Laporan Kasus Tuberculous Meningitis

1
CASE REPORT
TUBERCULOUS MENINGITIS
PRESENTED BY
MUKHAMAD FARIED
110100351
TESAR AKBAR NUGRAHA
110100511
SUPERVISED BY:
dr. Wisman Dalimunthe, Sp.A (K)
PEDIATRIC HEALTH DEPARTMENT

HAJI ADAM MALIK GENERAL HOSPITAL
UNIVERSITY OF NORTH SUMATERA
2015
ACKNOWLEDGMENTS
We are greatly indebted to the Almighty One for giving us blessing to finish this
case report about Tuberculous Meningitis. This case report is a requirement to
complete the clinical assistance program in Department of Child Health in H.
Adam Malik General Hospital, Medical Faculty of North Sumatra University.
We are also indebted to our supervisor and adviser, dr. Wisman
Dalimunthe, Sp.A (K) for much spent time to give us guidances, comments, and
suggestions. We are grateful because without him 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 comments and relevants suggestions from the
reviewers. Hopefully the content will be useful for everyone in the future.
Medan, 15th October 2015
Presentators
TABLE OF CONTENTS
ACKNOWLEDMENTS....................................................................................................
ii
TABLE OF CONTENTS...................................................................................................
1
CHAPTER 1 INTRODUCTION......................................................................................
2
CHAPTER 2 LITERATURE REVIEW..........................................................................
4
CHAPTER 3 CASE REPORT..........................................................................................
17
CHAPTER 4 DISCUSSION.............................................................................................
56
CHAPTER 5 SUMMARY.................................................................................................
58
REFERENCES..................................................................................................................
59
CHAPTER 1
BACKGROUND
1.1 Background
Tuberculosis (TB) is a significant bacterial disease which principally affects the
lungs. Its causal agent is Mycobacterium tuberculosis (Mtb) an intracellular
facultative organism which can produce progressive disease or latent
asymptomatic infection. Although TB is essentially a pulmonary disease, other
organs and tissues can be infected, being cerebral TB is the most severe form.1
There is high prevalence of tuberculous meningitis (TBM) in developing
countries, including indonesia, and the disease has a high mortality rate among
infants and children. Neurological complication are common, and early diagnoseis
and specific treatment for tuberculosis (TB) are essential for prevention of squelae
or fatal outcomes.2
TBM is the most severe complication of TB and frequently occurs in
childhood. Lympho-hematogenous spread from primary pulmonary focus leads to
the development of Rich focus in the brain. Rupturing of this cseous granuloma
into the subarachnoid space causes 3 features responsible for the clinical
manifestations
of
TBM:
development
of
further
tuberculomata;
basal
inflammatory exudates that cause cranial nerve palsies and obstruct cerebrospinal
fluid (CSF) passages, resulting in hydrocephalus; and obliterative vasculitis
leading to infarctions. Once the Rich focus has ruptured, a prodormal period of
nonspecific symptoms, such s fever, vomiting, and behavioral changes, develops.

As the disease progresses, neck stiffness, loss of consciousness, motor deficits,
and convulsions will follow. TBM diagnosis is often only considered once
irreversible neurologic damage has already occured.2
The outcome of TBM is known to be affected by age, stage of the disease
at admission, and whether riased intracranial pressure (ICP) caused by obstructive
hydrocephalus is actively treated.2
1.2 Objective
This paper is one of the requirements to fullfil in the senior clinical assistance
programs in Pediatric Department of Haji Adam Malik General Hospital,
University of North Sumatra. In addition, this paper can be used as reference to
know and understanding a litle about meningitis TB.
CHAPTER 2
LITERATURE REVIEW
2.1
Tuberculous Meningitis
2.1.1
Definition
Tuberculous meningitis is an inflammation of the meningen that cause by primary

tuberculosis (IKA UI, 2007). Tuberculous meningitis (TBM) is caused by
Mycobacterium tuberculosis (M. tuberculosis) and is the most common form of
central nervous system (CNS) tuberculosis (TB). 4 Central nervous system (CNS)
tuberculosis occurs in approximately 1% of all patients with active tuberculosis. It
results from the haematogenous dissemination of Mycobacterium tuberculosis
from primary pulmonary infection and the formation of small subpial and
subependymal foci (Rich foci) in the brain and spinal cord. In some individuals
foci rupture and release bacteria into the subarachnoid space causing meningitis.
In others, foci enlarge to form tuberculomas without meningitis. Tuberculous
meningitis (TBM) is the most dangerous form of infection with Mycobacterium
tuberculosis.5
2.1.2
Epidemiology
Tuberculosis of the central nervous system is the most severe manifestation of

extrapulmonary TB and constitutes approximately 1% of all new cases annually,
with Tuberculous Meningitis (TBM) being the commonest form of the disease.
Several studies have attempted to assess its epidemiology with variable
conclusions as the diseases incidence and mortality rates differ from country to
country according to their individual socioeconomic and public health statuses.

Mortality rates for instance have been described to range from 7 40% in
developed countries, while the percentages from TB endemic countries as well as
countries with high HIV prevalence have been found to be significantly higher,
reaching a 69% in South Africa. The key point in understanding the
epidemiological pattern of the disease is the fact that TBM and tuberculosis
infection are closely related in this aspect, so that it is generally accepted that
occurrence of the former in a community is correlated with incidence of the latter
and vice versa. It is therefore considered safe to assume that at a global level these
two entities share a common trend. According to the latest available data, in 2009
the global incidence of TB was 9.4 million cases which is equivalent to 137 cases
per 100.000 population with most of them occurring in Asia and Africa and a
smaller proportion occurring in Europe and the Region of the Americas.
Developing countries in particular account for more than 80% of the active cases
in the world. The global incidence rate after an initial fall during the 20th century
rose due to the HIV epidemic with a peak in 2004 and a subsequent slow but
steady decline that also involves the absolute number of TB related deaths. This
impact of HIV on TB has accordingly influenced the pattern of TBMs incidence
rates. In fact, HIV infection constitutes the most important determinant for the
development of TBM followed by age. As far as the latter is concerned it is in turn
determined by the socioeconomic status of a certain population. Therefore in
populations with a low TB prevalence adults seem to be more affected than
children. This is reversed in populations with a higher TB prevalence. Concerning
childhood disease, TBM appears to affect mainly children under the age of 5 years
with the mean age ranging from 23 to 49 months and according to literature close
contact with a confirmed case of pulmonary tuberculosis is usually the culprit.6
2.1.3
Etiology
Mycobacteria are aerobic, nonmotile, gram-positive rods ranging in appearance

from spherical to short filaments, which may be branched. Their cell wall contains
lipids, peptidoglycans, and arabinomannans. One distinct characteristic is their
ability to retain dyes that are usually removed from other microorganisms by
alcohols and dilute solutions of strong mineral acids such as hydrochloric acid.
This ability is attributed to a waxlike layer composed of mycolic acids in their
cell wall. As a result, they are termed acid-fast bacilli (AFB) after Ziehl-Neelsen
(ZN) staining. The causative agents of TBM are mainly the members of M.
tuberculosis complex and less commonly NTM. The incidence of CNS infection
due to the latter has increased substantially since the onset of the HIV epidemic.6
2.1.4
Pathogenesis
The initial point of tuberculosis infection is entry of the bacilli into the lungs via
inhalation of infectious droplets, whereupon the bacteria colonize macrophages
within the alveoli. During the progression of active pulmonary disease, bacteria
may disseminate to local lymph nodes and bloodstream, whereupon spread
throughout the systemic circulatory system may occur. It is also likely that
extensive bacteremia following dissemination from the lungs increases the
probability that a sub-cortical focus will be established in the CNS. Therefore,
higher numbers of bacilli in the circulatory system may be associated with
increased likelihood of CNS invasion and subsequent CNS TB.7
The CNS is protected from the systemic circulatory system by the
physiological blood brain barrier (BBB). This barrier is principally composed of
tightly apposed human brain microvascular endothelial cells (Fig. 1). The basal
portion of these endothelial cells is supported by astrocyte processes interspersed
with the extracellular matrix. Paracellular transport is limited by the presence of
endothelial cell tight junctions, while transcellular movement is restricted by the
relative paucity of endocytic vesicles. Such properties render the barrier
impermeable to many large, hydrophilic molecules and circulating pathogens.
Also protective of the CNS is the blood-cerebrospinal fluid (CSF) barrier,
providing spatial separation of the circulatory system from the CSF at the choroid
plexus. Cells lining the blood-CSF barrier share similar properties to those lining
the BBB, with enhanced tight junctions and more stringent regulation of
transcytosis. Despite the integrity of this barrier, however, there are a number of
bacterial and viral pathogens capable of crossing the BBB and causing subsequent
meningitis / encephalitis.7
Fig. (1). Blood Brain Barrier.7

