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CASE REPORT
TUBERCULOUS MENINGITIS

PRESENTED BY
MUKHAMAD FARIED

110100351

TESAR AKBAR NUGRAHA

110100362

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.3 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.

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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

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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.3
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.9
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.9
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.9
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

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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.9
Computed tomography (CT) scanning and magnetic resonance imaging
(MRI) lack specificity but help in monitoring complications that require
neurosurgery.9 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.9
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.9
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.9
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

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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.3
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. 9
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.9
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.9 The characteristic of CSF have a specific
presentation between bacterial, tuberculous, or viral meningitis.

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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,

increased
50-300,

0-5 lymphocyte,

count /L

cell/L),

mainly

lymphocyte

mainly

mainly

lymhocyte

PMN

1-3 PMN on 3first month,


30

lymphocyte

on neonatus, 20cell

20-125 (normal or

50 erytrocyte
15-35 (lumbal),

thousands
Very
decreased,

count increased
Very decreased,

slightly increased)
Normal or slightly

5-15 (ventricle)
50-80 (2/3 of

CSF/blood

CSF/blood

decreased

blood glucose)

Protein

Hundreds

(mg/dL)
Glucose
(mg/dL)

to

ratio

0,6 on neonatus,

45-1000,

ratio

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.9
2.1.9

Complication

Complication can occurred because of inadequate or late treatment. 9 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.9
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%.3

CHAPTER III
CASE REPORT

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3.1 Objective
The objective of this paper is to report a case of a 11 month old boy with a
diagnosis of bronkopneumonia.
3.2 Case
AS, a 11 month old boy, with 6,5 kg of BW and 66 cm of BH, came to Haji Adam
Malik General Hospital Medan on 12th November at 22.30. His chief complaint
was dyspnea.
History of disease:
AS, a 11 month old boy, with 6,5 kg of BW and 66 cm of BH, came to Haji Adam
Malik General Hospital Medan on 12th November at 22.30 with dyspnea as chief
complaint. The patients have been experienced this about 1 week before admitted
to hospital. Dyspnea was not directed with weather and activity. Cyanosis (-),
patient also experienced cough since 2 weeks ago followed by sputum. History of
contact with adult cough (-). Fever has been experienced by patient since 2 weeks
and the body temperature rises and drop. Shivering was not found. Vomiting (-)
and nausea (-). Defecation and urination is normal. History of weight loose is not
found.
History of medication:
O2, IVFD ringer lactate, nebule ventolin, inj meropenem, triamsinolon,
bromhexine an salbutamol
History of family:
There is no famiy history of similar disease found.

History of parents medication:


Not found
History of pregnancy:

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Patients mother was 31 years old during pregnancy. She regularly goes for
control. No history of complication neonate and maternal problem. Consumtion of
herbal medication (-)
History of birth:
Patient was first child. Gestational age was preterm (28 weeks). Body weight was
1200 gram, body length was not measured. Birth was assisted by traditional
midwife. Baby was born normally and cried spontaneously. Blusih was not found.
History of immunization:
Not complete
History of growth and development:
Patients mother explained that he grew normally. He was able to crawl and sit
appropriately based on his age.
Physical Examination:
Present status:
Sensorium : CM, body temperature: 37,6C, HR: 138 bpm, RR: 54 x/i, BW: 6,5
kg, BH: 66 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: within normal range
Nose: nasal flaring
Mouth : within normal range

Neck : lymph node enlargement (-)

19

Thorax : Symmetrical fusiform, retraction intercostal and epigastric


(+)
HR: 138 bpm, regular, murmur (-)
RR: 54x/i, regular, ronchi (+/+), wheezing (-/-)

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

normal
Extremities : pulse 138 bpm regular, adequate p/v, felt warm, CRT
< 3

Working diagnosis

: DD

bronkopneumonia

bronchiolitis

Laboratory finding
Complete blood analysis (12th November 2015 / 23.03)
Test
Result
Unit

