KEMENTRIAN RISET, TEKNOLOGI, DAN PENDIDIKAN TINGGI

UNIVERSITAS RIAU
FAKULTAS KEDOKTERAN
BAGIAN SARAF
Sekretariat : Gedung kelas 03, RSUD Arifin Achmad Lantai 04
JL. Mustika, Telp. 0761-7894000, Email : saraffkur@gmail.com

PATIENT’S STATUS
I. Patient’s identity
Name Mr. PP
Age 20 years old
Gender Male
Address Jl. Segar Tenayan Raya, pekanbaru
Religion Christian protest
Marital status Not married
Occupation seller
Date of hospital
15th September 2018
admission
Medical Records 9955XX

II. History of Illness (alloanamnesis)

Chief complaint
Loss of sudden unconsciousness since 1 hours before admitted to the hospital

Recent History
1 hour before admitted to the hospital patient got sudden
unconsciousness. He vomited for 1 time, containing food, Seizures 2 times for 10
minute. 1 week ago, he got high fever, persistently. The fever accompanied with
intense headache and vomiting. Vomit happened for 5 times in weak the patient
did not present any other complaint, including seizures, muscle weakness, facial
paralysis. He brought to general hospital arifin achmad and hospitalized for 4
days, and discharge himself. All of his complaints got worsen when he got home.

1
 Another symptom like History of shortness of breath, congestion, ear
pain, trauma, weak limbs, double vision, facial paralysis, dysartria, absence of
hearing loss and denied ringing of the ear.

Past Medical History

- History of unfinished TB treatment in 2 month ago
- History of brain tumor (-)

Family Disease History

- Completed TB treatment (+), which his uncle
Socioeconomic History
- patient his a tattoo on his chest
- history of smoking (+)
- history drug abuse (-)

RESUME
Mr.PP male, 20 years old has lost of unconsciuosness since 1 hours before
admitted to the hospital, seizures 2 times for 10 minutes. He also complained
headache, fever and vomitting. He has history of unfinished TB treatment in 2
month ago and comleted TB treatment which his uncle.
III. Physical Examination ( 15th September 2018 )
A. GENERAL APPEREANCE
Blood pressure : 120/70 mmHg
Pulse : 89 x / minute
Respiration Rate : 26 x / min
Nutritional status : Weight: 52 kg; Height: 160 cm; BMI: 20.31 kg
Temperature : 38.1o C

B. NEUROLOGIC STATUS

1) AWARENESS : Sopor GCS: (E2V1 M3)

2) COGNITIVE FUNCTION : Dificult to Aassess
3) Neck stiffness : (+)

2
 4) Cranial nerves :

N. I (Olfactorius )
Right Left Result
Sense of smell Difficult Difficult Not testable
to assess to assess
N.II (Opticus)
Right Left Result
Visual Acuity Difficult to Difficult to
Visual Fields assess assess Not testable
Color Recognition
N.III (Oculomotorius)
Right Left Result
Ptosis (-) (-) Pupil anisokor
Pupil Doll’s eye
shape Round Round right (+)
Size 4 mm 5 mm
Extraocular Doll’s eye (+) Doll’s eye (-)
movements
Pupillary Reflex (+) (-)
Direct (+) (-)
Indirect

N. IV (Trokhlearis)
Right Left Result
Eye Movement Doll’s Doll’s Doll’s eye right (+)
eye eye
(+) (-)

N. V (Trigeminus)
Right Left Result
Motorik Difficult Difficult
Sensibility to assess to assess Motoric and sensory
Cornea Reflex (+) (-) cannot be assessed

N. VI (Abduscens)
Right Left Result
Extraocular
movements Doll’s eye right (+)
Strabismus (-) (-)
Deviasi (-) (-)

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N. VII (Facialis)
Right Left Result
Tic (-) (-)
Motorik:
-Frowning Difficult to Difficult to
-Raised eye assess assess
-Brow Cannot be assess
-Close eyes
-Corners of the
mouth
-nasolabial fold

- Sense of taste
Chvostek Sign

N. VIII (Vestibulo-Coclearis)
Right Left Result
Hearing Difficult Difficult
Rhine Test to assess to assess Cannot be assess
Weber Test
Swabach Test

N. IX (Glossofaringeus)
Right Left Result
Pharyngeal Arch Normal Normal
Sense of Taste Normal Normal Normal
Gag Reflex (+) (+)

N. X (Vagus)
Right Left Result
Arcus farings Normal Normal Normal
Dysfonia (-) (-)

N. XI (Accesorius)
Right Left Result
Motor
Trophy Difficult Difficult Cannot be assessed
to assess to assess

N. XII (Hipoglossus)
Right Left Result
Motorik Difficult Difficult
Trofi to assess to assess Cannot be assessed
Tremor
Dysarthria

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IV. MOTOR SYSTEM
Right Left Result
Upper Extremity
Distal Drop tes Drop tes
Proximal Normal assess Lateralization
Tonus Eutrophy Normal to the left
Trophy (-) Eutrophy (weakness on
Involunter movement (-) left
Lower Extremity extremities)
Power
Distal Drop tes Drop tes
Proximal Normal Normal
Tonus Eutrophy Eutrophy
Trophy (-) (-)
Involunter movement
Body
Trophy (-) (-) Normal
Involunter movement (-) (-) Normal
Stomatch’s wall reflex (+) (+) Normal

V. SENSORY SYSTEM
Sensation Right Left Result
Touch Difficult to Difficult to
Pain assess assess Cannot be assessed
Temperature
Propioseptic

VI. REFLEXES
Reflex Right Left Result
Physiologic Physiologic Reflexes (+)
Biseps (+) (+)
Triseps (+) (+)
KPR (+) (+)
APR (+) (+)
Patologic Patologic Reflexes (+)
Babinski (+) (+)
Chaddock (-) (-)
Hoffman (-) (-)
Tromer (-) (-)

