1

PLEURAL EFFUSION ec PULMONARY TUBERCULOSIS

Presenters: Erwin Siahaan (060100090)
Yunny Safitri (060100158)
Day: Tuesday, December 28th 2010
Supervisor: Dr. Tina Christina L. Tobing, SpA

CHAPTER 1
INTRODUCTION

1.1. Background
A pleural effusion is always abnormal and indicates the presence of and
underlying disease.1 The accumulation of pleural fluid can usually be explained
by increased pleural fluid formation or decreased pleural fluid absorption, or
both.1,2 Increased pleural fluid formation can result from elevation of hydrostatic
pressure, decreased colloid osmotic pressure, increased capillary permeability,
passage of fluid through openings in the diaphragm, or reduction of pleural space
pressures.1,2 Decreased pleural fluid absorption can result from lymphatic
obstruction or from elevation of systemic venous pressures resulting in impaired
lymphatic drainage.1,2
The presence of fluid in the normally negative pressure environment of the
pleural space has a number of consequences for respiratory physiology.1,2 Pleural
effusions produce a restrictive ventilatory defect and also decrease the total lung
capacity, functional residual capacity, and forced vital capacity.2 They can cause
ventilation-perfusion mismatches and, when large enough, compromise cardiac
output.2
There is little accurate information about the epidemiology of childhood
tuberculosis in most parts of the world, particularly in developing nations where
tuberculosis rates are the highest.3 In most of these countries, the major method of
diagnosing tuberculosis in adults is by sputum microscopy; however, very few
children and almost no infants produce sputum in which organisms can be
 2

viewed.2,3 As a result, tuberculosis in children is vastly underreported and many

children die without being diagnosed or treated.3
In children, infection is the most common cause of pleural effusion.
Approxtimately 1,4 million people in the United States develop a pleural effusion
each year.4 Pleural effusion occurs in 6-12% of all cases of pulmonary
tuberculosis in chidren. There are 22,1% of spanish chidren with pulmonary
tuberculosis had pleural effusion. In the United States, tuberculosis is responsible
for approximately 2 percent of all pleural effusions.2,4
Children were even more greatly affected by this infection, with an
increase in reported cases in children 5 to 14 years of age of almost 40%. The
increase in cases of tuberculosis was thought to be the result of an increase in
medically underserved populations, an increased number of patients from endemic
areas, and an increase in patients infected with human immunodeficiency virus
(HIV) resulting in large numbers of contagious patients. Although infection
control efforts have been somewhat successful in controlling tuberculosis, it
remains a major cause of morbidity and mortality in selected areas of developed
country.4

1.2. Objective
This paper is done in order to complete the task in following the doctor’s
professional education program in the Departement of Pediatrics Haji Adam
Malik General Hospital, Faculty of Medicine North Sumatera University. In
addition, providing knowledge to the author and readers about tuberculosis pleural
effusion.
 3

CHAPTER 2
LITERATURE REVIEW

2.1. Tuberculous Pleural Effusion

2.1.1. Definition
Pleural effusion is the abnormal accumulation of fluid in the pleural space.
A pleural effusion is always abnormal and indicates the presence of an underlying
disease.1 The pleural cavity contains a relatively small amount of fluid,
approximately 10 mL on each side. A Pleural fluid volume is maintained by a
balance between fluid production and removal, and changes in the rates of either
can result in the presence of excess fluid, traditionally known as a pleural
effusion. Pleural effusion that caused by tuberculosis infection is called
tuberculosis pleural effusion.1,2,4

2.1.2. Etiology
Mycobacterium tuberculosis causes tuberculosis and is a very important
pathogen of humans.4,5 The mycobacteria are rod-shaped, aerobic bacteria that do
not form spores. Although they do not stain readily, once stained they resist
decolorization by acid or alcohol and are therefore called "acid-fast" bacilli.4,5,6
In tissue, tubercle bacilli are thin straight rods measuring about 0.4 x 3
µm.5 On artificial media, coccoid and filamentous forms are seen with variable
morphology from one species to another. Mycobacteria cannot be classified as
either gram-positive or gram-negative.5 Once stained by basic dyes they cannot be
decolorized by alcohol, regardless of treatment with iodine.5 True tubercle bacilli
are characterized by "acid-fastness", 95% ethyl alcohol containing 3%
hydrochloric acid (acid-alcohol) quickly decolorizes all bacteria except the
mycobacteria. Acid-fastness depends on the integrity of the waxy envelope. 5 The
Ziehl-Neelsen technique of staining is employed for identification of acid-fast
bacteria.5 In smears of sputum or sections of tissue, mycobacteria can be
demonstrated by yellow-orange fluorescence after staining with fluorochrome
stains (eg, auramine, rhodamine).5
 4

2.1.3. Epidemiology
The most frequent source of infection is the human who excretes,
particularly from the respiratory tract, large numbers of tubercle bacilli.4 Close
contact (eg, in the family) and massive exposure (eg, in medical personnel) make
transmission by droplet nuclei most likely.8 This risk is proportionate to the rate of
active infection in the population, crowding, socioeconomic disadvantage, and
inadequacy of medical care.4,8
The development of clinical disease after infection may have a genetic
component (proved in animals and suggested in humans by a higher incidence of
disease in those with HLA-Bw15 histocompatibility antigen).6 It is influenced by
age (high risk in infancy and in the elderly), by undernutrition, and by
immunologic status, coexisting diseases (eg, silicosis, diabetes), and other
individual host resistance factors.6,8
Infection occurs at an earlier age in urban than in rural populations.
Disease occurs only in a small proportion of infected individuals.4 In the United
States at present, active disease has several epidemiologic patterns where
individuals are at increased risk: minorities, predominantly African-Americans
and Hispanics; HIV-infected patients; homeless persons; and the very young and
very old.4 The incidence of tuberculosis is especially high in minority persons
with HIV infections.4,6 Primary infection can occur in any person exposed to an
infectious source.4,6 Patients who have had tuberculosis can be infected
exogenously a second time.6 Endogenous reactivation tuberculosis occurs most
commonly among persons with AIDS and elderly malnourished or alcoholic
destitute men.4,6,8

