0
not life threatening
• minor injury or illness
• ASA grade I