i

ACKNOWLEDGMENTS

We are greatly indebt to the Almighty One for giving us blessing to finish
this case report, Meningoencephalitis and Marasmus. This case report is
requirement to complete the clinical assistance program in Department of Child
Health in Haji Adam Malik General Hospital, Medical Faculty of North Sumatera
University.
We are also indebt to our supervisor and adviser, Dr. Supriatmo,
M.Ked(Ped), Sp.A(K), for spending time to give us guidance, comments, and
suggestions. We are grateful because without his role, this case report wouldnt
have taken its present shape.
This case report has gone through series of developments and corrections.
There were critical but constructive and relevants suggestions from the reviewers.
Hopefully the content will be useful for everyone the future.

Medan, February 2017

Writers

i
 CONTENTS

ACKNOWLEDGEMENTS ........................................................................ i
CONTENTS ................................................................................................. ii
CHAPTER 1 INTRODUCTION ............................................................... 1
1.1. Background ................................................................................ 1
1.2. Objective .................................................................................... 2
CHAPTER 2 LITERATURE REVIEW ................................................... 3
2.1. Anatomy of the brain ................................................................. 3
2.2. Meningoencephalitis .................................................................. 6
2.2.1 Definition .......................................................................... 6
2.2.2 Aetiology ........................................................................... 7
2.2.3 Pathophysiology ................................................................ 9
2.2.4 Diagnosis ........................................................................... 11
2.2.5 Differential Diagnosis ....................................................... 14
2.2.6 Management ...................................................................... 14
2.2.7 Prognosis ........................................................................... 16
2.3. Marasmus ................................................................................... 17
2.3.1 Definition .......................................................................... 17
2.3.2 Pathophysiology ................................................................ 17
2.3.3 Diagnosis ........................................................................... 18
2.3.4 Management ...................................................................... 19
2.3.5 Prognosis ........................................................................... 20
CHAPTER 3 CASE REPORT ................................................................... 21
CHAPTER 4 DISCUSSION ....................................................................... 31
CHAPTER 5 SUMMARY .......................................................................... 34
REFERENCE

ii
 CHAPTER 1

INTRODUCTION

1.1 Background

The Health efforts, diagnostic facilities and therapy are developing and continues to progress,
but the rate of infection still be the challenge in the health field.1 Both developing countries
and developed countries, infectious diseases are still a medical problem that is very important
because the death rate is still high. Central nervous system infection is one of the most
dangerous infection disease, such as Mengoencephalitis.2

Centers for Diseases Control and Prevention (CDC) reported that in 1998-2007 in the United
States reported 33 cases of Primary Amebic Meningoencephalitis (PAM) and as the cause of
death in 23 people in 1995-2004 and 6 people in 2007.3 In 2009, there were 103 cases of
meningoencephalitis and 14 deaths (CFR = 13.6%) in Mozambique.4 In 2011, WHO reported
that the case fatality rate (CFR) of meningoencephalitis in Asia caused by Togavirus is about
20%. 5

In Indonesia, meningitis / encephalitis is in the 17th position as the cause of death in all age
groups (0.8%) after malaria. Meningitis / Encephalitis is an infectious disease at all ages, with
the proportion 3.2%. While meningitis / encephalitis is in the 3rd position leading cause of
infant mortality at the age of 29 days-11 months, namely (9.3%) after diarrhea (31.4%) and
pneumonia (23.8%). The proportion of meningitis / encephalitis as the causes of death at the
age of 1-4 years about 8.8% and in the 4th position after Necroticans Entero Colitis (NEC),
about 0.7% .6

Malnutrition is the result of deficiency of protein, energy, minerals as well as vitamins

leading to loss of body fats and muscle tissues. Malnutrition is a significant public health
problem which is often neglected.7 Malnutrition is directly responsible for 300,000 deaths per
year in children younger than 5 years in developing countries and contributes indirectly to
8
more than half of all deaths in children worldwide. Protein-energy Malnutrition (PEM) in
children is still a problem of nutrition and public health in Indonesia. Based Health Research
in 2010, as many as 13.0% less nutritional status, of which 4.9% severe malnutrition. The
same data showed 13.3% of children underweight, of which 6.0% was emaciated children
and 17.1% of children have a very short category. Riskesdas 2013 there is an increased
prevalence of malnutrition-less, namely 19.6%, of which 5.7% severe malnutrition and 13.9%

1
less nutritional status. Protein-energy undernutrition (PEU), previously called protein-energy
malnutrition, is an energy deficit due to deficiency of all macronutrients. In children, chronic
primary PEU has 2 common forms: marasmus and kwashiorkor.7
Marasmus is one of severe acute malnutrition (SAM) condition and is primarily
caused by a deficiency in calories and energy which is characterized by skin and bones
appearance, old man face, prominent ribs, baggy pants. Based on body measurements,
marasmus is classified as moderately acutely malutrition and severely acutely malutrition.
This is determined by patients degree of wasting.9
Marasmus was identified through a combination of clinical and laboratory criteria.
Accurate diagnosis of marasmus is important because treatment can reduce mortality and
morbidity. Marasmus has many different symptoms but the common ones include old man
face, prominnent ribs, baggy pants. 10

1.2 Objectives

The objective of this paper is to report a case of a 3 years girl with diagnosis of
meningoencephalitis + marasmus. This paper provides a knowledge about
meningoencephalitis + marasmus that can be use for clinical practice. This paper is alsoone
of the requirement to complete the clinical assistant program in Child Health Department of
Haji Adam Malik General Hospital,University of Sumatera Utara.

2
 CHAPTER 2

LITERATURE REVIEW

2.1 Anatomy of the Brain11,12

In the discussion of meningoencephalitis, we will consider two anatomical parts,

namely meninges and the encephalon. Meninges is a membrane consisting of connective
tissue that lines and protects the brain. Lining of the brain or meninges consist of three parts:

1. Durameter

Durameter formed of fibrous connective tissue. Conventionally, durameter is composed of

two layers, namely endosteal and meningeal layer. These two layers are attached to the
meeting, except along certain places, separate and form venous sinuses. Actual endosteal
layer is a layer of the periosteum covering the surface of the skull bone. Durameter meningeal
layer is the actual layer of duramater , often referred as cranial durameter. Meningeal layer
consists of dense fibrous tissue that encloses the brain and strong and continued into the
spinal durameter after passing through the foramen magnum ends until the second segment of
the os sacrum. Meningeal layer formed in the septum, dividing the cranium cavity into spaces
that are interconnected with the free and accommodating parts of the brain. Septum function
is to secure the brain shift. The four septum include:

Falx cerebri is a crescent-shaped folds durameter located on the center line between
the two cerebral hemispheres. The tip of the anterior portion attached to the crista
galli. Widened posterior part, together with the upper surface of the tentorium
cerebelli.
Tentorium cerebelli is a crescent-shaped folds durameter that cover the fossa crania
posterior. This septum covering the upper surface of the cerebellum and sustain
occipital lobe cerebri.
Falx cerebelli is the durameter folds that attached to protuberantia occipital interna.
Sellae diaphragm is a small circular folds of durameter, which close the sella turcica
and the pituitary fossa sphenoidalis os. The diaphragm separates the hypothalamus
and pituitary gland of chiasma opticum. In the center, there is a hole pass by the
hypophyse shaft.