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VII. FUNCTION COORDINATION
Examination Right Left Result
Point finger to nose test NT NT
Nose-finger-nose test NT NT NT
Point finger-point finger test NT NT
Disdiadokonesia NT NT
Heel to knee test NT NT
Rebound test NT NT
Gait NT NT
Tandem NT NT
Romberg NT NT

VIII . SISTEM OTONOM

Bladder : Urine cathether (+)
Bowel : not assed yet

X. OTHER EXAMINATION
Laseque : (+)
Kernig : (+)
Patrick : (-)/(-)
Kontrapatrick : (-)/(-)
Valsava test : Unable to do
Brudzinski : brudzinski I-IV (-)

X. RESUME OF EXAMINATION
Awareness : Sopor, GCS : E2 M3V1
Blood Pressure : 123/69 mmHg
Pulse : 89 beat / minute, regular
RR : 30 time / minute
Kognitive Function : Cannot be assess
Meningeal sign : Stiff neck (+)
Cranial nerves : pupil anisokor, light reflex (+)/(-), left parese N.
III,IV,VI dan V
Motoric : lateralization to the left
Sensorik : Difficult to assess

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 coordination : Difficult to assess
autonomy : Normal
Reflex Physiologic : Within normal limit
Patologic : babinsky (+)
Other eximination : laseque (+), kerniq (+)

D. WORKING DIAGNOSIS
I. Clinical Diagnose :
Anamnesis : loss of consciusness, fever, headche, seizures, history of
unfinished th tretament in 2 month ago.
Physical eximination : meningeal sign neck stiffness (+), lateralization
to the left, reflex patologic babinsky (+), pupil anisokor, ligth reflex
(+)/(-), left parese N.III, IV, VI and V.
Topic Diagnose : leptomeningens
Etiology Diagnose : Susp tuberculosa (mycobacterium tuberculosa )
Differential Diagnose : mengitis purulenta

E. OTHER EXAMINATION
 Lumbal puncture
 Routine blood (haemoglobin, hematocryte, leukocyte, thrombocyte, LED,
DC)
 Electrolyte
 Head ct scan with contras
 Hiv test
 Sputum BTA

F. ADDITIONAL EXAMINATION RESULTS ( 14th September 2018 )

Routine blood (14 th September 2018)
- Hb : 10,6 g/dl
- Ht : 32 %
- WBC : 17.40 /ul
- PLT :451.000 /ul
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Hepatic function (14 th September 2018)
- AST : 52 U/L
- ALT: 16 U/L
Renal function (14th September 2018)
- Ureum : 19 mg/dl
- Creatinin: 0,49 mg/dl
Electrolyte serum level (14 th September 2018)
- Na + :
121 mmol/L
- K+ :
4,9 mmol/L
- CL - :
85 mmol/L
HIV rapid test (17 th September 2018)
- Non reaktif
Sputum Bta
- Bta( + 1)
X – photo thorax AP (9 th September 2018)

Interpretation :
Cor : within normal limits
Pulmo : specific proses

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 Head CT non contrast (9 th September 2018)

Interpretation : no intracerebral bleeding

Within nirmal limits
H. FINAL DIAGNOSIS
loss of consciousness ec meningitis tuberculosis
pulmonary TB
hyponatremia

I. THERAPY
- O2 nasal canul 3L/menit
- IVFD NACL 3% / 12 hours
- Inj. dexamethasone 3 x 5 mg iv
- Inj. ranitidine 2 x 50 mg iv
- Inj. Citicoline 2 x 500 mg iv
- paracetamol 4 x 1 gr iv
- inj. Ceftriaxone 2 x 1 gr iv

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 S A
Date
O P

16th Subjective: Assessment :

September
2018 Loss of consciousness (+), fever Loss of consciousness ec susp
(+), seizure (+) meningitis tuberculosa
Objective: Pulmonary tuberculosis
General condition : moderate Hyponatremi
illness
Consciousness : sopor, E2M3V1
Terapi :
Blood pressure : 150/100 mmHg
O2 nasal canul 3L/menit
Pulses: 150x/menit IVFD NACL 3% / 12 hours
Inj. dexamethasone 3 x 5 mg iv
Respiration: 40x/menit Inj. ranitidine 2 x 50 mg iv
Inj. Citicoline 2 x 500 mg iv
Temp: 37,80C
paracetamol 4 x 1 gr
General condition inj. Ceftriaxone 2 x 1 gr iv

PE thorax
Inspection : simetric between left
and right
Plan :
Palpation : -
Consul vct
Percussion : dullness at the right
and left lung Consul pulmonary

Auscultation : rhonci at the basal

right and left lung
Neurological status
a. N. cranialis :
N.III : Pupil anisokor,
light reflex (+)/(-), doll’s
eye right
N.IV : doll’s eye right
N.V : cornea reflex (-)/(+)

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 N.VI : doll’s eye (+)/(-)
b. Motoric : left
lateralisasition
c. Sensory : Difficult to
assess
d. Physiology reflex : (+/+)
e. Pathology reflex :
Babinski (+)

17th Subjective: Assessment :

September
2018 Loss of consciousness (+), fever Loss of consciousness ec susp
(+), seizure (+) meningitis tuberculosa
Objective: Pulmonary TB
General condition : moderate Hyponatremia
illness
Therapy
Consciousness : sopor, E2M3V1 O2 nasal canul 3L/menit
IVFD NACL 3%/ 12 hour
Blood pressure : 100/80 mmHg ,asering/ 8 hour
Inj. dexamethasone 3 x 5 mg iv
Pulses: 135x/menit
Inj. ranitidine 2 x 50 mg iv
Respiration: 24x/menit Inj. Citicoline 2 x 500 mg iv
paracetamol 4 x 1 gr
Temp: 380C inj. Ceftriaxone 2 x 1 gr iv
inj.meropenem 2 x 1 gr iv
General condition inj.omz 2 x 40 mg iv
PE thorax inj. Kalnex 3 x 500 mg iv
inj. Diazepam 5 mg /kp
Inspection : simetric between left the patient moves to HCU
and right
Palpation : -
Percussion : dullness at the right
and left lung
Auscultation : rhonci at the basal
right and left lung
Neurological status
a. N. cranialis
N.III : Pupil anisokor,
light reflex (+)/(-), doll’s

