Case Report Print

CASE REPORT
ENCEPHALITIS
Presenter : Debby Lidyanita Fachriza
Febrina Siregar
Day/Date : Tuesday, November 2,2010
Supervisor : Dr. Wisman Dalimunthe, Sp.A
CHAPTER I
Introduction
The death rate for encephalitis are still high, ranging between 35-50%. Patients
who live 20-40% have complications or sequelae involving the central nervous
system which can on intelligence, motor, psychiatric, epilepsy, vision or hearing
even the cardiovascular system. Babies who have experienced complications and
encephalitis due to residual heavier. Besides, there is no specific treatment for
encephalitis. Treatment is carried out so far are nonspecific and empirical aims to
maintain and sustain the life of every organ system affected. 4
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CHAPTER II
2.1. Epidemiology
Encephalitis is more common in children and young adults. About 1 in 200,000

people develop encephalitis each year in the United States. While anyone can
succumb, children, the elderly, and those with weakened immune systems are
more vulnerable. 2
Incidence of encephalitis throughout the world is difficult to determine

because the disease is often underreported. Approximately 150 to 3000 cases,
most of which are mild, may occur each year in the United States. Herpesvirus
accounts for most cases of encephalitis in the United States. Arboviral
encephalitis is more prevalent in warm climates and incidence varies considerably
from area to area and from year to year. St. Louis encephalitis is the most
prevalent type of arboviral encephalitis in the United States, and Japanese
encephalitis is the most prevalent type in other parts of the world. 2
2.2. Definition
Encephalitis is an inflammatory process of the brain parenchyma that usually is an

acute process, but maybe a postinfectious encephalomyelitis, a chronic
degenerative disease, or a slow viral infection. Encephalitis results from
inflammation of the brain parenchyma, leading to cerebral dysfunction.
Encephalitis may be diffuse or localized. Organisms cause encephalitis by one of
two mechansms : 1. Direct infection of the brain parenchyma or 2. An apparent
immunemediate response in the CNS tahat usually begins several days after the
appearance of extraneural manifestations of the infection. 2
2.3. Etiology
Viruses are the principal causes of acute infectious encephalitis. Encephalitis also
may result from other types infection and metabolic, toxic, and neoplastic
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disoerder. The most common viral causes of encephalitis in the U.S. are the
arboviruses, enteroviruses, and herpesviruses. HIV is an important cause of
encephalitis in children and adolescents and may presents as an acute febrile
illness, but more commonly is insidious in onset. 2
Acute disseminated encephalomyelitis (ADEM) is the abrupt development

of multiple neurologic signs related to an inflammatory, demyelinating disorder of
the brain and spinal cord. Acute disseminated encephalomyelitis follows
childhood viral infections, such as measles and chickenpox or vaccinations. Acute
disseminated encephalomyelitis resembles multiple sclerosis. 2
Primary Encephalitis—this type results from viral infection of the brain

and spinal cord. Primary encephalitis may occur in isolated cases (sporadic) or
occur in many people at the same time in the same area (epidemic). The most
common type of sporadic infection is herpes simplex encephalitis, which is caused
by the herpes virus. This type carries a high risk for serious neurological damage
and death and can occur in newborns if the virus is passed from the mother to the
infant during birth. Arthropod-borne viruses (transmitted through the bite of
insects and ticks) may cause arboviral encephalitis. Mosquitoes are the most
common agents of transmission and most cases occur during warmer weather,
when the insects are more active. Arboviral encephalitis and rabies encephalitis
(usually transmitted through the bite of an infected animal) may be sporadic or
epidemic. 3
Other types of arboviral encephalitis include the following; Japanese

(widespread in Asia), Murray Valley (endemic in Australia), Powassan
(transmitted by ticks; occurs in Canada and the northern United States), Tick-
borne (occurs throughout Europe; vaccine available) and Venezuelan equine
(common in Central and South America). 3
Secondary Encephalitis—this type develops as a complication of a viral

infection or reactivation of a latent virus. Viruses can become reactive when the
immune system is suppressed by other conditions (e.g., malnutrition, stress,
3
disease). Infections that may cause secondary encephalitis include influenza,
chickenpox (varicella-zoster), measles (rubeola), mumps, and German measles
(rubella). Secondary encephalitis that develops as a result of a variola virus
infection following smallpox vaccination or reactivation of another viral infection
(called acute disseminated encephalitis) is often fatal. 3
VIRAL NONVIRAL CAUSES OF