3
On separation of the two layers durameter, there is duramatris sinuses containing blood veins.
Sinus venosus / duramatris receives blood from the venous drainage of the brain and flows
into the internal jugular vein. The walls of the sinuses is limited by endothelium. Sinus on
calvaria that is superior sagittal sinus. The inferior sagittal sinus, sinus transversus and sinus
sigmoidea. Sinus on the basis crania, among others: occipital sinus, sinus sphenoidalis,
cavernous sinus, and sinus petrosal.

In this durameter layer there are many branches of blood vessels originating from the internal
carotid artery, a. maxilaris, a.pharyngeus ascendens, a.occipitalis and a.vertebralis. From the
point of clinical, the most important is a. meningeal (branch of a.maxillaris) because this
artery is generally often broke out in a state of trauma capitis. In durameter there are many
sensory nerve endings, and sensitive terhadapa rgangan so if there is stimulation of the nerve
endings can cause severe headaches.

2. Arachnoid

This layer is a membrane that is impermeable and smooth, that cover the brain and is located
between the pia mater and durameter. These membranes are separated from durameter by a
potential space that is spatium subdurale and from the pia mater by the subarachnoid cavity
that contains the cerebrospinal fluid. subarachnoid cavity (subarachnoid space) is a cavity /
space bounded by the outside of the arachnoid and the pia mater on the inside. Wall
subarachnoid space is covered by mesothelial cells were flattened. In certain areas arachnoid
protruding into the sinus venosus forming villi arachnoidales. This aggregation function as a
cerebrospinal fluid permeation into the blood stream.

The arachnoid associated with pia mater by delicate strands of fibrous tissue that crosses the
fluid in the subarachnoid cavity. The structure that runs to and from the brain to the skull or
foramen must go through subarachnoid cavity.

4
3. Pia mater

Pia mater layers are closely related to the brain and spinal marrow, follow each sulcus and
gyrus. The pia mater is a layer with many blood vessels and connective tissue made up of
smooth and passed by blood vessels that nourishes the nervous tissue. The central nervous
system astrocytes have endings that ended up as end feet in the pia mater to form the pia-glial
membrane. This membrane serves to prevent the harmful substances enters central nervous
system. Pia mater form tela choroidea, roof ventriculus tertius and Quartus and fused with
ependyma forming plexus choroideus in ventriculus lateralis, tertius and Quartus.

Figure 1. A cross section of brain tissue membrane layer

While encephalon is part of the central nervous system contained within the cranium; consists
of proencephalon (also called the forebrain that is part of the brain that develops from the
anterior three primary vesicles consist of diencephalon and telensefalon); mesencephalon
(also called the brainstem is the part of the brain that develops from the central part of the
three primary vesicles, consisting of tektum and peduncle); and rhombencephalon (also called
hindbrain, consists of metensefalon (cerebellum and pons) and mielensefalon (medulla
oblongata).

5
 Figure 2. Schematic distribution of brain tissue (encephalon)

Figure 3. brain tissue (encephalon)

2.2 Meningoencephalitis

2.2.1 Definition

Meningoencephalitis is an inflammation of the brain and meninges, the other names are
cerebromeningitis, encephalomeningitis, meningocerebritis13. Meningitis is an inflammation
caused by bacterial, viral, rickettsial, or protozoa which can be acute and chronic. While
encephalitis is an inflammation of the brain tissue that can be caused by bacteria, worms,
protozoa, fungi, rickets, or virus.14 Meningitis and encephalitis can be distinguished in many
cases based on the clinical manifestations, but they are often the same so-called
meningoencephalitis. The reason is that during bacterial meningitis, inflammation mediators
and the toxin produced in the subarachnoid cell spread into the brain parenchyma and cause

6
inflammatory responses of brain tissue. In encephalitis, inflammation reaction reach the
cerebrospinal fluid (CSS) and cause the symptoms of meningeal irritation in addition to
symptoms associated with encephalitis and in some etiologic agents can invade the meninges
and brain, for example enterovirus.15

2.2.2 Aetiology

The common caused agent of meningoencephalitis :

No Common Agent
1 Virus

Togaviridae
Alphavirus
Encephalitis Equine Eastern Virus
Encephalitis Equine Western Virus
Encephalitis Equine Venezuela Virus
Flaviviridae
Encephalitis St. Louis Virus
Powassan Virus

Bunyaviridae
Encephalitis California Virus
LaCrosse Virus
Jamestown Canyon Virus

Paramyxoviridae
Paramyxovirus
Parotitis Virus
Parainfluenza Virus

Morbilivirus
Measles Virus

Orthomyxoviridae
Influenza A
Influenza B

Arenaviridae
Lymphocytic choriomeningitis Virus

Picornaviridae
Enterovirus
Poliovirus
Coxsackie virus A
Coxsackie virus B
Echovirus

7
 Reoviridae
Orbivirus
Colorado dengue fever Virus

Rhabdoviridae
Rabies Virus

Retroviridae
Lentivirus
Human Immunodeficiency Virus Type 1 and 2
Oncornavirus
Human Lymphotropic Virus Type 1
Human Lymphotropic Virus Type 2

Herpesviridae
Herpes Virus
Herpes simplex Virus Type 1
Herpes simplex Virus Type 2
Varicella zoster Virus
Epstein Barr Virus
Cytomegalovirus
Human Cytomegalovirus

Adenoviridae
Adenovirus
2. Bakteri
Haemophilus influenza
Neisseria menigitidis
Streptococcus pneumonia
Streptococcus grup B
Listeria monocytogenes
Escherichia coli
Staphylococcus aureus
Mycobacterium tuberkulosa
3. Parasit
Protozoa
Plasmodium falciparum,
Toxoplasma gondii,
Naegleria fowleri (Primary amebic meningoencephalitis),
Granulomatous amebic encephalitis
Helminthes
Taenia solium,
Angiostrongylus cantonensis
Rickettsia
Rickettsia ( Rocky Mountain)
4. Fungi
Criptococcus neoformans
Coccidiodes immitis
Histoplasma capsulatum
Candida species
Aspergillus
Paracoccidiodes

