Case Report Tetanus Pediatric

1
CASE REPORT
PEDIATRIC TETANUS
Presenters
Day/ Date
Supervisor
: Fadillah Akbar S
(080100063)
Endah Galih Harina (080100086)
: Tuesday/ October 2 2012
: Prof. dr. Hj. Bidasari Lubis, Sp.A(K)
CHAPTER 1
INTRODUCTION
1.1.
Background
Tetanus is an acute, often fatal, disease caused by an exotoxin produced by
the bacterium Clostridium tetani. It is characterized by generalized rigidity and

convulsive spasms of skeletal muscles. The muscle stiffness usually involves the
jaw (lockjaw) and neck and then becomes generalized.
Although records from antiquity (5th century BCE) contain clinical
descriptions of tetanus, it was Carle and Rattone in 1884 who first produced
tetanus in animals by injecting them with pus from a fatal human tetanus case.
During the same year, Nicolaier produced tetanus in animals by injecting them
with samples of soil. In 1889, Kitasato isolated the organism from a human
victim, showed that it produced disease when injected into animals, and reported
that the toxin could be neutralized by specific antibodies. In 1897, Nocard
demonstrated the protective effect of passively transferred antitoxin, and passive
immunization in humans was used for treatment and prophylaxis during World
War I. A method for inactivating tetanus toxin with formaldehyde was developed
by Ramon in the early 1920's which led to the development of tetanus toxoid by
Descombey in 1924. It was first widely used during World War II.
C. tetani is a slender, gram-positive, anaerobic rod that may develop a
terminal spore, giving it a drumstick appearance. The organism is sensitive to heat
and cannot survive in the presence of oxygen. The spores, in contrast, are very
resistant to heat and the usual antiseptics. They can survive autoclaving at 249.8F
(121C) for 1015 minutes. The spores are also relatively resistant to phenol and
other chemical agents. The spores are widely distributed in soil and in the intestines and feces of horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens.
Manure-treated soil may contain large numbers of spores. In agricultural areas, a
significant number of human adults may harbor the organism. The spores can also
be found on skin surfaces and in contaminated heroin. C. tetani produces two
exotoxins, tetanolysin and tetanospasmin. The function of tetanolysin is not
known with certainty. Tetanospasmin is a neurotoxin and causes the clinical
manifestations of tetanus. On the basis of weight, tetanospasmin is one of the
most potent toxins known. The estimated minimum human lethal dose is 2.5
nanograms per kilogram of body weight, or 175 nanograms for a 70-kg human.
1.2.
Objective
This paper is done in order to complete the task in following the doctor's
professional education program in the department of pediatrics. In addition,

providing knowledge to the author and readers about empyema thoracic
CHAPTER 2
LITERATURE REVIEW
PEDIATRIC TETANUS
2.1.
Definition
Tetanus is an intoxication by increased muscle tone dan spams caused by
the release of the neurotoxin tetanospasmin by Clostridium tetani following

inoculation into a human host. Tetanus occurs in several clinical forms, including
generalzed, cephalic, localized, and neonatal disease. 1
Tetanus is disease with a spasm without major accompanied by impaired
consciousness. These symptoms caused directly, instead of germs but as impact
exotoxin (tetanospasmin) produced by germs at a synapse ganglion, the spinal
cord connection neuro muskular and nerve autonom. 2
Tetanus is an acute, spastic paralytic illness caused by tetanospasmin, a
neurotoxin produced by Clostridium tetani 4
2.2.
Epidemiology and Risk Factor

Although C. tetani is located everywhere, the disease is encountered
largely in underdeveloped, overcrowded, and economically disadvantaged