References

Hemoglobin

9.20

g%

11.3-14.1

Erythrocyte

3.51

106/mm3

4.40-4.48

Leucocyte

19.74

103/mm3

6.0-17.5

Thrombocyte

263

103/mm3

217-497

Hematocrite

28.70

37-41

Eosinophil

0.50

1-6

Basophil

0.500

0-1

Neutrophil

51.00

37-80

Lymphocyte

39.90

20-40

Monocyte

8.10

2-8

Neutrophil absolute

10.08

103/L

1.9-5.4

Lymphocyte

7.88

103/L

3.7-10.7

1.59

103/L

0.3-0.8

absolute
Monocyte absolute

20

Eosinophil absolute

0.09

103/L

0.20-0.50

Basophil absolute

0.10

103/L

0-0.1

MCV

81.80

Fl

81-95

MCH

26.20

Pg

25-29

MCHC

32.10

g%

29-31

Clinical chemistry (12 November 2015 / 23.03)


Test

Result

Unit

References

Blood Glucose

71.70

mg/dL

40-60

Ureum

14.70

mg/dL

< 50

Creatinine

0.23

mg/dL

0.17-0.41

Natrium

136

mEq/L

135-155

Potassium

5.3

mEq/L

3.6-5.5

Chloride

100

mEq/L

96106

Procalcitonin

0.42

ng/mL

<0.05

Gas blood analysis (12 November 2015 / 23.03)


pH

7.155

7.35-7.45

pCO2

38.7

mmHg

38-42

pO2

177.5

mmHg

85-100

Bicarbonate (HCO3) 13.4

mmol/L

2-26

Total CO2

14.5

mmol/L

19-25

Base Excess (BE)

-14.5

mmol/L

(-2) (+2)

O2 Saturation

98.8

95-100

21

Therapy:

- O2 1-2 L/ min via nasal cannula


- IVFD D5% NaCl 0,225% 25 gtt/menit (micro)
- Inj Ceftriaxone 300 mg/ 12 hours /iv
- Paracetamol 3x cth 1/2
- Fluid challenge 10 cc/kgBB (65 cc)

Follow Up
13th Novemember 2015
S
Dyspnea(+)
O
Sensorium: CM, Temp: 37,2C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Major was closed
-

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)


- Ear : within normal range
- Nose : nasal flaring
- Mouth : within normal range
Neck : lymph node enlargement
Thorax : symmetrical fusiform, retraction (+) intercostal, epigastric
A
P

HR: 140 bpm, regular, murmur (-)


RR : 52x/i, regular, ronchi (+/+), wheezing(-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable
Extremities : pulse 140 bpm, regular, adequate p/v , felt warm,

CRT < 3
DD/Broncopneumonia
Bronchiolitis
O2 1 L/min nasal canule
IVFD D5% NaCl 0,225 % 25gtt/i (micro)

22

Paracetamol 3x 75 mg
Inj Ampicilin 160 mg/6h
Inj Gentamycin 40 mg/24h
Nebule Ventolin 1 respul+ NaCl ,9 % /6h
Meylon 28 mEq, dosis I: 14 mEq meylon dalam 100cc D5% in 4 hours
Diet Su 650 kkal and 13 gr protein
At 22.30
S
dyspnea , fever (+)
O
Sensorium: GCS 13 (E4, V3, M6) , T= 38,8 C
Ear: yellow discharge (+)
Thorax: Simetris Fusiformis, retraksi (+) epigastrial
HR: 165x/i, reg, murmur (-)
RR: 65x/i, reg, stridor (+), ronchi (+)
P
Nebule Ventolin 1 respul+ NaCl 0,9% / 8 h
R
Check blood gas analysis, Check electrolite post correction
Advise from dr. Wisman Dalimunthe, SpA
-

Mucolitic :GE 3 x tab (pulv)


Analgetic Paracetamol: 4 x 10 mg (pulv)
Consult to THT
Cultur the ear discharge

Gas blood analysis (13 November 2015 / 20.59)


pH

7.427

7.35-7.45

pCO2

27.9

mmHg

38-42

pO2

165.0

mmHg

85-100

Bicarbonate (HCO3) 18.0

mmol/L

2-26

Total CO2

18.9

mmol/L

19-25

Base Excess (BE)

-5.5

mmol/L

(-2) (+2)

O2 Saturation

99.4

95-100

mg/dL

40-60

Carbohydrate Metabolism
Blood Glucose ad 108.3

23

random

Electrolyte
Calsium

8.0

mg/dL

8.4-10.4

Natrium

135

mEq/L

135-155

Potassium

4.8

mEq/L

3.6-5.5

Chloride

102

mEq/L

96106

Clinical Chemistry
Liver Function Test
Fosfatase Alkalase (ALP)