8
 The virus that causes meningoencephalitis has a large geographic variation in the
developing countries, the biggest causes are: herpes simplex type-1 (HSV-1), mumps virus,
enterovirus, herpes zoster, adenovirus and Epstein -Barr. In the United States there is a St.
Louis encephalitis, West Nile virus, Eastern equine virus and Weastern, bunyavirus including
California Encephalitis Virus. In Central and Eastern Europe, Tick-born encephalitis virus is
endemic. Herpes simplex type 2 is the cause of most diseases in neonates. In Asia, Japanese
encephalitis is the most cause encephalitis. Valley fever virus in Africa and the Middle East,
Latin America, and many parts of the world. Encephalomyelitis post infection can follow all
but the most often associated with measles. Guillane Barre syndrome have been associated
with Epstein Barr Virus infection, cytomegalovirus, coxsackie B, Herpes Virus zooster.
Patients with immunodeficiencies are very susceptible to certain viruses, namely those with a
weak immune cells including patients infected with the HIV virus can develop into
encephalitis caused by Herpes zoster or Cytomegalovirus.16
In general, fungal invasion into the brain is hematogenous spread of infection in the lungs.
Haematogenous spread from the lungs to the brain and membranes comparable with
metastatic germ tuberculosa into the intracranial space, either on the surface of the cortex and
in the arachnoid can be formed granulomas large or small, which eventually evolved into
abses.17
The cause for the bacteria reach the cerebrospinal fluid will multiply rapidly because of the
subarachnoid space and CSS do not have a complement, opsonin antibodies and phagocytic
cells. Proven on experimental infection by H. influenzae, only requires a live bacteria to
initiate infection in the CSS. Streptococcus bacteria can cause meningitis in all age groups,
and in patients aged over 40 years is the most causative agent.15

2.2.3 Pathophysiology

Meningoencephalitis caused by the bacterium enters through the bloodstream,

spread directly, the complications of penetrating wound. Spreading through the bloodstream
as sepsis or derived from focal inflammation in other parts near the brain. Spreading directly
through trombophlebilitis, osteomyelitis, an infection of the middle ear and sinus paranasales.
At first occurred suppurative inflammation of the lining / brain tissue. This inflammatory
process formed exudate, septic thrombosis in blood vessels, and the aggregation of
leukocytes dead. In areas experiencing inflammation arise edema, softening, and congestion

9
of the brain tissue with a bit of bleeding. The middle part then softened and formed a strong
wall forming concentric capsule. All around the abscess occur infiltration of
polymorphonuclear leukocytes, plasma cells and lymphocytes. The whole process takes less
than two weeks. Abscesses can be enlarged, then broke and entered into the ventricles or
subarachnoid space which can lead to meningitis.17
Meningoencephalitis caused by the virus occurs by the viruses through parotitis,
morbili, varicella, etc. into the human body through the respiratory tract. Poliovirus and
enterovirus through the mouth, herpes simplex virus through oral or genital mucosa. Other
viruses that enter the body through inoculation such as animal bites (rabies) or mosquitoes.
Babies in the womb through the placenta gets infection by the rubella virus or
cytomegalovirus. In the human body the virus has multiplied locally, then there viremia that
attacks the central nervous system through the capillary in the choroid plexus.
Another way is through the peripheral nerves or retrograde axoplasmic spread, for
example by herpes simplex viruses, rabies and herpes zoster. In the central nervous system
the virus spread directly or through the extracellular space. A viral infection in the brain can
cause aseptic meningitis and encephalitis (except rabies). In encephalitis, there is damage to
neurons and glia in which inflammation of the brain, brain edema, inflammation of the small
blood vessels, thrombosis, and mikroglia.17
Amoeba meningoencephalitis presumably enters through various ways, because the
causes are parasites that can live freely in nature. Most likely, the infection occurs through
the respiratory tract in patients when they swim in the warm water.18
Infection caused by the protozoan like Toxoplasma may arise from the mother-
fetus. Perhaps humans got toxoplasmosis because eating meat that is not overcooked. In
humans, these parasites can survive in the form of cysts, especially muscle and central
nervous system tissue. The fetus who gets toxoplasmosis through the mother-fetus
transmission may occur various manifestations of cerebral growth disorder, kidneys and other
body parts. And the manifestations of congenital toxoplasmosis can be: fetus died in utero,
neonatal congenital anomalies shows microcephaly, and etc.19

10
2.2.4 Diagnosis

1. History taking
1. History in bacterial meningitis
- History in children who have risk factors such as: the younger the child the
less likely he/she is to show the classic symptoms of fever, headache, and
meningeal; head trauma; splenectomy; chronic illness; and children with facial
cellulitis, periorbital cellulitis, sinusitis, and septic arthritis have an increased
risk of meningitis.
- Meningitis in the neonatal period is associated with maternal infection or
pyrexia in labor while meningitis in children <3 months may have symptoms
that are highly specific, including hyperthermia or hypothermia, changes in
sleeping habits or eating, iritable or lethargy, vomiting, crying high-pitched, or
seizures.
- After 3 months , children can show symptoms that are more commonly
associated with bacterial meningitis, with fever, vomiting, irritability, lethargy,
or changes in behavior
- After 2-3 year, children may complain of headache, stiff neck, and
photophobia.
2. History in viral meningitis
Children who are not immunized for measles, mumps and rubella are at risk of
viral meningoencephalitis
3. History in fungal meningitis
Immunocompromised patients at risk of meningoencephalitis due to fungal
infection.
4. History in aseptic meningitis
There is usually a history of taking anti-inflammatory drugs (NSAIDs), IVIG, and
antibiotics. Symptoms are similar to viral meningitis. Symptoms can occur within
minutes of swallowing the drug.
5. History for Encephalitis
Information such as the seasons of the year, trips, activities, and exposure to
animals helps diagnosis.

11
2. Physical Examination
Findings on physical examination varies based on the age and the infecting organism. It is
important to remember that young children, rarely showing specific symptoms.
- In young infants findings lead to meningitis rarely specific:
a. Hypothermia or fever
b. Bulging fontanelle, diastasis (separation) on the suture stitches, and a stiff neck
but usually these findings appear slow.

- As the child grows older, physical examination to more easily searchable.

a. Meningeal signs easier to observe (for example, a stiff neck, a Kernigs sign is
positive and Brudzinski also positive).
b. Focal neurological signs can be found up to 15% of patients and is associated
with a poor prognosis
c. Seizures occur in 30% of children with bacterial meningitis
d. Obtundation and coma occur in 15-20% of patients and more frequently with
pneumococcal meningitis.

- Can be found signs of increased intracranial pressure and the patient will
complain of headache, diplopia, and vomiting. Bulging fontanelle, ptosis, sixth
nerve palsy, anisocoria, bradycardia with hypertension, and apnea are signs of
increased intracranial pressure with brain herniation. Papilledema are rare, unless
there is a venous sinus occlusion, subdural empyema, or brain abscess.

- In acute encephalitis infections are usually preceded by a prodrome few days

specific symptoms, such as cough, sore throat, fever, headache, and abdominal
complaints, followed by typical symptoms of progressive lethargy, behavioral
changes, and neurological deficits. Seizures are common in the presentation.
Children with encephalitis may also have a maculopapular rash and severe
complications, such as fulminant coma, transverse myelitis, anterior horn cell
disease (polio-like illness), or peripheral neuropathy. Besides the physical findings
that are commonly found in encephalitis are fever, headache, and a decline in
neurological function. The decline in nerve function including altered mental
status, focal neurologic function and seizure activity.