MENINGITIS/ENCEPHALITIS ENCEPHALITIS
Herpesviruses Rocky Mountain spotted fever

- Herpes simplex Typhoid ,Typhus
- Varicella-zoster Mycoplasma
- Epstein Barr Brucellosis
- Cytomegalovirus Subacute bacterial endocarditis
Myxo/paramyxoviruses Syphilis (meningovascular)
- Influenza/parainfluenzae Relapsing fever
- Mumps Lyme disease
- Measles Leptospirosis
- Adenoviruses Tuberculosis
- Rabies Cryptococcus
- HIV Histoplasma
Naegleria
Enteroviruses Acanthamoeba
- Polioviruses Toxoplasma
- Coxsackieviruses Plasmodium falciparum
- Echoviruses Trypanosomiasis
- Toga viruses /flaviviruses Whipple’s disease
JEV /West Nile Behcet’s disease
4
- Eastern equine Vasculitis
- Western equine
- Venezuelan equine
- St. Louis. Powasson
- Miscellaneous California
Table 1. Pathogens of Encephalitis 3
2.4. Pathophysiology
There are at least two forms of infection-related encephalitis: primary and post- or
parainfectious. A primary encephalitis results from direct CNS invasion by the
offending agent, and the gray matter often is targeted. A postinfectious or
parainfectious encephalitis presents much like a primary encephalitis, but the
illness is not caused by direct CNS infection. In post/parainfectious encephalitis,
neurologic effects are the consequence of the host’s immune response, which
often affects the white matter. 3
The pathogenesis of primary encephalitis is diverse and incompletely

understood. Organisms infecting the brain directly first must gain entry to the
CNS. Some pathogens such as arboviruses initially cause bloodstream infection,
then enter the CNS via endothelial cell infection, endothelial cell transport, or
carriage in cells entering the CNS. Encephalitis tends to be a rare complication
after viremia because entry to the brain is carefully regulated at the blood-brain
barrier. An alternative mechanism used by herpes simplex virus (HSV), rabies,
and possibly poliovirus is retrograde transport in neurons. This strategy may be
successful because pathogens traveling inside neurons avoid immune surveillance.
An alternative mechanism used by the amoeba Naegleria fowleri is entry through
the olfactory mucosa. 3
Once an organism has entered the brain, a variety of anatomic sites can
become infected. For example, HSV typically infects neurons in the temporal
lobe; rabies predominantly affects the pons, medulla, cerebellum, and
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hippocampus; and Japanese encephalitis virus affects the brainstem and basal
ganglia. Neurologic signs and symptoms develop after infection as the result of
direct neuronal injury, the host inflammatory response, or both. Histologically, the
host response can include perivascular inflammation, gliosis, and brain edema.
Postinfectious encephalitis occurs days to weeks after the onset of an

infection. Currently in the United States, a minor respiratory tract infection is
likely to be the inciting event. Before the widespread use of viral vaccines, a
distinctive illness such as measles or varicella was likely to be the preceding
event, and encephalitis may follow these infections in regions where they remain
common. Because the inciting pathogen is not detected in the CNS in
postinfectious encephalitis, the illness is hypothesized to be caused by an aberrant
immune response against brain antigens such as myelin basic protein. Subsequent
demyelination causes focal or global CNS dysfunction. Postinfectious encephalitis
often is called acute disseminated encephalomyelitis (ADEM). 3
2.5. Diagnosis
History
- Ask about a viral prodrome with symptoms such as upper respiratory

infection, cough, coryza, malaise, anorexia, decreased enteral intake, diarrhea,
nausea, and vomiting.
- Encephalitis is often heralded by headaches, photophobia, a stiff neck,

increased sleeping, change in mental status, irritability, confusion,
hallucinations, seizures.
- Prodromal symptoms can range from hours to weeks; seizures or sudden

lapse of consciousness are uncommon as initial symptoms of encephalitis.
- Inquire about recent travel history, pets, and tick or mosquito bites. 3
Physical Exam
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Although the causes differ, the clinical symptoms of encephalitis is more or less
the same and unique so it can be used as diagnostic criteria. In general, symptoms
of encephalitis triad consisting of fever, convulsions and decreased
consciousness.7
After an incubation period of approximately 5-10 days there will be a

sudden increase in temperature, often occur hiperpireksia, big headache in
children, screaming at the child. Found signs of CNS stimulation (coma, stupor,
lethargy), stiff neck, increased tendon reflexes, tremors, muscle weakness and
sometimes paralysis. Clinical manifestations of bacterial encephalitis, in the
beginning there are no typical symptoms such as generalized infection, then
emerged signs of increased intracranial pressure headache, vomiting, no appetite,
fever, blurred vision, general or focal seizures and decreased consciousness.
Symptoms of cranial Nervi deficit, hemiparesis, increased tendon reflexes, stiff
neck, aphasia, hemianopia, nistagmus and ataxia. 8
Causes of neurological abnormalities (neurological deficit) is a direct