2.1.4. Pathogenesis
Infection with Mycobacterium tuberculosis (MTB) begins with the
inhalation of airborne bacilli.1 Mycobacteria in droplets 1–5 µm in diameter are
inhaled and reach alveoli.5 The disease results from establishment and
proliferation of virulent organisms and interactions with the host.1,4,6,8 After
inhalation, the bacilli reach the pulmonary alveoli and are transported through
 5

pulmonary lymphatic channels to hilar lymph nodes.8 They can then enter the
bloodstream by way of the thoracic duct.4 Although the entrance of MTB into the
host is respiratory, the organism can thus be spread to virtually every organ in the
body.1,4,6,8
Spread of small numbers of bacilli result in clinically inapparent foci of
infection.6,7 Regions most commonly seeded include the meninges, the pleura, and
the bone.6,7 A reaction involving macrophages, lymphocytes, and ingested
organisms then occurs, and tubercles are formed.8 When this reaction occurs, a
tuberculin skin test will become positive, indicating that exposure to MTB has
occurred.6,7 The production and development of lesions and their healing or
progression are determined chiefly by (1) the number of mycobacteria in the
inoculum and their subsequent multiplication, and (2) the resistance and
hypersensitivity of the host.6,7,8

The initial immune containment of clinically inapparent infection may not

be permanent, and reactivation is possible at any time. Infants younger than 1 year
of age have about a 50% chance of developing active disease.8 In children
younger than 5 years of age, the risk for reactivation to active disease is about
25%.8
Unlike adults, the vast majority of children with tuberculosis are not
infectious to others. In the early 1900s, several studies from European orphanages
showed that when an adult in the orphanage had tuberculosis, many of the
children developed tuberculosis as well; however, when only a child had
tuberculosis, none of the other children developed the disease.8 Subsequent
studies from children's hospitals and other environments where children are
separated from the adult from whom they acquired the organism have shown that
most children with the classic forms of childhood tuberculosis are not infectious
to others.8 However, those children who develop the adult type of tuberculosis,
including upper lobe infiltrates or cavities, and, particularly, having a positive
acid-fast smear of the sputum, can be infectious to others.8
It is commonly asked why young children with the childhood type of
tuberculosis are not infectious.4 Many children with tuberculosis do not have
 6

significant cough.8 When cough is present children rarely produce sputum. Even
when sputum is produced, organisms are sparse because they are in low
concentration in the endobronchial secretions of children.8 In addition, young
children lack tussive force necessary to suspend infectious particles of the correct
size in the air.4,8
Pleural effusion occurs in 2-38% of all cases of pulmonary tuberculosis in
children.8 Tuberculous pleural effusions can be either primary or results of
reactivation disease.4 Primary tuberculous pleural effusion results from direct
hematogenous invasion of the pleural space by mycobacterium tuberculosis, is
usually unilateral, and is often found in the absence of pulmonary parenchymal
disease.4,8 Tuberculous pleural effusion due to reactivation disease is typically
associated with focal parenchymal disease.4,8
Tuberculous pleural effusion is secondary to rupture of subpleural foci
into the pleural space.4,8 The rupture of subpleural foci into the pleural space 6 to
12 weeks after primary infection then promotes a delayed hypersensitivity
response to the mycobacterial proteins, resulting in a pleural effusion.4,8 It appears
that delayed hypersensitivity plays a large role in the pathogenesis of tuberculosis
pleural effusion.4,5 The hypersensitivity reaction is initiated when tuberculous
protein gains access to the pleural space.4,5,8
Tuberculous is pleural effusions are enriched with many potentially
immunoreactive cells and substances that comprise the vigorous local cell-
mediated immune-response.6 Compared with peripheral blood, pleural fluid is
enriched with T lymphocytes. The CD4+ to CD 8 ratio s 3:4 in pleural fluid.6,8

2.1.5. Sign and Symptoms

Many people with pleural effusion have no symptoms at all. 1,4 The most
common symptoms, regardless of the type of fluid in the pleural space or its
cause.1 Patients can present with fever, cough, and pleuritic pain.1 Night sweats
and hemoptysis are occasionally seen.4 The chest radiograph often reveals a
unilateral pleural effusion.6,8 The natural history of tuberculous pleural effusion is
complete or significant clearance of the effusion, even without treatment. 6,8
 7

However, untreated patients have a high rate of developing active pulmonary or

extrapulmonary disease within a year. Progression to active disease is greater in
young children and immunocompromised patients.4,6,8
Although tuberculosis is usually considered a chronic illness, tuberculous
pleuritis most commonly manifests as an acute illness.8 In one series of 71
patients, 35% had initial symptoms of less than 1 week in duration, whereas 70%
had been symptomatic for less than a month.8 In another series, 63% had an acute
illness that most commonly mimicked acute bacterial pneumonia.8 Most patients
have a cough, usually non productive, and most have chest pain, usually pleuritic
in nature.8 Most patients are febrile, but a normal temperature does not rule out
the diagnosis.8 Occasionally, the onset of TB is less acute, with only mild chest
pain, perhaps with low-grade fever and non productive cough, weight loss, and
easy fatigability.8

2.1.6. Diagnosis
The first step in evaluation of a pleural effusion is a detailed history and
physical examination.1,6 Diagnosis of the cause of many pleural effusions is based
on the clinical setting and exclusion of other alternative causes.1,6,8 The presence
of pleural fluid is suggested by a homogeneous density on chest x-ray that
obscures the underlying lung.1 It can be detected on X-ray when 300 mL or more
of fluid is present and clinically when 500 mL or more is present. Large effusions
may cause a shift of the mediastinum to the contralateral side.6 Small effusions
may only blunt the costophrenic angle.6 Lateral decubitus x-rays may help to
detect freely movable fluid by demonstrating a layering-out effect. If the fluid is
loculated, no such effect is perceived. Ultrasonography can be extremely valuable
in localizing the fluid and detecting loculations, especially when thoracentesis is
contemplated.1,6,8
 8