12
3. Other Examination
If suspected bacterial meningitis and encephalitis, a lumbar puncture should be
performed. Lumbar puncture should be avoided in the presence of cardiovascular instability
or signs of increased intracranial pressure. Routine CSF examination included WBC count,
differential, protein and glucose levels, and gram stain. Bacterial meningitis is characterized
by neutrophilic pleocytosis, with real high protein and low sugar. Viral meningitis is
characterized by lymphocytic pleocytosis protein mild to moderate, normal or slightly higher,
and normal glucose. While in encephalitis showed lymphocytic pleocytosis, a little height
protein levels, and normal glucose levels. Increased erythrocytes and CSF protein may occur
in HSV. Extreme increase in protein and low glucose levels showed an infection of
tuberculosis, cryptococcal infection, or meningeal carcinomatosis. Cerebrospinal fluid should
be cultured to determine bacteria, fungi, viruses, and mycobacteria that infect. PCR is used to
diagnose enterovirus and HSV because it is more sensitive and faster than the virus culture.
Leukocytosis is common. Blood cultures are positive in 90% of cases.
Examination of electroencephalogram (EEG) can confirm encephalitis component.
EEG is the definitive test and showed slow wave activity, although there may be a focal
changes. Neuroimaging studies may be normal or may show swelling of the brain
parenchyma diffuse or focal abnormalities.
Brain biopsy may be required for the definitive diagnosis of the cause of
encephalitis, especially in patients with focal neurologic findings. A brain biopsy may be
appropriate for patients with severe encephalopathy that do not show clinical improvement if
the diagnosis remains unclear. HSV, rabies encephalitis, prion-associated disease
(Creutzfeldt-Jakob disease and kuru) can be diagnosed by routine examination of culture or
biopsy pathologic brain tissue. A brain biopsy may be necessary to identify arbovirus and
enterovirus infections, tuberculosis, fungal infections, and non-communicable diseases,
especially primary CNS vasculopathies or malignancy.20

13
2.2.5 Differential Diagnoses

1. Febrile Convulsion
Febrile convulsion are convulsion that occur in the increase in body temperature
(rectal temperature> 38 C) that is caused by a process of extracranial. Febrile
convulsion are divided into simple febrile convulsion and complex febrile convulsion.
Complex febrile convulsion s are focal febrile convulsion, more than 15 minutes, or
repeated in 24 hours. In simple febrile convulsion are common convulsions, brief, and
only once in 24 hours.21
2. Cerebral Infarction
Cerebral infarction is the death of neurons, glia and vascular caused by lack of oxygen
or nutrients or metabolic disturbance. Each cause of infarction (anoxia, ischemia, or
hypoglycemia) have a description of its own, so the pattern of predilection zone and
its histopathologic. Myocardial anoxia caused by lack of oxygen although the blood
circulation is normal. Hypoglycemic infarction occurs when blood glucose levels fall
below a critical number for a prolonged period. Of the three types of infarction was,
the most frequently encountered are the cause hypoxic ischemic infarction secondary
to disruption of cellular nutrition, and the death of brain cells.22
3. Cerebral Hemorrhage
Primary bleeding from blood vessels in the parenchyma and not caused by trauma.23

2.2.6 Management

1. Convulsion, treated with:

Anti-convulsion
- Give Diazepam iv at a dose of 0.3-0.5 mg / min at a speed of 1-2 mg / min or
within 3-5 minutes, with a maximum dose of 20mg.
Drugs are practically given that rectal diazepam at a dose of 0.5-0.75 mg / kg,
or Rectal Diazepam 5mg for children with weight less than 10kg; Rectal
Diazepam 10mg for more than 10kg; Rectal Diazepam 5mg for children under
3 years of age; Rectal Diazepam 7.5 mg for children over 3 years.
- After administration of rectal diazepam convulsion has not stopped, could be
repeated in the same way and with the same dose interval 5 minutes. If after 2
times diazepam rectal administration still cnvulsion, it is recommended to go

14
 to the hospital, in order to be given diazepam intravenously at a dose of 0.3-
0.5 mg / kg.
- When the convulsion still have not stopped, then given phenytoin iv with an
initial dose of 10-20 mg / kg / times at a speed of 1 mg / kg / min or less than
50mg / min. When the seizure stops, the next dose is 4-8mg / kg / day, starting
12 hours after the initial dose.
- When the administration of phenytoin seizures have not stopped, the patient
should be treated in the intensive care unit.23
2. Source of infection that causes meningitis eradicated with drugs or with surgery.
3. The increase of intracranial pressure can be treated with
- Mannitol
The dose of 1 - 1.5 mg / kg IV within 30-60 minutes and can be repeated 2
times at intervals of 4 hours.
- Corticosteroid
Usually used dexamethasone IV 10 mg then repeated with 4 mg every 6 hours.
Corticosteroids are still causing controversy. Anyone agree to use it but there
also said there was no point to use it.
- If there is obstructive hydrocephalus, do shunting.
- Physiotherapy is given to prevent and reduce defects.24
4. Antibiotics
Broad-spectrum antibiotic should be given as soon as possible without waiting for
culture results. Only when there is culture results, we can replaced with
appropriate antibiotics. Antibiotic therapy in meningitis required far greater than
the minimum bactericidal concentration, therefore:
- When organisms penetrate into the sub-arachnoid space, it means the host has
decreased immunity.
- Cerebrospinal liquor conditions unfavorable for leukocytes and phagocytosis
is ineffective.
Antibiotics intravenous is recommended which has broad spectrum
that can against gram positive, gram negative and anaerobic bacteria; also can
pass through the blood brain barrier. urthermore, antibiotics are given based
on the results of test sensitivity23.
Antibiotics are often used for purulent meningitis are:

15
 1. Ampicilin, given intravenously
Neonates: 50-100 mg / kg / day divided into two times/day.
Age 1-2 months: 100-200 mg / kg / day divided into three times/day.
Age> 2 months: 300-400 mg / kg / day divided into four times/day.
2. Gentamicin, given intravenously
Premature: 5 mg / kg / day divided into two times/day.
Neonates: 7.5 mg / kg / day divided into three times/day.
Baby and adult: 5 mg / kg / day divided into three times/day.
3. Chloramphenicol, given intravenously
Premature: 25 mg / kg / day divided into two times/day.
Babies even months: 50 mg / kg / day divided into two times/day.
Children: 100 mg / kg / day divided into 4 times/day.
4. Ceftriaxon
- Children> 12 years and children BB> 50 kg: 1-2 gram once a day.
- Babies 14 days: 20-50 mg / kg body weight should not be more than 50 mg /kg,
once a day.
- Babies 15 days -12 years: 20-80 mg / kg, once a day. Intravenous doses> 50 mg / kg
should be administered intravenously at least 30 minutes.22,23
Supportive therapy involves treatment for dehydration with fluid replacement
and treatment of shock, disseminated intravascular coagulation, inappropriate secretion of
antidiuretic hormone, convulsions, increased intracranial pressure, apnea, arrhythmia, and
coma. Supportive therapy also involves the maintenance of an adequate cerebral perfusion
before cerebral edema.23

2.2.7 Prognosis
The prognosis varies depending on:
1. Age: The younger the better the prognosis
2. Germs cause
3. Duration of disease before being given antibiotics
4. The type and dose of antibiotics given
5. diseases that predispose.
In many cases, patients with mild meningitis can recover completely although the
healing process takes a long time. Meanwhile, in severe cases, brain damage can occur and
nerves permanently, and usually requires long-term therapy20.

