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CASE REPORT

TETANUS

Presented by:
Shinta Pedia Dinanti (110100324)
Elvira (110100333)

Supervisor:
dr. Rizky Ardiansyah, M.Ked (Ped), Sp.A(K)

DEPARTMENT OF PEDIATRICS
H. ADAM MALIK CENTRAL GENERAL HOSPITAL
FACULTY OF MEDICINE
UNIVERSITY OF SUMATERA UTARA
MEDAN
2016

FOREWORD
All praises to Allah swt for His grace and blessing that provide this opportunity
and grant us the capability to complete a case report titled Tetanus. This case report is
written as a requirement to complete the clinical rotation in Department of Pediatrics,
Faculty of Medicine, University of Sumatera Utara.
We would like to offer our sincere appreciation to our supervisor, dr. Rizky
Ardiansyah, M.Ked(Ped), Sp.A(K), for his supervision and constant support. His
invaluable help of constructive comments and suggestions throughout the process have
contributed to the completion of this case report. We would also like to offer our
appreciation to all the residents in Department of Pediatrics for their support and
contribution to our case report.
We realize that this case report is still far from perfection. Therefore, we would
like to look forward to suggestions from the readers for the improvement of further
works in the future. We hope that this case report can be of use and everybody is able to
take a benefit from it. Thank you.
Medan, January 2016

Writers

CONTENTS
FOREWORD ............................................................................................................. i
CONTENTS .............................................................................................................. ii
CHAPTER 1 INTRODUCTION ............................................................................. 1
CHAPTER 2 LITERATURE REVIEW ................................................................. 3
2.1. Definition ........................................................................................................... 3
2.2. Etiology ............................................................................................................. 3
2.3. Epidemiology .................................................................................................... 3
2.4. Pathophysiology ................................................................................................ 4
2.5. Clinical Manifestations ...................................................................................... 5
2.6. Diagnostic Evaluation ....................................................................................... 7
2.7. Differential Diagnosis ........................................................................................ 7
2.8. Treatment ........................................................................................................... 8
2.9. Prevention ........................................................................................................ 10
2.10.......................................................................................................Complications
.......................................................................................................................... 12
2.11...............................................................................................................Prognosis
.......................................................................................................................... 12
CHAPTER 3 CASE REPORT ............................................................................... 13
CHAPTER 4 DISCUSSION ................................................................................... 26
CHAPTER 5 CONCLUSION ................................................................................ 31
REFERENCES 32

CHAPTER I
INTRODUCTION

Tetanus is a neurologic disorder; an acute, spastic paralysis illness, characterized


by generalized rigidity and convulsive spasms of skeletal muscles that is caused by
tetanospasmin, a powerful neurotoxin produced by Clostridium tetani. Tetanus occurs in
several clinical forms, including generalized, neonatal, and localized disease. C. tetani is
a motile, gram-positive, spore-forming obligate anaerobe whose natural habitat
worldwide is soil, dust, and the alimentary tracts of various animals. It forms spores
terminally, thus producing a drumstick or tennis racket appearance microscopically1-4.
The word tetanus originates from the Greek language tetanos which means
to contract4. The most common form, neonatal tetanus, is associated with
unimmunized mother. In addition, maternal tetanus results from postpartum,
postabortal, or postsurgical wound infection with C. tetani. Most non-neonatal cases of
tetanus are associated with a traumatic injury, often a penetrating wound inflicted by a
dirty object, such as a nail, splinter, fragment of glass, or unsterile injection, but a rare
case may have no history of trauma 1. Although tetanus affects all ages, the highest
prevalence is found in newborn and young people. Tetanus occurs sporadically and
almost always affects unimmunized persons, partially immunized persons, or fully
immunized individuals who fail to maintain adequate immunity with booster doses of
vaccine3.
In anaerobic environment, the clostridia produce tetanospasmin, a potent
neurotoxin, which inhibits the release of inhibitory neurotransmitters in the central
nervous system (CNS), resulting in muscle rigidity 1-6. The diagnosis of tetanus is made
solely by clinical findings and there are no confirmatory laboratory tests 5. Treatment
strategies involve three management principles: organisms present in the body should
be destroyed to prevent further toxin release; toxin present in the body, outside the CNS
should be neutralized; and the effects of toxin already in the CNS should be minimized 4.
The prognosis is dependent on incubation period. In general, shorter intervals indicate
more severe tetanus and a poorer prognosis4.

The records that contain clinical descriptions of tetanus date back to antiquity
(5h century BC); however, the ones who first discovered the etiology 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
1920s which led to the development of tetanus toxoid by Descombey in 1924. It was
first widely used during World War II7.
Since the invention of tetanus vaccine, the incidence of tetanus has declined
significantly. It is strongly recommended to get an immunization of tetanus vaccine
because inadequate immunization may result in an increase in the incidence of tetanus 8.
Based on these facts, the writers are interested to present a case report of a patient with
tetanus in the H. Adam Malik Central General Hospital.

CHAPTER II
LITERATURE REVIEW
2.1.

Definition
Tetanus is a neurologic disorder; an acute, spastic paralysis illness, characterized

by generalized rigidity and convulsive spasms that is caused by tetanospasmin, a


powerful neurotoxin produced by Clostridium tetani1-4. Tetanus occurs in several
clinical forms, including generalized, neonatal, and localized disease3.
2.2.

Etiology
Clostridium tetani is a motile, gram-positive, spore-forming obligate anaerobe

whose natural habitat worldwide is soil, dust, and the alimentary tracts of various
animals. It forms spores terminally, thus producing a drumstick or tennis racket
appearance microscopically. Tetanus spores are extremely stable; they can survive
boiling for 15 minutes, but not autoclaving at 120C, 1.5 bar, for 15 minutes, which
ensures sterility. Meanwhile, the vegetative cells are killed by antibiotics, heat, and
standard disinfectants1-4.
2.3.