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 eye right
N.IV : doll’s eye right
N.V : cornea reflex (+)/(-)
N.VI : doll’s eye (+)/(-)
b. Motoric : left
lateralisasition
c. Sensory : Difficult to
assess
d. Physiology reflex : (+/+)
e. Pathology reflex :
Babinski (+)

18 th Loss of consciousness (+), fever Assessment :

September (+), seizure (+)
2018 Meningitis ec susp tuberculosa
Objective:
Pulmonary TB
General condition : moderate
illness Hyponatremia

Consciousness : sopor, E2M3V1 Therapy

Blood pressure : 150/100 mmHg
Pulses: 150x/menit
Respiration: 42x/menit
Temp: 37,80C
General condition
PE thorax
Inspection : simetric between left
and right
Palpation : -
Percussion : dullness at the right
and left lung
Auscultation : rhonci at the basal
right and left lung
Neurological status
O2 NRM 10 L/menit
IVFD RL 20 tpm
IVFD penamin G : Triofusin 1: 1
Inj. dexamethasone 3 x 5 mg iv
Inj. ranitidine 2 x 50 mg iv
Inj. Citicoline 2 x 500 mg iv
paracetamol 4 x 1 gr
inj. Ceftriaxone 2 x 1 gr iv
inj.meropenem 2 x 1 gr iv
inj.omz 2 x 40 mg iv
inj. Kalnex 3 x 500 mg iv
inj. Diazepam
inj. Methylprednisolon 2 x 62,5
mg iv
Combivent + pulmicort nebulizer
4x1

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a. N. cranialis
N.III : Pupil anisokor,
light reflex (+)/(-), doll’s
eye right
N.IV : doll’s eye right
N.V : cornea reflex (+)/(-)
N.VI : doll’s eye (+)/(-)
b. Motoric : left
lateralisasition
c. Sensory : Difficult to
assess
d. Physiology reflex : (+/+)
e. Pathology reflex :
Babinski (+)

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 BAB II

DISCUSSION

2.1 Meningitis

2.1.1 Definition

Meningitis is inflammation of the membrane that covers the organs of

the central nervous system, which is usually known as meningens (inflammation
of the arachnoid and pyramid). Meningitis is caused by infection, chemicals that
irritate if injected or inserted into the subarachnoid space and cause inflammation
in the meninges. Meningitis caused by infection is classified as acute pyogenic
(usually caused by bacteria), aseptic meningitis (usually due to viral) and chronic
meningitis (tuberculous, spirochetal, or cryptococcal). This classification is made
based on the characteristics of CSF and clinical examination of the disease1.

2.1.2 Anatomy of the meningens layer

The brain and spinal cord are lined with meninges. Besides lining the
brain and spinal cord, meningen also serves to protect nerve structures, carry
blood vessels and secrete cerebrospinal fluid (CSS). Mening membrane consists
of 3 layers2.
1. Duramater
Duramater is conventionally composed of two layers, the endosteal layer
and the meningeal layer. Duramater is a hard membrane, consisting of fibrous
connective tissue that is firmly attached to the inner surface of the cranium.
Because it is not attached to the arachnoid membrane below it, there is a potential
space (subdural space), where bleeding often occurs3.

2. Arachnoid
Arachnoid is a thin and translucent layer, located between the inner
piamater and the outer dura mater which includes the brain. This membrane is
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separated from the duramater by potential space, called the subdural spatium, and
from the piamater by the subarachnoid spatium filled with CSS. Subarachnoid
hemorrhage is generally caused by head injury.

3. Piamater
The piamater is firmly attached to the surface of the cerebral cortex. The
piamater is the vascular membrane that tightly encases the brain,
encompassing the gyrus and entering the deepest sulci. This membrane
encapsulates the brain nerve and merges with the epineurium. The arteries that
enter the brain are also covered by piamater.

Picture 1. Layout of Meningen Layer2

2.1.2 classification of meningitis

A. Meningitis is divided into 2 groups based on changes that occur in brain

fluid :
 Serous meningitis
Serous meningitis is characterized by elevated cell and protein counts
with clear cerebrospinal fluid. The most common causes are
Tuberculosis bacteria and viruses. Tuberculosis is often xantocromic.2
 Purulent meningitis
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 Purulent meningitis or bacterial meningitis is acute meningitis and
produces pus-shaped exudates and is not caused by specific bacteria or
viruses. Causes include: Diplococcus pneumonia (pneumococci),
Neisseria meningitis (meningococci), Streptococcus haemolyticuss,
Staphylococcus aureus, Haemophilus influenzae, Escherichia coli,
Klebsiella pneumoniae, Peudomonas aeruginosa.3
B. Meningitis based on causative microorganisms
 Bacterial meningitis
Bacterial meningitis is a characteristic of inflammation in all
meninges, where organisms enter the arachnoid and subarachnoid spaces.
Bacterial meningitis is a neurological emergency with a mortality rate of
around 25%. Bacterial meningitis if detected quickly and get the right
treatment will get good results. Bacterial meningitis is often referred to as
purulent meningitis or septic meningitis. The bacteria that can cause
meningitis attacks are; Streptococcus pneuemonia (pneumococcus),
Neisseria meningitidis, Haemophilus influenza, (meningococcus),
Staphylococcus aureus and Mycobacterium tuberculosis.3,4
 Viral meningitis
Viral meningitis is usually called aseptic meningitis. Often
occurs as a result of a variety of diseases caused by viruses, including;
measles, mumps, herpes simplex, and herpes zoster. Viruses that cause
meningitis can be divided into two groups, namely RNA (ribonuclear acid)
virus and DNA virus (deoxyribo nucleid acid). Examples of RNA viruses
are enterovirus (polio), arbovirus (rubella), flavivirus (dengue) and
mixovirus (influenza, parotitis, morbili). While examples of DNA viruses
include the herpes virus, and retroviruses (AIDS). Viral meningitis can
usually heal itself and return to its original state (complete healing). In the
case of acute viral infections, clinical features such as acute meningitis,
acute meningo-encephalitis or acute encephalitis. A mild degree of acute
meningo-encephalitis may occur in many acute viral infections, usually in
children, whereas in adult patients it is not identified.3,4