invasion and destruction of brain tissue by a virus that is being breed; nerve tissue
reaction against viral antigens that will result in demyelination, vascular damage,
and paravaskular; and because the activation reaction neurotrophic virus that is
latent.7
In viral encephalitis early symptoms of mild headache, fever, symptoms of

upper respiratory infections or gastrointestinal tract for a few days later came the
signs of CNS inflammation, such as stiff neck, a sign of positive kernig, anxiety,
weakness and difficulty sleeping. Neurologic deficits that arise depending on
where the damage. Furthermore, consciousness begins to decline until the coma,
or focal seizures may occur commonly, hemiparesis, impaired coordination,
personality disorders, disorientation, impaired speech and mental disorders.
Clinical findings in encephalitis is determined by (1) weight and anatomical
localization of nervous system that looks (2) pathogenicity agents that attack (3)
immunity and reactive mechanisms other patients.6
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Diagnostic Test
Typically, a doctor will ask for a blood sample and order a lumbar puncture
(sometimes called a spinal tap), in which a needle is inserted into the lower back
and a small amount of fluid (called CSF or cerebral-spinal fluid) is taken from the
spinal canal. Some hospitals are also equipped to take a biopsy, where a tiny
amount of tissue is taken from the brain while the patient is under general
anesthesia. Doctors also frequently order a CT scan or Magnetic Resonance Image
(MRI), in which computerized images of the brain are obtained that show the
extent of the swelling and damage to the brain. Another test sometimes used to
help confirm a diagnosis is an electroencephalogram (EEG), which records
electrical events in the brain.6
2.6. Differential Diagnosis
- Meningitis
- Encephalopathy
- Brain Abscess
- Subarachnoid hemorrhage
- Brain tumor. 6
2.7. Complication
Neurological complications that may be permanent or improve as the infection

runs its course include the following; Altered mental state (e.g., disorientation,
personality changes), convulsions, drooping eyelids (ptosis), double vision
(diplopia), crossed eyes (strabismus), hyperactive deep tendon reflexes, increased
intracranial pressure, loss of consciousness, mental retardation, motor
dysfunction, partial paralysis (paresis) of the extremities, projectile vomiting,
pupil irregularities, restlessness, seizures and tremor. 3
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2.7. Treatment
Treatment for encephalitis depends on the cause. Some cases of viral encephalitis
can be treated successfully if medication is started as soon as possible. If herpes
simplex encephalitis is suspected, antiviral medication such as acyclovir
(Zovirax®) or ribavirin (Virazole®) is often administered immediately to improve
chances for recovery and prevent complications. Side effects of these medications
include nausea, vomiting, and headache. Treatment for viral encephalitis also
includes palliative care. There is no cure for arboviral encephalitis and the goal of
treatment is to relieve symptoms (palliative). 2,3,6
Palliative care may include intravenous fluids (to prevent dehydration),

antibiotics (to prevent secondary infections), and other medications (to prevent
complications). Diuretics (e.g., furosemide, mannitol) may be administered to
reduce intracranial pressure and benzodiazepines (e.g., lorazepam [Ativan®]) may
be administered to prevent seizures. 2,3,6
New patients with possible encephalitis should be hospitalized until the

disappearance of neurologic symptoms. Management objective is to maintain
organ function by laboring airway remains open, enteral or parenteral feeding,
maintaining fluid and electrolyte balance and acid-base disorders correction of
blood. Governance is done as follows 4:
1. Overcoming cramps are vital action, because seizures in encephalitis is usually

severe. Giving Phenobarbital mg/kgBB/24 5-8 hours. If seizures occur frequently,
should be given diazepam (0.1 to 0.2 mg / kg) IV, in the form of infusion for 3
minutes.
2. Improving homeostasis, with intravenous fluids D5 - 1 / 2 S or D5 - 1 / 4 S
(depending on age) and oxygen delivery.
3. Reduce cerebral edema and to reduce the impact by anoksia cerebral with
dexamethasone 0.15 to 1.0 mg / kg / day iv divided into 3 doses.
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4. Lowering the intracranial pressure rises with Mannitol is given intravenously at
a dose of 1.5 to 2.0 g / kg for 30-60 minutes. Giving can be repeated every 8-12
hours. Glycerol can also, through the pipe nasogastrik, 0.5 to 1.0 ml / kg diluted
with two parts orange juice. This material is not toxic and can be repeated every 6
hours for a long time.
5.Causative treatment.
Before etilogi got rid of bacteria, especially brain abscess (bacterial encephalitis),
it must be given parenteral antibiotic treatment. Treatment for encephalitis due to
herpes simplex virus infection Acyclovir is given intravenously, 10 mg / kg to 30
mg / kg per day for 10 days. If there is tolerance then given Adenine arabinose
(vidarabin). So also when there is recurrence after treatment with Acyclovir. With
the exception of the use of Adenine arabinosid to patients by herpes simplex
encephalitis, the treatment is done is non-specific and empirical in order to sustain
life and support every organ system affected. The effectiveness of various
treatments are recommended not been assessed objectively.
6. Physiotherapy and rehabilitative efforts after the patient recovered
7. Foods high in protein calorie diet therapy.
8. Other, better treatment, early consulting with an anesthesiologist to anticipate

