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

1

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

2

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 MENINGITIS/ENCEPHALITIS

NONVIRAL CAUSES OF ENCEPHALITIS

Herpesviruses

- Herpes simplex

- Varicella-zoster

- Epstein Barr

- Cytomegalovirus

Myxo/paramyxoviruses

- Influenza/parainfluenzae

- Mumps

- Measles

- Adenoviruses

- Rabies

- HIV

Enteroviruses

- Polioviruses

- Coxsackieviruses

- Echoviruses

- Toga viruses /flaviviruses

JEV /West Nile

Rocky Mountain spotted fever

Typhoid ,Typhus

Mycoplasma

Brucellosis

Subacute bacterial endocarditis

Syphilis (meningovascular)

Relapsing fever

Lyme disease

Leptospirosis

Tuberculosis

Cryptococcus

Histoplasma

Naegleria

Acanthamoeba

Toxoplasma

Plasmodium falciparum

Trypanosomiasis

Whipple’s disease

Behcet’s disease

4

- Eastern equine

- Western equine

- Venezuelan equine

- St. Louis. Powasson

- Miscellaneous California

Vasculitis

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 5

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

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 6

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

7

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

8

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 9 th 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 :

12

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

14

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

15

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 :


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

18

LCS Result

- 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 :


Ears : normal

19

Nose : NGT




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.



20


(150cc/4 jam/NGT)

Follow Up September 17th _ 19 th, 2010

S : Unconciousness (+), Seizure (+), Fever (-)


Head :


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/kgBB30cc/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 :


22

Ears : normal

Nose : NGT

Mouth : normal











-Meningoencephalitis + Miliaria Rubra

-Meningitis + Miliaria Rubra





- Inj. Manitol 20% 0,5 gr/kgBB 30cc/24 jam (H3 aff)

- Phenytoin 2 x 50 mg



23

- Resperidon 0,3mg 1x1 (night) for 3 days


(150cc/4 jam/NGT)

Follow Up September 21th _ 23th, 2010



Head :


Ears : normal

Nose : NGT

Mouth : normal












24



- Inj. Ampicillin 650 mg/6 jam/IV


- 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 :


Ears : normal

Nose : NGT

25

Mouth : normal

Neck : Lymph nodes enlargement (-), neck stifness (-)















- Gentamycin Zalf

- Urdafalk 3x40mg (H1)


(150cc/4 jam/NGT)

Follow Up September 27th, 2010

S : Unconciousness (+), Fever (-), Uncontrolled movement (+)

26


Head :


Ears : normal

Nose : NGT

















27

- Gentamycin Zalf



(150cc/4 jam/NGT)

Follow Up September 28th – 31 th, 2010

S : Unconciousness (+), Fever (+), Uncontrolled movement (+)


Head :


Ears : normal

Nose : NGT

Mouth : normal











28


- Inj. Cefotaxim 650 mg/6 jam/IV aff

- Inj. Ampicillin 650 mg/6 jam/IVaff



- Gentamycin Zalf


- 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 :


Ears : normal

Nose : NGT



29




Extremities: Pulse 120 bpm, regularly, BP : 100/60 mmhg, Pressure/Volume was adequate.





P : - Head Elevated 30°




- Gentamycin Zalf


- Cetrizin 1 x ½ tab

- Hydrocortison cream 2,5%


(150cc/4 jam/NGT)

- Fisioterapi

Follow Up October 2nd – 6 th, 2010


30

O : Sens: CM, T: 37,0ºC, BW: 14kg, BL: 92cm

Head :


Ears : normal

Nose : NGT

Mouth : normal





Extremities: Pulse 120 bpm, regularly, BP : 100/60 mmhg, Pressure/Volume

was adequate.









- Gentamycin Zalf


31

- 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

Follow Up October 2nd – 6 th, 2010


O : Sens: CM, T: 37,0ºC, BW: 14kg, BL: 92cm

Head :


Ears : normal

Nose : NGT

Mouth : normal





32


was adequate.









- Gentamycin Zalf


- 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 :

Eyes: light reflexes (+/+), isochoric pupil, lower eyelids pale were not

33

confirmed.

Ears : normal

Nose : normal, NGT (+)

Mouth : normal






was adequate.





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

34


- 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

- 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

35

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.

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

36

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

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.

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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

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.

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http://emedicine.medscape.com/article/1166498-overview

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