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2.1.3 Etiology of Meningitis

The most common causes of meningitis are microorganisms such as

bacteria, viruses, parasites and fungi. These microorganisms infect the blood and
cerebrospinal fluid. Meningitis can also be caused by non-infectious causes, such
as AIDS, malignancy, diabetes mellitus, physical injury or certain drugs that can
weaken the immune system (immunosuppressive).5
Meningitis can occur due to infection by viral, bacteria, fungi or
parasites:
 Viral :
Viral meningitis is generally not too severe and can heal naturally
without specific treatment. The case of viral meningitis in the United States,
especially during the summer is caused by enteroviruses; although only a few
cases develop into meningitis. Other viral infections that can cause meningitis :
1) Mumps viral
2) Herpes viral, including Epstein-Barr viral, herpes simplexs, varicella-
zoster, Measles, and Influenza
3) Viruses that spread through mosquitoes and other insects (Arboviruses)
4) nother rare case of LCMV (lymphocytic choriomeningitis virus), spread
through mice.5
 Bacterial :
One of the main causes of bacterial meningitis in children and young
adults in the United States is the Neisseria meningitidis bacteria. Meningitis
caused by this bacteria is known as meningococcal disease. Bacteria that cause
meningitis also vary by age group.4 During the first month of age, bacteria that
cause meningitis in normal infants are obtained from maternal flora or the baby's
environment (including group B Streptococcus, gram-negative enteric bacilli and
Listeria monocytogenes). Meningitis in this group can sometimes be due to
Haemophilus influenzae and other pathogens found in older patients.

Bacterial meningitis in children aged 2 months - 12 years is usually due

to H. influenzae type B, Streptococcus pneumoniae or Neisseria meningitidis.

17
Diseases caused by H. influenzae type B can occur at any age but often occur
before the age of 2 years. .
Klebsiella, Enterobacter, Pseudomonas, Treponema pallidum, and
Mycobacterium tuberculosis can also cause meningitis. Citrobacter diversus is an
important cause of brain abscess.
Tabel 1. The causative bacteria are most common according to age and
predisposing factors 5

Risk and/or Predisposing

Bacterial Pathogen
Factor

Age 0-4 weeks Streptococcus agalactiae (group B

streptococci)
E coli K1
Listeria monocytogenes

Age 4-12 weeks S agalactiae

E coli
H influenzae
S pneumoniae
N meningitides

Age 3 months to 18 years N meningitidis

S pneumoniae
H influenza

Age 18-50 years S pneumoniae

N meningitidis
H influenza

Age older than 50 years S pneumoniae

N meningitidis
L monocytogenes
Aerobic gram-negative bacilli

Immunocompromised state S pneumoniae

N meningitidis
L monocytogenes
Aerobic gram-negative bacilli

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 Intracranial manipulation, Staphylococcus aureus
including neurosurgery Coagulase-negative staphylococci
Aerobic gram-negative bacilli, including
P aeruginosa

Basilar skull fracture S pneumoniae

H influenzae
Group A streptococci

CSF shunts Coagulase-negative staphylococci

S aureus
Aerobic gram-negative bacilli
Propionibacterium acnes

2.1.4 Epidemiology

In bacterial meningitis, pneumococci, influenza (H. influenzae) and

forms of meningococcal meningitis have a worldwide distribution. influenzae
meningitis, previously often occurs in infants and young children which is
reduced by vaccination programs in developed countries. However, this case often
occurs in less developed countries and its frequency increases in adults (in the
United States there are 15,000 cases each year). Meningococcal meningitis often
occurs in children and adolescents but is also found in adults, with a decrease in
the number of cases after the age of 50 years. Pneumococcal meningitis mainly
occurs at a very young age and in older adults. Changes in the epidemiology of
bacterial meningitis may occur due to an increased incidence of nosocomial
infections, apart from occurring due to the influx of H influenzae.5

2.1.5 Patofisiology Meningitis

Meningitis in general as a result of the spread of disease in other organs

or tissues of the body. Viruses or bacteria spread hematogenously to the lining of
the brain, for example in pharyngitis, tonsillitis, pneumonia, bronchopneumonia
and endocarditis. The spread of bacteria or viruses can also be done by
percontinuitatum from inflammation of organs or tissues near the lining of the
19
brain, such as brain abscesses, otitis media, mastoiditis, cavernous sinus
thrombosis and sinusitis. The spread of germs can also occur due to head trauma
with open fractures or complications of brain surgery. Invasion of germs into the
subarachnoid space causes an inflammatory reaction in the pia and arachnoid,
CSS (cerebrospinal fluid) and ventricular system. At first a small and hyperemic
meningeal blood vessel, in a very short time there was spread of
polymorphonuclear leukocytes into the subarachnoid space, then exudate formed.4
Within a few days lymphocyte formation and histiocytes occur and in the second
week of cellplasma. The exudate formed consists of two layers, the outer part
contains polymorphonuclear leukocytes and fibrin, while in the layer there are
macrophages. Inflammatory processes other than arteries also occur in veins in the
cortex and can cause thrombosis, brain infarction, brain edema and degeneration
of neurons. Thrombosis and fibrino-purulent perineural exudate organization
cause cranial abnormalities. In meningitis caused by viruses, cerebrospinal fluid
appears clearer than meningitis caused by bacteria In TB meningitis occurs due to
the spread of hematogenous infections to meninges. In the course of TB
meningitis through 2 stages. Initially, lesions in the brain or meninges occur due
to hematogenous spread of bacilli during primary infection. Hematogenous spread
can also occur in chronic TB, but this condition is rarely found. Furthermore,
meningitis occurs due to the release of bacilli and TB antigens from caseose focus
(initial brain lesions) due to trauma or immunologic processes, directly into the
subarachnoid space. TB meningitis usually occurs 3–6 months after primary
infection.4
Most bacteria enter the spinal cerebro fluid in the form of colonization
of the nasopharynx or hematogenously spread to the choroid plexus, brain
parenchyma, or meninges. Veins experiencing blockages can cause retrograde
flow of transmission from infection. Damage to the duramater layer can be caused
by fractures, post neurosurgery, epidural steroid injection, anesthesia, presence of
foreign objects such as cochlear implants, VP shunts, etc. Often the colonization
of organisms on the skin can cause meningitis. Although meningitis is said to be
inflammation of the meninges, damage to the meninges can result from infection
which can result in brain edema, venous blockage and blocking the flow of