the need for artificial respiration
2.8. Prognosis
The prognosis for encephalitis varies depends on the type of encephalitis, the
patient's age, overall health, and status of the immune system. Some cases are
mild, short and relatively benign and patients have full recovery. Other cases are
severe, and permanent impairment or death is possible. The acute phase of
encephalitis may last for 1 to 2 weeks, with gradual or sudden resolution of fever
and neurological symptoms. Neurological symptoms may require many months
before full recovery. With early diagnosis and prompt treatment, most patients
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recover from meningitis. However, in some cases, the disease progresses so
rapidly that death occurs during the first 48 hours, despite early treatment. 2,4,9
2.9. Objective
The aim of this paper is to report a case of Encephalitis in a boy aged 1 years and
9 months old.
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CHAPTER III
3.1. Case Report
R, a 1 year and 9 months old boy, weight 7kg with the height of 99cm was
admitted to H. Adam Malik Hospital on September 9th 2010, with the chief
complain is unconsciousness. This has been experienced by the patient since last 2
days. This patient been having seizure 7 days in a row, frecuency >3 times per day
for ±10-20 minutes. History of seizure before (+).Fever was found since 2 weeks
ago. It was very high fever but shiverring was not found. Cough (-), flu (-).
Urination and defecation was normal. History of contact with TBC patients
negatif. There is yellowish fluid, thick and no odor was found from left ear since 3
weeks ago.
History of delivery was normal and aided by a midwife, crying spontaneously,

and cyanosis was not found, her wight is 2500 gram and lenght was forgotten.
History of pregnancy was normal. History of immunization was complete.
Feeding history : 0-5 months with breast milk.
Before she was admitted to HAM General Hospital, she was consulted from
puskesmas Karang Rejo. The patient was initially diagnosed with high fever and
seizure.
Physical examination
On physical examination, the following findings were confirmed.
A boy, with body weight 7 kg, body length was 99 cm, and EID index was 82,35
%, nutritional status was normoweight; body temperature was 37,3˚ C. The level
of consciousness of this patient was GSC11 (E4V2M5), anemia (-) dyspnoe (-),
edema (-), cyanotic (-), jaundice (-).
Head :
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Eye : light reflexes (+/+), isochoric pupil. Pale inferior palpebra
conjunctive (-/-)
Ears : normal
Nose : normal
Mouth : ulcus (+) in mucosa and lips
Neck : normal, no lymph nodes enlargement
Chest : Symmetrical fusiform, retraction (+) epigastrial, suprasternal
HR : 116 bpm, regular, no murmur
RR : 20 tpm, regular, no rales
Abdominal : soepel, peristaltic was normal. H/L : impalpable
Extremities : Pulse was 116 tpm, regular, normal tone and volume
Spastic (+) at four extremities
Lymph nodes enlargement was not found
Physiology Reflex: APR +/+↑ ; KPR +/+↑
Pathologic Reflex: Babinsky (-), Oppenheim (-),
Meningeal Reflex: (-)
Genitalia : Boy, there were no abnormalities present
Laboratory findings (September 9, 2010):
Routine Blood Examination
- WBC : 5.85 x 103/uL - RBC : 4.75 x 106/uL
13
- Hb : 12.0 g/dL - PLT : 293 x 103/uL
Blood Electrolic
- Na : 138 mEq/L
-K : 3,4 mEq/L
- Cl : 108 mEq/L
Liver Profile
- SGOT (AST) : 217 u/L
- SGPT (ALT) : 213 u/L
Kidney Profile
- Ureum : 14 mg/dl
- Creatinine : 0,64 mg/dl
Arterial Blood Gas
- pH : 7.471 - Pco2 : 29.0 mmHg
- Po2 : 196.5 mmHg - Bicarbonate : 20.7
- Total CO2 : 21,5 - Base Exes : -1.9
- O2 Saturation : 99,7 %
Working Diagnosis :
- Encephalitis
- Meningoencephalitis
- Meningitis
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Further Examinations :
- Complete blood, LFT, RFT, Electrolit, AGDA
- LP
- X-ray
- Head CT scan
Medication :
- Head elevated 30°
- O2 1-2 L/i
- IVFD D5% NaCl 0,9% ; 48gtt/i micro
- Inj. Cefotaxim 650mg / 6 hours / IV
- Inj. Phenytoin loading dose 20mg/kgbb in 20 cc NaCl 0,9% (if seizure)
- Kenalog in orabase 2x1 applic
- Gentamycin zalf 3x1 applic
- Diet SV 1560 kkal + 26 gr protein
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3.2. Daily Follow Up
Follow Up September 10th, 2010
S : Unconciousness (+), Seizure (-), Fever (-)
O : Sens: GSC 6 (E1V1M4), T: 37,3ºC, BW: 13kg, BL: 92cm BW/BL:96,29%
Head :
Eyes: light reflexes (+/+), isochoric pupil, lower eyelids pale were not
confirmed.
Ears : normal
Nose : normal
Mouth : ulcus (+) at lips and mouth
Neck : Lymph nodes enlargement (-)
Axilla : pustule (+)
Chest : Symmetrical fusiformic, HR : 110 bpm, regularly, murmurs (-)
RR : 48 tpm, regularly, rales (-),