Epidemiology
Tetanus occurs worldwide and is endemic in 90 developing countries, but its

incidence varies considerably. The most common form, neonatal (umbilical) tetanus,
kills approximately 500,000 infants each year because the mother was not immunized;
about 80% of these deaths occur in just 12 tropical Asian and African countries. In
addition, an estimated 15,000-30,000 unimmunized women worldwide die each year of
maternal tetanus that results from postpartum, postabortal, or postsurgical wound
infection with C. tetani1.
Most non-neonatal cases of tetanus are associated with a traumatic injury, often
a penetrating wound inflicted by a dirty object, such as a nail, splinter, fragment of
glass, or unsterile injection, but a rare case may have no history of trauma. Tetanus is
also associated with illicit drug injection, middle-ear infection, animal bites, abscesses
(including dental abscesses), body piercing, chronic skin ulceration, burns, compound
fractures, frostbite, gangrene, intestinal surgery, ritual scarification, infected insect bites,
and female circumcision1, 3. Although tetanus affects all ages, the highest prevalence is

found in newborn and young people. Tetanus occurs sporadically and almost always
affects unimmunized persons, partially immunized persons, or fully immunized
individuals who fail to maintain adequate immunity with booster doses of vaccine3.
In the study that conducted at several hospitals in Indonesia between 1991 and
1996, it was found that almost all hospitals are found in the age group 5-9 years. Also,
the risk of being exposed to tetanus for boys is greater than girls, because of differences
in the daily activities of boys who prefer to play outdoors 5. In 1997-2000, the
prevalence of tetanus is 1.6-1.8/100,000; the mortality caused by neonatal tetanus is
7.9%4.
Table 1. Age Group Distribution of Tetanus Cases in 1991-19965

2.4.

Pathophysiology
Contamination of wounds with spores of C. tetani is probably a frequent

occurrence. Germination and toxin production; however, take place only in wounds with
low oxidation-reduction potential, such as those with devitalized tissue, foreign bodies,
or active infection. C. tetani itself does not evoke inflammation, and the portal of entry
retains a benign appearance unless infection with other organisms is present because C.
tetani is not an invasive organism1, 3.
C. tetani releases two toxins: tetanospasmin and tetanolysin. Only tetanospasmin
causes the clinical manifestations of tetanus, whereas tetanolysin is not related to the
disease1-4, but is thought to enhance the effect of tetanus toxin 2. Tetanospasmin, a zinc
metalloprotease, released in the wound binds to peripheral motor neuron terminals,
enters the axon, and is transported to the nerve-cell body in the brainstem and spinal
cord by retrograde intraneuronal transport.1-4 Tetanospasmin is formed in vegetative

cells under plasmid control. It is a single polypeptide chain. With autolysis, the singlechain toxin is released and cleaved to form a heterodimer consisting of a heavy chain
(100 kDa), which mediates binding to nerve-cell receptors and entry into these cells,
and a light chain (50 kDa), which acts to block neurotransmitter release. The amino acid
structure of C. tetani toxin has been known to be partially homologous with botulinum
toxin1, 3-4.
The toxin then migrates across the synapse to presynaptic terminals, where it
blocks release of the inhibitory neurotransmitters glycine and -aminobutyric acid
(GABA). The blocking of neurotransmitter release involves the cleavage of protein(s)
critical to proper function of the synaptic vesicle release apparatus. With diminished
inhibition, the resting firing rate of the motor neuron increases, producing rigidity.
With lessened activity of reflexes that limit polysynaptic spread of impulses (a
glycinergic activity), agonists and antagonists may be recruited rather than inhibited,
with the 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 circulating catecholamine levels.
Tetanospasmin, like botulinum toxin, may block neurotransmitter release at the
neuromuscular junction and produce weakness or paralysis; recovery requires sprouting
of new nerve terminals1, 3-4, 6.
In local tetanus, only the nerves supplying the affected muscles are involved.
Generalized tetanus occurs when toxin released in the wound enters the lymphatics and
bloodstream and is spread widely to distant nerve terminals; the blood-brain barrier
blocks direct entry into the central nervous system. If it is assumed that intraneuronal
transport times are equal for all nerves, short nerves are affected before long nerves: this
fact explains the sequential involvement of nerves of the head, trunk, and extremities in
generalized tetanus1.
2.5.

Clinical Manifestations
The incubation period typically is 2-14 days, but it may be as long as months

after the injury1. In general, the further the injury site is from the central nervous
system, the longer is the incubation period5. Shorter incubation periods are associated
with a higher chance of death7.
1. Generalized tetanus

It is the most common form of the disease, and it is characterized by increased muscle
tone and generalized spasms. Trismus (masseter muscle spasm, or lockjaw) is the
presenting symptom in about half of cases. Early symptoms include headache,
restlessness, and irritability, and then often followed by stiffness, difficulty chewing,
dysphagia, and neck muscle spasm. Sustained contraction of the facial muscles results
in a grimace or sneer (risus sardonicus), and contraction of the back muscles produces
an arched back (opisthotonos). Opisthotonos is an equilibrium position that results from
unrelenting total contraction of opposing muscles, all of which display the typical
board-like rigidity of tetanus. The subsequent involvement of other muscles produces a
rigid abdomen and stiff proximal limb muscles; the hands and feet are relatively spared.
A constant threat during generalized spasms is reduced ventilation or apnea or
laryngospasm, which can lead to airway obstruction and asphyxiation1-5.
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. The smallest disturbance by sight, sound, or touch may
trigger a tetanic spasm.
Fever is common because of the substantial metabolic energy consumed by
spastic muscles. Autonomic dysfunction commonly complicates severe cases and
includes tachycardia, arrhythmias, labile hypertension, diaphoresis, and cutaneous
vasoconstriction1, 3.
2. Neonatal tetanus
It is the infantile form of generalized tetanus, typically manifests within 3-12 days of
birth, averaging about 7 days 3, 7. It is usually fatal if left untreated, and develops in
children born to inadequately immunized mothers. Poor feeding, rigidity, and spasms
are typical features of neonatal tetanus. The umbilical stump may frequently hold
remnants of dirt, dung, clotted blood, or serum, or it may appear relatively benign
because of the unsterile treatment1.
3. Local tetanus
It is an uncommon form in which manifestations are restricted to muscles near the
wound. The prognosis is excellent3. This form results in painful spasms of the muscles