Much of the current understanding of the pathogenesis of CNS TB and
subsequent meningitis comes from the meticulous work of Arnold Rich and
Howard McCordock, who demonstrated upon autopsy that the majority of TB
meningitis patients displayed a caseating focus in the brain parenchyma or the
meninges. Rich postulated that these foci, also termed as Rich foci, develop
around bacteria deposited in the meninges and brain parenchyma during the initial
bacteremic phase. Much later, the rupture of these foci allowed dissemination of
the bacilli into the subarachnoid space, causing diffuse, inflammatory meningitis
(Fig. 2). Since the meninges and the brain parenchyma are anatomically and
physiologically protected from the systemic circulation by the BBB, the
mechanism by which the bacilli initially invade this barrier need to be elucidated.
Theoretically, M. tuberculosis can cross the BBB as a free (extra-cellular)

organism or via infected monocytes/neutrophils. While the latter hypothesis seems
attractive, such cellular traffic is severely restricted into the CNS prior to invasion
by the offending pathogen. Intravenous inoculation of free M. tuberculosis or M.
bovis in guinea pigs and rabbits has been shown to produce CNS invasion as
evidenced by the formation of tuberculomas in their brain parenchyma. Further,
one report utilizing CD18 leukocyte adhesion deficient mice, suggests that free
mycobacteria may transverse the BBB independent of leukocytes or macrophages.
Finally, it is unclear whether, after invading the CNS, M. tuberculosis reside
primarily within the parenchyma of the brain, the vessel wall, or the endothelial
cells lining the microvasculature. Significant vasculitis associated with CNS
tuberculosis and robust human endothelial cell invasion observed in vitro may
suggest that M. tuberculosis reside, at least initially, in the endothelial cells lining
the microvasculature.7
Fig. (2). Pathogenesis of Central Nervous System tuberculosis and

subsequent tuberculous meningitis.7
The spread of M. tuberculosis into the subarachnoid space following
rupture of a Rich focus triggers a robust inflammatory T cell response. Studies of
CSF cytokine levels in patients with TB meningitis have found elevated levels of
TNF- and IFN-. The clinical manifestation of CNS tuberculosis is primarily a
consequence of the inflammation which develops in response to M. tuberculosis in
the CNS. Obstruction of the CSF by inflammatory infiltrate leads to
hydrocephalus, and vasculitis contributes to infarction, causing potentially
irreparable neurological damage. Inhibition of this inflammation may therefore
help in preventing the sequelae of CNS TB. Though thalidomide, which inhibits
TNF-, has not be shown to be beneficial for the treatment of TB meningitis in
children, corticosteroids such as dexamethasone which suppress the production of
inflammatory cytokines and chemokines lead to better outcomes and are
recommended as adjunctive treatment for patients with TB meningitis.7
2.1.5
Clinical manifestation
Generally, the progression of tuberculous meningitis has 3 stage:8

1. Stage I: Prodormal
This stadium will progress in 1 3 week without any special
clinical symptoms and without any neurological disorder. Experienced
symptoms include fever, malaise, anorexia, abdominal pain and headaches,
sleep cycles change, nausea, vomiting, constipation, irritable to apathy, but
without loss of consciousness. Physical examination showed the large
fontanelle bulging in infants. older children will experience a change of
mood and decreased school performance. intermittent seizures may arise.8
Prodromal stage may last a very short when tubercles broke into
the subarachnoid space arrived - arrived so the trip can last clinical jump
to the next stage quickly.8
2. Stage II: Transitional
At this stage exudate was collected in cerebral gyrus which make
the meningeal refleks positive, ie a stiff neck, Kernig, and brudzinsky
(except in infants frequently meningeal refleks is negative). Decreased of
consciousness (but not coma or delirium), hydrocephalus, papilaedema
light, and the presence of tubercles in the choroid, and cranial nerve palsy.
10
Cranial nerve that most commonly affected are N. VI that was followed by
N. III, N. IV, and N. VII which can cause strabismus, diplopia, ptosis, and
decreased pupil reaction to light. Older children will complain of severe
headache and vomiting, while the baby would seem irritable and vomiting.
The child may have symptoms of encephalitis in the form of a real focal
neurological deficits accompanied by involuntary movements and speech
disorders. Hydrocephalus that occure before symptoms of encephalitis is
one characteristic of tuberculous meningitis.8
3. Stage III: Terminal.
This stage takes place quickly, as long as 2-3 weeks. brainstem
infarction due to vascular lesions or strangulation by exudates which
experienced organization. Consciousness decreased to stupor or coma,
more severe form of focal neurological deficits (hemiplegia to paraplegia).
hyperpyrexia, papilaedema, hyperglycemia, opistotonus, decerebrate
posture, pulse and irregular breathing, dilated pupils, and not react to light,
or even death.8
2.1.6
Diagnosis
The diagnosis of tuberculous meningitis is not a simple work up especially on

mild stage. It cannot be made or excluded on the basis of clinical findings2.
Suspecting a tuberculous meningitis is a must if there is prolonged fever (>14
days, or >7 days if there is contact history with TB-confirmed family), patient still
unconscious after antimicrobial treatment, positive meningeal sign, hydrocephalus
and stroke with unclear etiology.8
Evaluate contact history to TB-confirmed family, immunodeficiency
possibility or drug-induced immunodepression. Evaluate BCG vaccination history,
because BCG vaccination can decrease tuberculous meningitis risk until 50-80%.8
Positive tuberculin test and chest radiography can confirm the suspicion,
but the negative result doesnt eliminate the suspicion because non-reactive
tuberculin and normal chest radiography is found at almost 50% patient. A
11
complete blood count testing should be performed, and the erythrocyte