20
cerebrospinal fluid which can end with hydrocephalus, increased intracranial, and
herniation.4

2.1.6 Diagnosis Meningitis

History
he onset of acute symptoms (<24 hours) is accompanied by trias of
meningitis, namely fever, severe headache and stiff neck. Other symptoms include
nausea, vomiting, photophobia, focal or generalized seizures, impaired
consciousness. You may find a history of lung, ear, sinus, or heart valve
infections. In infants or neonates, symptoms are nonspecific such as fever,
iribility, lethargy, vomiting and seizures.

Neurological physical examination

a. Physical examination
Physical examination has a very important value to strengthen the
history findings. Consists of inspection, palpation, percussion, and auscultation.
The attitude of courtesy and respect for the body and the person of the patient
being punched must be considered carefully by the examiner.4
Physical examination must always begin with an assessment of the
general condition of the patient. By assessing this general condition, it can be
obtained the impression whether the patient is in an acute distress condition that
needs immediate help, or the patient is in a relatively stable state so that help can
be given after a more complete physical examination.
1. Vital symptoms. Examination of the airway, state of respiration and
circulation. Make sure that the airway is open and the patient can breathe.
The brain needs a continuous supply of oxygen, so glucose. Without
oxygen the brain cells will die within 5 minutes. Therefore, there must be a
circulation of blood to deliver oxygen and glucose to the brain. So the time
to restore breathing and blood circulation is short
2. Skin. Pay attention to signs of trauma, see liver disease, injections, wet
skin due to sweat (for example hypoglycemia, shock), dry skin (eg diabetic
coma), bleeding such as dengue fever, DIC)
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 3. Head. Note signs of trauma, scalp hematoma, hematoma around the eyes,
bleeding in the ear canal and nose.
4. Thorax, heart, lung, abdomen, extremities.
b. Neurogical examination6
In each patient with a coma or decreased consciousness, a neurological
examination must be performed, paying attention to the attitude of the patient
when lying down whether calm and relaxed which indicates that the decrease in
consciousness is not deep. The presence of evaporating movements and
swallowing indicates that the decrease in consciousness is not deep. Open eyelids
and dependent tendencies are obtained in a deep decrease in consciousness. Keep
in mind that there are no strict boundaries between levels of awareness. In general,
the data is said that the stronger the stimulus needed to generate answers, the
deeper the level of consciousness decreases.4
a. GCS (Glasgow Coma Scale)
GCS is used to pay attention to the response (response) of patients to
stimuli and give value to the response.6
b. Kranial nerve 1-12
Cranial nerves come directly from the brain and leave the skull through
holes in the bone called foramina, there are 12 pairs of cranial nerves that are
expressed by name or by Roman numerals. These nerves are olfactory (I),
optic (II), oculomotor (III), trochlearis (IV), trigeminal (V), abdusens (VI),
facial (VII), cochlear vestibule (VIII), glossopharyngeal (IX) , vagus (X),
asesorius (XI), hypoglossus (XII). Cranial nerves I, II, VII are pure sensory
nerves, cranial nerves III, IV, XI and XII are motor nerves, but also contain
proprioceptive fibers from the muscles they innervate. Cranial nerves V, VII,
X are mixed nerves, cranial nerves III, VII and X also contain some nerve
fibers from parasympathetic branches of the autonomic nervous system.
.
c. Stiff neck
Stiff neck is a symptom that is often found in kelianan brain membrane
stimuli. There are 3 ways to perform rigid neck checks:

22
 1. Head Flexion. For cervical rigid examination can be done with the
examiner's hand placed under the head of the patient who is lying down.
Then the head is flexed and attempted to get the chin to reach the chest.
During this bending, detainees were noticed. If there is a stiff neck, we get
a prisoner and the chin cannot reach the chest. Stiff neck can be mild or
severe. In a stiff neck, the head cannot be bent, but often the head is
shaken back.
2. Brudzinski I (Brudzinski's neck sign)
To check this sign is done with the hand placed under the head of the
patient who is lying down, we bend the head as far as possible until the
chin reaches the chest. The other hand should be placed on the patient's
chest to prevent lifting the body. If the brudzinski sign is positive, this
action results in flexion of both legs. Previously it should be noted
whether the limbs are not paralyzed, of course the legs will not be flexed
3. Brudzinski II (Brudzinski's contralateral leg sign)
In patients who are lying down, one leg is flexed on the pelvic joints,
while the other leg is in a state of extension (straight). If this one leg is
also flexed, it is called a positive brudzinski II sign
4. Kernig sign
On this examination, the patient who is lying on his thigh is flexed on the
hip joint to make an angle of 90°. After that the limbs are extended on the
knee joint. Usually we can do this extension to an angle of 135°, between
the lower limbs and the upper limbs. If there is resistance and pain before
this angle is reached, then it is said that the sign kernig is positive. In
meningitis the signs are usually bilateral positive
5. Lasegue sign
Examination is carried out by means of the patient who is lying down
straightened (extension) both legs. Then one leg is lifted straight, bent
(flexed) on the hip joint. The other leg must be straight (extension). Under
normal circumstances we can reach an angle of 70° before pain and
resistance arise. If there is pain and resistance before we reach 70°, then the
lasegue sign is positive.7

23
Additional examination

a. Lumbar puncture
Lumbar puncture is usually performed to analyze the number of cells
and proteins of the cerebrospinal fluid, provided that there is no increase in
intracranial pressure.
1. In Serous Meningitis there are varying pressures, clear fluid, increased white
blood cells, glucose and normal protein, culture (-).
2. In Purulenta Meningitis there is increased pressure, cloudy fluid, the number of
white blood cells and protein increases, glucose decreases, culture (+) some types
of bacteria.