adjacent to the wound site and may precede generalized tetanus 1. It is usually mild, lasts
for months, and is self-limited4.
4. Cephalic tetanus
It is a rare form of local tetanus, follows head injury or ear infection such as chronic
otitis media. The incubation period is a few days and the mortality is high. Cephalic
tetanus is characterized by retracted eyelids, deviated gaze, trismus, risus sardonicus,
and spastic paralysis of tongue and pharyngeal musculature1, 3.
2.6.

Diagnostic Evaluation
The diagnosis of tetanus is based solely on clinical findings. The history of

injury or bite, the characteristic facial appearance, and spasms may help us diagnosing
tetanus. Most cases occur in unimmunized individuals. Tetanus is unlikely if a reliable
history indicates the completion of a primary vaccination series and the receipt of
appropriate booster doses3. The WHO definition of tetanus requires at least one of the
following signs: trismus (inability to open the mouth) or risus sardonicus (sustained
spasm of the facial muscles), or painful muscular contractions. Although this definition
requires a history of injury or wound, tetanus may also occur in patients who are unable
to recall a specific wound or injury5, 8. The typical setting is an unimmunized patient
(and/or mother) who was injured or born within the preceding 2 wk and who presents
with trismus, other rigid muscles, and a clear sensorium 1. Routine laboratory studies are
usually normal. A peripheral leukocytosis may result from a secondary bacterial
infection of the wound or may be stress induced from the sustained tetanic spasms. The
cerebrospinal fluid (CSF) is normal, although the intense muscle contractions may raise
intracranial pressure. C. tetani is not always visible on Gram stain of wound material,
and it is isolated in only about one third of cases1.
2.7.

Differential Diagnosis
The differential diagnosis includes local conditions also producing trismus, such

as alveolar abscess, strychnine poisoning, dystonic drug reactions (e.g., to


phenothiazines and metoclopramide), and hypocalcaemic tetany. Other conditions
sometimes confused with tetanus include meningitis/encephalitis, rabies, and an acute
intraabdominal process because of the rigid abdomen 3. 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
tetany, characterized by laryngeal and carpopedal spasms, but trismus is absent1.
Table 2. Differential diagnosis of tetanus9
Differential diagnosis
Manifestation
Infection
Meningoencephalitis
Fever (+), trismus (-), depressive sensorium, abnormal CSF
Polio
Trismus (-), flaccid paralysis, abnormal CSF
Rabies
Animal bite (+), trismus (-), just oropharyngeal spasms
Oropharyngeal lesion
Local, spasms (-)
Peritonitis
Trismus/spasms (-)
Metabolic disorders
Tetany
Carpopedal and laryngeal spasms (+), hypocalcaemia
Strychnine poisoning
Complete relaxation within spasms
Phenothiazine reaction
Dystonia, response to diphenhydramine
CNS disease
Hemorrhage
Trismus (-),depressive sensorium,
Status epilepticus
Depressive sensorium
Psychiatric disorders
Hysteria
Inconstant trismus, complete relaxation within spasms
Musculoskeletal disorders
Trauma
Local
2.8.

Treatment
Treatment for tetanus includes:

1. General measures
Treatment strategies involve three management principles: organisms present in the
body should be destroyed to prevent further toxin release; toxin present in the body,
outside the CNS should be neutralized; and the effects of toxin already in the CNS
should be minimized4. The goals of therapy are to eliminate the source of toxin,
neutralize unbound toxin, and prevent muscle spasms, monitoring the patients
condition and providing supportespecially respiratory supportuntil recovery2-3. A
supportive care in a quiet, dark, secluded setting is most desirable. Because tetanic
spasms may be triggered by minor stimuli, the patient should be sedated and protected
from all unnecessary sounds, sights, and touch; and all therapeutic and other

manipulations must be carefully scheduled and coordinated1, 8. Protection of the airway


is vital. Wounds should be explored, carefully cleansed, and thoroughly debrided3, 8.
2. Antibiotic therapy
Antibiotic therapy is administered to eradicate vegetative cells as the source of toxin.
Penicillin G (100,000-200,000 IU/kg/24 hr divided in 2-4 doses for 7-10 days) has been
recommended because of its effective clostridiocidal action and its diffusibility1, 8, but
metronidazole (500 mg every 6 h or 1 g every 12 h) is preferred by some experts
because of its excellent antimicrobial activity, higher survival rate, and the absence of
activity antagonistic to GABA, as seen with penicillin 3. Clindamycin and erythromycin
are also alternatives for the treatment of penicillin-allergic patients1, 3.
3. Antitoxin
Antitoxin is administered to neutralize circulating toxin and unbound toxin in the
wound; however, toxin already bound to neural tissue is unaffected 1, 3. Human tetanus
immunoglobulin (TIG) is the preparation of choice and should be given promptly. The
dose is 3000-6000 units intramuscularly, usually in divided doses because the volume is
large; however, the optimal dose is not known 3. If TIG is unavailable, use of human
intravenous immunoglobulin (IVIG), or of equine- or bovine-derived tetanus antitoxin
(TAT), may be necessary. The optimal dosage of IVIG is not known, while 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 1. TAT is cheaper than human
antitoxin, but its half-life is shorter and its administration commonly elicits
hypersensitivity and serum sickness3, 10.
4. Control of muscle spasms
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 weeks before its tapered withdrawal. Other options include lorazepam,
midazolam, barbiturates, and chlorpromazine1, 3-4.
5. Respiratory care
Intubation or tracheostomy, with or without mechanical ventilation, may be required for
hypoventilation due to oversedation or laryngospasm or for the avoidance of aspiration
by patients with trismus, disordered swallowing, or dysphagia 3. However, endotracheal
intubation and suctioning easily provoke reflex tetanic seizures and spasms 1, so the need