countries. Because immunization is totally eff ective in preventing tetanus, it is
most frequently noted in countries or in ethnic groups in which effective
immunization is less likely to be achieved. In the United States, tetanus is
encountered more frequently in blacks in the rural South, where a combination of
more extensive exposure to spores and incomplete immunity are predisposing
factors. 3
Tetanus is an entirely preventable disease; the first vaccine was produced
in 1924. Routine vaccination began in the UK in 1961. It is given as a combined
vaccine along with diphtheria and pertussis (DPT). Unfortunately, immunity to
tetanus may not be life-long and booster injections may be required after
individuals sustain tetanus-prone wounds. Tetanus immunization guidelines are
available in the British National Formulary. Poor access to a programme of
immunization accounts for the high prevalence of the disease in the developing
world. Implementation of global tetanus immunization has been a target of the
World Health Organization since 1974. Recently there has been a cluster of
tetanus cases amongst injecting drug-users in the UK. Twenty-four cases were
reported between 2003 and 2004. The majority of these had no record of (or, at
best, incomplete) immunization. This outbreak is thought to be a result of a batch
of contaminated heroin.2 I.M or s.c. drug-use is a particularly high risk activity
for developing tetanus. 5
A marked decrease in mortality from tetanus occurred from the early
1900s to the late 1940s. In the late 1940s, tetanus toxoid was introduced into
routine childhood immunization and tetanus became nationally notifiable. At that
time, 500600 cases (approximately 0.4 cases per 100,000 population) were
reported per year. 6
After the 1940s, reported tetanus incidence rates declined steadily. Since
the mid-1970s, 50100 cases (~0.05 cases per 100,000) have been reported
annually. From 2000 through 2007 an average of 31 cases were reported per year.
The death-to-case ratio has declined from 30% to approximately 10% in recent
years. An all-time low of 18 cases (0.01 cases per 100,000) was reported in 2009.
6
During 2001 through 2008, the last years for which data have been
compiled, a total of 233 tetanus cases was reported, an average of 29 cases per
year. Among the 197 caes with known outcomes the case-fatality rate was 13%.
Age of onset was reported for all 233 cases, of which, 49% were among persons
50 years of age or older. The median age was 49 years (range 5-94 years). A total
of 138 (59%) were male. Incidence was similar by race. The incidence among
Hispanics was almost twice that among non-Hispanics. However, when
intravenous drug users (IDUs) were excluded the incidence was almost the same
among Hispanics compared with non-Hispanics. 6
Almost all reported cases of tetanus are in persons who have either never
been vaccinated, or who completed a primary series but have not had a booster in
the preceding 10 years. Heroin users, particularly persons who inject themselves
subcutaneously, appear to be at high risk for tetanus. Quinine is used to dilute
heroin and may support the growth of C. tetani. Neonatal tetanus is rare in the
United States, with only two cases reported since 1989. Neither of the infants'
mothers had ever received tetanus toxoid.6
Tetanus toxoid (TT) vaccination status was reported for 92 (40%) of the
233 patients. A total of 37 patients (41%) received no TT doses, 26 (28%)
received 1 dose, five (5%) received 3 doses, and 24 (26%) received 4 or more
doses. Seven (24%) of 29 patients with 3 or more doses of TT had received their
last dose within 10 years, 18 (62%) from 10 to 54 years previously, and four
(14%) reported an unknown interval since their last dose. 6
Among 195 patients whose medical history was known, 30 (15%.) were
reported to have diabetes. Twenty-seven (15%) of 176 patients whose status was
known were IDUs, of whom 16 (59%) were Hispanic. An acute wound preceded
disease onset in 167 (72%) patients. Of those patient wounds, 132 (79%) were
punctures, or contaminated, infected, or devitalized wounds considered tetanusprone and eligible to receive tetanus immune globulin (TIG). Case reports for 51
(84%) of those who sought care were sufficiently complete to evaluate
prophylaxis received; 49 (96%) did not receive appropriate TT prophylaxis or TT
plus TIG as is currently recommended. Among all 233 patients, 31 (13%) reported
a chronic wound or infection before disease onset, including diabetic ulcers and
dental abscesses. Twenty-two (9%) reported no wounds or infections; of these, 14
were IDUs. 6
2.3.
Etiology
The tetanus bacillus is a long, thin (2 to 5 m 3 to 8 m), motile, gram-
positive anaerobic rod. Older cultures of these organisms and smears from
wounds frequently stain as gram-negative microbes, and this result may be
confusing to the uninitiated. These organisms may develop a terminal spore that
does not take the Gram stain and gives the bacterium a drumstick appearance. The
spores are very resistant to heat and the usual antiseptics, and they may persist in
tissues for many months in a viable, although dormant, state. Under anaerobic
conditions the organisms are easily isolated on blood agar or in cooked meat
broth. The organism does not ferment carbohydrates, does not usually liquefy
gelatin, and produces little change in litmus milk. The bacilli are widely
distributed in soil; street dust; and the feces of some horses, sheep, cattle, dogs,
cats, rats, guinea pigs, and chickens. Consequently, manure-containing soil may
be highly infectious. In agricultural areas a significant number of normal human
adults may harbor the organisms, and agricultural workers have a higher incidence
of infection. The spores have also been found in contaminated heroin.Tetanus
bacilli produce a potent neurotoxin that is one of the most toxic substances
known; the mouse LD50 of highly purified preparations is between 0.1 and 1
ng/kg (Schiavo et al., 1995 ). Tetanus neurotoxin derives its potency by virtue of
its absolute specificity for neuronal cells and its target intracellular catalytic
activity. 10
2.4.
Etiopathogenesis
Tetanus result from infection with Clostridium tetani. Clostridium tetani is
an obligate of anaerobic gram positive bacteria, mobile, nonencapsulated, and

forms spores, which are resistant to heat, desiccation, and disinfectants. The
spores are found in soil, house dust, animal intestines, and human feces. They
need tissue with the proper anaerobic conditions to germinate; the ideal media are
wounds with tissue necrosis. And the bacillus are found in or on soil, manure,
dust, clothing, skin, and 10-25% of human GI tracts.7
Most cases of tetanus are caused by direct contamination of wounds with
the clostridial spores (Tolan, 2012). But these spores can persist in normal tissue
for months to years.4 Clostridium tetani is not a tissue-invasive organism and
cannot evoke an inflammatory reaction, unless co-infection with other organisms
develops, so it has a benign appearance. 2 If the conditions become anaerobic
caused of low oxidationreduction potential, such as dead or devitalized tissue, a
foreign body, or active infection,the spores in the tissue germinate and elaborate
toxins in low oxidation-reduction potential (Eh) of an infected injury site.8
2.5.
Pathophysiology
There are two kind of toxins produced by C. tetani, they are tetanospasmin
and tetanolysin. Tetanolysin is not believed to be of any significance in the clinical