sedimentation rate should be determined.8 Positive tuberculin test, chest
radiography abnormal finding and the finding of infection source in family only
can support the diagnoses. Tuberculin test often negative because of anergy,
especially on terminal stage.9
The gold standard of diagnosis is to find M. tuberculosis bacilli on
cerebrospinal fluid (CSF) culture, but to growing the bacteria up needs long time
at least 3-6 weeks and the positive result is found only on 50-75% cases if the
CSF is enough (5-10 ml). So the therapy can be given based on CSF analysis
result or the finding of acid-resistant bacteria on the microscopic test. 8 Spinal tap
carries some risk of herniation of the medulla in any instance when intracranial
pressure (ICP) is increased, but if meningitis is suspected, the procedure must be
performed regardless of the risk, using suitable precautions and obtaining
informed consent before the procedure. Use manometrics to check CSF pressure.
Typically, the pressure is higher than normal.10
CSF analysis result show xhantochromic color, with fibrin sediment,
leucocyte count increases to 10-500 cell/mm 3 (almost of them is lymphocyte, but
on early stage PMN is dominantly found), protein is very increased (0,4-1,3 g/dL)
low glucose (<40 mg/dL, infrequently to <20 mg/dL, or glucose-serum/CSF ratio
0.4).8 So the serum glucose level should be measured as comparison with the
glucose level measured in the CSF. Hemorrhagic CSF also has been recorded in
proven cases of TBM, this is attributed to fibrinoid degeneration of vessels
resulting in hemorrage.10
CSF acid-resistant staining can detect acid-resistant bacteria only on 30%
cases and needs high CSF amount as on culture. Low CSF amount can lowering
detection rate.8 Ziehl neelsen stain uses the properties of the cell wall to form a
complex that prevents decolorization by acid or alcohol. Fluorochrome tissue
stains also can be helpful in the diagnosis of tuberculous meningitis.10
Ziehl-Neelsen staining lacks sensitivity, and culture results are often too
late to aid clinical judgment. Semi-automated radiometric culture systems, such as
Bactec 460, and automated continuously monitored system have reduced culture
12
times. Newer methods involving amplification of bacterial DNA by polymerase

chain reaction (PCR) and comparable system have not been assessed completely
and may not be suitable for laboratories in developing countries with limited
resources.10
Computed tomography (CT) scanning and magnetic resonance imaging
(MRI) lack specificity but help in monitoring complications that require
neurosurgery.10 CT-scan or MRI testing is the most useful diagnosis on terminal
stage because it can detect complications, like communicans hydrocephalus,
cerebral oedem, ischemia, lesion on basal and tuberculoma. Tuberculoma can be
single or multiple, on CT scan or MRI is seen as lesion with clear border
surrounded by oedematous tissue. Strengthening with contrast will show ring-like
lesion.8
In one study, findings from electroencephalography (EEG) were abnormal
in some cases. EEG findings correlated with severity of meningitis and degree of
coma. Brainstem auditory evoked potential abnormalities were observed in some
cases. Motor and somatosensory evoked potentials may be helpful in objective
documentation of respective motor and sensory functions in patients with TBM
and altered sensorium.10
Electrolyte
concentrations
should
be
assessed.
Mild-to-moderate
hyponatremia is present roughly 45% of patients, in some cases constituting a true

syndrome of inappropriate diuretic hormone secretion (SIADH). Blood urea
nitrogen (BUN) and creatinine levels should be measured as well. Urinalysis
should be performed.10
2.1.7 Treatment
Tuberculous meningitis therapy based on Indonesia guideline is given on 12
months and also follow general tuberculosis therapy concept.8
Intensive phase
This phase is given on 2 months, using 4 or 5 anti-tuberculosis drugs, that
is isoniazid (INH) rifampin (RIF), pyrazinamide (PZA), ethambutol (E)
13
and streptomycin (SM). Streptomycin is given if there is anti-tuberculosis

drugs resistance.8
Advanced phase
This phase is given on next 10 months, using 2 anti-tuberculosis drugs that
is INH and RIF.8
The dosage of anti-tuberculosis drugs given is:
Isoniazid 5-15 mg/kgBW/day, max 30 mg/day
Rifampin 10-20 mg/kgBW/day, max 600 mg/day
Pyrazinamide 20-40 mg/kgBW/day, max 2 g/day
Ethambutol 15-25 mg/kgBW/day, max 1,25 g/day
Streptomycin 15-40 mg/kgBW/day, max 1 g/day

The second-line therapy is ethionamide, cycloserine, ofloxacin, and para-
aminosalicylate acid (PAS).8 The best anti-tuberculosis treatment of tuberculous

meningitis include isoniazid, rifampin, pyrazinamide, and streptomycin, all of
which enter CSF readily in presence of meningeal inflammation. Ethambutol is
less effective in meningeal disease unless used in high doses. INH, RIF, and PZA
are bactericidal. RIF and SM achieve optimal CSF levels when the meninges are
inflamed.10
Although anti-tuberculosis drug therapy have been started, culture and
sensitivity test are still performed to get a suitable therapy for the bacteria
sensitivity.8
During anti-tuberculosis therapy, monitoring must be performed every
month
to
evaluate
patients
commitment,
diseases
progressivity
and
manifestation, and adverse effect of the drugs. Liver function test is evaluated
when anti-tuberculosis therapy is started, then evaluate on weeks 2, 4, 6, 8 and
every month.8
On the first weeks therapy, PMN count increasing and hypersensitivity
reaction can be found caused by releasing of bacterial cell wall protein when the
bacteria is lysis. So corticosteroid can be given to suppress inflammation process
and reducing oedem, that is prednisone with dosage 11-2 mg/kgBW/day on 4-6
14
weeks and tapered off until 2-4 weeks. Steroid therapy can reduce mortality rate,
long-term complications, and permanent sequelae.8 The use of corticosteroids may
be indicated in the presence of increased intracranial pressure (ICP), altered
consciousness focal neurological findings, spinal block, and tuberculous
encephalopathy. Treatment of tuberculoma consist of high dose steroids and
continuation of anti-tuberculosis therapy, often for a prolonged course. 8
Symptomatic therapy can be given if there is seizure, correction of dehydration
caused by low nutritional intake or vomiting, and phisiotherapy.9
If there is a sign of obstructive hydrocephalus and neurologic worsening
surgical action such as ventriculo-peritoneal shunt (VPS) may be needed.8 Studies
suggest that prompt ventriculo-atrial or ventriculo-peritoneal shunting improves
outcome, particularly in patients presenting with minimal neurological deficit. 10
Surgical therapy for tuberculoma isnt important because it will be a resolution
with pharmacologic therapy. Unfortunately, tuberculoma can resist for a long
time, for months or for years.8
BCG vaccination offers a protective effect (approximately 64%) againts
tuberculous meningitis. Improvement in weight for age was associated with a
decreased risk of the disease, however, further studies are needed to evaluate the
association, if any, between nutritional status and vaccine effeicacy.10
2.1.8 Differential Diagnoses
The differential diagnoses of this cases is every condition that induced fever and
sensory changes, in which CNS infection by bacteria, fungi (such as
histoplasmosis, cryptococcus) virus (aseptic meningoencephalitis), spiroseta or
parasite. It must be considered of malignancy metastasis possibility, lymphoma,
epidural abscess, subdural hematoma or subdural empyema. 8 Diagnostic confuion
often exists between tuberculous meningitis and other meningoencephalitides, in
particular partially treated meningitis.10 The characteristic of CSF have a specific
presentation between bacterial, tuberculous, or viral meningitis.
15
Table.1. CSF Characteristic on Bacterial, Tuberculous, and Viral Meningitis.8