10

for these procedures should be anticipated, and they should be undertaken electively and
early3.
6. Autonomic dysfunction
The optimal therapy for sympathetic overactivity has not been defined, but it is
regulated by standard - and - (or both) blocking agents; morphine has also proved
useful1. Hypotension or bradycardia may require volume expansion, use of vasopressors
or chronotropic agents, or pacemaker insertion3.
7. Vaccine
Patients recovering from tetanus should be actively immunized because immunity is not
induced by the small amount of toxin that produces disease3.
8. Additional measures
Additional therapeutic measures include hydration to control insensible and other fluid
losses, which may be significant; the meeting of the patients increased nutritional
requirements by enteral or parenteral means due to tetanus spasms resulting in high
metabolic demands and a catabolic state; physiotherapy to prevent contractures; and
administration of heparin or another anticoagulant to prevent pulmonary emboli. Bowel,
bladder, and renal function must be monitored. Gastrointestinal bleeding and decubitus
ulcers must be prevented, and intercurrent infection should be treated3, 8.
2.9.

Prevention
Prevention measures for tetanus include:

1. Active immunization
All partially immunized and unimmunized adults should receive vaccine, as should
those recovering from tetanus. The primary series for adults consists of three doses: the
first and second doses are given 4 to 8 weeks apart, and the third dose is given 6 to 12
months after the second. A booster dose is required every 10 years and may be given at
mid-decade ages35, 45, and so on. Combined tetanus and diphtheria toxoid, adsorbed
(Td, for adult use), rather than single-antigen tetanus toxoid, is preferred for persons <7
years of age. Adsorbed vaccine is preferred because it produces more persistent
antibody titers than fluid vaccine3-4.
2. Wound management

11

Proper wound management requires consideration of the need for (1) passive
immunization with TIG and (2) active immunization with vaccine, preferably Td in
persons over age 7. The dose of TIG for passive immunization of persons with wounds
of average severity is 250 units intramuscularly, which produces a protective antibody
level in the serum for at least 4-6 weeks; the appropriate dose of TAT, an equine-derived
product, is 3000-6000 units. Vaccine and TAT should be administered at separate sites
with separate syringes3.
3. Neonatal tetanus
Measures aimed at preventing neonatal tetanus include maternal vaccination even
during pregnancy (two doses are given 4 weeks apart), efforts to increase the proportion
of birth that take place in the hospital, and the provision of training for nonmedical birth
attendants3-4.
Table 3. Guidelines for tetanus prophylaxis in wound management1, 3
Vaccination status
Clean, minor wounds
Tetanus-prone woundsa
b
Td
TIG
Tdb
TIG
Unknown or <3 Yes
No
Yes
No
doses
3 dosesc
No, unless >10 No
No, unless >5 No
years since last
years since last
done
done
a Such as, but not limited to, wounds contaminated with dirt, feces, soil, and saliva; puncture
wounds; avulsions; and wounds resulting from missile or crushing injuries, burns, and frostbite.
b For children <7 years old, DTP (or DT, if pertussis vaccine is contraindicated) is preferred to
tetanus toxoid alone. Td is preferred to tetanus toxoid alone in adults.
c If only three doses of fluid toxoid have been received, then a fourth dose of toxoid
preferably an adsorbed toxoidshould be given.
Note: DT, diphtheria and tetanus vaccine; DTP, diphtheria, tetanus, and pertussis vaccine; Td,
tetanus-diphtheria toxoid, adsorbed; TIG, tetanus immune globulin.
Source: Modified from Centers for Disease Control and Prevention: Diphtheria, tetanus, and
pertussis: Recommendations for vaccine use and other preventive measures: Recommendations
of the Immunization Practices Advisory Committee (ACIP). MMWR 40(RR- 10):1, 1991.

2.10.
Complications
The most dangerous complication of tetanus is severe airway obstruction due to
laryngospasm (spasm of the vocal cords) and/or spasm of the muscle of respiration,
leading to interference with breathing and intervention with ventilator. Fracture of spine
or long bones may result from sustained contractions and convulsions. Hyperactivity of

12

the autonomic nervous system causes uncontrollable release of catecholamines and may
lead to hypertension and tachycardia and/or an abnormal heart system1-4.
2.11.

Prognosis

The prognosis is dependent on incubation period, the time from spore incubation
to first symptom, and the time from first symptom to first tetanic spasm. In general,
shorter intervals indicate more severe tetanus and a poorer prognosis 4. Recovery in
tetanus occurs through regeneration of synapses within the spinal cord and thereby the
restoration of muscle relaxation. However, active immunization with tetanus toxoid at
discharge with provision for completion of the primary series is mandatory because an
episode of tetanus does not result in the production of toxin-neutralizing antibodies1.