course of tetanus. Tetanospasmin is a neurotoxin and causes the clinical
manifestation of tetanus. Tetanospasmin that is released by the maturing bacilli is
distributed via the lymphatic and vascular circulation to the end plates of all
nerves.12
A plasmid carries the toxin gene; the toxin is released with vegetative
bacterial cell death and subsequent lysis. Tetanus toxin (tetanospasmin) are 150kd simple proteins consisting of a heavy (100 kd) and a light (50 kd) chain joined
by a single disulfide bond. Tetanus toxin binds at the neuromuscular junction and
enters the motor nerve by endocytosis, after which it undergoes retrograde axonal
transport to the cytoplasm of the alpha-motoneuron. In the sciatic nerve, the
transport rate was found to be 3.4mm/hr. The toxin exits the motoneuron in the
spinal cord and next enters adjacent spinal inhibitory interneurons, where it
prevents release of the neurotransmitter -aminobutyric acid (GABA) by cleaving
proteins crucial for the proper functioning of the synaptic vesicle release
apparatus. The phenomenal potency of tetanus is enzymatic in nature. The light
chain of tetanus is a zinc-containing endoprotease (zinc metalloprotease) whose
substrate is synaptobrevin, a constituent protein of the docking complex that
enables the synaptic vesicle to fuse with the terminal cell membrane. 5 This
diminished inhibition result in an increase in the resting firing rate of the motor
neuron, which is responsible for the observed muscle rigidity.1
The lessened activity of reflexes limits the polysynaptic spread of impulses
(a glycinergic activity). Agonists and antagonists may be recruited rather than
inhibited, with consequent production of spasms. Loss of inhibition may also
affect preganglionic sympathetic neurons in the lateral gray matter of the spinal
cord and produce sympathetic hyperactivity and high levels of circulating
catecholamines. Finally, tetanospasmin can block neurotransmitter release at the
neuromuscular junction, causing weakness and paralysis. The autonomic nervous
system is also rendered unstable in tetanus. 1
Localized tetanus develops when only the nerves supplying the affected
muscle are involved. Generalized tetanus develops when the toxin released at the
wound spreads through the lymphatics and blood to multiple nerve terminals. The
blood-brain barrier prevents direct entry of toxin to the CNS. 1
2.6.
Diagnosis
The diagnosis of tetanus may be established clinically.

History
Most cases occur in patients with a history of only partial immunization.
Persons who inject drugs also constitute a high-risk group. Symptoms usually
begin 8 days (2-14 days) after the infection, but it may be as long as months after
the injury, then the onset may range from 3 days to 3 weeks (Hinfey,2011).
Tetanus may be either generalized, which is more common, or localized (Nelson).
Patients may report a sore throat with dysphagia (early sign). The initial
manifestation may be local tetanus, in which the rigidity affects only 1 limb or
area of the body where the clostridium-containing wound is located.7
Generalized Tetanus
The extent of the trauma in generalized tetanus varies from trivial injury to
contaminated crush injury. The incubation period is 7-21 days, largely depending
on the distance of the injury site from the CNS. Trismus is the presenting
symptom in 75% of cases; a dentist or an oral surgeon often initially sees the
patient. Other early features include irritability, restlessness, diaphoresis, and
dysphagia with hydrophobia, drooling, and spasm of the back muscles. These
early manifestations reflect involvement of bulbar and paraspinal muscles,
possibly because they are innervated by the shortest axons. 1 Muscle rigidity
spreads in a descending pattern from the jaw and facial muscles over the next 2448 hours to the extensor muscles of the limbs.12
The simptom called sardonic smile of tetanus (risus sardonicus) results
from intractable spasm of facial and buccal muscles. When the paralysis extends
to abdominal, lumbar, hip, and thigh muscles, the patient may assume an arched
posture of extreme hyperextension of the body, opisthotonos, with the head and
the heels bent backward and the body bowed forward with only the back of the
head and the heels touching the supporting surface. Opisthotonos is an
equilibrium position that results from unrelenting total contraction of opposing
muscles, all of which display the typical boardlike rigidity of tetanus.8
Because tetanus toxin does not affect sensory nerves or cortical function,
the patient unfortunately remains conscious, in extreme pain, and in fearful
anticipation of the next tetanic seizure. These seizures are characterized by
sudden, severe tonic contractions of the muscles, with fist clenching, flexion, and
adduction of the arms and hyperextension of the legs. Without treatment, the
seizures range from a few seconds to a few minutes in length with intervening
respite periods, but as the illness progresses, the spasms become sustained and
exhausting. The smallest disturbance by sight, sound, or touch may trigger a
tetanic spasm. The tetanic paralysis usually becomes more severe in the 1st wk
after onset, stabilizes in the 2nd wk, and ameliorates gradually over the ensuing 14 wk (Nelson). The condition may progress for 2 weeks despite antitoxin therapy
because of the time needed for intra-axonal antitoxin transport.1
Localized Tetanus
Localized tetanus causes painful spasms of muscle at the site of
contaminated wound where spore inoculate.7 This is an unusual form of tetanus
and the prognosis for survival is excellent. 1 But localized tetanus may precede
generalized tetanus. Cephalic tetanus is a rare form of localized tetanus involving
the bulbar musculature that occurs with wounds or foreign bodies in the head,
nostrils, or face. It also occurs in association with chronic otitis media. Cephalic
tetanus is characterized by retracted eyelids, deviated gaze, trismus, risus
sardonicus, and spastic paralysis of tongue and pharyngeal musculature. 8 The
prognosis for survival is usually poor.1
Tetanus Neonatorum
Neonatal tetanus (tetanus neonatorum), the infantile form of generalized
tetanus, typically manifests within 3-12 days of birth as progressive difficulty in
feeding (i.e., sucking and swallowing), with associated hunger and crying. 8 The
10
usual cause is the use of contaminated materials to sever or dress the umbilical
cord in newborns of unimmunized mothers. The usual incubation period after
birth is 3-10 days, which is why it is sometimes referred to as the disease of the
seventh day. Paralysis or diminished movement, stiffness to the touch, and
spasms, with or without opisthotonos, characterize the disease. The umbilical
stump may hold remnants of dirt, dung, clotted blood, or serum, or it may appear
relatively benign (Nelson). The mortality rate exceeds 70%.1
Physical diagnostic
Generilized tetanus
In the inspection, sardonic smile (risus sardonicus) in the face and
persistent spasm of the back musculature (opisthotonus) are found. Waves of
opisthotonus are highly characteristic of the disease. With progression, the
extremities become involved in episodes of painful flexion and adduction of the
arms, clenched fists, and extension of the legs. Noise or tactile stimuli may
precipitate spasms and generalized convulsions. Involvement of the autonomic
nervous system may result in severe arrhythmias, oscillation of the blood
pressure, profound diaphoresis, hyperthermia, rhabdomyolysis, laryngeal spasm,
and urinary retention. In most cases, the patient remains lucid. Other symptoms
include elevated temperature, sweating, elevated blood pressure, and episodic
rapid heart rate.12 Fever, occasionally with a temperature as high as 40C, is
common because of the substantial metabolic energy consumed by spastic
muscles. Laryngeal and respiratory muscle spasm can lead to airway obstruction
and asphyxiation. Dysuria and urinary retention result from bladder sphincter
spasm; forced defecation may occur.8
Tetanus Neonatorum
This is generalized tetanus that results from infection of a neonate. It
primarily occurs in underdeveloped countries and accounts for up to one half of
11
all neonatal deaths. Physical examination findings are similar to generalized