stridor (+)
Abdomen : Soepel, normal peristaltic. H/L : inpalpable
Extremities: Pulse 110 bpm, regularly, Pressure/Volume was adequate.
Spastic (+) at 4 extremities, pustule (+)
Pathologic Reflex: Babinsky (-), Oppenheim (-), Gordon (-)
Meningeal Reflex : (-)
A : -Encephalitis + stomatitis + impetigo bulosa
-Meningoencephalitis + stomatitis + impetigo bulosa
-Meningitis + stomatitis + impetigo bulosa
P : - Head elevated 30°
16
- IVFD D5% NaCl 0,9% 36 gtt/i mikro
- Inj. Cefotaxim 650 mg/6 jam/IV
- Inj. Ampicillin 650 mg/6 jam/IV, skin test
- phenytoin loading dose 260 mg in 30 cc NaCl 0,9% in 30 minutes,
12 hours later maintenance 35 mg/12 jam/IV in 10 cc NaCl 0,9% in 30
minutes.
- Kenalog inorabase 2x1 applic
- Gentamycin Zalf 3x1 applic
- Diet SV 1150 kkal dengan 20 gr protein dalam 900cc cairan
(150cc/4 jam/NGT)
Follow Up September 11th - 14 th, 2010
Head :
confirmed.
Ears : normal
Nose : normal
Axilla : pustule (+)
17
RR : 18 tpm, regularly, rales (-),
A : -Encephalitis + stomatitis + impetigo bulosa
-Meningoencephalitis + stomatitis + impetigo bulosa
-Meningitis + stomatitis + impetigo bulosa
P : - Elevasi kepala 30°
- Phenytoin maintenance 35 mg/12 jam/IV diencerkan dalam 10 cc NaCl
0,9% habis dalam 30 menit (if seizure)
- Diet SV 1150 kkal with 20 gr protein in 900cc fluid
(150cc/4 jam/NGT)
X-Ray Result
Abnormality radiological of the heart and lung were not found
LCS Result
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- Colour : clear
- LDH : 111 U/L
- Protein : 10,0 mg/dL
- Total of cel : 1,0 mm3
- Glucose : 57,0 mg/dL
- pH :7
- PMN : difficult to analize
- MN : difficult to analize
- Culture : Staphylococcus Saprophyticus
Mantoux Test Result
Induration (-)
Hiperemis (-)
Result : (-)
Follow Up September 15th _ 16 th, 2010
S : Unconciousness (+), Seizure (+), Fever (-)
Head :
confirmed.
Ears : normal
Nose : NGT
19
RR : 48 tpm, regularly, rales (-)
A : -Encephalitis + Miliaria Rubra + Stomatitis
-Meningoencephalitis + Miliaria Rubra + Stomatitis
-Meningitis + Miliaria Rubra + Stomatitis
- Jika kejang phenytoin loading dose 260 mg diencerkan dalam 30
cc NaCl 0,9% habis dalam 30 menit, 12 jam kemudian maintenance 35
mg/12 jam/IV diencerkan dalam 10 cc NaCl 0,9% habis dalam 30 menit.
(150cc/4 jam/NGT)
20
Follow Up September 17th _ 19 th, 2010
S : Unconciousness (+), Seizure (+), Fever (-)
Head :
confirmed.
Ears : normal
Nose : NGT
A : -Encephalitis + Miliaria Rubra
-Meningoencephalitis + Miliaria Rubra
-Meningitis + Miliaria Rubra
21
- Jika kejang phenytoin loading dose 260 mg diencerkan dalam 30
cc NaCl 0,9% habis dalam 30 menit, 12 jam kemudian maintenance 35
mg/12 jam/IV diencerkan dalam 10 cc NaCl 0,9% habis dalam 30 menit.
- Inj. Manitol 20% 0,5 gr/kgBB30cc/24 jam
(150cc/4 jam/NGT)
Head CT Scan result
Atrofi cerebral cortex, hidrosefalus comunicans, ischemic, and infark
bilateraloccipital lobes e.c meningitis
Follow Up September 20th , 2010
O : Sens: GSC 11 (E4V2M5), T: 36,5ºC, BW: 14kg, BL: 92cm
Head :
confirmed.
Ears : normal
Nose : NGT
Mouth : normal
22
-Meningoencephalitis + Miliaria Rubra
-Meningitis + Miliaria Rubra
- Inj. Manitol 20% 0,5 gr/kgBB 30cc/24 jam (H3 aff)
- Phenytoin 2 x 50 mg
- Resperidon 0,3mg 1x1 (night) for 3 days
(150cc/4 jam/NGT)
23
Follow Up September 21th _ 23th, 2010
Head :
confirmed.
Ears : normal
Nose : NGT
Mouth : normal
- Inj. Ampicillin 650 mg/6 jam/IV
24
- Urdafalk 3x40 mg
(150cc/4 jam/NGT)
- Fisioterapi
EEG Result
Normal
Banyak dijumpai artefak ECG
Follow Up September 24th _ 26th, 2010
S : Unconciousness (+), Fever (-), Uncontrolled movement (+)
Head :
confirmed.
Ears : normal
Nose : NGT
Mouth : normal
Neck : Lymph nodes enlargement (-), neck stifness (-)
25
- Gentamycin Zalf
- Urdafalk 3x40mg (H1)
(150cc/4 jam/NGT)
Follow Up September 27th, 2010
S : Unconciousness (+), Fever (-), Uncontrolled movement (+)
Head :
confirmed.
Ears : normal
26
Nose : NGT
- Gentamycin Zalf
(150cc/4 jam/NGT)
Follow Up September 28th – 31 th, 2010
27
S : Unconciousness (+), Fever (+), Uncontrolled movement (+)
Head :
confirmed.
Ears : normal
Nose : NGT
Mouth : normal
- Inj. Cefotaxim 650 mg/6 jam/IV aff
- Inj. Ampicillin 650 mg/6 jam/IVaff
- Gentamycin Zalf
28
- Diet SV 1150 kkal with 20 gr protein in 900cc fluid
(150cc/4 jam/NGT)
- Fisioterapi
Follow Up October 1st , 2010
O : Sens: GSC 12 (E4V3M5), T: 37,9ºC, BW: 13,5kg, BL: 92cm
Head :
confirmed.
Ears : normal
Nose : NGT
Extremities: Pulse 120 bpm, regularly, BP : 100/60 mmhg, Pressure/Volume