Old tuberculin is a concentrated filtrate of broth in which tubercle bacilli

have grown for 6 weeks.6,8 In addition to the reactive tuberculoproteins, this
material contains a variety of other constituents of tubercle bacilli and of growth
medium.6,8 A purified protein derivative (PPD) is obtained by chemical
fractionation of old tuberculin. PPD is standardized in terms of its biologic
reactivity as "tuberculin units" (TU).6 A large amount of tuberculin injected into a
hypersensitive host may give rise to severe local reactions and a flare-up of
inflammation and necrosis at the main sites of infection (focal reactions).6,8 The
volume is usually 0.1 mL injected intracutaneously. In an individual who has not
had contact with mycobacteria, there is no reaction to PPD-S.6,8
An individual who has had a primary infection with tubercle bacilli
develops induration, edema, erythema in 24–48 hours, and, with very intense
reactions, even central necrosis.1,6,8 The skin test should be read in 48 or 72 hours.
It is considered positive if the injection of 5 TU is followed by induration 10 mm
or more in diameter.1,3,4 Positive tests tend to persist for several days.4 Weak
 9

reactions may disappear more rapidly.4 The tuberculin test becomes positive
within 4–6 weeks after infection (or injection of avirulent bacilli).4 It may be
negative in the presence of tuberculous infection when "anergy" develops due to
overwhelming tuberculosis, measles, Hodgkin's disease, sarcoidosis, AIDS, or
immunosuppression.4 A positive tuberculin test may occasionally revert to
negative upon isoniazid treatment of a recent converter.4,6 After BCG vaccination,
people convert to a positive test, but this may last for only 3–7 years.4 Only the
elimination of viable tubercle bacilli results in reversion of the tuberculin test to
negative.1,6,8

A positive tuberculin test indicates that an individual has been infected in

the past.4 It does not imply that active disease or immunity to disease is present. 4
Tuberculin-positive persons are at risk of developing disease from reactivation of
the primary infection, whereas tuberculin-negative persons who have never been
infected are not subject to that risk, though they may become infected from an
external source.4 In 30 percent of patients with tuberculous pleural effusion, the
initial tuberculin skin test is negative.6 However, a repeat test, within 8 weeks of
the development of symptoms, is likely to be positive.1,6,8
 10

General laboratory tests such as a complete blood count and cell

differential are usually normal in children with tuberculosis.3,4 Cultures are
positive in only 30 to 70% of cases.3,4 Biopsy of the pleura is more likely to yield
a positive acid-fast stain or culture, and evidence of granuloma formation can be
demonstrated.3,4
The diagnosis is suggested in a patient with a unilateral pleural effusion
who has a history of exposure to tuberculosis.3,4 A one-time thoracentesis is
usually indicated because it allows examination of the pleural fluid for diagnostic
purposes and can help exclude other etiologies.3,4,6 When pleural tuberculosis is
present, pleural fluid is usually yellow and occasionally tinged with blood. 3 The
chemistry results are indicative of a mild exudate; specific gravity is usually 1.012
to 1.025, the protein level is usually 2 to 4 g/dL, and the glucose may be low,
although it is often in the low-normal range (20-40 mg/dL). 3,4,6,8 Most typically,
there are several hundred to several thousand white blood cells/mm3 with an early
predominance of polymorphonuclear cells followed by a high proportion of
lymphocytes.3,4 The pleural fluid usually reveals several hundred cells, most of
which are lymphocytes.4 Less than one third of patients have a positive acid-fast
stain or acid-fast culture from pleural fluid.4,6 Acid-fast smears of the fluid are
usually negative because of the relative paucity of organisms.4,6,8 Yield of pleural
biopsy is significantly higher and approaches 75%.3,4,6,8
Adenosine deaminase (ADA) is an enzyme involved in purine catabolism
that catalyzes thhe conversion of adenosine to inosine; high levels of ADA have
been reported in pleural fluid of patients infected with tuberculosis.1,4,6,8 Elevated
levels of ADA can also be found in patients with an increased number of
lymphocytes in the pleural fluid; thus, patients with leukemias and lymphomas
can have misleading results.1,4 Polymerase chain reaction for the detection of
mycobacterial DNA in pleural effusions is increasingly performed and has a
sensitivity of 70% with a specificity of 100%.1,4,6 Most patients with tuberculous
pleural effusion have strongly reactive skin tests, and empiric treatment is often
given to a patient with a unilateral pleural effusion, a strongly reactive
tuberculosis skin test, and no other obvious etiology for the effusion.1,4,6,8
 11

Another test that is useful in the diagnosis of tuberculosis pleural effusion

is the level of interferon-gamma in the pleural fluid.4,8 Interferon-gamma is
produced by the CD4+ lymphocytes from patients with tuberculous pleuritis.4,8
Patient with tuberculous pleuritis tend to have higher pleural fluid interferon-
gamma levels than do patients with pleural effusions of other etiologies.4 In the
largest series published until now.4,6 The pleural fluid interferon-gamma levels
were elevated in immunocompromised patient and transplantation patient with
tuberculous pleuritis.4,6,8
In recent years, the posssibility of establishing the diagnosis of tubercuous
pleuritis by demonstration of tuberculous antigens or specific antibodies against
tuberculous proteins in the pleural fluid has been investigted. 1,4 None of these tests
have proved to be to use in the diagnosis of tuberculous pleuritis.1,4,8 The presence
of antituberculous antibodies in the pleural space appears to result from their
passive diffusion from the serum rather than local antibody production. 6
Therefore, it is unlikely that measurement of such antibodies in the pleural fluid
will ever be diagnostically useful.1,4,6,8
Children were categorized as bacteriologically confirmed tuberculosis,
radiologically certain tuberculosis, probable tuberculosis or not tuberculosis.9
Bacteriologically confirmed tuberculosis was defined as the presence of acid fast
bacilli on sputum microscopy and/or M. tubeculosis cultured from a respiratory
secimen.5,9 Radologically certain tuberculosis was defined as agreement between
both independent experts that the chest x-ray indicated certain tuberculosis in the
absence of bacteriologic confirmation.9 Probable tubercuosis was defined as the
presence of suggestive radiologic signs and good clinical response to
antituberculosis treatment in the absence of bacteriologic confirmation or
radiologic certainty.9 Good clinical response was defined as complete symptom
resolution and weight gain of > 10 % of body weight at diagnosis, within 3 month
of starting antituberculosis treatment.9 Not tuberculosis was defined as spontaneus
symptom resolution or no response to antituberculosis therapy in the absence of
bacteriologic confirmation or radiologic signs suggestive of tuberculosis.9
 12