tetanus findings. The newborn usually exhibits irritability, poor feeding, rigidity,
facial grimacing, and severe spasms with touch. 8
Localized Tetanus
In mild cases, patients may have weakness of the involved extremity,
presumably due to partial immunity. In more severe cases, intense painful spasms
occur and usually progress to generalized tetanus. In cephalic tetanus, cranial
nerve findings and rapid progression are typical. This form may remain localized
or progress to generalized tetanus.1
Laboratory test
Wounds should be cultured in suspected cases. However, C tetani can be
cultured from wounds of patients without tetanus and frequently cannot be
cultured from wounds of patients with tetanus.The leukocyte count may be high.
Cerebrospinal fluid examination yields normal results.1
Serum antitoxin levels of 0.01 or higher are considered protective and
make tetanus unlikely, although rarely cases have been reported despite the
presence of protective antitoxin levels. Serum muscle enzyme levels (eg, creatine
kinase, aldolase) may be elevated. 1
2.7.
Differential Diagnosis
Fully developed, generalized tetanus cannot be mistaken for any other
disease. However, trismus may result from parapharyngeal, retropharyngeal, or

dental abscesses, or rarely, from acute encephalitis involving the brainstem. Either
rabies or tetanus may follow an animal bite, and rabies may present as trismus
with seizures. However, rabies may be distinguished from tetanus by its
hydrophobia, marked dysphagia, predominantly clonic seizures, and CSF
pleocytosis. Although strychnine poisoning may result in tonic muscle spasms and
generalized seizure activity, it seldom produces trismus, and unlike tetanus,
general relaxation usually occurs between spasms. Hypocalcemia may produce
12
tetany, characterized by laryngeal and carpopedal spasms, but trismus is absent.

Occasionally, epileptic seizures, narcotic withdrawal, or other drug reactions may
suggest tetanus.5 And, the other differential diagnosis are meningitis which found
meningens signs and bacteria or different CSF composition.1
2.8.
Managament
Management of tetanus requires eradication of C. tetani and the wound
environment conducive to its anaerobic multiplication, neutralization of all