16
2.3 Marasmus
2.3.1 Defenition
The World Health Organization (WHO) defines malnutrition as the cellular
imbalance between the supply of nutrients and energy and the bodys demand for them to
ensure growth, maintenance, and specific functions. 25
Marasmus is a condition primarily caused by a deficiency in calories and energy
(PEM). Typical characteristics of a wasted (marasmic) child include: 26
Skin and bones apperance
A thin old man face
Front view: ribs easily seen, skin of upper arms loose, skin of thighs loose.
Back view: Ribs and shoulder bones easily seen, flesh missing from buttocks
resulting in loose skin or baggy pants
Usually active and may appear to be alert

2.3.2 Pathophysiology
Protein-energy malnutrition will occur when the body's need for calories, protein,
or both are not fulfilled by diet. In a state of lack of food, the body is always trying to
preserve life by meeting basic needs or energy. The ability of the body to use carbohydrates,
proteins and fats is very essential to maintain life, carbohydrates (glucose) can be used by all
body tissues as fuel, unfortunately the body's ability to store carbohydrates very little, so that
after 25 hours was possible shortage. As a result, protein catabolism occurs after a few hours
to produce amino acids are immediately converted into carbohydrates in the liver and
kidneys. Diving fasting fat tissue are broken down into fatty acids, glycerol and ketone
bodies. Muscles can use fatty acids and ketone bodies as an energy source that is running a
chronic food shortage. The body will defend itself not to break down proteins again after
losing roughly half of the body.25

17
2.3.3 Diagnosis
Malnutrition for an individual child should be diagnosed based on the anthropometric
parameters and their cutoffs.27

Table 1. Anthropometric criteria to identify severe, moderate, and at risk categories of acute malnutrition for
infants and 10 year-old children.

Marasmus is a condition primarily caused by a deficiency in calories and energy,

whereas kwashiorkor indicates an associated protein deficiency, resulting in an edematous
appearance. Typical characteristics of a wasted (marasmic) child include:
Skin and bones apperance (emaciated ; severely wasted)
A thin old man face; wrinkled appearance; sparse hair
Front view: ribs easily seen, skin of upper arms loose, skin of thighs loose.
Back view: Ribs and shoulder bones easily seen, flesh missing from buttocks resulting
in loose skin or baggy pants
Usually active and may appear to be alert
Since marasmus is one of severe acute malnutrition (SAM) condition, marasmus,
based on body measurements, is classified as moderately acutely malutrition and severely
acutely malnutrition.
Mid-Upper Arm Circumference (MUAC) is often the screening tool used to determine
malnutrition for children in the community under five years old. A very low MUAC (<11cm
for children under five years) is considered a high mortality risk and is a criteria for
admission with severe acute malnutrition.

Table 2. MUAC criteria to identify malnutrition of children under five years in the
community 18
 Lists that must be paid attention in diagnosing marasmus:26
Complete history, including a detailed dietary history
Growth measurements, including weight and length/height; head circumference in
children younger than 3 years
Complete physical examination
Height-for-age or weight-for-height measurements greater than 2 standard deviations
below the mean for age
Height-for-age or weight-for-height measurements more than 2 standard deviations
less than the mean for age
Height-for-age measurements less than 95% of expected value
Height-for-height measurements less than 90% of expected value
Less than 5 cm/y of growth in children older than 2 years
Body mass index (BMI), although this is not established by the Centers for Disease Control
and Prevention (CDC) as a criteria for failure to thrive.

2.3.4 Management
Management of the child with severe malnutrition is divided into three phases.
These are:28
Initial (Stabilization) treatment : life-threatening problems are identified and treated
in a hospital or a residential care facility, specific deficiencies are corrected, metabolic
abnormalities are reversed and feeding is begun.
Rehabilitation: intensive feeding is given to recover most of the lost weight,
emotional and physical stimulation are increased, the mother or carer is trained to
continue care at home, and preparations are made for discharge of the child.
Follow-up: after discharge, the child and the childs family are followed to prevent
relapse and assure the continued physical, mental and emotional development of the
child.

19
 Table 3. Time-frame for the management of a child with severe malnutrition

2.3.5 Prognosis
Except for complications mentioned above, prognosis of even severe marasmus is
good if treatment and follow-up care are correctly applied. Since teaching parents how to
prevent malnutrition is of high importance to prevent recurrence, they must understand the
causes of malnutrition, how to prevent its recurrence (including correct feeding), and how to
treat diarrhea and other infections.28

20
 CHAPTER 3

CASE REPORT

3.1 Objective
The objective of this paper is to report a case of a 3 years old and 4 months old girl
with a diagnosis of meningoencephalitis + marasmus.

3.2 Case
A 3 years and 4 months years old girl with a 17 kg of BW and 85 cm of BH was
admitted to emergency room in Haji Adam Malik General Hospital Medan on 2nd February
2017 at 12.20 p.m with the main complain of loss of conciousness.

3.3 History of Disease

Patient FA, a girl, the second child of two children, born normally by midwives with
term pregnancy. Birth weight was 3500 grams and with body length of 51cm.
Patient presented with loss of conciousness which experienced since 5 days before
entering Adam Malik hospital. Before the patient experienced loss of consciousness, she had
convulsion 3 times with duration about 15 minutes per times. When the patient had
convulsion, her entire body was rigid and her eyes widened to top. The patient also had fever.
The fever happened for a month but showed a decrement in temperature by giving anti-
pyretic medicine. The parents reported that fever was not so high in temperature (subfebris)
with the highest temperature was 37,8 C. The temperature rose again without administration
of anti-pyretic medicine. The history of chills was not found. The history of convulsion just
after the fever was not found. The patient also had coughs for 10 days and happened
intermittent for 2 months. The coughs comes with phlegm. The colour of the phlegm was
white, but as time goes by the phlegm colour was greenish. The consistency of the phlegm
was viscous. Bleeding coughs was not found. The history of body weight loss was found. The
patient lost 5 kilograms in a month. The patient was hospitalized in Mitra Medika Hospital
for a week. The parents took the patient there because of her intermittent fever, and cough.
The patient was referral from Mitra Medika Hospital by a pediatrician with diagnosis
Meningitis TB + Hidrocephalus Communicans and the mantoux test result showed positive.