Pulmonary tuberculosis was defined as a symptomatic child with :1)

bacteriologically confirmed tuberculosis; 2) radiologically confirmed tuberculosis;
or 3) probable tuberculosis (as defined), excluding isolated pleural effusion.9

2.1.7. Differential Diagnosis

Parapneumonic fluids the most common complication of bacterial
pneumonia in children and the most common cause of pleural effusion.1,2 An
estimated 2% of pneumonia are complicated by empyema.1,2 Approximately 40%
of children who are hospitalized with pneumonia have pleural effusion. 1,2
Bacterial pneumonias are frequently associated with pleural effusions (as
often as 50 % of the time) and when they become complicated, require drainage.1
Complicated parapneumonic effusions include empyema (the finding of gross pus
in the pleural space), those with positive pleural fluid cultures or Gram stains, and
those in which the microbiology is negative but the patient continues to show
signs of infection with fever, severe pleuritic pain and leukocytosis.1 In this last
category the pleural fluid usually shows high white blood cell counts with
polymorphonuclear predominance, glucose <30 mg/dl, and high LDH (>500
units/dl).1,2

2.1.8. Treatment
The same general principles that apply to the treatment of tuberculosis in
adults also apply to children.4,8 However, children, in general, have smaller
mycobacterial loads than adults and the risk of developing secondary drug
resistance is less in children.4 Of course, children or adolescents who develop the
adult type of pulmonary tuberculosis, with a cavity or extensive infiltrate in the
upper lobes, have a large burden of organisms and a higher propensity to develop
drug resistance while on treatment.4,8
Historically, recommendations for treating children with tuberculosis have
been extrapolated from clinical trials of adults with pulmonary tuberculosis.4
 13

However,over the past 2 decades, over a dozen studies and clinical trials of
treatment of tuberculosis in children have been published.4 These trials have
shown that the basic regimen of 6 months of isoniazid and rifampin,
supplemented during the first 2 months with pyrazinamide, cures over 99% of
cases of drug-susceptible pulmonary tuberculosis in children, with an incidence of
clinically significant adverse reactions of < 2%.4,8 Although a short period of daily
administration of medications (the first 2-6 weeks) may be desirable, several
studies have shown that giving two or three times per week intermittent treatment
from the very beginning is effective in the vast majority of cases of pulmonary
tuberculosis in children.4 Several studies have shown that regimens containing
only isoniazid and rifampin for 6 to 9 months are effective in some of the milder
forms of pulmonary tuberculosis in children, but most experts feel that the
additional use of pyrazinamide in the initial phase is warranted in case the child
absconds from treatment early.4,8
Many adults with tuberculosis are routinely given four drugs as initial
therapy, with ethambutol being the most common fourth drug.4 However, in small
children, addition of extra drugs leads to problems with tolerance, especially
because there are few pediatric dosage forms available, and treatment involves the
crushing of pills or creation of suspensions that are difficult to administer.4,8
There is little information published about the treatment of drug-resistant
tuberculosis in children.4,8 Again, the principles are similar to those used to treat
adults with drug-resistant tuberculosis.4,8 At least two bactericidal drugs must be
 14

used and the complete regimen usually includes at least three drugs for cases of
isoniazid-resistant tuberculosis (most commonly rifampin, pyrazinamide, and
ethambutol) and at least four drugs and usually five or six for cases of multi-drug-
resistant tuberculosis.1 Patterns of drug resistance among children tend to mirror
those found among adults in the same population.4,8 However, because the
organism is isolated from, at best, 40% of children with tuberculosis, it is
imperative to try to link a child with tuberculosis to the adult from whom the child
acquired the organism so that that adult isolate's susceptibility tests can be used to
correctly treat the child.1,4,8
Corticosteroids are useful in the treatment of some children with
tuberculosis under the cover of effective antituberculosis drugs and probably are
used more commonly for children than adults with tuberculosis.1,2,4,8 The most
commonly prescribed regimen is prednisone 1 to 2 mg/kg/day for 4 to 6 weeks
with gradual tapering.4 Corticosteroids are beneficial when the host inflammatory
reaction contributes significantly to tissue damage or impairment of organ
function.4,8 Evidence is convincing that corticosteroids decrease mortality rates
and long-term neurological sequelae in patients with tuberculous meningitis. 4
Short courses of corticosteroids also may be effective for children with enlarged
hilar lymph nodes that compress the tracheal bronchial tree causing respiratory
distress, localized emphysema, or severe segmental pulmonary disease.4,8 Several
clinical trials have shown that corticosteroids can help relieve symptoms and
tamponade associated with tuberculous pericardial effusion in children.1,2,4,8
Isoniazid therapy is clearly indicated for children with tuberculosis
infection with no clinical or radiographic evidence of disease.1,4 A chest
radiograph that shows only a granuloma or a small fibrotic lesion constitutes
infection and the child should be treated accordingly.4 The currently
recommended length of therapy for children is 9 months and the isoniazid can be
given either daily under self-supervision or twice weekly under directly observed
therapy (DOT).4,8 DOT may be particularly indicated for children with high risk
infections, such as infants and newborns, immunocompromised children, and
 15