accessible tetanus toxin, control of seizures and respiration, palliation and
provision of meticulous supportive care, and, finally, prevention of recurrences. 8
All patients should be admitted to a medical or neurological intensive care unit
where they can be monitored and observed continuously. Some hospitals in which
tetanus is frequently encountered have specially constructed, quiet, dark rooms to
minimize extrinsic stimuli that might trigger paroxysmal spasms. Patients must be
allowed to rest quietly to limit peripheral stimuli, and they must be positioned
carefully to prevent aspiration pneumonia. Intravenous fluids should be instituted,
and electrolytes and blood gases are essential to guide therapy.3
Surgical wound excision and debridement is often needed to remove the
foreign body or devitalized tissue that created anaerobic growth conditions.
Surgery should be done promptly, after the administration of human tetanus
immunoglobulin (TIG) and antibiotics. Excision of the umbilical stump in
neonatal tetanus is no longer recommended.8
Once tetanus toxin has begun its axonal ascent to the spinal cord, it cannot
be neutralized by TIG. Accordingly, TIG is given as soon as possible to neutralize
toxin that diffuses from the wound into the circulation before the toxin can bind at
distant muscle groups. An optimal dose of TIG has not been determined. A single
intramuscular injection of 500 U of TIG is sufficient to neutralize systemic tetanus
toxin, but total doses as high as 3,000-6,000 U are also recommended. Infiltration
of TIG into the wound is now considered unnecessary. If TIG is unavailable, use
of human intravenous immunoglobulin (IVIG), which contains 4-90 U/mL of
TIG, or of equine- or bovine-derived tetanus antitoxin (TAT), may be necessary.
13
However, the optimal dosage of IVIG is not known, and it is not approved for this
indication. The usual dose of TAT is 50,000-100,000 U, with half given
intramuscularly and half intravenously, but as little as 10,000 U may be sufficient.
TAT is not available in the United States. Approximately 15% of patients given
the usual dose of TAT experience serum sickness. When using TAT, it is essential
to check for possible sensitivity to horse serum and desensitization may be
needed. The human-derived immunoglobulins are much preferred because of their
longer half-life (30 days) and the virtual absence of allergic and serum sickness
adverse effects. Intrathecal TIG, given to neutralize tetanus toxin in the spinal
cord, is not effective.8
Penicillin is the standard therapy for tetanus in most parts of the world,
although antibiotics for C.tetani probably play a relatively minor role in the
specific treatment of this disease. Recommended dose is 100,000200,000 IU/day
intramuscularly or intravenously for 710 days. In 1945, it was first noted that
intravenous administration of penicillin could produce convulsions. The animal
models had myoclonic convulsions caused penicillin when applied directly to the
cortex. Penicillin became the standard model for producing experimental focal
epilepsy.3
Metronidazole has been considered the first line of therapy and is a safe
alternative to penicillin. Rectal administration of metronidazole is rapidly
bioavailable and produces fewer spasms than repeated intravenous or
intramuscular injections. Dose is 400 mg rectally or 500 mg intravenously every 6
hours for 710 days.3
All patients with generalized tetanus need muscle relaxants. Diazepam
provides both relaxation and seizure control; the initial dose of 0.1-0.2/kg q 3-6 hr
given intravenously is then titrated to control the tetanic spasms, after which it is
sustained for 2-6 wk before its tapered withdrawal. Magnesium sulfate, other
benzodiazepines (e.g., midazolam), chlorpromazine, dantrolene, and baclofen are
also used. Intrathecal baclofen produces such complete muscle relaxation that
apnea often ensues; like most other agents listed, baclofen should be used only in
an intensive care unit setting. The best survival rates in generalized tetanus are
14
achieved with neuromuscular blocking agents such as vecuronium and

pancuronium, which produce a general flaccid paralysis that is then managed by
mechanical ventilation. Autonomic instability is regulated with standard - and (or both) blocking agents; morphine has also proved useful.8
2.9.
Prevention
Because there is essentially no natural immunity to tetanus toxin, the only
effective way to control tetanus is by prophylactic immunization. Thus, universal

primary immunization with subsequent maintenance of adequate antitoxin levels
by means of appropriately timed boosters is necessary to protect all age groups.3
Table 1 Clinical guideline for tetanus prophylaxis10
History of
Full TT
Course
or
TT Booster
No or
unknown
Full TT course
< 5 years
Full TT course
5 10 years
Full TT course
> 10 years
Simple Wounds
(non-Tetanus prone)
Complicated wounds
TT
HTIG
TT
HTIG
Full course
No
Full Course
Consider
No
No
No
No
No
No
Booster
No
Booster
No
Booster
Consider
Human Tetanus Immune Globulin (HTIG) should be reserved for

protecting non-immunised patients or patients having existing immune deficient
conditions with wounds that are considered to be Tetanus-prone. Advice from
senior medical staff should be sought when in doubt. HTIG is safe and indicated
for patients with a contraindication to TT (such as anaphylaxis) and have a
Tetanus-prone wound.11
Table 2 Tetanus prone wounds and Non-tetanus prone wounds11
Clinical Features
Tetanus prone wounds
Age of wound
> 6 hours
Non-tetanus prone
wounds
< 6 hours
15
Configuration
Depth
Mechanism of injury
Signs of infection
Devitalized tissue
Contaminants
Denervated and/or
ischemic tissue
2.10.
Stellate wound, avulsion

> 1 cm
Missile, crush, burn,
frostbite
Present
Present
Present
Present
Linear wound, abrasion

< 1 cm
Sharp surface
Absent
Absent
Absent
Absent
Complications
The seizures and the severe, sustained rigid paralysis of tetanus predispose
the patient to many complications. Aspiration of secretions and pneumonia may

have begun before the first medical attention was received. Maintaining airway
patency often mandates endotracheal intubation and mechanical ventilation with
their attendant hazards, including pneumothorax and mediastinal emphysema. The
seizures may result in lacerations of the mouth or tongue, in intramuscular
hematomas or rhabdomyolysis with myoglobinuria and renal failure, or in long
bone or spinal fractures. Venous thrombosis, pulmonary embolism, gastric
ulceration with or without hemorrhage, paralytic ileus, and decubitus ulceration
are constant hazards. Excessive use of muscle relaxants, an integral part of care,
may produce iatrogenic apnea. Cardiac arrhythmias, including asystole, unstable
blood pressure, and labile temperature regulation reflect disordered autonomic
nervous system control that may be aggravated by inattention to maintenance of
intravascular volume needs.8
2.11.Prognosis
The most important factor influencing outcome is the quality of supportive
care. Mortality is highest in the very young and the very old. A favorable
prognosis is associated with a long incubation period, with the absence of fever,
and with localized disease. An unfavorable prognosis is associated with a week or
less between the injury and the onset of trismus and with 3 days or less between
trismus and the onset of generalized tetanic spasms. Sequelae of hypoxic brain
injury, especially in infants, include cerebral palsy, diminished mental abilities,
16
and behavioral difficulties. Most fatalities occur within the 1st wk of illness.
Reported case fatality rates for generalized tetanus range between 5% and 35%
and for neonatal tetanus extend from <10% with intensive care treatment to >75%
without it. Cephalic tetanus has an especially poor prognosis because of breathing
and feeding difficulties.
CHAPTER III
CASE REPORT
Name
: Gilang Ramadhan
Age
: 3 tahun
Sex
: Male
Address
: Jl. L Sujono G Palapa I LK VIII Bandar Selamat Medan
Date of Admission
: 1 September 2012
Major Complaint
: difficulty in opening the mouth
17
History
: Patient has been experiencing this condition for the past 5
days, rigidity of abdominal muscle is found to be experiencing for past 5 days,
rigidity of limbs muscle is found to be experiencing for past 5 days. Spasm after
stimulation is found to be experiencing for past 5 days. Cough and shortness of
breath is found to be experiencing for past 5 days. Fever is not found. Generalized
spasticity is found, freq 1x, it is experiencing for past 1 day. History of tooth
carries is found. History of wound on right sole of foot is found but patient
doesnt know when and what caused.
History of birth
History of immunization
History of nutrition
History of medications
: patient is single son in family