Condition
Bacterial
Tuberculous
Viral Meningitis
Normal
Stain
Meningitis
Purulent, cloudy
Meningitis
Xanthochrome,
Clear (except cell
Clear
Pressure
200-750+
fibrin clots
150-750+
count >300/L)
Normal or slightly
<160
(mmH2O)
Cell
Thousands (>1000
200-500, mainly
increased
50-300, mainly
0-5 lymphocyte,
count /L
cell/L), mainly
lymphocyte
lymhocyte
1-3 PMN on 3-
PMN
first month,
30 lymphocyte
on neonatus, 20-
Protein
Hundreds to
45-1000, cell
20-125 (normal or
50 erytrocyte
15-35 (lumbal),
(mg/dL)
Glucose
thousands
Very decreased,
count increased
Very decreased,
slightly increased)
Normal or slightly
5-15 (ventricle)
50-80 (2/3 of
(mg/dL)
CSF/blood ratio
CSF/blood ratio
decreased
blood glucose)
0,6 on neonatus,
0,4
0,4 on older child
Tuberculous meningitis must be differentiated not only from other forms

of acute and subacute meningitis but also from conditions such as viral infection
and cerebral abscess. The radiological differential diagnoses includes cryptococcal
meningitis, cytomgalovirus encephalitis, sarcoidosis, meningeal metastases, and
lymphoma.10
2.1.9
Complication
Complication can occurred because of inadequate or late treatment3. Tuberculous

meningitis got high complication rate, major or minor, even after treated and has
been confirmed healed. Permanent major neurologic symptom such as cerebral
palsy, mental retardation, epileptic, paraplegia, and sensory changes on extremity.
Minor neurologic symptom such as cranial nerve palsy, nystagmus, ataxia, and
mild changes of coordination and spastiity.8
Mental retardation rate is almost 70%, intracranial calcification about
30%, and endocrine changes such as precocious puberty, hyperprolactinemia,
growth hormone deficiency, diabetes insipidus, corticotrophin, and gonadotropin
16
caused by hypofisis and hypothalamic disturbances is about 20% of cases. The

complication can affect eye that caused optical atrophy and blindness, and affect
ear that caused hearing loss.8
Tuberculous radiculomyelitis (TBRM) is a rare complication of
tuberculous meningitis. It develops at various intervals after tuberculous
meningitis, even in adequately treated patients after sterilization of the CSF. The
most common symptoms are subacute paraparesis, radicular pain, bladder
disturbance, and subsequent paralysis.10
2.1.10 Prognosis
The prognosis depends on patients stage when diagnosed and treated. On early
stage the prognosis is great, but most of patients on late stages experienced
permanent neurologic symptoms. Patients age under 3 years got worse prognosis.
Untreated patient can caused patients death.8 Before anti-tuberculosis drugs had
been found, tuberculous meningitis mortality is almost 100%. With antituberculous treatment, mortality can be reduced even still high that is about 1050%.9
CHAPTER III
CASE REPORT
17
3.1 Objective
The objective of this paper is to report a case of a 3 years 1 month old girl with a
diagnosis of tuberculous meningitis.
3.2 Case
DM, a 3 years 1 month old girl, with 7 kg of BW and 78 cm of BH, came to Haji
Adam Malik General Hospital Medan on 8th September at 20.25. Her main
complaint was loss of consciousness.
History of disease:
DM, a girl, 3 years 1 month old, with 7 kg of BW and 78 cm of BH, came to Haji
Adam Malik General Hospital Medan on 8th September at 11 PM. The chief
complaint was loss of consciousness. It has been experienced by patient for 5 days
before admitted to hospital, loss of consciousness begins with seizure. Seizure is
experienced by patient since 1 week. Seizure has been experienced three times,
the duration of seizure at least 5 minutes. When she got seizure her hands and foot
stomp, her eyes stare upward. Seizure found coincide with fever. Fever has been
experienced by patient since 1 week with high temperature. Fever recur in this 1
year, fever is usually followed by yellow-greenish liquid out from her ears. The
liquid out from her ears in this 1 year, intermittent, the liquid is yellow-greenish
and smell odor. Cough experienced in 2 months, history of contact with adult
cough is found. Her mother said she is consuming anti-tuberculosis drugs for 1
month. Headache was experienced by patient since 1 month ago. Vomiting is not
found. She has not defecate for 5 days, urination is normal. History of loose of
weight is found in 1 month.
History of medication:
O2, IVFD ringer lactate, inj streptomycin, anti-tuberculosis drugs first line early
phase 1x1.
History of family:
Patients mother is diagnosed as lung tuberculosis.
History of parents medication:
18
Patients mother is consuming anti-tuberculosis drugs.

History of pregnancy:
Patients mother was 42 years old during pregnanc gestational age was aterm.
History of birth:
Birth was assisted by traditional midwife. Baby was born normally and cried
spontaneously. Body weight was 4000 gram, body length was not measured.
History of feeding:
18 months of breast feeding, family food was given from 18 months onwards.
History of immunization:
None
History of growth and development:
Patients mother explained that he grew normally. He was able to talk, crawl and
walk appropriately based on his age.
Physical Examination:
Present status:
Sensorium : GCS 9 (E2 M2 V5), body temperature: 36.8C, HR: 130 bpm, RR: 32
x/i, BW: 7 kg, BH: 78 cm, BW/A: Z score < -3 , BL/A: Z score < -3, BW/BL: Z
score < -3, anemic (-), icteric (-), dyspnea (+), cyanosis (-), edema (-).
Localized status:
Head : Face: within normal range
Eyes: light reflex +/+, isochoric pupil, pale inferior
palpebral conjunctiva-/-, superior and inferior palpebra
edema-/-,.
Ears: secretion of yellow-greenish liquid
Nose: nasal cannula applied
Mouth : within normal range
Neck : Stiff neck (-) lymph node enlargement (-)

Thorax : Symmetrical fusiform, retraction (-)
HR: 130 bpm, regular, murmur (-)
RR: 32x/i, regular, ronchi (-/-)
19
Abdomen: Symmetric, supple, normal peristaltic, liver and spleen:
undeterminable
Extremities : pulse 120 bpm regular, adequate p/v, felt warm, CRT
< 3 edema pretibial (+).

Physiologic reflex: APR/KPR (+)/(+)
Pathologic reflex : Chaddock (-) / babinski (+) / oppenheim (-)
Meningeal sign : Kernig sign (-) / Brudzinski I / II (-)
Anogenital : Female
Differential diagnosis :
Tuberculous meningitis (dd bacterial meningitis, viral meningoencephalitis) +
Lung TB + chronic suppurative otitis media + malnutrition
Working diagnosis
Tuberculous meningitis + Lung TB +
chronic suppurative otitis media +
malnutrition
Laboratory finding
Complete blood analysis (8th September 2015 / 20:55)
Test
Result
Unit
References
Hemoglobin
9.30
g%
11.3-14.1
Erythrocyte
5.40
106/mm3
4.40-4.48
Leucocyte
4.17
103/mm3
6.0-17.5
Thrombocyte
259
103/mm3
217-497
Hematocrite
30.40
37-41
Eosinophil
0.50
1-6
Basophil
0.200
0-1
Neutrophil
62.80
37-80
Lymphocyte
23.00
20-40
Monocyte
13.70
2-8
Neutrophil absolute
2.61
103/L
1.9-5.4
20
0.96
103/L
3.7-10.7
Monocyte absolute
0.57
103/L
0.3-0.8
Eosinophil absolute
0.02
103/L
0.20-0.50
Basophil absolute
0.01
103/L
0-0.1
MCV
56.30
Fl
81-95
MCH
17.20
Pg
25-29
MCHC
30.60
g%
29-31
Result
Unit
References
Blood Glucose
89.40
mg/dL
< 200
Ureum
12.00
mg/dL
< 50
Creatinine
0.28
mg/dL
0.24-0.41
Calsium
8.3
mg/dL
8.4-10.4
Natrium
134
mEq/L
135-155
Potassium
2.4
mEq/L
3.6-5.5
Chloride
95
mEq/L
96106
Lymphocyte
absolute
Clinical Chemistry
Test
Carbohydrate Metabolism
Electrolyte
Cerebrospinal fluid analysis (10th September 2015)

Color
Clear
Clear
LDH
286
U/L
<200
Total Protein
96.00
Mg/dL
<45
Leucocyte count
0.617
103 u/L
<3
21
Erythrocyte count
0.001
106 u/L
Glucose
38
mg/dL
pH
8.0
MN cell
25.1
PMN cell
74.9
40-76
7-8
Gas blood analysis (11 September 2015 / 21:18)

pH
7.39
7.35-7.45
pCO2
19.0
mmHg
38-42
pO2
202.0
mmHg
85-100
Bicarbonate (HCO3) 11.5
mmol/L
2-26
Total CO2
12.1
mmol/L
19-25
Base Excess (BE)
-11.2
mmol/L
(-2) (+2)
O2 Saturation
100.0
95-100
Unit
References
Complete blood analysis