148

U/L

<4,62

AST/SGOT

46

U/L

<38

ALT/SGPT

22

U/L

<41

Renal Function Test


Ureum
Creatinin

11,6
0,22

mg/dL
mg/dL

<50
0.17-0,42

Immunoserology
Autoimmune (CRP Kuantitatif)
Other Test (Procalcitonin)

5,6
0.17

mg/dL
ng/mL

<0,05

24

14th Novemember 2015


S
dyspnea (+)
O
Sensorium: CM, Temp: 37C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Major was closed
-

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)


- Ear : within normal range
- Nose : nasal flaring
- Mouth : within normal range
Neck : lymph node enlargement
Thorax : symmetrical fusiform, retraction (+) intercostal, epigastric
-

HR: 140 bpm, regular, murmur (-)


RR : 50x/i, regular, ronchi (+/+), wheezing(-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable
Extremities : pulse 140 bpm, regular, adequate p/v , felt warm,

CRT < 3
DD/Broncopneumonia

Bronchiolitis
O2 1 L/min nasal canule

IVFD D5% NaCl 0,225 % 25gtt/i (micro)


Paracetamol 3x 75 mg
Inj Ampicilin 160 mg/6 jam/iv
Inj Gentamycin 40 mg/24 jam/iv
Inj Dexametason 2,5 mg/8 jam/iv
Nebule Ventolin 1 respul+ NaCl ,9 % /8 jam
Diet Su 650 kkal dengan 13 gr protein
Answer from ENT division
S
Fluid in left ear (-), pain (+), cough and flu (about 1 week)
O
left ear: secret (+), thick, yellowish, central perforation
A
Acute Otitis Media
P
Result of Radiology examination
-

Both of sinus costophrenicus are sharp. Diafragma is smooth


Infiltrate on suprahilar, perihiler, dan parakardial paru bilateral
No cardiomegaly (CTR 45%)
Trachea in middle
Bones and soft tissue normal
Conclusion : Bronkopneumonia bilateral

25

15th Novemember 2015


S
O

Shortness of breath (+)


Sensorium: CM, Temp: 37,1C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Mayor was closed
-

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)


- Ear : within normal range
- Nose : pernafasn cuping hidung
- Mouth : within normal range
Neck : lymph node enlargement
Thorax : symmetrical fusiform, retraction (+) intercostal, epigastric
A
P

HR: 138 bpm, regular, murmur (-)


RR : 46x/i, regular, ronchi (+/+), wheezing(-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable
Extremities : pulse 138 bpm, regular, adequate p/v , felt warm,

CRT < 3 , blood pressure: mmHg.


DD/Broncopneumonia
Bronchiolitis
O2 1 L/min nasal canule
IVFD D5% NaCl 0,225 % 25gtt/i (micro)
Paracetamol 3x 75 mg
Inj Ampicilin 160 mg/6 jam
Inj Gentamycin 40 mg/24 jam
Inj Dexametason 2,5 mg/8 jam/iv
Inj Aminophylline MD 1 cc/12 jam/iv diencerkan in 5 cc NaCl 0,9 %
bolus pelan
Nebule Ventolin 1 respul+ NaCl ,9 % /6 jam

16thNovemember 2015
S
O

Shortness of breath (+)


Sensorium: CM, Temp: 37C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella mayor was closed
-

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

26

palpebra (-/-), sclera icteric (-/-)


- Ear : within normal range
- Nose : nasal flaring
- Mouth : within normal range
Neck : lymph node enlargement
Thorax : symmetrical fusiform, retraction (+) intercostal, epigastric
-

HR: 120 bpm, regular, murmur (-)


RR : 40x/i, regular, ronchi (+/+), wheezing(-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable
Extremities : pulse 138 bpm, regular, adequate p/v , felt warm,

CRT < 3 , blood pressure: mmHg.