13

CHAPTER III
CASE REPORT
3.1. Objective
The objective of this paper is to report a case of a 17-year-old boy with a diagnosis of
tetanus.
3.2. Case
AAR, a 17-year-old boy, with body weight of 50 kg and body height of 164 cm, came to
Haji Adam Malik Central General Hospital Medan on January 11, 2016 at 23:00 pm.
His chief complaint was history of seizures.
History of disease:
AAR, a 17-year-old boy came to Haji Adam Malik Central General Hospital Medan on
January 11, 2016 at 23:00 pm with history of seizures as the chief complaint. The
patient suffered from seizures for one day with a frequency of two times in a day, with
duration of no more than five minutes for each seizure. There was no loss of
consciousness during each seizure. He also had whole body spasm and stiff in each
seizure. He had no history of previous seizures.
The patient had a history of ear discharge from right ear of his ear since two
weeks ago, with the characteristics of the discharge having white color, watery
consistency, no odor, and low volume. His uncle revealed that the patient frequently
cleaned out his ear canals by using cotton buds, wood, pen, etc. The history of bloody
ear discharge was not known.
The patient had difficulties in opening his mouth for one week, maximum width
2cm. He did not have a pain in swallowing
The patient had fever for one week. His body temperature was not too high. The
fever went up and down, and could be relieved with fever-reducing drugs.
The patient had shortness of breath for one week. Shortness of breat not related
to the weather.
The patient history exposed sharp objects denied. Defecation and urination were
normal.

14

The patient is referrals from general hospital Rantauprapat by an internist


diagnosed tetanus.
History of medication:
Valium, Dexamethasone, Tetagam 500 IU, Ceftriaxone Injection, Metrodinazole
Injection.
History of family:
None
History of parents medication:
None
History of pregnancy:
The age of the patients mother was 30 years old during pregnancy. The gestation age
was 9 months.
History of birth:
Birth was assisted by a midwife. The patient was born per vaginam and cried
immediately after birth. Body weight, body length, and head circumference at birth was
unclear. There was no history of cyanosis and jaundice.
History of feeding:
Not clear.
History of growth and development:
The patients uncle reported that patient grew normally. The patient had developed
talking, crawling, and walking skills on time.
History of immunization:
Not clear.

15

Physical Examination:
Present status:
Sensorium: compos mentis

Body temperature: 36.7C

Heart rate: 90 bpm

Respiratory rate : 20 bpm

Body weight: 50 kg

Body height: 164 cm

BW/A: 78.1%

BL/A: 93.7%

BW/BL: 98%
Anemic (-), icteric (-), dyspnea (-), cyanosis (-), edema (-).
Local status:

Head
Face
Eye

: Risus sardonicus (+)


: Light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-),

icteric sclerae (-/-)


Ears
: both ear lobes in normal morphology, right membrane perforation (+)
Nose
: septum deviation (-)
Mouth
: trismus (+) 3 cm
Neck
Lymph node enlargement (-)
Thorax
Symmetrical fusiform, retraction (-); HR: 90 bpm, regular, murmur (-/-); RR: 20
bpm, regular, rhonchi (-/-), wheezing (-/-)
Abdomen
Muscular defense (+), normal peristaltic, liver and spleen impalpable,
Extremities
Pulse 90 bpm, regular, adequate pressure/volume, warm, CRT < 3, pitting edema
(-/-)
Physiologic reflexes: KPR (+/+), APR (+/+)
Pathologic reflexes: Babinski sign (-), Chaddock sign (-), Oppenheim sign (-),

Gordon sign (-)


Anogenital
Male

Differential diagnosis:
1. Tetanus
2. Pediatric febrile seizures
3. Epilepsy
Working diagnosis:

16

Tetanus
Laboratory finding:
Complete blood analysis (December 11, 2015 / 23:53)
Test
Hemoglobins
Erythrocytes
Leukocytes
Platelets
Hematocrits
Eosinophils
Basophils
Neutrophils
Lymphocytes
Monocytes

Result
14.40
4.62
9.84
348
40.60
0.00
0.100
87.00
9.70
3.20

Clinical Chemistry
Test
Result
Carbohydrate Metabolism
Random Blood Glucose 116.20
Renal
Ureum
16.60
Kreatinin
0.79
Electrolytes
Natrium
138
Potassium
4.1
Chloride
104

Unit
g%
106/mm3
103/mm3
103/mm3
%
%
%
%
%
%

References
12.0-14.4
4.40-4.48
4.5-13.5
150-450
37-41
1-6
0-1
37-80
20-40
2-8

Unit

References

mg/dL

40-60

mg/dL
mg/dL

<50
0.7-1.20

mEq/L
mEq/L
mEq/L

135-155
3.6-5.5
96106

Therapy:

Isolated care
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diet via nasogastric tube (NGT) 2250 kcal/day
Tetagam 3000 IU IM single dose
Metronidazole injection 375 mg/6 hr/IV
Diazepam injection 15 mg/3 hr/IV (when in seizure)

17

FOLLOW UP
January 12, 2016
S
O

Seizure (+)
Sensorium: compos mentis; temperature: 36.7o C BW: 50 kg, BH: 164 cm
BW/A: 78.1% ; BH/A: 93.7% ; BW/BH: 98%
Head
Face: Risus sardonicus
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-), icteric
sclerae (-/-)
Ears: right mebran perforatin (+)
Nose
: within normal range, NGT (+)
Mouth
: trismus (+) 3 cm
Neck
Lymph node enlargement (-)
Thorax
Symmetrical fusiform, retraction (-)
HR: 90 bpm, regular, murmur (-/-)
RR: 20 bpm, regular, rhonchi (-/-), wheezing (-/-)
Abdomen
Muscular defense (+), normal peristaltic, liver and spleen impalpable
Extremities
Pulse 90 bpm, regular, adequate pressure/volume, warm extremities, CRT < 3,

A
P

S
O

pitting edema (-/-), muscle rigidity (+)


Tetanus + Chronic suppurative otitis media
Isolated care
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diet via nasogastric tube (NGT) 2250 kcal/day
Tetagam 3000 IU IM single dose
Metronidazole injection 375 mg/6 hr/IV
Diazepam injection 15 mg/3 hr/IV (when in seizure)
January 13, 2016
Seizure (+), fever (-), history of yellowish discharge (+) from right ear.
Sensorium: compos mentis; temperature: 37.1o C
Head
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-),