Tabel 2. Differences in CSF changes in meningitis

Bacterial
Tes Viral meningitis Meningitis TBC
meningitid

pressure LP Increase normal variation

color murky clear Xanthochromia
cell count > 1000/ml < 100/ml variation
cell Predominant PMN Predominant MN Predominant MN
differential
increase Normal/increase increase
Protein
Normal/decreas Normal low
Glucosa

24
Tabel 3. Typical CSF Finding in Meningitis8

b. Routine blood test

Examination of hemoglobin level, leukocyte count, blood sedimentation
rate (LED), glucose level, urea level, electrolyte and culture were examined.
1) In Serous Meningitis there is an increase in leukocytes and glucose.
2) Tuberculous Meningitis is also found to increase LED.
3) In Purulenta Meningitis there is an increase in leukocytes, proteins, neutrophils.

c. Radiology examinitation
On plain head examination, it can be determined whether there is a skull
fracture and infection of the paranasales sinuses, as a cause or risk factor for
meningitis. Chest photo examination was performed to determine the presence of
pneumonia, lung abscess, specific processes, and tumor mass. CT Scan and MRI
can be done with the aim to determine whether there is brain edema, ventriculitis,
hydrocephalus, and tumor mass.
1) In Serous Meningitis a chest photo, head photo is taken, if possible, do a CT
scan.
25
2) In Purulenta Meningitis a head photo is taken (mastoid check, sinusitis,
dentition) and chest photos.
d. Tuberculin test
A tuberculin test is performed to determine the existence of a specific
process. Electrolyte examination needs to be done in bacterial meningitis because
dehydration and hyponatremia can occur especially in the first 48-72 hours.7
Bacterial meningitis9

- Complete peripheral blood and blood culture. Examination of blood sugar and
electrolytes if indicated.
- Lumbar puncture is very important to make a diagnosis and determine the
etiology:
• Obtain cloudy or opalesens with Nonne (-) / (+) and Pandy (+) / (++).
• The number of cells is 100-10,000 / m3 by calculating the type of
polymorphonuclear predominant, protein 200-500 mg / dl, glucose <40 mg
/ dl. In the early stages the number of cells can be normal with lymphocyte
predominance.
• If you have received antibiotics before, the CSF picture can be non-
specific.
- In severe cases, lumbar puncture should be delayed and still given empirical
antibiotics (2-3 days delay does not change the diagnostic value except
identification of germs, and even if antibiotics are sensitive)
- If it is strongly suspected towards meningitis, although there are signs of
increased intracranial pressure, lumbar puncture can still be done as long as you
are careful. Use of a spinal needle can minimize complications of herniation.
- Absolute contraindication to lumbar puncture only if signs and symptoms of
increased intracranial pressure are found due to space pressure lesions.
- CT scan with contrast or MRI of the head (in severe cases or suspected
complications such as subdural empyema, hydrocephalus and brain abscess)
- On electroencephalography examination can be found general slowdown.

26
Tuberculosis meningitis 9

- Examination includes complete peripheral blood, blood sedimentation

rate, and blood sugar. Peripheral blood leukocytes often increase (10,000-
20,000 cells / mm3). Hyponatraemia and hypochloremia are often found
due to inadequate hormone antidiuretic secretion.
- Lumbar puncture:
• Cerebrospinal Liquor (LCS) is clear, cloudy or xantochrome
• The number of cells increases between 10-250 cells / mm3 and rarely
exceeds 500 cells / mm3. Calculate the type of predominant lymphocyte
cells even though in the early stages polymorphonuclear can be
dominant.
• Protein increases above 100 mg / dl while glucose decreases below 35
mg / dl, the CSF and blood glucose ratio is below normal
• Examination of BTA (acid resistant bacillus) and M. tuberculosis
culture is still carried out.
• If the first CSF examination results are doubtful, a repeat lumbar
puncture can strengthen the diagnosis at 2 weeks intervals.
- Polymerase Chain Reaction (PCR), enzyme-linked immunosorbent assay
(ELISA) and Latex particle agglutination can detect Mycobacterium
bacteria in the cerebrospinal fluid (if possible).
- Contrast CT-scan or MRI imaging can show parenchymal lesions in the
basal area of the brain, infarction, tuberculoma, or hydrocephalus.
- Chest X-rays can show a picture of Tuberculosis.
- Tuberculin test can support diagnosis
- Electroencephalography (EEG) is carried out if possible can show
slowing of the rhythm of the base rhythm.
Viral meningitis

- Hematological and chemical examination must be carried out

- LCS examination is an important examination in the examination of the causes
of meningitis. CT scan must be performed in cases related to abnormal
neurological signs to exclude intracranial lesions or obstructive hydrocephalus