DD/Broncopneumonia

Bronchiolitis
O2 1 L/min nasal canule

IVFD D5% NaCl 0,225 % 25gtt/i (micro)


Inj Ampicilin 160 mg/6 jam
Inj Gentamycin 40 mg/24 jam
Inj Dexametason 2,5 mg/8 jam/iv
Inj Aminophylline MD 1 cc/12 jam/iv diencerkan in 5 cc NaCl 0,9 %
bolus pelan
Paracetamol 75 mg (k/p)
GE 3x tab
Advise from dr. Wisman Dalimunthe, SpA
-

Aff NGT
Consul for Cardiology Division (echocardiography)
Tappering off Inj dexamethasone

17th Novemember 2015


S
O

Shortness of breath (+)


Sensorium: CM, Temp: 37C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Mayor was closed
-

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)


- Ear : within normal range
- Nose : within normal range
- Mouth : within normal range
Neck : lymph node enlargement

27

Thorax : symmetrical fusiform, retraction (+) intercostal, epigastric


A

HR: 118 bpm, regular, murmur (-)


RR : 35x/i, regular, ronchi (+/+), wheezing(-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable
Extremities : pulse 118 bpm, regular, adequate p/v , felt warm,

CRT < 3
DD/Broncopneumonia
Bronchiolitis
O2 1 L/min nasal canule (intermitten)

IVFD D5% NaCl 0,225 % 25gtt/i (micro)


Inj Ampicilin 160 mg/6 jam/iv
Inj Gentamycin 40 mg/24 jam/iv
Inj Dexametason 2mg/12 jam/iv (tapering off)
Inj Aminophylline (MD) 1 cc/12 jam/iv diencerkan in 5 cc NaCl 0,9 %
bolus pelan
Paracetamol 75 mg (k/p)
Nebule Ventolin 1 respul+ NaCl ,9 % /8jam

18th Novemember 2015


S
O

Dyspnea (-)
Sensorium: CM, Temp: 37C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Mayor was closed
-

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)


- Ear : within normal range
- Nose : within normal range
- Mouth : within normal range
Neck : lymph node enlargement
Thorax : symmetrical fusiform, retraction (-)
A

HR: 118 bpm, regular, murmur (-)


RR : 35x/i, regular, ronchi (+/+), wheezing(-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable
Extremities : pulse 118 bpm, regular, adequate p/v , felt warm,

CRT < 3
DD/Broncopneumonia

28

Bronchiolitis
IVFD D5% NaCl 0,225 % 25gtt/i (micro)

Inj Ampicilin 160 mg/6 jam/iv


Inj Gentamycin 40 mg/24 jam/iv
Inj Dexametason 2mg/12 jam/iv (tapering off)
Inj Aminophylline (MD) 1 cc/12h /iv diluted in 5 cc NaCl 0,9 % bolus
slowly
Paracetamol 75 mg (if needed)
Nebule Ventolin 1 respul+ NaCl ,9 % /8jam
19th Novemember 2015
S
O

dyspnea (-)
Sensorium: CM, Temp: 37C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Mayor was closed
-

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)


- Ear : within normal range
- Nose : within normal range
- Mouth : within normal range
Neck : lymph node enlargement
Thorax : symmetrical fusiform, retraction (-)
A
P

HR: 116 bpm, regular, murmur (-)


RR : 22x/i, regular, ronchi (+/+), wheezing(-/-)
Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable
Extremities : pulse 110 bpm, regular, adequate p/v , felt warm,

CRT < 3
Broncopneumonia
IVFD D5% NaCl 0,225 % 25gtt/i (micro)
Inj Ampicilin 160 mg/6h/iv
Inj Gentamycin 40 mg/24h/iv
Paracetamol 75 mg (if needed)
Nebule Ventolin 1 respul+ NaCl ,9 % /8h

CHAPTER IV

29

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

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

Experienced
symptoms
of
bronchopneumonia include fever,
shortness of breath

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
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

30

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

CHAPTER V
SUMMARY

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

31

DM, a girl, 3 years and 1 months old, weighted 7 kg and heighted 78 cm,
from General Hospital Medan on September 11th 2015 at 20.25 PM develops loss
of consciousness. Patient was diagnosed as tuberculous meningitis. Patient was
treated with Phenytoin, Ceftriaxsone, Paracetamol, Furosemide, spironolactone,
diamox, rifampicin, INH, pyrazinamide, ethambutol, prednisone, vit. B complex,
and Vit. C.

REFERENCES

32

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. Hassan R, Buku Kuliah Ilmu Kesehatan Anak edisi 11, Bagian Ilmu Kesehatan
Anak Fakultas Kedokteran Universitas Indonesia, 2007.
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.
7. Be NA, Pathogenesis of Central Nervous System Tuberculosis, Curr Mol Med.
2009; 9(2): 94-99.
8. Tanto C, Kapita Selekta Kedokteran, Media Aesculapius, 2014.
9. Ramachandran TS, Tuberculous Meningitis, Emedicine Medscape, 2014.