children who are contacts of cases of recently diagnosed pulmonary

tuberculosis.1,2,4,8
Careful monthly monitoring of the clinical and bacteriologic responses to
therapy is important.3 With DOT, clinical evaluation is an integral component of
each visit for drug administration.3,4 For patients with pulmonary tuberculosis,
chest radiographs should be obtained after 2 months of therapy to evaluate
response.3,4,8 Even with successful 6-month regimens, hilar adenopathy can persist
for 2 to 3 years; normal radiographic findings are not necessary to discontinue
therapy.8 Follow-up chest radiography beyond termination of successful therapy
usually is not necessary unless clinical deterioration occurs. 1,3,4,8
If therapy has been interrupted, the date of completion should be
extended.4 Although guidelines cannot be provided for every situation, factors to
consider when establishing the date of completion include the following: (1)
length of interruption of therapy; (2) time during therapy (early or late) when
interruption occurred; and (3) the patient’s clinical, radiographic, and bacteriologic
status before, during, and after interruption of therapy.4 The total doses
administered by DOT should be calculated to guide the duration of therapy.
Consultation with a specialist in tuberculosis is advised. 4,8
Untoward effects of isoniazid therapy, including severe hepatitis in
otherwise healthy infants, children, and adolescents, are rare.1,4 Routine
determination of serum transaminase concentrations is not recommended.1
However, for children with severe tuberculosis disease, especially children with
meningitis or disseminated disease, transaminase concentrations should be
monitored approximately monthly during the first several months of treatment. 3,4,6
Other indications for testing include the following: (1) having concurrent or recent
liver or biliary disease; (2) being pregnant or in the first 6 weeks postpartum; (3)
having clinical evidence of hepatotoxic effects; or (4) concurrently using other
hepatotoxic drugs (eg, anticonvulsant or HIV agents).3,4,6 In most other
circumstances, monthly clinical evaluations to observe for signs or symptoms of
hepatitis and other adverse effects of drug therapy without routine monitoring of
transaminase concentrations is appropriate follow-up.1,2,4 In all cases, regular
 16

physician-patient contact to assess drug adherence, efficacy, and adverse effects is

an important aspect of management.4,8 Patients should be advised to call a
physician immediately if signs of adverse effects, in particular hepatotoxicity (eg,
vomiting, abdominal pain, jaundice), develop. 1,2,3.,4,8

2.1.9. Complication
Possible complications include respiratory failure caused by massive fluid
accumulation, septicemia, bronchopleural fistula, pneumothorax, or pleural
thickening.2

2.1.10. Prevention
In much of the world, the only method available to prevent tuberculosis in
children is administration of a bacille Calmett-Guérin (BCG) vaccine.4 When
considering the total body of literature of BCG vaccination of children, the
general conclusion is that the BCG vaccines prevent 60 to 90% of serious
tuberculosis cases in children.4 Clearly, the BCG vaccines are better than no
method of prevention, but they are not capable of completely preventing
tuberculosis disease in a population of children.4,8 BCG vaccination has worked
better in some situations than others.4 In the United States, the presence of HIV
infection in the child is an absolute contraindication to giving BCG vaccine;
internationally, the presence of asymptomatic HIV infection is not considered a
contraindication to BCG vaccination.4,8
In the United States, the major method of preventing tuberculosis in
children is interrupting transmission through a community-based contact
investigation with appropriate chemotherapy, and the treatment of tuberculosis
infection to prevent the development of disease.4,6 The contact investigation is the
most important activity for preventing tuberculosis in children because the yield is
high for finding infection and it finds the most recent infections, which are most
likely to develop soon into cases of tuberculosis disease in children.4,6 Several
investigations have shown that when contact investigations are not conducted well
or completely, preventable cases of tuberculosis in children inevitably occur.4,6,8
 17

Effusions that are enlarging or compromising respiratory function in a

febrile unwell child require drainage.2 Other risk predictors indicating the need for
chest tube placement include frank pus on thoracentesis, a positive pleural fluid
gram stain and culture finding, pleural fluid pH level of less than 7, a glucose
concentration of less than 40 mg/dL, or an LDH level of more than 1000 IU.2
Controversy still remains about the optimum chest tube size.2 Although
use of a small-bore tube (eg, pigtails) for free-flowing fluid and large-bore tubes
for thick pus are commonly used, good quality data to recommend one size of
chest tube over another are lacking.2 In the absence of evidence that large bore
chest drains confer any advantage, the British Thoracic Society (BTS) guidelines
recommend using small bore chest tubes (including pigtail catheters) whenever
possible to minimize patient discomfort.2 When combined with fibrinolytic
therapy, the use of small chest tubes was found to have some advantages over
large tubes.2
The timing of elective removal of the drain depends on numerous factors,
including the amount of fluid draining, the child’s overall clinical condition, the
presence of fever, and radiographic and ultrasonographic appearance of the chest,
as well as a fall in acute phase reactants.2 In most cases, the chest tube may be
removed when the pleural drainage becomes minimal (<10-15 ml/24 h) and the
fluid is clear or yellow.2
A current controversy in involves how to find children with tuberculosis
infection so they can be treated to prevent future disease.8 When tuberculosis
infection was more common, mass skin testing of children made sense.8 The new
approach being developed by pediatricians is to screen children with a
questionnaire to determine if risk factors for tuberculosis infection are present,
then subsequently skin test only those children who have risk factors.8 In several
published studies, four major questions have emerged that probably account for
over 95% of the attributable risk of tuberculosis infection for children (1) Was the
child born in a country with a high prevalence of tuberculosis? (2) Has the child
traveled (nontourist, > 2 weeks) to a country with a high prevalence of
tuberculosis? (3) Has the child been exposed to an adult with pulmonary
 18

tuberculosis? (4) Do other family members have positive tuberculin skin tests?
Applying skin tests only to children with one of these risk factors will
significantly decrease the number of tests performed and decrease the number of
false-positive tuberculin skin tests but insure that children with real risk factors
are tested and given appropriate treatment when necessary.8