18

icteric sclerae (-/-)


Ears: white discharge (-) from right ear
Nose
: within normal range, NGT (+)
Mouth
: trismus (+) 3cm
Neck
Lymph node enlargement (-)
Thorax
Symmetrical fusiform, retraction (-)
HR: 96 bpm, regular, murmur (-/-)
RR: 20 bpm, regular, rhonchi (-/-), wheezing (-/-)
Abdomen
Soepel, normal peristaltic, liver and spleen impalpable, opisthotonos (-)
Extremities
Pulse 96 bpm, regular, adequate pressure/volume, warm extremities, CRT <
A
P

3, muscle rigidity (-)


Tetanus
Isolated care
O2 1 L/min via nasal cannula (when in seizures)
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diazepam injection MD 15mg/3hr/IV
Diazepam injection 15mg/IV (when in seizures)
Metrodinazole injection 400mg/6hr/IV (D2)
Diet SV 2100 kcal + 100 gr protein via NGT

R/ Consult otorhinolaryngologist and dentist


Consultation reply from otorhinolaryngologist
S: A 17-year-old patient complained of the white and watery discharge coming out of
right ear of his ear in the last two weeks. Headache (-), seizure (-), fever (-).
O: Ear

Right

Left

Auricles

Normal

Normal

Ear canals

Serumen prop (+)

Serumen prop (+)

Tympanic membrane

Perforation & dry

Intact, light reflex (+)

A: Acute otitis media auricular dextra


P: - H2O2 3% 3gtt VI AD

S
O

January 14, 2016


Seizure (+), fever (-)
Sensorium: compos mentis; temperature: 36.7o C

19

Head
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-),
icteric sclerae (-/-)
Ears: right membrane perforation (+)
Nose
: within normal range, NGT (+)
Mouth
: trismus (+) 3cm
Neck
Lymph node enlargement (-)
Thorax
Symmetrical fusiform, retraction (-)
HR: 92 bpm, regular, murmur (-/-)
RR: 20 bpm, regular, rhonchi (-/-), wheezing (-/-)
Abdomen
Soepel, normal peristaltic, liver and spleen impalpable
Extremities
Pulse 92 bpm, regular, adequate pressure/volume, warm extremities, CRT <
A
P

S
O

3, muscle rigidity (-)


Tetanus + Acute otitis media auricular dextra
Isolated care
O2 1 L/min via nasal cannula (when in seizures)
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diazepam injection MD 17.5mg/3hr/IV
Diazepam injection 15mg/IV (when in seizures)
Metrodinazole injection 400mg/6hr/IV (D3)
Diet SV 2100 kcal + 100 gr protein via NGT
January 15, 2016
Seizure (-), fever (-)
Sensorium: compos mentis; temperature: 36.9o C
Head
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-), icteric
sclerae (-/-)
Ears: right membrane perforation (+)
Nose
: within normal range, NGT (+)
Mouth
: trismus (+) 3cm
Neck
Lymph node enlargement (-)
Thorax

20

Symmetrical fusiform, retraction (-)


HR: 92 bpm, regular, murmur (-/-)
RR: 24 bpm, regular, rhonchi (-/-), wheezing (-/-)
Abdomen
Soepel, normal peristaltic, liver and spleen impalpable
Extremities
Pulse 92 bpm, regular, adequate pressure/volume, warm extremities, CRT < 3,
A
P

muscle rigidity (-)


Tetanus + Acute otitis media auricular dextra
Isolated care
O2 1 L/min via nasal cannula (when in seizures)
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diazepam injection MD 17.5mg/3hr/IV
Diazepam injection 15mg/IV (when in seizures)
Metrodinazole injection 400mg/6hr/IV (D4)
Diet SV 2100 kcal + 100 gr protein via NGT
Giving diazepam MD transformed into continuous with a syringe pump, a dose of 3
mg / bw / day = 150mg / day
5 ampoules of diazepam + 40cc D5% 50cc = 50mg 1cc = 1mg
150mg / 24hr = 6.5cc / hr
Giving diazepam MD 5 ampoules + 40cc D5% 6.5cc / hr
Giviing diazepam eradicate spasms continued as before

S
O

January 16, 2016


Seizure (-), fever (-)
Sensorium: compos mentis; temperature: 37.0o C
Head
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-), icteric
sclerae (-/-)
Ears: right membrane perforation (+)
Nose
: within normal range, NGT (+)
Mouth
: trismus (+) 3cm
Neck
Lymph node enlargement (-)
Thorax
Symmetrical fusiform, retraction (-)
HR: 96 bpm, regular, murmur (-/-)

21

RR: 24 bpm, regular, rhonchi (-/-), wheezing (-/-)


Abdomen
Soepel, normal peristaltic, liver and spleen impalpable
Extremities
Pulse 96 bpm, regular, adequate pressure/volume, warm extremities, CRT < 3,
A
P

muscle rigidity (-)


Tetanus + Acute otitis media auricular dextra
Isolated care
O2 1 L/min via nasal cannula (when in seizures)
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diazepam injection MD 6.5mg/hr/IV
Diazepam injection 15mg/IV (when in seizures)
Metrodinazole injection 400mg/6hr/IV (D5)
Diet SV 2100 kcal + 100 gr protein via NGT
Giving diazepam MD with a syringe pump, a dose of 3mg /bw/d = 150mg /d
Giving diazepam MD 5 ampoules + 40cc D5% 6.5cc / hr
January 17, 2016

S
O

Seizure (-), fever (-)