21
History of medication: IVFD NaCl 0.9%, Inj.Meropenem 360 mg/ 12 hrs, Inj.Phenytoin 1
amp/ 12 hrs, Paracetamol drips, Anti-Tuberculosis Drugs (H4), Prednison.

History of family:.There was no history of the same disease in family.

History of parents medication: Unclear

History of Pregnancy: The age of mother was 31 years old during pregnancy. The gestation
was 38 weeks.

History of Birth: Birth was assisted by a midwife. The patient was born pervaginal and cried
immediately after birth. Body weight at birth was 3500 gram, body length was 51 cm but the
head circumference was unclear.

History of feeding: Patient was given breast milk from birth to 2 months, then given
formulated milk from 2 months until now. Porridge strain from 6 months to 12 months and
family meals since the age of 1 year until now.

History of immunization: Not Complete.

History of growth and development: The patients mother reported that FA grew normally.
FA had developed talking, crawling, and walking skills on time.

Physical Examination:
Present Status: Level of consciousness: Sopor (E=4 V=1 M=3)
Body temperature: 38,8 C, BW: 8 kg, BH: 85 cm. BW/A: Z-Score < -3 SD ,
BL/A: Z-Score < -3 SD, anemic (+/+), ikteric (-/-), dyspnea (-), cyanosis(-),
edema (-).
Localized Status
- Head:
Old mans face (+)
Eye: light reflex +/+, isochoric pupil, conjunctiva palpebra inferior pale (-/-)
Ear: within normal range
Nose: NGT and Oxygen via nasal canule
Mouth: within normal range
22
 - Neck:
Jugular Vein Pressure: (R+2) cmH2O
Stiff Neck: (+)
Enlarged Lymph Nodes: (+)Multiple, : 0.5 cm colli dextra et sinistra
- Thorax:
Symetrical fusiformis, Retractions (-), RR: 40x/minute, regular, respiratory
sound: vesicular,ronchi (+/+), HR: 128 x/minute, regular, murmur (-).
- Abdomen:
Soepel, Peristaltic (+) N, Hepar and Lien: unpalpable.
- Extremities:
Pulse: 124x/minute, regular, tension/volume: enough, warm acral, CRT < 3,
edema pretibial (-), Plantar palmar et pedis pales (+/+) blood pressure: 90/60 mmHg,
Spastic (+).
Neurologist Examination:
Physiologic reflex:
APR/KPR : +/+
Pathologic reflex:
Babinski : +/+
Oppenheim: +/+
Chaddock: +/+
Gordon: +/+
Meningeal Reflex:
Kernig: +/+
Brudzinski I : -
Brudzinski II: +
Laboratory Findings:
2nd February 2017
Complete blood count:
Test Result Unit Referal
Hemoglobin 12.8 g% 11.7-15.5

Erythrocyte 5.04 106/mm3 4.20-4.87

Leucocyte 15.9 103/mm3 4.5-11.0
Thrombocyte 495 103/mm3 150-450
Hematocrite 39 % 38-44
Eosinophil 0.00 % 1-6
Basophil 0.10 % 0-1

Neutrophil 87.20 % 37-80

Lymphocyte 8.20 % 20-40

23
Monocyte 4.50 % 2-8

Neutrophil 13.88 103/L 2.7-6.5

absolute
Lymphocyte 1.30 103/L 1.5-3.7
absolute
Monocyte absolute 0.71 103/L 0.2-0.4

Basophyl absolute 0.01 103/L 0-0.1

MCV 77 fL 85-95

MCH 25.4 Pg 28-32

MCHC 33.1 g% 33-35

Blood Glucose mg/dL <200

9.70
Sodium 132 mEq/L 135-155

Kalium 4.3 mEq/L 3.6-5.5

Chloride 96 mEq/L 96-106

Differential Diagnosis :
1. Meningoencephalitis + Marasmus
2. Meningitis + Marasmus
3. Encephalitis + Marasmus

Diagnosis: Meningoencephalitis + Marasmus

Therapy:
- Head elevation 300 and midline position
- O2 via nasal canule 1 L/minute
- IVFD NaCl 0.9% 20cc/ hour
- IVFD NaCl 3% 0.1 cc/kg/hr -> 0.8 cc/ hour
- Inj. Ceftriaxone 50mg/kg/ 24 hrs divided into 2 dose = 200mg/ 12hr
- Inj. Phenytoin loading dose 10 mg/ kg -> 80 mg in 20 cc NaCl 0.9% for 20 minutes
then 12 hrs later maintenance dose 25 mg in 20 cc NaCl/ 12 hrs
- Inj. Dexamethasone 0.6 mg/ kg/ 24 hrs divided into 3 dose = 1.6 mg/ 8hr
- Inj. Furosemide 8mg/ 24hrs

Planning :
- X-ray
- Head CT-Scan

24
 - Lumbal Punction and CSF culture
Follow Up:

3th Feb 2017

S O A P
Seizure (-), Sensorium: GCS : 8 ( Meningoencephalitis -Head elevation 300
Fever (+), E4V1M3), T: 38.4 oC, + marasmus and midline
loss of BW: 8 kg, BH: 85 cm. position
consciousness Head: eye reflect +/+,
(+) isochoric pupil, conj. -O2 via nasal canule
palpebral inferior pale -/-, 1 L/minute
mouth/nose/ear:
normal/NGT and oxygen -IVFD NaCl 0.9%
via NC/ normal 20cc/ hour
Neck:Jugular Vein
Pressure:(R+2) cmH2O -IVFD NaCl 3% 0.8
Stiff Neck:(+) cc/ hour
Enlarged Lymph
Nodes:(+)Multiple, : 0.5 Inj. Ceftriaxone
cm colli dextra et sinistra 50mg/kg/ 24 hrs
Thorax: Symetrical divided into 2 dose
fusiformis, Retractions (-), = 200mg/ 12hr
RR: 36x/min, regular,
respiratory sound: -Inj. Phenytoin
vesicular,ronchi (-/-), maintenance dose
stridor (+/+) HR: 130 25 mg in 20 cc
x/min, regular, murmur (-) NaCl/ 12 hrs
Abdomen: Soepel, Normal
peristaltic, Hepar -Inj. Dexamethason
unpalpable, Lien: 1.6 mg/ 8hr
unpalpable.
Extremities: Pulse: -Inj. Furosemide
130x/min, regular, 8mg/ 24hrs
adequate, warm acral,
CRT < 3, edema pretibial -Diamox 3 x 70 mg
(-), BP : 100/60 mmHg.
Neurologist Examination: -F75 150cc/ 3hrs
Physiologic reflex: with 3cc mineral
APR/KPR : +/+ msx
Pathologic reflex:
Babinski : +/+ -Vit.A 1x200.00 IU
Oppenheim: +/+
Chaddock: +/+ -Vit.C 1x100 mg