: not complete
: 0-6 months : breast milk
:-
Physical examination
Presence Status : Sensorium: compos mentis. Temperature: 36,8C.
Anemic (-), dyspnea (-), cyanotic (-), edema (-), icteric (-).
Body weight (BW): 12 kg. Body length (BL): 65 cm
CDC: BW/Age = 95.8%, BL/Age = 98.5%, BW/BL = 97.5%
Localized status :
Head
: Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-). Ear: within normal limit. Nose:
within normal limit. Mouth: trismus (+) 0.5 cm. Face: risus
Abdomen
sardonicus (+).
: Lymph node enlargement (-).
: symmetries fusiform, retraction (-)
HR: 112 bpm, regular, murmur (-)
RR : 22 x/minute, regular, ronkhi (-/-)
: Peristaltic (+), muscular rigidity (+), liver and spleen not
Extremities
palpable.
: Pulse = 112 bpm, regular, adequate pressure/volume, warm
Neck
Thorax
axilla, capillary refill time (CRT) < 3, clubbing finger (-),

BCG scar (-) right arm.
Genitalia
: Male, within normal limit and anus (+).
Laboratory Result: September 1st 2012
Test
Complete
Results
Normal
Value
Unit
18
Blood Count
Hemoglobin
(Hb)
Erytrocyte
(RBC)
Leukocyte
(WBC)
Hematocrite
Trombocyte
(PLT)
MCV
MCH
MCHC
RDW
MPV
PCT
PDW
Neutrofil
Limfosit
Monosit
Eosinophil
Basophil
Neutrophil
absolute
Limfosit
absolute
Monosit
absolute
Eosinophil
absolute
Basophil
absolute
Parameters
Faal Hemostasis
PT + INR
Protombin Time
Control
Pasient
10.70
11.3
14.1
g%
4.82
106/mm3
16.31
4.40
4.48
4.5 13,5
33.30
584
37 41
150 450
%
10 /mm3
69.20
22.20
32.10
17.40
81 - 95
25 29
29 31
11.6
14.8
7.0 10.2
fL
pg
g%
%
9.50
8.30
8.6
84.30
12.80
2.80
0.00
0.100
13.75
103/mm3
37 80
20 40
28
16
01
2,4 7,3
fL
%
fL
%
%
%
%
%
103/L
2.09
1.5 5,1
103/L
0.46
0.2 0.6
103/L
0.00
0.10
0.30
0 0.1
103/L
0.01
Results
12.30
11.80
Normal Value
103/L
Unit
Second
Second
19
INR
APTT
Control
Patient
Trombin Time
Control
Patient
Clinical Chemistry
Liver
AST/SGOT
ALT/SGPT
Carbohdyrat Metabolism
Glucosa
Renal
Ureum
Creatinin
Electrolit
Natrium (Na)
Kalium (K)
Clorida (Cl)
0.94
30.2
28
Second
Second
17.8
18
Second
Second
95
36
<38
<41
U/L
U/L
102.10
<200
mg/dL
16.80
0.27
<50
0.24 0.41
mg/dL
mg/dL
131
5.0
102
135 155
3.6 5.5
96 106
mEq/L
mEq/L
mEq/L
Differential Diagnosis:
-
Tetanus
Rabies
Ensefalitis
Working Diagnosis:
Tetanus
Management:
-
Activity: Bedrest
Diet SV 1100 kkal + 36 gr protein
O2 1/2 L/i nasal canule
IVFD D5% NaCl 0.45% 20 gtt / minute micro
NGT
Injection of diazepam 10mg / iv, continous 3mg / kgBW / 3 hours / iv
Injection of Penicilin Procain 600000 IU / 12 hours / im
20
ATS 40000 IU / im (Inj. ATS 20.000 IU im & Inj. ATS 20.000 IU in 200 cc
Nacl 0.9% for 30-45 mnt)

TT 0.5cc / im
Clean the wound with H2O2, alcohol, betadine
Diagnostic Planning:
-
Consultation with infection

Consultation with dentist
Consultation with THT
September 2th 2012

S Difficulty in opening the mouth (+ ) Fever (-), excitative spasm (-), spasm (-)
O Sens: CM, Temp: 37C, Body weight: 12 kg
Head
: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-) Ear: within normal limit. Nose: within normal limit.
Neck
Thorax
A
P
Mouth: trismus (+) 0,5 cm. Face: risus sardonicus (+).