was adequate.
P : - Head Elevated 30°
29
- Gentamycin Zalf
- Cetrizin 1 x ½ tab
- Hydrocortison cream 2,5%
(150cc/4 jam/NGT)
- Fisioterapi
Follow Up October 2nd – 6 th, 2010
O : Sens: CM, T: 37,0ºC, BW: 14kg, BL: 92cm
Head :
confirmed.
Ears : normal
Nose : NGT
Mouth : normal
30
was adequate.
- Gentamycin Zalf
- Caladin cream
- Urdafalk 3x40mg
R/ : - Physiotherapy 3x/minggu
Lab Finding October 5 th, 2010
Routine Blood Examination
- WBC : 3.77 x 103/uL - RBC : 3.97 x 106/uL
- Hb : 9.78 g/dL - PLT : 269 x 103/uL
31
Follow Up October 2nd – 6 th, 2010
O : Sens: CM, T: 37,0ºC, BW: 14kg, BL: 92cm
Head :
confirmed.
Ears : normal
Nose : NGT
Mouth : normal
was adequate.
- Gentamycin Zalf
32
- Caladin cream
- Urdafalk 3x40mg
Follow Up October 7th – 8 th, 2010
S : Unconciousness (+), Fever (+), Seizure (+), generalized, freq 2x, duration 5
Minutes, papule erythema (+)
O : Sens: GCS 6 (E2V2M2), T: 38,2ºC, BW: 14kg, BL: 92cm
Head :
confirmed.
Ears : normal
Nose : normal, NGT (+)
Mouth : normal
was adequate.
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P : - Head elevated 30°
- Phenytoin loading dose 280mg in 28cc NaCl 0,9% maintenance inj.
Phenytoin 50mg/12 jam in 5cc NaCl 0,9%
- Carmabazepin 5mg/kgBB
- Gentamycin Zalf
- Caladin cream
- Urdafalk 2x40mg
Lab Findings October 9th, 2010
Arterial Blood Gas
- pH : 7.230 - Pco2 : 25.0 mmHg
- Po2 : 132.0 mmHg - Bicarbonate : 10
- Total CO2 : 11.0 - Base Exes : -15
- O2 Saturation : 96.0 %
Blood Electrolic
34
- Na : 157 mEq/L
-K : 3,3 mEq/L
- Cl : 125 mEq/L
Glucose
- Blood : 132 mg/dL
- Urine : -
The patient passed away on Oktober 9th 2010 at 17.10 p.m.
CHAPTER IV
4.1. Discussion
Encephalitis is irritation and swelling (inflammation) of the brain. It often coexists