27
before a lumbar puncture (LP). LCSD culture remains the standard criterion for
examination of bacterial or pyropharyngeal aseptic meningitis. Again, patients
who are partially treated with bacterial meningitis can develop with gram-negative
staining and aseptic appearance. The following are characteristics of CSF that are
used to support the diagnosis of viral meningitis:
• Cells: Pleocytosis with a WBC count in the range of 50 to> 1000x 109
/ L blood has been reported in viral meningitis. Predominant
mononuclear cells are the rule, but PMN can be the main cell in the first
12-24 hours; Cell count is usually then dominated by lymphocytes in
classic CSF patterns in meningitisviral. This helps to distinguish
bacterial meningitis from viral, which has a higher cell count and
predominant PMN in cells in cell differences; this is not an absolute rule
anyway.
• Protein: CSF protein levels are usually slightly increased, but can vary
from normal to as high as 200 mg / dL.
- Imaging studies: Imaging for suspected viral meningitis and encephalitis can
include head CT scans with and without contrast, or brain MRI with gadolinium.
Contrast CT scans help in removing intracranial pathology. Contrast scans must
be obtained to evaluate for addition along the mening and to rule out the
cerebrum, intracranial abscess, subdural empyema, or other lesions. Alternatively,
and if available, brain MRI with gadolinium can be done. MRI with contrast is a
criterion standard for visualizing intracranial pathology in viral encephalitis.
HSV-1 more often affects the basal frontal and temporal lobes with a frequent
picture of diffuse bilateral lesions.
- Other tests: All patients whose condition does not improve clinically within 24-
48 hours must be carried out a work plan to determine the cause of meningitis. In
cases of suspected encephalitis, MRI with added contrast and adequate
visualization of the basal frontal and temporal area is needed. EEG can be
performed if encephalitis or subclinical seizures are suspected in disturbed
patients. Periodic lateralized epileptiform discharge (PLEDs) is often seen in
herpetic encephalitis.

28
- Procedure: Lumbar puncture is an important procedure used in diagnosing viral
meningitis. Another potential procedure, depending on individual indications and
the severity of the disease, includes monitoring intracranial pressure, brain biopsy,
and ventricular drainage or shunting.
Tabel 3 Description of cerebrospinal fluid in meningitis based on the etiological
agent

2.1.8 Diagnosis

Bacterial meningitis

The diagnosis of bacterial meningitis cannot be made only by looking at

symptoms and signs. Clinical manifestations such as fever, headache, vomiting,
stiff neck and meningeal excitatory signs may also occur in meningismus,
tuberculous meningitis and aseptic meningitis. Almost all authors say that a
definitive diagnosis of meningitis can only be made by examining cerebrospinal
fluid through a lumbar puncture. Therefore every patient with suspicion of
meningitis must have lumbar puncture.10
Generally opalesen-colored cerebrospinal fluid until cloudy, but at an
early stage can be obtained clear fluid. Nonne and Pandy reactions are generally
found to be strong positive. The cell count is generally thousands per cubic
millimeter of fluid which consists mostly of polimorphonuclear (PMN) cells. In
29
the early stages, the number of cells is only hundreds of cubic permilimeters by
counting more lymphocytes than segments. Therefore in such a situation, a lumbar
puncture needs to be repeated the next day to establish a definitive diagnosis. This
condition is also found in the stage of healing purulent meningitis. Increased
levels of protein in CSS. Sugar levels decrease but not as low as tuberculous
meningitis. Chloride levels are sometimes low.
From the examination of the preparation directly under a microscope, it
may be possible to find the germs that cause it, although this is rare. Reliable
differentiation of germs is only determined by culture and animal experiments. No
germs found on direct preparations are not contra-indications of diagnosis. On
examination of peripheral blood, high leukocytosis is found with a shift to the left
(Shift to the left). Generally there is megaloblastic anemia.
Tuberculosis meningitis

The diagnosis can be determined on the basis of the clinical picture and
the most important is the description of CSS. Definitive diagnosis can only be
made if tuberculosis bacteria are found in CSS. A positive tuberculin test, a
radiological abnormality seen in thoracic radiographs and the presence of a source
of infection in the family can only contribute to the diagnosis. The tuberculin test
in tuberculous meningitis is often negative because of an allergic reaction (false-
negative), especially in terminal stages.

Meningitis Viral

Etiological diagnosis can only be made by isolating the virus. In

practice, serological examinations are not done due to the many types of viruses
that can cause this disease.
Diagnosis can usually be made based on clinical symptoms, CSS
abnormalities and a self-limited disease course. CSS culture for possible causes of
other microorganisms must be done (fungus, leptospira, mycobacterium) so that
the possibility of other causes of microorganisms can be removed.

30
 In addition to CSS cultures, other tests such as tuberculin tests, photos of
Roentgen thoracic, looking for sources of tuberculosis must be done in order to
rule out the possibility of tuberculous meningitis.

2.1.9 clinical symptoms

Meningitis has the characteristic of sudden onset of fever, headache and

stiff neck. Usually it is also accompanied by several other symptoms, such as:
 Nausea
 Gag
 photopobia
 Change or decrease in awareness

Bacterial meningitis

Nonem of the clinical features are pathognomonic for bacterial

meningitis. Signs and clinical manifestations of bacterial meningitis are so
widespread that they are often found in children who are either meningitis or not.
Clinical signs and features vary greatly depending on the patient's age, illness at
home before diagnosis and the body's response to infection.
Meningitis in newborns and premature babies is very difficult to diagnose, the
clinical picture is very blurred and not typical. The fever in newborn meningitis
only occurs in half of the number of cases. Usually the patient looks weak and
lazy, does not want to eat, vomiting, decreased consciousness , the large fontanel
is tense and bulging, neck is limp, irregular respiration, sometimes accompanied
by jaundice if sepsis. Generally if it is found sepsis in newborns we must suspect
meningitis.
Babies aged 3 months - 2 years rarely give a classic picture of
meningitis. Usually manifestations that arise only in the form of fever, vomiting,
restlessness, recurrent seizures, sometimes also obtained high pitch cry (in
infants). The physical mark that is clearly visible is the crown and tension, while
the sign Kernig and Brudzinsky are difficult to evaluate. Because the incidence of
meningitis at this age is very high, the presence of central nervous system
31
infection should be suspected in children with persistent fever that cannot be
explained.
In large children and adult meningitis sometimes provides a classic
picture.Symptoms usually begin with fever, chills, vomiting and
headache.Sometimes the first symptoms are seizures, restlessness, behavioral
disorders.Energy decreases such as delirium, stupor, coma can also Clinical signs
commonly found are stiff neck, Brudzinski and Kernig marks. Headache results
from meningial vascular inflammation, often accompanied by photophobia and
hyperesthesia, cervical stiffness accompanied by spinal rigidity due to meningic
irritation and spinal root.
Brain nerve disorders are caused by local inflammation in perineurium,
also due to disruption of vascular supply to the nerves. Cranial nerves VI, VII, and
IV are the most frequently affected. Focal cerebral signs are usually secondary to
cortical necrosis or occlusive vasculitis, most commonly due to thrombosis
cortical vein. Cerebral vasculitis causes spasms and hemiparesis.10
Clinical manifestations that can arise are:8
1. Symptoms of acute infection
a. Lethargy.
b. Irritabilitas.
c. fever.
d. gag.
e. Anoreksia.
f. Headache
g. Petechia and Herpes Labialis (untuk infeksi Pneumococcus).
2. Symptoms of high intracranial pressure
a. gag.
b. headache.
c. Moaning cry
d. conciousness.
e. seizures.
f. Bulging fontanel
g. . Hemiparesis, Paralisis, Strabismus.