25
 Gordon: +/+
Meningeal Reflex: -Vit. Bcomp 1x1
Kernig: +/+ tab
Brudzinski I : -
Brudzinski II: + -Folic Acid 1x5mg

Follow Up:

4th 5th Feb

2017
S O A P
Seizure (-), Sensorium: Meningoencephalitis -Head elevation 300
th
Fever (+), 4 Feb 2017 + marasmus and midline
loss of GCS : 8 ( E4V1M3), T: position
consciousness 37.7 oC , BW: 8 kg, BH:
(+) 85 cm. -O2 via nasal canule
1 L/minute
5th Feb 2017
GCS : 8 ( E4V1M3), T: -IVFD NaCl 0.9%
37.7 oC , BW: 8 kg, BH: 20cc/ hour
85 cm.
Head: eye reflect +/+, -IVFD NaCl 3% 0.8
isochoric pupil, conj. cc/ hour
palpebral inferior pale -/-,
mouth/nose/ear: Inj. Ceftriaxone
normal/NGT and oxygen 50mg/kg/ 24 hrs
via NC/ normal divided into 2 dose
Neck:Jugular Vein = 200mg/ 12hr
Pressure:(R+2) cmH2O
Stiff Neck:(+) -Inj. Phenytoin
Enlarged Lymph maintenance dose
Nodes:(+)Multiple, : 0.5 25 mg in 20 cc
cm colli dextra et sinistra NaCl 0.9%/ 12 hrs
Thorax: Symetrical
fusiformis, Retractions (-), -Inj.
Dexamethasone 1.6
4th Feb 2017 mg/ 8hr -> aff
RR: 30x/min, regular, (5/02/17)
respiratory sound: -Inj. Furosemide
vesicular,ronchi (-/-), 8mg/ 24hrs
stridor (+/+) HR: 116

26
x/min, regular, murmur (-) -Diamox 3 x 70 mg

5th Feb 2017 -Diet F75 150cc/

RR: 36x/min, regular, 3hrs with 3cc
respiratory sound: mineral mix
vesicular,ronchi (-/-),
stridor (+/+) HR: 120 -Vit.C 1x100 mg
x/min, regular, murmur (-)
Abdomen: Soepel, Normal -Vit. Bcomp 1x1 tab
peristaltic, Hepar
unpalpable, Lien: -Folic Acid 1x1mg
unpalpable.
Extremities: Pulse:
116x/min, regular,
adequate, spastic, warm
acral, CRT < 3, pretibial
edema (-), BP : 100/60
mmHg.
Neurologist Examination:
Physiologic reflex:
APR/KPR : +/+
Pathologic reflex:
Babinski : +/+
Oppenheim: +/+
Chaddock: +/+
Gordon: +/+
Meningeal Reflex:
Kernig: +/+
Brudzinski I : -
Brudzinski II: +

27
Follow Up:

6th Feb 2017

S O A P
Seizure (-), Sensorium: GCS : 8 ( Meningoencephalitis -Head elevation 300
Fever (+), E4V1M3), T: 38.1 oC, + marasmus and midline
loss of BW: 8 kg, BH: 85 cm. position
consciousness Head: eye reflect +/+,
(+) isochoric pupil, conj. -O2 via nasal canule
palpebral inferior pale -/-, 1 L/minute
mouth/nose/ear:
normal/NGT and oxygen -IVFD NaCl 0.9%
via NC/ normal 20cc/ hour micro
Neck:Jugular Vein
Pressure:(R+2) cmH2O -IVFD NaCl 3%
Stiff Neck:(+) 0.8 cc/ hour
Enlarged Lymph
Nodes:(+)Multiple, : 0.5 Inj. Ceftriaxone
cm colli dextra et sinistra 50mg/kg/ 24 hrs
Thorax: Symetrical divided into 2 dose
fusiformis, Retractions (-), = 200mg/ 12hr
RR: 32x/min, regular,
respiratory sound: -Inj. Phenytoin
vesicular,ronchi (-/-), maintenance dose
stridor (+/+) HR: 112 25 mg in 20 cc
x/min, regular, murmur (-) NaCl/ 12 hrs
Abdomen: Soepel, Normal
peristaltic, Hepar -Inj. Furosemide
unpalpable, Lien: 8mg/ 24hrs
unpalpable.
Extremities: Pulse: -Diamox 3 x 70 mg
112x/min, regular,
adequate, warm acral, -F75 150cc/ 3hrs
CRT < 3, edema pretibial with 3cc mineral
(-), BP : 100/60 mmHg. mix
Neurologist Examination:
Physiologic reflex: -Vit.C 1x100 mg
APR/KPR : +/+
Pathologic reflex: -Vit. Bcomp 1x1
Babinski : +/+ tab
Oppenheim: +/+
Chaddock: +/+ -Folic Acid 1x1mg
Gordon: +/+ -NaCl 0.9% nebule/

28
 Meningeal Reflex: 8hrs
Kernig: +/+
Brudzinski I : -
Brudzinski II: +

7th - 8th Feb

2017
S O A P
Seizure (-), Sensorium: Meningoencephalitis -Head elevation 300
th
Fever (+), 7 Feb 2017 + marasmus and midline
loss of GCS : 10 ( E4V3M3), T: position
consciousness 38 oC , BW: 8.1 kg, BH:
(+) 85 cm. -O2 via nasal canule
1 L/minute
8th Feb 2017
GCS : 10 ( E4V3M3), T: -IVFD NaCl 0.9%
37.7 oC , BW: 8.1 kg, BH: 20cc/ hour micro
85 cm.
-IVFD NaCl 3%
Head: eye reflect +/+, 0.1cc/ kgbb/ hr
isochoric pupil, conj.
palpebral inferior pale -/-, - Inj. Ceftriaxone
mouth/nose/ear: 50mg/kg/ 24 hrs
normal/NGT and oxygen divided into 2 dose
via NC/ normal = 200mg/ 12hr
Neck:Jugular Vein
Pressure:(R+2) cmH2O -Inj. Phenytoin
Stiff Neck:(+) maintenance dose
Enlarged Lymph 25 mg in 20 cc
Nodes:(+)Multiple, : 0.5 NaCl/ 12 hrs
cm colli dextra et sinistra
Thorax: Symetrical -Inj. Furosemide
fusiformis, Retractions (-), 8mg/ 24hrs
7th Feb 2017
RR: 30x/min, regular, -Diamox 3 x 70 mg
respiratory sound:
vesicular,ronchi (-/-), -F100 150cc/ 3hrs
stridor (+/+) HR: 116 with 3.5cc mineral
x/min, regular, murmur (-) mix