with inflammation of the covering of the brain and spinal cord (meningitis) and
most cases are caused by viral infection. Inflammation changes the normal blood
flow in the brain. It usually results from an infection, most often by a virus, but
sometimes by bacteria, a fungus, or parasites. In rare cases, it is caused by brain
injury, a drug or vaccine reaction, or poison.
Base on theory the symptoms of encephalitis may very widely depending

on the cause and severity. They range from no symptoms in very mild cases, to
more severe symptoms, including muscle weakness (unsteadiness standing up or
trouble walking), headache, fatigue, fever, neck pain, stiff neck, nausea and
vomiting, a foul mood, irritability, aversion to light (squinting), seizures,
clumsiness, mental confusion, drowsiness, and a coma (in severe cases). Most
people infected with an arthropod-borne virus do not develop encephalitis.
35
Infection is usually does not produce symptoms (called asymptomatic) or causes
flu-like symptoms such as fever, headache, and malaise.
In this case, the diagnosis is established based on historical taking and clinical
examination that lead to encephalitis. Historical taking gained an unconsciousness
that has been experienced by the patient since last 2 days. Fever was found with
the temperature around 37,5 -38,5˚C. This patient been having seizure 7 days in a
row before admitted, frequency >3 times per day for ±10-20 minutes, rigid hand
was found. Other then that, the physiology reflexes of this patient are higher then
usual.
To confirm the diagnosis a doctor will ask for a blood sample and order a lumbar
puncture, in which a needle is inserted into the lower back and a small amount of
fluid (called CSF or cerebral-spinal fluid) is taken from the spinal canal. Some
hospitals are also equipped to take a biopsy, where a tiny amount of tissue is taken
from the brain while the patient is under general anaesthesia. Doctors also
frequently order a CT scan or Magnetic Resonance Image (MRI), in which
computerized images of the brain are obtained that show the extent of the swelling
and damage to the brain. Another test sometimes used to help confirm a diagnosis
is an electroencephalogram (EEG), which records electrical events in the brain.
For this patient we had done several procedures such as LFT, Blood culture,
Lumbar Puncture, mantoux test, X-ray, EEG, and Head CT scan. The result for
the lumbar puncture is LCS analize within normal limits. The result for EEG is
normal. For radiology the result is normal and Mantoux test was negatif. Finally
Head CT result are atrofi cerebral cortex, hidrosefalus comunicans, ischemic, and
infark bilateraloccipital lobes e.c meningitis.
Treatment for viral encephalitis also includes palliative care. There is no cure for
arboviral encephalitis and the goal of treatment is to relieve symptoms (palliative).
Palliative care may include intravenous fluids (to prevent dehydration), antibiotics
(to prevent secondary infections), and other medications (to prevent
complications). Diuretics (e.g., furosemide, mannitol) may be administered to
36
reduce intracranial pressure and benzodiazepines (e.g., lorazepam [Ativan®]) may
be administered to prevent seizures.
The patient was given oxygen, IVFD D5% NaCl 0,225%, Inj. Cefotaxime, inj.
Ampicillin, inj. Phenytoin, Inj. Manitol, Paracetamol tablet, Risperidon tablet, and
Cetrizine tablet.
4.2. Summary
It has been reported a case of a boy, 1 year and 9 months years old with
encephalitis. The diagnosis was established based on anamnesis, clinical sign,
symptoms, and physical examination. The prognostic of this patient was not good.
Finally, the patient passed away on the 9th of march 2010 at 17.15 with cause of
death being metabolic asidosis.
REFERENCES
1.
2. Kliegman, Jenson, Marcdante, Behrman 2006, Essentials of pediatrics,

Fifth edition, H : 483-486, Ste1800, Philadelphia.
3. Lewis, P. Glaser, CA, Pediatrics in review, Encephalitis. Official Journal