Test
Result
Hematology (15th September 2015 / 11:45)

LED
13
Urinalysis (18th September 2015 / 09:42)
mm/hour
< 20
22
Urine volume / 24
1500
mL/ 24 hours
< 1200-2000
Protein Urine
79 (-)
mg %
<150
Protein Urine / 24
1195
mg / 24 hours
hours
hours
Therapy:
- Head elevation 30 midline position

- IVFD NaCl 0,9% 20 gtt (micro) + KCl 15 mEq 10 gtt / min
(threeway)
- Inj. Phenytoin MD 22,5 mg / 1 hours in 20 cc NaCl 0,9%
(finished in 20 minutes)
- O2 1-2 l/min via nasal cannula
- Inj Ceftriaxone 350 mg/ 8 hours /iv
- Paracetamol100 mg / 8 hours / iv
- Inj. Furosemide 10 mg / 12 hours / iv
- Spironolactone 2x6,25 mg
- Diamox 3x200 mg
- Rifampicin 1x150 mg
- INH 1x100 mg
- Ethambutol 1x200 mg
- Pirazinamid 1x 200 mg
- Prednisone 3x7 mg
- Vit. B complex 1x1
- Vit. C 1x100 mg
- Folic acid 1x1 mg
- Diet F75 140 cc + min mix 2,8 cc/ 3 hours / NGT
23
Planning Assesment:
- CSF analysis
- CSF culture
- Thorax radiography
- Consult to THT department
- Liver Function Test
- Renal Function test
- Eye function test
- Ear Function test
- CT scan
- MRI
- Urinalysis
- EEG
24
Follow Up
S
O
8-10th September 2015

Loss of consciousness, convulsions (-)
Sensorium: GCS 9 (E2V2M5), Temp: 36,5oc/37,9c/38c, BW: 9 kg
Head : Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra
(-/-)
- Ear : discharge yellow-black
- Nose : within normal range
- Mouth : within normal range
Neck : stiff neck (-)
Thorax : symmetrical fusiform, retraction (-),
-
HR: 104/124/ 118bpm, regular, murmur (-)

RR : 24/30/30x/i, regular, ronchi (-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable

Extremities : pulse 104/124/ 118bpm, regular, adequate p/v , felt warm, CRT < 3 ,
blood pressure: 100/60mmHg.
Physiological Reflex: APR (+) / KPR (+)
Pathological Reflex: Babinski (+), Oppenheim (-), chaddock (-),Gordon(-)
A
Meningeal Reflex: stiff neck (-), brudzinski I/II (-/-), Kernig sign (-)
DD/ Meningitis
+ Miliary TB + OMSK + Malnutrition
Ensefalitis
Meningoensefalitis
Head Elevation 30 midline position
O2 1-2 L/min nasal canule
IVFD NaCl 0,9% 30gtt/i (three way)
Inj Ceftriaxone 1g/daily/iv
Inj. Phenytoin MD 22,5 mg /24 hrs in 20cc NaCl 0,9% (finished in 20 minute)
Inj. Paracetamol 100mg/8 hrs/iv
25
Laboratory finding
Complete blood analysis (8th September 2015 / 20:55)
Test
Result
Unit
References
Hemoglobin
9.30
g%
11.3-14.1
Erythrocyte
5.40
106/mm3
4.40-4.48
Leucocyte
4.17
103/mm3
6.0-17.5
Thrombocyte
259
103/mm3
217-497
Hematocrite
30.40
37-41
Eosinophil
0.50
1-6
Basophil
0.200
0-1
Neutrophil
62.80
37-80
Lymphocyte
23.00
20-40
Monocyte
13.70
2-8
Neutrophil absolute
2.61
103/L
1.9-5.4
Lymphocyte
0.96
103/L
3.7-10.7
Monocyte absolute
0.57
103/L
0.3-0.8
Eosinophil absolute
0.02
103/L
0.20-0.50
Basophil absolute
0.01
103/L
0-0.1
MCV
56.30
Fl
81-95
MCH
17.20
Pg
25-29
MCHC
30.60
g%
29-31
Unit
References
absolute
Clinical Chemistry
Test
Result
26
Blood Glucose
89.40
mg/dL
< 200
Ureum
12.00
mg/dL
< 50
Creatinine
0.28
mg/dL
0.24-0.41
Calsium
8.3
mg/dL
8.4-10.4
Natrium
134
mEq/L
135-155
Potassium
2.4
mEq/L
3.6-5.5
Chloride
95
mEq/L
96106
Electrolyte
Cerebrospinal fluid analysis (10th September 2015)

Color
Clear
LDH
286
U/L
<200
Total Protein
96.00
Mg/dL
<45
Leucocyte count
0.617
103 u/L
<3
Erythrocyte count
0.001
106 u/L
Glucose
38
mg/dL
pH
8.0
MN cell
25.1
PMN cell
74.9
S
O
Clear
40-76
7-8

Loss of consciousness, Convulsion (-)
Sensorium: vegetative state, Temp: 37,8oc/37,8oc/37,8oc. BW: 9kg,
Head Circumference: 44cm
Head : Eye : Light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-)
-
Ear : discharge yellow-black
27
- Nose : within normal range

- Mouth : within normal range
-
HR: 114/124/118 bpm, regular, murmur (-)

RR : 34/26/24x/i, regular, ronchi (-/-)

Extremities : pulse 114/124/118 bpm, regular, adequate p/v , felt warm,
CRT < 3. Blood pressure 100/90mmHg.
Pathological Reflex: Babinski (-), Oppenheim (-), chaddock (-)
A
P
Meningitis TB + Miliary TB + OMSK + Marasmus
O2 1 L/min nasal canule
IVFD NaCl 0,9% + KCl 15 mEq 20gtt/i (three way)
Inj Ceftriaxone 1g/24hrs/iv( in 50cc NaCl 0,9%)
Inj. Phenytoin MD 22,5 mg /12 hrs in 20cc NaCl 0,9% (finished in 20
minute)
Inj. Furosemide 10mg/12hrs /iv
Inj. Sibital LD 180mg, MD 20mg/12hrs (if convulsion)
Spironolakton 2x6,25mg
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Pyrazinamide 1x200mg
Etambutol 1x200mg
Prednisone 3x7mg
vit. B Complex 1x1
vit. C 1x100mg
Asam folat 1x1mg
Diet F75 140 cc + min mix 2,8cc/3jam/NGT
Resomal 50 cc jika muntah/mencret
Konsul THT
Jawaban: OMSK ADS + Meningitis + TB + Marasmus
Anjuran: kultur secret telinga kanan & kiri
Gas blood analysis (11 September 2015 / 21:18)
28
pH
7.39
7.35-7.45
pCO2
19.0
mmHg
38-42
pO2
202.0
mmHg
85-100
mmol/L
2-26
Total CO2
12.1
mmol/L
19-25
Base Excess (BE)
-11.2
mmol/L
(-2) (+2)
O2 Saturation
100.0
95-100
Result
Unit
References
Natrium
135
mEq/L
135-155
Potassium
4,0
mEq/L
3.6-5.5
Chloride
103
mEq/L
96106
Clinical Chemistry (13th september 2015)

Test
Electrolyte

S
Sensorium: vegetative state, Temp: 37,2oc/37,6oc/37,1oc. BW: 9kg

-
Nose : within normal range
29

-
RR : 26/36/34 x/i, regular, ronchi (-/-)