2.1.11. Prognosis
The prognosis of pleural diseases depends on the underlying cause and
ranges from very poor (for example, when cancer had spread to the pleura) to very
good (for example, when an otherwise healthty person develops fluid associated
with a treatable infection).3 Most tuberculosis effusions completely resolve with
the use of proper antituberculosis agents. Residual pleural thickening can occur in
50% of patients.2

2.2. Mild Malnutrition

The traditional approach to nutritional assessment measures only the
physical manifestations of the problem (i.e., clinical, anthropometric, and
biochemical indicators) and, perhaps, some of the immediate causes related to
dietary intake.10 These indicators may be adequate for estimating the magnitude of
the problem, but additional methods and approaches are needed to assess the
broader nutrition situation. These approaches include consideration not only of
dietary intake but also of health care and control of resources at household,
community, and national levels.10
Despite the need for additional methods and approaches, a number of
anthropometric indices have been used successfully for many years to estimate the
prevalence of undernutrition among preschool-aged children.10 These include
height for age, weight for age, and weight for height.10 The first is an index of the
cumulative effects of undernutrition during the life of the child, the second
reflects the combined effects of both recent and longer-term levels of nutrition,
and the last reflects recent nutritional experiences10. Values below 80–90% of
expected are considered abnormally low.10
 19

These indices are reasonably sensitive indicators of the immediate and

underlying general causes of undernutrition, but they are not specific for any
particular cause.10 They do not reveal the relative importance of dietary intake,
infectious diseases, food insecurity, inadequate health/environmental services, low
birthweight, suboptimal childcare practices, income constraints, or disparities in
control of resources.10 These factors are part of the assessment of the overall
nutrition situation and are distinct from the biochemical and/or anthropometric
indicators that merely reflect the severity and extent of the problem, its
distribution across geographic and social groups, and trends over time.10
The cumulative evidence suggests that undernutrition has pervasive effects
on immediate health and survival as well as on subsequent performance.10 These
include not only acute effects on morbidity and mortality but also longer-term
effects on cognitive and social development, physical work capacity, productivity,
and economic growth.10 The magnitude of both the acute and longer-term effects
are considerable.10 Prospective studies suggest that severely underweight children
(<60% of reference weight for age) have more than an eight-fold greater risk for
mortality than normally nourished children, that moderately underweight children
(60–69% of reference weight for age) have a four- to five-fold greater risk, and
that even mildly underweight children (70–79% of reference weight for age) have
a two- to three-fold greater risk.10 The high prevalence of mortality in those with
mild and moderate undernutrition suggests that more than half of child deaths
may be caused directly or indirectly by undernutrition.10 Moreover, 83% of these
deaths result from mild to moderate forms of undernutrition. A major factor is the
potentiation of infectious diseases by undernutrition.10
Survivors of childhood undernutrition frequently have deficits in height
and weight that persist beyond adolescence into adulthood.10 These deficits are
often accompanied by deficits in frame size as well as muscle circumference and
strength.10 The implications of these deficits with respect to the work capacity of
both men and women and to women's reproductive performance are obvious.
Survivors of childhood malnutrition also have deficits in cognitive function and
school performance relative to normally nourished children from the same
 20

environment.10 Mean deficits in scores on standard tests of cognition range from

5–15 points.10 The fact that severely undernourished children, as assessed by low
length-for-age, have greater deficits in cognitive performance than children with
mild or moderate undernutrition strongly suggests that the intellectual deficits are
related to the severity of undernutrition.10
The extent to which intellectual deficits can be decreased by dietary
intervention alone is not clear.10 However, these deficits can be decreased by a
combination of dietary and behavioral interventions coupled with improvements
in the overall quality of the home and/or school environment.10 Such interventions
appear to be much more effective if instituted in early life.10
Undernutrition ranges from a lower than desired intake of one or more
nutrients with either no symptoms or only vague symptoms to severe
malnutrition.10 The approach to treating mild undernutrition is the same as that
suggested for food insecurity of sufficient severity to result in low intake of
specific nutrients.10
 21

The guidelines highlight 10 steps for routine management of children with

malnutrition, as follows:10
• Prevent and treat the following:
o Hypoglycemia
o Hypothermia
o Dehydration
o Electrolyte imbalance
o Infection
o Micronutrient deficiencies
• Provide special feeds for the following:
o Initial stabilization
o Catch-up growth
o Provide loving care and stimulation
 22

o Prepare for follow-up after discharge

CHAPTER 3
CASE REPORT

3.1. Objective
The aim of doing this paper is to report a case of tuberculosis pleural
effusion in a 7 years old boy that was admitted to Infection Unit of Pediatrics
Departement in Haji Adam Malik General Hospital.

3.2. Case
Y, 7 years old boy, body weight 21 kg, and 125 cm of height, was
admitted to infection unit of pediatrics departement, Haji Adam Malik General
Hospital on December 3rd 2010 at 10.45 am with chief complain breathlessness.
Breathlessness occurs since 1 week ago and subsided when the patient lie down
 23

on right side. This complain was followed by cough. The cough occurs since 1
month ago with yellow phlegm and no bloody streak. These chief complain also
followed by night hyperperspiration, decreased of body weight and lessen of
appetite. Night hyperperspiration occurs since 1 week ago. Decreased of body
weight and lessen of appetite occurs since 1 month ago.
The patient also complained having fever since 1 month ago, the fever is
subfebrile, the temperature falls with the adminstration of paracetamol. Fever
always occur at night and subsided in the morning. History of having contact to
tuberculosis patient was not found. History of immunization is complete
(according to his mother) and a BCG scar was found.
He had history to be inpatient in RB4 with diagnoses dengue fever 2
weeks later before his chief complain for his medical problem now.