Sensorium: compos mentis; temperature: 36.8o C
Head
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-), icteric
sclerae (-/-)
Ears: right membrane perforation (+)
Nose
: within normal range, NGT (+)
Mouth
: trismus (+) 3cm
Neck
Lymph node enlargement (-)
Thorax
Symmetrical fusiform, retraction (-)
HR: 92 bpm, regular, murmur (-/-)
RR: 24 bpm, regular, rhonchi (-/-), wheezing (-/-)
Abdomen
Soepel, normal peristaltic, liver and spleen impalpable
Extremities
Pulse 92 bpm, regular, adequate pressure/volume, warm extremities, CRT < 3,
muscle rigidity (-)

22

A
P

Tetanus + Acute otitis mediaauricular dextra


O2 1 L/min via nasal cannula (when in seizures)
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diazepam injection MD 6.5mg/hr/IV
Diazepam injection 15mg/IV (when in seizures)
Metrodinazole injection 400mg/6hr/IV (D6)
Diet SV 2100 kcal + 100 gr protein via NGT
Giving diazepam MD with a syringe pump, a dose of 3mg /bw/d = 150mg /d
Giving diazepam MD 5 ampoules + 40cc D5% 6.5cc / hr

S
O

January 18, 2016


Triggered seizure (-), fever (-)
Sensorium: compos mentis; temperature: 37.3o C
Head
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-), icteric
sclerae (-/-)
Ears: right membrane perforation (+)
Nose
: within normal range, NGT (+)
Mouth
: trismus (+) 4cm
Neck
Lymph node enlargement (-)
Thorax
Symmetrical fusiform, retraction (-)
HR: 100 bpm, regular, murmur (-/-)
RR: 20 bpm, regular, rhonchi (-/-), wheezing (-/-)
Abdomen
Soepel, normal peristaltic, liver and spleen impalpable
Extremities
Pulse 100 bpm, regular, adequate pressure/volume, warm extremities, CRT < 3,

A
P

muscle rigidity (-)


Tetanus + Acute otitis mediaauricula dextra
O2 1 L/min via nasal cannula (when in seizures)
Intravenous fluid (IVFD) D5% NaCl 0.45% 20 gtt/minutes (macro)
Diazepam injection MD 6.5mg/hr/IV via Syring pump
Diazepam injection 15mg/IV (when in seizures)
Metrodinazole injection 400mg/6hr/IV (D7)
Diet SV 2100 kcal + 100 gr protein via NGT

23

CHAPTER 4
DISCUSSION
We present a case about AU, a 17-year-old boy who came to Haji Adam Malik
Central General Hospital Medan on 12 January , 2016 at 4:30 am with the diagnosis of
tetanus. On clinical history, the patient had seizures as the chief complaint. There was
no loss of consciousness during each seizure. The patient also had rigid extremities in
each seizure. He experienced trismus, mouth was opened two centimeter. He also had
fever and a history of ear discharge right ear since three weeks ago. The history of
immunization was not clear. On physical examination, the vital signs showed no
abnormalities. The findings included discharge from his ears, trismus and muscle
rigidity. Physiologic reflexes were normal, and there were no pathologic reflexes.
Laboratory results were normal. Based on these findings, BG was diagnosed with
tetanus.
Tetanus affects all ages; however, the highest prevalence is found in newborn
and young people. Tetanus occurs sporadically and almost always affects unimmunized
persons, partially immunized persons, or fully immunized individuals who fail to
maintain adequate immunity with booster doses of vaccine 3. In the study that conducted
at several hospitals in Indonesia between 1991 and 1996, it was found that almost all
hospitals are found in the age group 5-9 years. Also, the risk of being exposed to tetanus
for boys is greater than girls, because of differences in the daily activities of boys who
prefer to play outdoors5. In this case, the patient is a 17-year-old boy. His history of
immunization was unclear. In the United States from 1995 to 1997, 54% of the reported
cases of tetanus had an unknown tetanus vaccination history11.
Most non-neonatal cases of tetanus are associated with a traumatic injury, often a
penetrating wound inflicted by a dirty object, such as a nail, splinter, fragment of glass,
or unsterile injection, but a rare case may have no history of trauma. Tetanus is also
associated with illicit drug injection, middle-ear infection, animal bites, abscesses
(including dental abscesses), body piercing, chronic skin ulceration, burns, compound
fractures, frostbite, gangrene, intestinal surgery, ritual scarification, infected insect bites,
and female circumcision1, 3. In this case, the patient had a history of middle-ear infection
(acute otitis media) since three weeks ago, with the characteristics of the discharge

24

having white color, watery consistency, no odor, low volume.. However, five days
before hospital admission, the discharge became yellowish-white in color, viscous in
consistency, having a smelly odor and increased volume. The patient often cleaned out
his ear canals by using cotton buds too often (one pack of cotton buds was spent in only
one week) and everything such as wood, pen, etc.
The most common form of tetanus is generalized tetanus, which is characterized
by increased muscle tone and generalized spasms. Trismus (masseter muscle spasm or
lockjaw) is the presenting symptom in about half of cases. Early symptoms include
headache, restlessness, and irritability, and then often followed by stiffness, difficulty
chewing, dysphagia, and neck muscle spasm. Sustained contraction of the facial
muscles results in a grimace or sneer (risus sardonicus), and contraction of the back
muscles produces an arched back (opisthotonos). The subsequent involvement of other
muscles produces a rigid abdomen and stiff proximal limb muscles; the hands and feet
are relatively spared1-5.
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. The smallest disturbance by sight, sound, or
touch may trigger a tetanic spasm. Fever is common because of the substantial
metabolic energy consumed by spastic muscles. Autonomic dysfunction commonly
complicates severe cases and includes tachycardia, arrhythmias, labile hypertension,
diaphoresis, and cutaneous vasoconstriction1, 3.
In this case, the patient had seizures as the chief complaint. The seizures were
triggered by touch and did not occur spontaneously. There was no loss of consciousness
during each seizure. The patient had rigid extremities in each seizure and trismus, and.
He also had a fever. In conclusion, he had the clinical manifestations of a generalized
tetanus. Generalized tetanus makes up approximately 85-90% of all tetanus cases 11. it is
characterized by increased muscle tone and generalized spasms1.
The diagnosis of tetanus is based solely on clinical findings 3. The WHO
definition of tetanus requires at least one of the following signs: trismus (inability to
open the mouth) or risus sardonicus (sustained spasm of the facial muscles), or painful
muscular contractions5, 8. Routine laboratory studies are usually normal. A peripheral