CRT < 3.
Pathological Reflex: Babinski (-), Oppenheim (-), chaddock (-), gordon
(-).
A
P
Meningitis TB + TB Milier + OMSK + Gizi Kurang
minute)
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Prednisone 3x7mg
vit. B Complex 1x1
vit. C 1x100mg
Asam folat 1x1mg
Diet F75 140 cc + min mix 2,8cc/3jam/NGT
Consul to Respirologi (15/9/15)
Answer: dd/Miliary TB
Suggestion: mantoux test, gastric lavage, repeated thorax photo (AP
Lateral)
Clinical Chemistry (15th september 2015)
30
Test
Result
Unit
References
145.20
mg/dL
< 200
Calsium
6,8
mg/dL
8.4-10.4
Natrium
130
mEq/L
135-155
Potassium
3,8
mEq/L
3.6-5.5
Chloride
99
mEq/L
96106
Blood Glucose
Electrolyte

S
O

Sensorium: vegetative state, Temp: 37,2oc/37oc/37,9oc. BW: 8,1kg
-

-

CRT < 3.
Pathological Reflex: Babinski (-), Oppenheim (-), chaddock (-).
A
Meningitis TB + TB Milier + OMSK + Marasmus
31

minute)
Ibuprofen syr 4x100mg
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Prednisone 3x7mg
vit. B Complex 1x1
vit. C 1x100mg
Asam folat 1x1mg
Diet F100 170 cc/3jam + min mix 3,4 cc/3jam/NGT

S
Loss of consciousness, Convulsion (-), spastik (+), diare (+) date
22/9/15
Sensorium: vegetative state, Temp: 36,4oc/38oc/37,6oc. BW: 8,1kg
-

-

32
CRT < 3.
Pathological Reflex: Babinski (+), Oppenheim (-), chaddock (-).
A
P
minute)
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Prednisone 3x7mg
vit. B Complex 1x1
vit. C 1x100mg
asam folat 1x1mg
Diet F100 170 cc/3jam + min mix 3,4 cc/3jam/NGT
Laboratory finding
Complete blood analysis (21th September 2015)
Test
Result
Unit
References
Hemoglobin
7.80
g%
11.3-14.1
Erythrocyte
4.32
106/mm3
4.40-4.48
Leucocyte
10.18
103/mm3
6.0-17.5
Thrombocyte
964
103/mm3
217-497
Hematocrite
23.60
37-41
Eosinophil
0.30
1-6
Basophil
0.300
0-1
Neutrophil
69.10
37-80
33
Lymphocyte
16.80
20-40
Monocyte
13.50
2-8
Neutrophil absolute
7.04
103/L
1.9-5.4
Lymphocyte
1.71
103/L
3.7-10.7
Monocyte absolute
1.37
103/L
0.3-0.8
Eosinophil absolute
0.03
103/L
0.20-0.50
Basophil absolute
0.03
103/L
0-0.1
MCV
54.60
Fl
81-95
MCH
18.10
Pg
25-29
MCHC
33.10
g%
29-31
absolute

S
O

Sensorium: vegetative state, Temp: 36,4oc/36,5oc/37,6oc. BW: 8,5kg
LK: 44cm. PB: 81cm. LLAM: 12cm. LLAS: 12cm. BB/U: Z Score<3SD. PB/U: <-3SD. BB/PB: -3<SD<-2.
-

-

34
CRT < 3.
A
P
minute)
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Prednisone 3x7mg
vit. B Complex 1x1tab
vit. C 1x100mg
asam folat 1x1mg
Diet F100 200 cc/3jam + min mix 4 cc/3jam/NGT
PRC Transfusion 70cc from 150cc
consult to Neuro Surgery Department (23/9/15)
answer: Diversi CSF
S
O

-
35

-

CRT < 3.
A
P
minute)
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Prednisone 3x7mg
vit. C 1x100mg
asam folat 1x1mg
PRC Transfusion 70cc from 150cc
36
Laboratory finding
Complete blood analysis (26th September 2015)
Test
Result
Unit
References
Hemoglobin
15.50
g%
11.3-14.1
Erythrocyte
6.75
106/mm3
4.40-4.48
Leucocyte
6.19
103/mm3
6.0-17.5
Thrombocyte
390
103/mm3
217-497
Hematocrite
46.30
37-41
Eosinophil
0.30
1-6
Basophil
0.200
0-1
Neutrophil
64.80
37-80
Lymphocyte
23.40
20-40
Monocyte
11.30
2-8
Neutrophil absolute
4.01
103/L
1.9-5.4
Lymphocyte
1.45
103/L
3.7-10.7
Monocyte absolute
0.70
103/L
0.3-0.8
Eosinophil absolute
0.02
103/L
0.20-0.50
Basophil absolute
0.01
103/L
0-0.1
MCV
68.60
Fl
81-95
MCH
23.00
Pg
25-29
MCHC
33.50
g%
29-31
absolute
Faal Hemostase (26th September 2015)

APTT
Patient
27.7
37
Control
Renal
Trombin Time
Ureum
Patient
Creatinine
Control
s
mg/dL
Mg/dL
33.0
24.30
s
s0.12
< 50
15.5
0.31 17.5
0.47
Liver
Albumin
g/dL
4.0
Electrolyte
Natrium
137
mEq/L
135-155
Potassium
3.9
mEq/L
3.6-5.5
Chloride
109
mEq/L
96106
29th September 1st October 2015
3.8 5.4
38
S
O
Loss of consciousness, Spasm (+)

-

-

CRT < 3.
A
P
Hydrocephalus ec Meningitis TB + TB Milier + OMSK + Marasmus
minute)
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
39
Etambutol 1x200mg
Prednisone 3x7mg
vit. C 1x100mg
asam folat 1x1mg
consult to PICU (29/9/15)
consult to Anasthesion (29/9/15)
Clinical Chemistry (1st October 2015)

Blood Glucose
119.60
mg/dL
< 200
Calsium
7.7
mg/dL
8.4-10.4
Natrium
140
mEq/L
135-155
Potassium
4.1
mEq/L
3.6-5.5
Chloride
106
mEq/L
96106
Electrolyte
Gas blood analysis

pH
7.280
7.35-7.45
pCO2
19.0
mmHg
38-42
pO2
227.0
mmHg
85-100
mmol/L
2-26
Total CO2
9.5
mmol/L
19-25
Base Excess (BE)
-15.9
mmol/L
(-2) (+2)
40
O2 Saturation
100.0
95-100
1.22
0.2 2.5
Haematology
Reticulosit
S
O
2-4 Oktober 2015

LK: 44cm. PB: 81cm. LLA: 12cm. BB/U: Z Score<-3SD. PB/U: <3SD. BB/PB: -3<SD<-2.
-
Ear /Nose /Mouth : within normal range

-

CRT < 3.
Konsul anestesi: (4/10/15)
A
P
Acc to measure anesthesia and suggest to lokal EVD

Hidrocepalus + Meningitis TB + Miliary TB + OMSK + Marasmus
41
minute)
Ibuprofen 4x100mg
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Prednisone 3x7mg
Nystatin drop 4x0,5cc
vit. C 1x100mg
asam folat 1x1mg
Diet F100 200 cc/2jam + min mix 4 cc/NGT
Physiotheraphy
Laboratory finding
Complete blood analysis (4th October 2015)
Test
Result
Unit
References
Hemoglobin
14.50
g%
11.3-14.1
Erythrocyte
6.36
106/mm3
4.40-4.48
Leucocyte
6.08
103/mm3
6.0-17.5
Thrombocyte
340
103/mm3
217-497
Hematocrite
44.20
37-41
Eosinophil
0.00
1-6
Basophil
0.500
0-1
Neutrophil
49.40
37-80
Lymphocyte
33.70
20-40
Monocyte
16.40
2-8
Neutrophil absolute
3.00
103/L
1.9-5.4
42
2.05
103/L
3.7-10.7
Monocyte absolute
1.00
103/L
0.3-0.8
Eosinophil absolute
0.00
103/L
0.20-0.50
Basophil absolute
0.03
103/L
0-0.1
MCV
69.50
Fl
81-95
MCH
22.80
Pg
25-29
MCHC
32.80
g%
29-31
Lymphocyte
absolute
Faal Hemostase (4th October 2015)