: symmetries fusiform, retraction (-).
RR : 25 x/minute, regular, ronkhi (-)

Abdomen
: Peristaltic (+), muscular rigidity (+), liver and spleen not palpable
Extremities : Pulse = 115 bpm, regular, adequate pressure/volume, warm axilla, BCG
capillary refill time (CRT) < 3, clubbing finger (-).
Genital
: Male
- Tetanus
Management:
-

Injection of diazepam 3mg / kgBW / 3 hours /iv
Injection of penicilin procain 600000 IU / 12 hours / im
September 3th 2012
21
S Difficulty in opening the mouth (+) Fever (-), excitative spasm (-), spasm (-)
O Sens: CM, Temp: 36,8C, Body weight: 12 kg
Head

Neck
Thorax
A
P


Abdomen
Genital
: Male
- Tetanus
Management:
-

September 4th 2012

Head

Neck
Thorax
A
P


Abdomen
Genital
: Male
- Tetanus
Management:
22
- O2 1/2 L/i nasal canule

- IVFD D5% NaCl 0.45% 20 gtt / minute micro
- Injection of diazepam 3mg / kgBW / 3 hours /iv
- Injection of penicilin procain 600000 IU / 12 hours / im
- Diet SV 1100 kkal + 36 gr protein
R - Consul dentistry : teeth care with cotton
September 5th 2012

O Sens: CM, Temp: 37C, Body weight: 12 kg
Head

Neck
Thorax

Abdomen
Genital
: Male
- Tetanus
A
P
Mouth: trismus (+) 2 cm. Face: risus sardonicus (+).

Management:
-

R - Consul THT : : trismus (+), patients can open his mouth 2 cm
-
Advice : H2O2 6x8 drops both ears
September 6th 2012

Head

23
Neck
Thorax
A
P


Abdomen
Genital
: Male
- Tetanus
Management:
-

September 7th 2012

Head

Neck
Thorax
A
P

RR : 24x/minute, regular, ronkhi (-)

Abdomen
Genital
: Male
- Tetanus
Management:
-

24
September 8th 2012

Head

Neck
Thorax
A
P


Abdomen
Genital
: Male
- Tetanus
Management:
-

Injection of diazepam mg / kgBW / 3 hours /iv
Diet MII 1400 kkal + 60 gr protein
September 9th 2012

Head

Neck
Thorax
A
P


Abdomen
Genital
: Male
- Tetanus
Management:
25

September 10th 2012

Head

Neck
Thorax
A
P


Abdomen
Genital
: Male
- Tetanus
Management:
-

September 11th 2012

Head

Neck
Thorax

26
A
P

Abdomen
Genital
: Male
- Tetanus
Management:
-

September 12th 2012

Head

Neck
Thorax
A
P


Abdomen
Genital
: Male
- Tetanus
Management:
-

27
CHAPTER IV
DISSCUSSION
28
Almost all reported cases of tetanus are in persons who have either never
been vaccinated. Tetanus is more extensive in incomplete immunity person as a
predisposing factors. From the case, this patients history of immunisation is not
complete.
Symptoms usually begin 8 days (2-14 days) after the infection, but it may
be as long as months after the injury, then the onset may range from 3 days to 3
weeks. From the case, this patient has History of tooth carries and history of
wound on right sole of foot but patient doesnt know when and what caused.
Trismus is the presenting symptom in 75% of cases, sardonic smile of
tetanus (risus sardonicus) results from intractable spasm of facial and buccal
muscles, when the paralysis extends to abdominal, lumbar, hip, and thigh muscles,
the patient may assume an arched posture of extreme hyperextension of the body
called opisthotonos. From the case, trismus and spasm of the back muscles was
found.
Penicillin is the standard therapy for tetanus in most parts of the world,
although antibiotics for C.tetani probably play a relatively minor role in the
specific treatment of this disease. Metronidazole has been considered the first line
of therapy and is a safe alternative to penicillin. From the case, the patient was
administered with penicillin 600.000 IU
All patients with generalized tetanus need muscle relaxants. Diazepam
provides both relaxation and seizure control. From the case, patients was
administered with diazepam.
Summary
GR, male, 11 years old, was diagnosed with pediatric tetanus. The diagnosis was
established based on history taking, clinical manifestations, and laboratory
findings. Patient had been hospitalized at Adam Malik General Hospital and
29
discharged by own request. The patient was administered with antispasm, ATS,
antibiotic, and palliative treatment.
REFERENCE
1. Tolan, Robert W.2012. Pediatric Tetanus. Available from:
www.emedicine.medscape.com/article/972901 [Accesed: September, 12th
2012]
2. Soedarmo S, dkk. Tetanus .Buku Ajar Infeksi dan Pediatri
Tropis.2010.Jakarta : Badan Penerbit IDAI. 322-330
30
3. Edlich, Richard F, et al.2003.Management and Prevention of Tetanus.