25

leukocytosis may result from a secondary bacterial infection of the wound or may be
stress induced from the sustained tetanic spasms. The cerebrospinal fluid (CSF) is
normal, although the intense muscle contractions may raise intracranial pressure. C.
tetani is not always visible on Gram stain of wound material, and it is isolated in only
about one third of cases1.
In this case, the patient presented with trismus and painful muscular
contractions. The laboratory results were normal. Cerebrospinal fluid analysis and Gram
stain of wound material was not performed. Trismus is the most common presenting
symptom in tetanus, accounting for approximately 75-98% of tetanus cases. Muscle
stiffness accounts for 95%, and muscle spasm is seen in 46% of cases. Fever is seen in
only 8% of cases12.
The treatment for tetanus includes:
1. General measures
A supportive care in a quiet, dark, secluded setting is most desirable because tetanic
spasms may be triggered by minor stimuli, so the patient should be sedated and
protected from all unnecessary sounds, sights, and touch; and all therapeutic and other
manipulations must be carefully scheduled and coordinated1, 8. In this case, the patient
was given an isolated care.
2. Antibiotic therapy
We can choose either penicillin G or metronidazole1, 3, 8. In this case, the patient was
given metronidazole injection 375 mg/6 hr/IV. Metronidazole is preferred because of its
excellent antimicrobial activity, higher survival rate, and the absence of activity
antagonistic to GABA, as seen with penicillin3.
3. Antitoxin
The preparation of choice is human tetanus immunoglobulin (TIG), which should be
given promptly. If TIG is unavailable, human intravenous immunoglobulin (IVIG), or of
equine- or bovine-derived tetanus antitoxin (TAT) is used, and the dose is given half
intramuscularly and half intravenously1. In this case, the patient was given human
tetanus immunoglobulin (HTIG) 3.000 IU intramuscularly.
4. Control of muscle spasms
The preparation of choice is diazepam (0.1-0.2/kg q 3-6 hr given intravenously) 1, 3-4. In
this case, the patient was given diazepam injection 15 mg/3 hr/IV (seizure-eradicating
dose = 15 mg/IV when in seizure).
5. Respiratory care
Intubation or tracheostomy, with or without mechanical ventilation, may be required for

26

hypoventilation due to oversedation or laryngospasm or for the avoidance of aspiration


by patients with trismus, disordered swallowing, or dysphagia3. In this case, the only
respiratory support that was given to the patient is O2 1 L/min via nasal cannula.
6. Autonomic dysfunction
The optimal therapy for sympathetic overactivity has not been defined, but it is
regulated by standard - and - (or both) blocking agents; morphine has also proved
useful1. Hypotension or bradycardia may require volume expansion, use of vasopressors
or chronotropic agents, or pacemaker insertion 3. In this case, there were no signs of
autonomic dysfunction; therefore, no associated therapy was given.
7. Vaccine
Patients recovering from tetanus should be actively immunized because immunity is not
induced by the small amount of toxin that produces disease 3. In this case, a dose of
tetanus toxoid (TT) 0,5 cc was administered once intramuscularly. Basic immunization
of DPT (diphtheria, pertussis, tetanus) is administered three times since 2 months of
age, with an interval of 4-6 weeks. This will grant an immunity for 1-3 years. This is
equal to two doses of tetanus toxoid (TT) in older children or adults. Fourth dose of
DPT can be given at 18-24 months of age; it will prolong the immunity for 5 years more
until the child is 6-7 years old and is equal to the third dose of TT. Fifth dose of DPT, if
given at school age (around 5 years old), will prolong the immunity for 10 years more
until the child is 17-18 years old and is equal to four doses of TT. The booster doses is
administered every ten years. Each dose of tetanus toxoid is given 0,5 cc
intramuscularly13. In this case, for persons of 7-18 years old who are not fully
immunized, the doses of DPT are started at minimum age of 7 years, with an interval of
6 months if the first dose was administered at or after the 1st birthday14.
8. Additional measures
Additional therapeutic measures include hydration to control insensible and other fluid
losses, which may be significant; and the meeting of the patients increased nutritional
requirements by enteral or parenteral means due to tetanus spasms resulting in high
metabolic demands and a catabolic state3, 8. The patient was given IVFD NaCl 0.45% 20
gtt/minutes (micro). The patients nutritional requirement was initially given via
nasogastric tube (NGT).

27

CHAPTER 5
CONCLUSION

AU, a boy, 17 years old, with body weight of 50 kg and body height of 164 cm, came to
Haji Adam Malik Central General Hospital Medan on 12 january 2016 at 4:30 am with
seizures as the chief complaint. Extremities rigidity, trismus, fever, and ear discharge
were found. The patient was diagnosed with tetanus and treated with isolated care, O2 1
L/min via nasal cannula, IVFD NaCl 0.45 % 20 gtt/minutes (micro), diet via nasogastric
tube (NGT), Tetanus immunoglobulin (HTIG) 3.000 IU via IM, tetanus toxoid (TT) 0,5
cc via IM (once), metronidazole injection 375 mg/6 hr/IV, diazepam injection 15 mg/3
hr/IV (seizure-eradicating dose = 15 mg/IV when in seizure).

28

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