PT + INR
Protrombin Time
Patient
Control
s
s
INR
APTT
Patient
Control
Trombin Time
Patient
Control
14.80
14.10
1.05
s
s
31.6
33.8
s
s
16.9
17.2
Blood Glucose
70.00
mg/dL
< 200
Calsium
8.2
mg/dL
8.4-10.4
Natrium
135
mEq/L
135-155
Potassium
3.8
mEq/L
3.6-5.5
Electrolyte
43
Chloride
S
O
106
mEq/L
96106
5-7 Oktober 2015

Sensorium: vegetative state, Temp: 37,3oc/37oc/37oc. BW: 9,3kg
LK: 44cm. PB: 81cm. LLA: 13cm. BB/U: Z Score<-3SD. PB/U: <3SD. BB/PB: -3<SD<-2. TD: 118/84mmHg
-

-

CRT < 3.
Konsul anestesi: (4/10

Hidrocepalus ec Meningitis TB + Miliary TB + OMSK ADS +
Marasmus
44
minute)
Ibuprofen 4x100mg
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Nystatin drop 4x0,5cc
vit. C 1x100mg
asam folat 1x1mg
Diet F100 225 cc/3jam + min mix 4,5 cc/NGT
Fisioterapi
Planning: VP Shunt installation (6/10/15)
Patient moved to PICU (7/10/15)
Cerebrospinal fluid analysis (7th October 2015)

Color
Clear
Clear
LDH
36
U/L
<200
Total Protein
23.00
Mg/dL
<45
Leucocyte count
0.001
103 u/L
<3
Erythrocyte count
0.000
106 u/L
Glucose
61
mg/dL
pH
8.0
MN cell
40-76
7-8
45
PMN cell
100
Laboratory finding
Complete blood analysis (7th October 2015)
Test
Result
Unit
References
Hemoglobin
11,90
g%
11.3-14.1
Erythrocyte
5,18
106/mm3
4.40-4.48
Leucocyte
9,74
103/mm3
6.0-17.5
Thrombocyte
327
103/mm3
217-497
Hematocrite
37,10
37-41
Eosinophil
0.10
1-6
Basophil
0.100
0-1
Neutrophil
80,20
37-80
Lymphocyte
12.20
20-40
Monocyte
7.40
2-8
Neutrophil absolute
7.81
103/L
1.9-5.4
Lymphocyte
12.20
103/L
3.7-10.7
Monocyte absolute
0.72
103/L
0.3-0.8
Eosinophil absolute
0.01
103/L
0.20-0.50
Basophil absolute
0.01
103/L
0-0.1
MCV
71.60
Fl
81-95
MCH
23.00
Pg
25-29
MCHC
32.10
g%
29-31
absolute
Faal Hemostase
PT + INR
Protrombin Time
46
Patient
Control
s
s
INR
APTT
Patient
Control
Trombin Time
Patient
Control
22.9
13.50
1.74
s
s
29.5
33.5
s
s
17.8
17.0
Gas blood analysis

pH
7.32
7.35-7.45
pCO2
16.0
mmHg
38-42
pO2
202.0
mmHg
85-100
mmol/L
2-26
Total CO2
8.7
mmol/L
19-25
Base Excess (BE)
-16.3
mmol/L
(-2) (+2)
O2 Saturation
100.0
95-100
3.5
3.8 5.4
Liver
Albumin
g/dL
Blood Glucose
75.40
mg/dL
< 200
47
Renal
Ureum
mg/dL
12.90
< 50
Creatinine
Mg/dL
0.23
0.31 0.47
Electrolyte
Calsium
8.3
mg/dL
8.4-10.4
Natrium
136
mEq/L
135-155
Potassium
388
mEq/L
3.6-5.5
Chloride
111
mEq/L
96106
48
S
O
8-10 Oktober 2015

Febris ()
Sensorium:
GCS
11,
Temp:
36,9oc/37oc/37,2oc.
LK: 44cm.
Head : Eye : Light reflex (+/+),
isochoric
pupil,
pale
inferior

-
Ear /Nose /Mouth : within

normal range

Thorax
symmetrical
fusiform,
retraction (-),
-
HR: 128/98/116 bpm, regular,

murmur (-)
RR : 24/24/28 x/i, regular,

ronchi (-/-)
Abdomen : supple, peristaltic (+)N,

Liver and Spleen: no palpable
Extremities : pulse 111/110/116 bpm,
regular, adequate p/v , felt warm, CRT
< 3.
Physiological Reflex: APR (+) / KPR
(+)
Pathological Reflex: Babinski (-),
Oppenheim (-), chaddock (-).
Meningeal Reflex: stiff
neck (-),
brudzinski I/II (-/-), Kernig sign (-)

49
A
P
Post VP Shunt a/i Hidrocepalus ec

Meningitis TB + Miliary TB
Inj. Ceftriaxone 500mg/12hrs
Inj. Phenytoin MD 25 mg /12 hrs in 20cc NaCl 0,9% (finished in 20
minute)
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
vit. B 6 1x1tab
vit. C 1x100mg
physiotherapy
Diet Pediasure 80cc/3hrs
Gas blood analysis (8th October 2015)

pH
7.150
7.35-7.45
pCO2
14.0
mmHg
38-42
pO2
187.0
mmHg
85-100
mmol/L
2-26
Total CO2
5.3
mmol/L
19-25
Base Excess (BE)
-21.7
mmol/L
(-2) (+2)
O2 Saturation
99.0
95-100
145.20
mg/dL
< 200
Metabolic
Blood Glucose
50
11-13 Oktober 2015

S
O
Febris ()
Sensorium: GCS11, Temp: 37,2oc/36,9oc/37,1oc.
LK: 44cm.
-

-

CRT < 3.
A
P

Post VP Shunt a/i Hidrocepalus ec Meningitis TB + Miliary TB
Inj. Ceftriaxone 500mg/12hrs
Inj. Phenytoin MD 25 mg /12 hrs in 20cc NaCl 0,9% (finished in 20
minute)
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
51
Etambutol 1x200mg
vit. B 6 1x1tab
vit. C 1x100mg
Fisioterapi
14-15 Oktober 2015

S
O
Febris ()
Sensorium: GCS11, Temp: 37oc/36,9oc/37,1oc.
LK: 44cm.
-

-
HR: 120/106 bpm, regular, murmur (-)
RR : 30/26 x/i, regular, ronchi (-/-)