Physical Examination
Presence Status
Sens : Compos Mentis Temp : 37,60C
BW : 21 kg BL : 125 cm
Anemic (-) Cyanosis (-) Dypsnoe (-) Oedema (-) Icteric (-)
Localized Status
Head: - Eye: light reflexes (+/+), isochoric pupil, conjunctiva palpebra inferior
pale (-/-)
- Ear/Mouth/Nose: within normal limit
Neck : lymph node enlargement (+) at sinistra and dextra colli regio, size + 1
cm, multiple, soft, mobile and without pain pressure.
Thorax : asymmetric, seems like right dominant, retraction (+) epigastrial. HR 112
bpm, regular, without murmur. RR 32 tpm, regular, weakness breathing
soundwas found at left side pulmonary regio and dull in percussion.
Abdomen: symmetric, soepel, peristaltic (+). With no palpable of liver and spleen.
Extremities: pulse 122 bpm, regular,adequate pressure and volume, warm acral,
BP 100/60 mmHg. Physiological reflexes: within normal limit,
pathological reflexes (-) and meningeal reflexes (-).
 24

Differential Diagnose:
Pneumonia
Sinistra pleural effusion ec ?

Working Diagnose: Pneumonia

Management:
IVFD D5% NaCl 0,225% 10 gtt/I micro

Futher Examination:
CBC
Chest X-Ray
LFT
RFT
3 times Direct Smear Sputum
Tuberculin Skin Test
FOLLOW UP

Follow Up December 3 rd 2010

S: Breathless (+), fever (+), cough (+)
O: Sens: CM, T: 39,2, BL= 125 cm, BW= 22 kg, BW/ BL= 89, 79%
Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+)
E/N/T: within normal limit
Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: asymmetric, seems like right dominant, retraction (+) epigastrial. HR: 110
bpm, regular, without murmur. RR: 38 tpm, regular, weakness breathing
soundwas found at left side pulmonary regio and dull in percussion.
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
 25

Extremities: Pols: 120 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities. BP: 100/70 mmHg.
A: Pleural effusion ec: DD: 1. Pneumonia + Mild malnutrition
2. Pulmonary TB
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225% 10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
- Inj. Cefotaxime 600 mg/ 8 hours/ IV
- Inj. Chloramphenicol 600 mg/ 8 hours/ IV
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg (if fever)
R: - Consult to respirology department
- Sputum analysis
- AFB direct smear
- Pleural tapping

Laboratory Finding (December 3rd 2010) – Emergency Unit

Test Result Normal Value
Complete Blood Count
Hemoglobin (Hb) 10,70 11,3-14,1
Erytrocytes (RBC) 4,37x10 6 4,40-4,48
Leucoytes (WBC) 9,75x10 4,5-13,5
Hematocrite (Ht) 33,00 37-41
Trombocytes (Plt) 503x10³ 150-450
MCV 75,50 81-95
MCH 24,50 25-29
MCHC 32,40 29-31
RDW 14,10 11,6-14,8
MPV 7,90 7,0-10,2
PCT 0,40
 26

PDW 7,8

Chest X-Ray finding:

Massive pleura effusion on the left hemithorax.
CTR < 50%

Follow Up December 4 th 2010

S: Breathless (+), fever (-), cough(+)
O: Sens: CM, T: 37,3, BL= 125 cm BW= 22 kg
Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+). E/N/T: within normal limit
Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: asymmetric, seems like right dominant, retraction (+) epigastrial. HR : 98
bpm, regular, without murmur. RR: 30 tpm, regular, weakness breathing
soundwas found at left side pulmonary regio and dull in percussion.
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
Extremities: Pols: 98 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities. BP: 100/50 mmHg.
A: Pleural effusion ec: DD: 1. Pneumonia + Mild malnutrition
2. Pulmonary TB
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225%10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
- Inj. Cefotaxime 600 mg/ 8 hours/ IV (Day 1)
- Inj. Chloramphenicol 600 mg/ 8 hours/ IV (Day 1)
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg (if fever)
R: - Consult to respirology department
- Sputum analysis
 27

- AFB direct smear

- Montoux Test
- Pleural tapping
- Pleural fluid analysis

Follow Up December 5 th 2010

S: Breathless (+), fever (-),cough(+)
O: Sens: CM, T: 36,8, BL= 125 cm, BW= 22 kg
Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+). E/N/T: within normal limit
Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: asymmetric, seems like right dominant, retraction (+) epigastrial. HR: 98
bpm, regular, without murmur. RR: 38 tpm, regular, weakness breathing
soundwas found at left side pulmonary regio and dull in percussion.
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
Extremities: Pols: 120 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities.
BP: 100/60 mmHg.
A: Pleural effusion ec: DD: 1. Pneumonia + Mild malnutrition
2. Pulmonary TB
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225% 10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
- Inj. Cefotaxime 600 mg/ 8 hours/ IV (Day 2)
- Inj. Chloramphenicol 600 mg/ 8 hours/ IV (Day 2)
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg (if fever)

Follow Up December 6 th 2010

S: Breathless (+), fever (-), cough (+)
 28

O: Sens: CM, T: 36,7, BL= 125 cm, BW= 22 kg

Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+). E/N/T: within normal limit
Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: Asimetric, seems like right dominant with minimal epigastrial retraction
(+) epigastrial. HR: 100 bpm, regular, without murmur. RR: 26 tpm,
regular, weakness breathing soundwas found at left side pulmonary regio
and dull in percussion.
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
Extremities: Pols: 100 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities. BP: 100/60 mmHg.
A: Pleural effusion ec: DD: 1. Pneumonia + Mild malnutrition
2. Pulmonary TB
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225% 10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
- Inj. Cefotaxime 600 mg/ 8 hours/ IV (Day 3)
- Inj. Chloramphenicol 600 mg/ 8 hours/ IV (Day 3)
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg
R: - Consult to respirology department
- Sputum analysis
- AFB direct smear
- Pleural tapping
- Pleural fluid analysis

Montoux Test Result: - Positive

- Undulation (+) hyperemis, size 12 mm.