32
 h. Crack pot sign.
i. Cheyne Stokes.
j. Hypertension and Choked disc papila N. optik
3. Meningeal stimulation symptoms.
a. Siffnes neck (+).
b. Kernig, Brudzinsky I dan II positif(+)
In children less than 1 year of age, meningeal symptoms cannot be relied
upon as a diagnosis. When there are symptoms above, a lumbar puncture
is needed to get cerebrospinal fluid (CSS).
Tuberculosis meningitis

Clinically there are sometimes no symptoms of real meningitis even

though the lining of the brain has been affected. This is the case with miliary
tuberculosis so that in the spread of billions, lumbar puncture should be done even
though the symptoms of meningitis have not yet been seen.

Staging Clinical manifestation

Stage 1 Fully consciousness, did not have focal neurological signs
Stage2 Inattentive, confused, sign of clouding consciousness or focal
neurological signs
Stage 3 Coma, stupor, multiple cranial nerve palsies, completes
hemiplegia or paraplegia

Meningitis Viral

Usually the symptoms of viral meningitis are not as severe as meningitis

and can heal naturally without specific treatment. Generally the onset of the
disease is sudden, although sometimes it is preceded by heat for several days.
Symptoms found in large children are heat and sudden headache accompanied by
stiff neck. Other symptoms that can arise are sore throat, nausea, vomiting,
decreased consciousness, pain in the neck and back, fotophobia, paresthesia,
myalgia. Symptoms in infants are not typical. Babies are easily aroused and

33
become restless. Nausea and vomiting are common but symptoms of seizures are
rare. If the cause is Echovirus or Coxsackie, it can be accompanied by a rash with
heat that will disappear after 4-5 days. When the examination was found stiff, the
sign of Kernig and Brudzinski was sometimes positive.
Other variations of viral infection can help diagnosis, such as:
• Gastroenteritis, rash, pharyngitis and pleurodynia in enterovirus infection
• Skin manifestations, such as zoster eruption of VZV, maculopapular rash from
measles and enterovirus, vesicular eruption of herpes simplex and herpangina
from coxsackie A virus infection
• Pharyngitis, lymphadenopathy and splenomegaly lead to EBV infection
• Immunodeficiency and pneumonia, leading to adenovirus, CMV or HIV
infection
• Parotitis and orchitis towards the Mumps virus

2.1.10 Treatment

Viral meningitis

Viral meningitis is a self-limiting disease, so what needs to be done is to

treat or treat the underlying disease of meningitis.11

34
Bacterial meningitis

T
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Meningitis Tuberculosis treatment 12

35
 BASIC DIAGNOSIS

1. basic of clinical diagnose : loss of consciousness ec susp. Meningitis

tuberculosis ?
According to anamnesis, a 20 years old male patient had loss of
consciousness, there is fever, headache and from physical eximination
there are meningeal sign. Loss of consciousness can be caused by :
 Decreased consciousness without focal abnormalities and without
stiff neck. Examples : ischemic disorders, metabolic disorders,
intoxication, systemic infections, hyperthermia and epilepsy
 Decreased consciousness without focal abnormalities and with stiff
neck. Examples : subarachnoid hemorrhage, meningitis and brain
tissue ( meningoenchepalitis).
 Decreased awereness with focal abnormalities. Examples : brain
tumor, cerebral hemorrhage, cerebral infarction and brain abcess.
Based on symptoms of possible decreased awereness experienced
by patient today due to meningitis tuberculosis due to in the
absence of lateralization and found fever that indicates the
existence of an infection reaction.
Meningitis is inflammation of the membrane that covers the organs
of the central nervous system, which is usually known as
meningens (inflammation of the arachnoid and piamater). This can
lead to diffuse and / or focal neuro[hysichological dysfunction that
causes interference with ARAS resulting in a decrease in
consciousness. Headache caused by stimulation of nociceptor
pain the head.

2. basic topic diagnose :leptomeningens

Meningitis is inflammation of the membrane that covers the

organs of the central nervous system, which is usually known as
meningens (inflammation of the arachnoid and piamater).
3. basic of etiologycal diagnose : susp. Tuberculosis (mycobacterium
tuberculosis)

Meningitis can be caused by bacteria, viruses, or some cases that

are rarely caused by fungi. Bacterial that often cause bacterial meningitis
are tuberculosis bacteria.

4. Final diagnosis

The final diagnosed of this patients is loss of consciousness ec susp

meningitis tuberculosa (mycobacterium tuberculosis ), pulmonary TB and
hyponatremia.
 DAFTAR PUSTAKA

1. Israr YA.Meningitis. Faculty of Medicine, University of Riau, Arifin Achmad

General Hospital of Pekanbaru: 2008; 1-6.
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3. Mesranti. Meningitis. Sumatera Utara: Fakultas Kedokteran Universitas
Sumatera Utara. 2011. Diunduh dari:
http://repository.usu.ac.id/bitstream/123456789/23705/4/Chapter%20II.pdf.
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