Extremities : pulse 120/106 bpm, regular, adequate p/v , felt warm, CRT
< 3.
A
P

Post VP Shunt a/i Hidrocepalus ec Meningitis TB + Miliary TB
O2 1 L/min nasal canule (14/10/15)
Ciprofloxacin 2x125mg
Phenytoin 2x25 mg
52
Diamox 3x200mg
Rifampicin 1x150mg
INH 1x100mg
Etambutol 1x200mg
Prednisone 3x5mg
vit. B 6 1x1tab
vit. C 1x100mg
OUT PATIENT (15/10/15)
CHAPTER IV
DISCUSSION
Case
Theory
The chief complaint of this patient

was loss of consciousness. Seizure has
been experienced three times, the
duration of seizure at least 5 minutes.
Fever is experienced by patient with
high temperature. Cough experienced,
History of loose of weight is found.
Patient has history of fever, since 1

week before admitted to hospital with
high temperature
Experienced
symptoms
of
tuberculous meningitis include
fever, malaise, anorexia, abdominal
pain and headaches, sleep cycle
changes,
nausea,
vomiting,
constipation, irritable to apathy, loss
of
consciousness,
intermittent
seizure may arise.
Suspecting a tuberculous meningitis
is a must if there is prolonged fever
(>14 days, or >7 days if there is
contact history with TB-confirmed
family
53
Patients mother is diagnosed as lung

tuberculosis
Patient has no history of immunization
Based on Chest X-Ray The Patient has

abnormal inhomogeneous infiltrate
tuberculosis impression
CSF acid resistant staining test on this

patient shows negative result
The patient is treated with rifampicin,

INH, pyrazinamide and ethambutol
Patient is treated with corticosteroid

prednisone
Symptomatic therapy of this patient is

head elevation, IVFD NaCl + KCl,
phenytoin, O2, paracetamol,
furosemide, spironolactone, and
additional therapy is vit. B complex,
vit. C, folic acid and diet F75
Evaluate contact history to TBconfirmed

family,
immunodeficiency possibility or
drug-induced immunodepression.
Evaluate BCG vaccination history,
because BCG vaccination can
decrease tuberculous meningitis
risk until 50-80%
Positive tuberculin test, chest
radiography abnormal finding and
the finding of infection source in
family only can support the
diagnoses
CSF acid-resistant staining can
detect acid-resistant bacteria only
on 30% cases and needs high CSF
amount as on culture. Low CSF
amount can lowering detection rate
Anti-tuberculosis drug given is
isoniazid (INH), rifampin (RIF),
pyrazinamide (PZA), ethambutol
(E) and streptomycin (SM).
Streptomycin is given if there is
anti-tuberculosis drugs resistance
Corticosteroid can be given to
suppress inflammation process and
reducing oedem, that is prednisone
Symptomatic therapy can be given
if there is seizure, correction of
dehydration
caused
by
low
nutritional intake or vomiting, and
phisiotherapy
54
CHAPTER V
SUMMARY
DM, a girl, 3 years and 1 months old, weighted 7 kg and heighted 78 cm, from
pediatric cardiology polyclinic in H. Adam Malik General Hospital Medan on
September 11th 2015 at 11.00 PM develops loss of consciousness that was
experienced by the patient for 5 days before admitted to hospital, loss of
consciousness begins with seizure. Seizure is experienced by patient since 1 week.
Seizure has been experienced three times, the duration of seizure at least 5
minutes. When she got seizure her hands and foot stomp, her eyes stare upward.
Seizure found coincide with fever. Fever has been experienced by patient since 1
week with high temperature. Fever recur in this 1 year, fever is usually followed
by yellow-greenish liquid out from her ears. The liquid out from her ears in this 1
year, intermittent, the liquid is yellow-greenish and smell odor. Cough
experienced in 2 months, history of contact with adult cough is found. Her mother
said wass consuming anti-tuberculosis drugs for 1 month. Patient was treated with
55
Phenytoin, Ceftriaxone,
Paracetamol, Furosemide, spironolactone, diamox,
rifampicin, INH, ethambutol, prednisone, vit. B complex, and Vit. C.
REFERENCES
1. Isabel BE, Pathogenenesis and Immune Response in Tuberculous Meningitis,
Malays J Med Sci. Jan-Feb 2014; 21(1): 4-10.
2. Dimyati Y, Outcomes of tuberculous meningitis in children: a case review
study, Pediatricia Indonesiana, Vol. 51, No. 5, 2011.
3. IKA
4. Marx GE, Tuberculous Meningitis: Diagnosis and Treatment Overview,
Tuberculosis Research and Treatment, Volume 2011.
5. Thwaites G, British Infection Society guidelines for the diagnosis and treatment
of tuberculosis of the central nervous system in adults and children, Journal of
Infection. 2009; 167-187.
6. Kechagia M, Tuberculous Meningitis, InTech, 2012.
56
7. Be NA, Pathogenesis of Central Nervous System Tuberculosis, Curr Mol Med.

2009; 9(2): 94-99.
8. Tanto, C., Liwang, F., Hanifati, S., Pradipta, E., 2014. Kapita Selekta
Kedokteran. Jakarta: Media Aesculapius.
9. Hassan, R., Alatas, H., 2002. Buku Kuliah Ilmu Kesehatan Anak.
Jakarta:Bagian Ilmu Kesehatan Anak Fakultas Kedokteran Universitas Indonesia.
10. Emedicine Medscape, 2014. Tuberculous Meningitis. Available at:
http://emedicine.medscape.com/article/11166190-overview

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1

TESAR AKBAR NUGRAHA

PEDIATRIC HEALTH DEPARTMENT

Medan, 15th October 2015

nonspecific symptoms, such s fever, vomiting, and behavioral changes, develops.

Tuberculous meningitis is an inflammation of the meningen that cause by primary

Tuberculosis of the central nervous system is the most severe manifestation of

country according to their individual socioeconomic and public health statuses.

Mycobacteria are aerobic, nonmotile, gram-positive rods ranging in appearance

Fig. (1). Blood Brain Barrier.7

Theoretically, M. tuberculosis can cross the BBB as a free (extra-cellular)

Fig. (2). Pathogenesis of Central Nervous System tuberculosis and

Generally, the progression of tuberculous meningitis has 3 stage:8

The diagnosis of tuberculous meningitis is not a simple work up especially on

complete blood count testing should be performed, and the erythrocyte

times. Newer methods involving amplification of bacterial DNA by polymerase

hyponatremia is present roughly 45% of patients, in some cases constituting a true

and streptomycin (SM). Streptomycin is given if there is anti-tuberculosis

The dosage of anti-tuberculosis drugs given is:

Isoniazid 5-15 mg/kgBW/day, max 30 mg/day

Rifampin 10-20 mg/kgBW/day, max 600 mg/day

Pyrazinamide 20-40 mg/kgBW/day, max 2 g/day

Ethambutol 15-25 mg/kgBW/day, max 1,25 g/day

Streptomycin 15-40 mg/kgBW/day, max 1 g/day

aminosalicylate acid (PAS).8 The best anti-tuberculosis treatment of tuberculous

Table.1. CSF Characteristic on Bacterial, Tuberculous, and Viral Meningitis.8

Clear (except cell

0,4 on older child

Tuberculous meningitis must be differentiated not only from other forms

Complication can occurred because of inadequate or late treatment3. Tuberculous

caused by hypofisis and hypothalamic disturbances is about 20% of cases. The

Patients mother is consuming anti-tuberculosis drugs.

Neck : Stiff neck (-) lymph node enlargement (-)

Abdomen: Symmetric, supple, normal peristaltic, liver and spleen:

< 3 edema pretibial (+).

Tuberculous meningitis + Lung TB +

chronic suppurative otitis media +

Cerebrospinal fluid analysis (10th September 2015)

Gas blood analysis (11 September 2015 / 21:18)

Bicarbonate (HCO3) 11.5

Base Excess (BE)

Complete blood analysis

Hematology (15th September 2015 / 11:45)

Urinalysis (18th September 2015 / 09:42)

- Head elevation 30 midline position

8-10th September 2015

HR: 104/124/ 118bpm, regular, murmur (-)

Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable

Cerebrospinal fluid analysis (10th September 2015)

11-13th September 2015

Ear : discharge yellow-black

- Nose : within normal range

HR: 114/124/118 bpm, regular, murmur (-)

Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable

Gas blood analysis (11 September 2015 / 21:18)

Bicarbonate (HCO3) 11.5

Base Excess (BE)

Clinical Chemistry (13th september 2015)

14-16th September 2015

Loss of consciousness, Convulsion (-)

Sensorium: vegetative state, Temp: 37,2oc/37,6oc/37,1oc. BW: 9kg

Ear : discharge yellow-black

Nose : within normal range

Mouth : within normal range