8th Feb 2017 -Vit.C 1x100 mg

RR: 32x/min, regular,
respiratory sound: -Vit. Bcomp 1x1

29
vesicular,ronchi (-/-) HR: tab
128 x/min, regular,
murmur (-) -Folic Acid 1x1mg
-NaCl 0.9% nebule/
Abdomen: Soepel, Normal 8hrs
peristaltic, Hepar
unpalpable, Lien:
unpalpable.
Extremities: Pulse:
130x/min, regular,
adequate, warm acral,
CRT < 3, edema pretibial
(-), BP : 100/60 mmHg.
Neurologist Examination:
Physiologic reflex:
APR/KPR : +/+
Pathologic reflex:
Babinski : +/+
Oppenheim: +/+
Chaddock: +/+
Gordon: +/+
Meningeal Reflex:
Kernig: +/+
Brudzinski I : -
Brudzinski II: +

30
 CHAPTER 4
DISCUSSION

The patient in this case report is a 3 years old and 4 months old girl. According with
the previous epidemiological study, the meningoencephalitis is one of the most dangerous
infection disease in children.2 In Indonesia, meningitis / encephalitis is in the 17th position as
the cause of death in all age groups (0.8%) after malaria. The proportion of meningitis /
encephalitis as the causes of death at the age of 1-4 years about 8.8% and in the 4th position
after Necroticans Entero Colitis (NEC), about 0.7% .6
Patient presented with loss of conciousness which experienced since 5 days before
entering Adam Malik hospital. Before the patient experienced loss of consciousness, she had
convulsion. The patient also had fever. The patient also had coughs for 10 days and happened
intermittent for 2 months. The coughs comes with phlegm The history of body weight loss
was found. The patient lost 5 kilograms in a month. The patient had pathologic reflex such as
Babinski, Oppenheim, Chaddock, Gordon and meningeal reflex such as Kernigs sign and
Bruzinski II.
Findings on physical examination varies based on the age and the infecting
organism. It is important to remember that young children, rarely showing specific
symptoms. As the child grows older, physical examination to more easily searchable such as
Meningeal signs easier to observe (for example, a stiff neck, a Kernigs sign is positive and
Brudzinski also positive), focal neurological signs, seizures occur in 30% of children with
bacterial meningitis, obtundation and coma. In acute encephalitis infections are usually
preceded by a prodrome few days specific symptoms, such as cough, sore throat, fever,
headache, and abdominal complaints, followed by typical symptoms of progressive lethargy,
behavioral changes, and neurological deficits. Seizures are common in the presentation.
Children with encephalitis may also have a maculopapular rash and severe complications,
such as fulminant coma, transverse myelitis, anterior horn cell disease (polio-like illness), or
peripheral neuropathy. Besides the physical findings that are commonly found in encephalitis
are fever, headache, and a decline in neurological function. The decline in nerve function
including altered mental status, focal neurologic function and seizure activity.

31
 Management for meningoencephalitis:
1. Convulsion, treated with Anti-convulsion
- Give Diazepam iv at a dose of 0.3-0.5 mg / min at a speed of 1-2 mg / min or within
3-5 minutes, with a maximum dose of 20mg. Drugs are practically given that rectal
diazepam at a dose of 0.5-0.75 mg / kg.
- After administration of rectal diazepam convulsion has not stopped, could be repeated
in the same way and with the same dose interval 5 minutes. If after 2 times diazepam
rectal administration still cnvulsion, it is recommended to go to the hospital, in order
to be given diazepam intravenously at a dose of 0.3-0.5 mg / kg.
- When the convulsion still have not stopped, then given phenytoin iv with an initial
dose of 10-20 mg / kg / times at a speed of 1 mg / kg / min or less than 50mg / min.
When the seizure stops, the next dose is 4-8mg / kg / day, starting 12 hours after the
initial dose.
- When the administration of phenytoin seizures have not stopped, the patient should be
treated in the intensive care unit.23
2. The increase of intracranial pressure can be treated with
- Corticosteroid
Usually used dexamethasone IV 10 mg then repeated with 4 mg every 6 hours.
Corticosteroids are still causing controversy. Anyone agree to use it but there also said there
was no point to use it..
- Physiotherapy is given to prevent and reduce defects.24
3. Antibiotics
Broad-spectrum antibiotic should be given as soon as possible without waiting for
culture results. Only when there is culture results, we can replaced with appropriate
antibiotics.
Antibiotics intravenous is recommended which has broad spectrum that can against
gram positive, gram negative and anaerobic bacteria; also can pass through the blood brain
barrier. Furthermore, antibiotics are given based on the results of test sensitivity23.
Supportive therapy involves treatment for dehydration with fluid replacement and
treatment of shock, disseminated intravascular coagulation, inappropriate secretion of
antidiuretic hormone, convulsions, increased intracranial pressure, apnea, arrhythmia, and
coma. Supportive therapy also involves the maintenance of an adequate cerebral perfusion
before cerebral edema.23

32
 Management for this patient:
- Head elevation 300 and midline position
- O2 via nasal canule 1 L/minute
- IVFD NaCl 0.9% 20cc/ hour
- IVFD NaCl 3% 0.8 cc/ hour
- Inj. Phenytoin loading dose 10 mg/ kg -> 80 mg into 20 cc NaCl 0.9% for 20
minutes then 12 hrs later maintenance dose 25 mg in 20 cc NaCl/ 12 hrs
- Inj. Dexamethasone 0.6 mg/ kg/ 24 hrs divided into 3 dose = 1.6 mg/ 8hr
- Inj. Furosemide 8mg/ 24hrs
- Diamox 3 x 70 mg

33
 CHAPTER 5
SUMMARY

A 3 years and 4 months years old girl, BW 8.5 kg and a BH 85 cm, admitted to emergency
room in Haji Adam Malik General Hospital medan on 2nd February 2017 with the main
complain of loss of consciousness since 5 days ago. Symptoms such as seizures, fever,
history of chronic cough were also found. Sign of old mans face, stiff neck, lymph nodes
enlargement, rigid extremities, pathologic neurologic examination, meningeal reflex were
positive. Leukocytosis and Thrombocytosis were also found. The patient was decided to be
hospitalized and further follow up suggested meningoencephalitis with marasmus as
diagnosis. The patient was monitored throughly the hospitalization and was in theraphy with
Head elevation 300 and midline position, O2 via nasal canule 1 L/minute, IVFD NaCl 0.9%
20cc/ hour, IVFD NaCl 3% 0.8 cc/ hour, Inj. Phenytoin loading dose 10 mg/ kg -> 80 mg
dalam 20 cc NaCl 0.9% for 20 minutes then 12 hrs later maintenance dose 25 mg in 20 cc
NaCl/ 12 hrs, Inj. Dexamethasone 1.6 mg/ 8hr , Inj. Furosemide 8mg/ 24hrs, Diamox 3 x 70
mg . After 7 days hospitalization, the patient showed obvious clinical improvement and still
on treatment in hospital.

34
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