Of The American Academy Of Pediatrics. 2005.
4. Anonim 1985, Ensefalitis dalam Hasan R., Ilmu Kesehatan Anak, h : 622-
624, Fakultas Kedokteran Universitas Indonesia. Jakarta.
5. Gondim, FAA. Oliveira, G. Thomas, FP. Viral Encephalitis [ cited 2008

October 4]. Available from: URL:
http://emedicine.medscape.com/article/1166498-overview.
Accessed October 25, 2010
6. Nelson, dkk. Meningoensefalitis Virus, Ilmu Kesehatan Anak Nelson, h :

882-884. ECG. Jakarta
37
7. Anonim 2000, Ensefalitis dalam Arif M, Kapita Selekta Kedokteran, Edisi
3, Jilid 2, h: 60-66, Medik Aesculapius FK UI, Jakarta.
8. Kempe, C.H., 1982, Infections, bacterial and Spirochaetal In Jerry L. Eller,

Current Pediatric Diagnosis and Treatment, 7 ed., p : 732-733, Lange
Medical Publications, Los Atlos, California.
38

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CASE REPORT

Day/Date : Tuesday, November 2,2010

Supervisor : Dr. Wisman Dalimunthe, Sp.A

Encephalitis is more common in children and young adults. About 1 in 200,000

Incidence of encephalitis throughout the world is difficult to determine

Encephalitis is an inflammatory process of the brain parenchyma that usually is an

Acute disseminated encephalomyelitis (ADEM) is the abrupt development

Primary Encephalitis—this type results from viral infection of the brain

Other types of arboviral encephalitis include the following; Japanese

Secondary Encephalitis—this type develops as a complication of a viral

VIRAL NONVIRAL CAUSES OF

Herpesviruses Rocky Mountain spotted fever

Table 1. Pathogens of Encephalitis 3

The pathogenesis of primary encephalitis is diverse and incompletely

Postinfectious encephalitis occurs days to weeks after the onset of an

- Ask about a viral prodrome with symptoms such as upper respiratory

- Encephalitis is often heralded by headaches, photophobia, a stiff neck,

- Prodromal symptoms can range from hours to weeks; seizures or sudden

After an incubation period of approximately 5-10 days there will be a

Causes of neurological abnormalities (neurological deficit) is a direct

In viral encephalitis early symptoms of mild headache, fever, symptoms of

2.6. Differential Diagnosis

Neurological complications that may be permanent or improve as the infection

Palliative care may include intravenous fluids (to prevent dehydration),

New patients with possible encephalitis should be hospitalized until the

1. Overcoming cramps are vital action, because seizures in encephalitis is usually

6. Physiotherapy and rehabilitative efforts after the patient recovered

7. Foods high in protein calorie diet therapy.

8. Other, better treatment, early consulting with an anesthesiologist to anticipate

3.1. Case Report

History of delivery was normal and aided by a midwife, crying spontaneously,

On physical examination, the following findings were confirmed.

Mouth : ulcus (+) in mucosa and lips

Neck : normal, no lymph nodes enlargement

Chest : Symmetrical fusiform, retraction (+) epigastrial, suprasternal

HR : 116 bpm, regular, no murmur

RR : 20 tpm, regular, no rales

Abdominal : soepel, peristaltic was normal. H/L : impalpable

Spastic (+) at four extremities

Lymph nodes enlargement was not found

Physiology Reflex: APR +/+↑ ; KPR +/+↑

Pathologic Reflex: Babinsky (-), Oppenheim (-),

Meningeal Reflex: (-)

Genitalia : Boy, there were no abnormalities present

Laboratory findings (September 9, 2010):

Routine Blood Examination

- WBC : 5.85 x 103/uL - RBC : 4.75 x 106/uL

- SGOT (AST) : 217 u/L

- SGPT (ALT) : 213 u/L

- Creatinine : 0,64 mg/dl

Arterial Blood Gas

- pH : 7.471 - Pco2 : 29.0 mmHg

- Po2 : 196.5 mmHg - Bicarbonate : 20.7

- Total CO2 : 21,5 - Base Exes : -1.9

- Complete blood, LFT, RFT, Electrolit, AGDA

- Head elevated 30°

- IVFD D5% NaCl 0,9% ; 48gtt/i micro

- Inj. Cefotaxim 650mg / 6 hours / IV

- Inj. Phenytoin loading dose 20mg/kgbb in 20 cc NaCl 0,9% (if seizure)

- Kenalog in orabase 2x1 applic

- Gentamycin zalf 3x1 applic

- Diet SV 1560 kkal + 26 gr protein

Follow Up September 10th, 2010