Follow Up December 7 th 2010

 29

S: Breathless (+), fever (-), cough (+)

O: Sens: CM, T: 36,8, BL= 125 cm, BW= 22 kg
Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+). E/N/T: within normal limit
Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: asymmetric, seems like right dominant, retraction (+) epigastrial. HR: 108
bpm, regular, without murmur. RR: 38 tpm, regular, weakness breathing
soundwas found at left side pulmonary regio and dull in percussion.
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
Extremities: Pols: 108 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities. BP: 100/60 mmHg.
A: Pleural effusion ec: DD: 1. Pneumonia + Mild malnutrition
2. Pulmonary TB
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225% 10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
- Inj. Cefotaxime 600 mg/ 8 hours/ IV (Day 4)
- Inj. Chloramphenicol 600 mg/ 8 hours/ IV (Day 4)
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg (if fever)

Advice from Pediatric Pulmonology Departement:

- - Pleural tapping
- Pleural fluid analysis

Follow Up December 8 th 2010

S: Breathless (+), fever (-), cough (+)
O: Sens: CM, T: 39,2, BL= 125 cm , BW= 22 kg
Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+). E/N/T: within normal limit
 30

Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: asymmetric, seems like right dominant, retraction (+) epigastrial. HR: 100
bpm, regular, without murmur. RR: 40 tpm, regular, weakness breathing
soundwas found at left side pulmonary regio and dull in percussion.
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
Extremities: Pols: 100 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities. BP: 100/70 mmHg.
A: Pleural effusion ec: DD: 1. Pneumonia + Mild malnutrition
2. Pulmonary TB
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225% 10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
- Inj. Cefotaxime 600 mg/ 8 hours/ IV (Day 5)
- Inj. Chloramphenicol 600 mg/ 8 hours/ IV (Day 5)
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg (if fever)

Until 22.00 WIB AFB direct smear result is negative.

Follow Up December 9 th 2010

S: Breathless (+), fever (-), cough (+)
O: Sens: CM, T: 36,2, BL= 125 cm, BW= 22 kg
Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+). E/N/T: within normal limit
Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: asymmetric, seems like right dominant, retraction (+) epigastrial. HR: 110
bpm, regular, without murmur. RR: 38 tpm, regular, weakness breathing
soundwas found at left side pulmonary regio and dull in percussion.
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
 31

Extremities: Pols: 120 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities. BP: 100/70 mmHg.
A: Pleural effusion ec: DD: 1. Pneumonia + Mild malnutrition
2. Pulmonary TB
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225% 10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
- Inj. Cefotaxime 600 mg/ 8 hours/ IV (Day 6)
- Inj. Chloramphenicol 600 mg/ 8 hours/ IV (Day 6)
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg (if fever)

Follow Up December 10 th 2010

S: Breathless (+), fever (-), cough (-)
O: Sens: CM, T: 39,2, BL= 125 cm, BW= 22 kg
Head: Eye: pupil reflex (+/+), isochoric pupil (+), pale palpebra inferior
conjunctiva (+). E/N/T: within normal limit
Neck: Lymph node enlargement (+) bilateral, size ± 1 cm, multiple, consistency
soft, mobile (+), tenderness (+).
Chest: Asimetric with minimal epigastical retraction.
HR: 100 bpm, regular, mur-mur (-)
RR: 48 rpm, regular
Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.
Extremities: Pols: 100 bpm, regular, pressure and volume was adequate, cyanotic
(-), with warm extremities. BP: 100/70 mmHg.
A: Pleural effusion ec: DD: 1. Pulmonary TB + Mild malnutrition
2. Pneumonia
P: - Oxygen 1 L/ minutewith nasal canule
- IVFD D5% NaCl 0,225% 10 gtt/minute micro
- Reguler diet 1540 kkal with 44gr protein
 32

- Inj. Cefotaxime 600 mg/ 8 hours/ IV (Day 7)

- Inj. Chloramphenicol 600 mg/ 8 hours/ IV (Day 7)
- Rifampicin 1 x 240 mg
- INH 1 x 240 mg
- Pirazinamid 2 x 40 mg
- Ambroxol syrup 3 x Cth1
- Paracetamol 3 x 250 mg (if fever)

December, 11 th 2010 Patient discharge from RSUP HAM.

CHAPTER 4
DISCUSSION

A pleural effusion is always abnormal and indicates the presence of and

underlying disease.1 The accumulation of pleural fluid can usually be explained
by increased pleural fluid formation or decreased pleural fluid absorption, or
both.1,2 In thiscase the pleural effusion is caused by Mycobacterium tubercuosis a
microoorganism obigate aerob which caused caseous necrosis.
Based on Pleural effusion occurs in 2-38% of all cases of pulmonary
tuberculosis in children.8 Tuberculous pleural effusions can be either primary or
results of reactivation disease.4 in this case, it maybe caused by result of
reactivation disease as we found from the clinical history of the patient had adjust
recover from dengue fever. So, the immune system is decreased.
Primary tuberculous pleural effusion results from direct hematogenous
invasion of the pleural space by mycobacterium tuberculosis, is usually unilateral,
 33

and is often found in the absence of pulmonary parenchymal disease. 4,8

Tuberculous pleural effusion due to reactivation disease is typically associated
with focal parenchymal disease.
Based on physical examination on pleural efusion we can find on
inspection the asymetrical chest expantion, on palpation we can find the decreased
of stem fremitus on the left side chest. On auscultation we can find the decreased
of vesicular breath sound. The acid fast bacilli staining result was negative, so we
can not confirm this patient had a pulmonary tuberculosis. But, tuberculin skin
test was positive with 12 mm induration witdh. So, we start the adjuvantibus
therapy to confirm the diagnosis. The result can be evaluated on 2 weeks to see
the outcome as subsided of clinical manifestation and the increase of body weight.

SUMMARY
It has been reported a case of an 7 years old boy with pleural effusion.
Who was suspected as pleural effusion caused by M. tuberculosis infection. The
diagnosis was established based on history taking, clinical manifestation,
radiology finding and laboratory findings. Treatment for this patient was based on
underlying disease, symptomatic and supportive treartment.
 34

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2. Assefa, Dagnachew. 2010. Pleural Effusion. Available from:
http://emedicine.medscape.com/article/1003121-print [accessed December
10th 2010].
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 35

5. Jawetz, MZ. 2007. Mycobacteria. In: Jawetz, Melnick, & Adelberg's

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