Professional Documents
Culture Documents
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
i
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.
Writers
ii
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
1
CHAPTER I
INTRODUCTION
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.
3
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 120°C, 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,
4
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.
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,
5
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 single-
chain 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 γ-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 α 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.
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 days3, 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.
7
3. Local tetanus
It is an uncommon form in which manifestations are restricted to muscles near the
wound. The prognosis is excellent 3. 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.
2.8. 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 patient’s
condition and providing support—especially respiratory support—until recovery 2-3. A
9
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 diffusibility 1, 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 known3. 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
10
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 ages—35, 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
11
2.10. Complications
12
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
History of medication:
Valium, Dexamethasone, Tetagam 500 IU, Ceftriaxone Injection, Metrodinazole
Injection.
History of family:
None
History of pregnancy:
The age of the patient’s 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 immunization:
Not clear.
15
Physical Examination:
Present status:
Sensorium: compos mentis Body temperature: 36.7°C
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 : Risus sardonicus (+)
Eye : 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
16
Differential diagnosis:
1. Tetanus
2. Pediatric febrile seizures
3. Epilepsy
Working diagnosis:
Tetanus
Laboratory finding:
Complete blood analysis (December 11, 2015 / 23:53)
Test Result Unit References
Hemoglobins 14.40 g% 12.0-14.4
Erythrocytes 4.62 106/mm3 4.40-4.48
Leukocytes 9.84 103/mm3 4.5-13.5
Platelets 348 103/mm3 150-450
Hematocrits 40.60 % 37-41
Eosinophils 0.00 % 1-6
Basophils 0.100 % 0-1
Neutrophils 87.00 % 37-80
Lymphocytes 9.70 % 20-40
Monocytes 3.20 % 2-8
Clinical Chemistry
Test Result Unit References
Carbohydrate Metabolism
Random Blood Glucose 116.20 mg/dL 40-60
Renal
Ureum 16.60 mg/dL <50
Kreatinin 0.79 mg/dL 0.7-1.20
Electrolytes
Natrium 138 mEq/L 135-155
Potassium 4.1 mEq/L 3.6-5.5
Chloride 104 mEq/L 96–106
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
17
FOLLOW UP
S Seizure (+), fever (-), history of yellowish discharge (+) from right ear.
O Sensorium: compos mentis; temperature: 37.1o C
Head
Eye : light reflex (+/+), isochoric pupil, pale palpebral conjunctivae (-/-),
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 <
3”, muscle rigidity (-)
A Tetanus
P 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
20
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”, muscle rigidity (-)
A Tetanus + Acute otitis mediaauricula dextra
P 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
25
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
26
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
27
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 metronidazole 1, 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
28
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).
31
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