Available
from
:
http://www.google.co.id/url?
sa=t&rct=j&q=&esrc=s&source=web&cd=3&cad=rja&ved=0CDwQFjAC
&url=http%3A%2F%2Fplasticosfoundation.org%2Farticles%2Ftetanusarticle.pdf&ei=oP1LUIjAPMzHrQeIyoG4Dg&usg=AFQjCNFMr-LmXPL9wPT-aaCuA_CU5FlZg [Accesed: September, 13th 2012]
4. Ismoedijanto, M. Nassiruddin. Wahyu Prajitno, 2004. Diazepam in Severe
Tetanus Treatment. Available from:
http://www.google.co.id/#hl=id&sclient=psyab&q=CASE+REPORT+DIAZEPAM+IN+SEVERE+TETANUS+TREAT
MENT&oq=CASE+REPORT+DIAZEPAM+IN+SEVERE+TETANUS+T
REATMENT&gs_l=hp.3...2167341.2179871.3.2181220.46.6.6.0.0.0.0.0..
0.0...0.0...1c.1j2.Sfkb60LYdXY&psj=1&bav=on.2,or.r_gc.r_pw.r_qf.&fp=
1b646a699d9d3356&biw=1280&bih=646. [Accesed: September, 13th
2012]
5. Andrew Michael Taylor FRCA, 2006. Tetanus. Available from:
http://ceaccp.oxfordjournals.org/content/6/3/101.extract
[Accesed:
th
September, 13 2012]
6. CDC (Centers for Disease Control and Prevention).2012.Tetanus. The Pink
Book:
Course
Text
Book-12th
edition
http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/tetanus.pdf
7. Hinfey, Patrick B.2011.Tetanus.Available from:
2012]
8. Arnon S.S. Tetanus. In: Nelson Textbook of Pediatrics. 19 th Edition. USA:
Saunders Elsevier, Philadelphia, 2007; p. 951-953
9. Dire, Daniel J.2012.2011.Tetanus in Emergency Medicine.Available from:
2012]
10. Chan, K H & Lau, C C.2004. Wound Management and Tetanus
Prophylaxis. Available from: http://www.google.co.id/url?
sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CB4QFjAA&url=http
%3A%2F%2Fwww3.ha.org.hk%2Fidctc%2Fdocument%2FWound
%2520Management%2520%2520Tetanus
%2520Prophylaxis.pdf&ei=AYdNUNiwKZHJrQfAs4CwAg&usg=AFQjC
NETZ0t9eYSeKVZqRK-M3a39gV8Gsw [Accesed: September, 6th 2012]
11. Ross,Steven E.1995.Prophylaxis Against Tetanus in Wound Management.
Available
from:
http://www.google.co.id/url?
sa=t&rct=j&q=&esrc=s&source=web&cd=4&ved=0CEAQFjAD&url=htt
p%3A%2F%2Fpdfs.journals.lww.com%2Fjtrauma
%2F1966%2F07000%2FProphylaxis_Against_Tetanus_in_Wound_Manag
ement.7.pdf&ei=Z4dNUPvnKI3PrQeQgIH4DQ&usg=AFQjCNEVWOZx
4g8wGBmupn6bwktC-Q1E0g [Accesed: September, 6th 2012]
31
12. Krugman.2004.Krugmans Infection Diseases of

Edtion.USA: Mosby, Philadelphia, 2004; p. 655 - 663
Children
11th

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1

the bacterium Clostridium tetani. It is characterized by generalized rigidity and

professional education program in the department of pediatrics. In addition,

the release of the neurotoxin tetanospasmin by Clostridium tetani following

Epidemiology and Risk Factor

largely in underdeveloped, overcrowded, and economically disadvantaged

an obligate of anaerobic gram positive bacteria, mobile, nonencapsulated, and

and tetanolysin. Tetanolysin is not believed to be of any significance in the clinical

The diagnosis of tetanus may be established clinically.

all neonatal deaths. Physical examination findings are similar to generalized

disease. However, trismus may result from parapharyngeal, retropharyngeal, or

tetany, characterized by laryngeal and carpopedal spasms, but trismus is absent.

environment conducive to its anaerobic multiplication, neutralization of all

achieved with neuromuscular blocking agents such as vecuronium and

effective way to control tetanus is by prophylactic immunization. Thus, universal

Human Tetanus Immune Globulin (HTIG) should be reserved for

Tetanus prone wounds

Stellate wound, avulsion

Linear wound, abrasion

the patient to many complications. Aspiration of secretions and pneumonia may

: Jl. L Sujono G Palapa I LK VIII Bandar Selamat Medan

: difficulty in opening the mouth

: patient is single son in family

axilla, capillary refill time (CRT) < 3, clubbing finger (-),

Nacl 0.9% for 30-45 mnt)

Consultation with infection

September 2th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

Mouth: trismus (+) 0,5 cm. Face: risus sardonicus (+).

RR : 25 x/minute, regular, ronkhi (-)

O2 1/2 L/i nasal canule

September 3th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

Mouth: trismus (+) 0,75 cm. Face: risus sardonicus (+).

RR : 24 x/minute, regular, ronkhi (-)

O2 1/2 L/i nasal canule

September 4th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

Mouth: trismus (+) 1,5 cm. Face: risus sardonicus (+).

RR : 23 x/minute, regular, ronkhi (-)

- O2 1/2 L/i nasal canule

September 5th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

RR : 21 x/minute, regular, ronkhi (-)

Mouth: trismus (+) 2 cm. Face: risus sardonicus (+).

O2 1/2 L/i nasal canule

Advice : H2O2 6x8 drops both ears

September 6th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

: Lymph node enlargement (-).

RR : 26 x/minute, regular, ronkhi (-)

O2 1/2 L/i nasal canule

September 7th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

Mouth: trismus (+) 2 cm. Face: risus sardonicus (+).

RR : 24x/minute, regular, ronkhi (-)

O2 1/2 L/i nasal canule

September 8th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva

Mouth: trismus (+) 2 cm. Face: risus sardonicus (+).

RR : 23 x/minute, regular, ronkhi (-)

O2 1/2 L/i nasal canule

September 9th 2012

: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva