lapkas erwin-yunny

8/7/2019 Lapkas Erwin-Yunny

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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

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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 doctors

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.

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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

m.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

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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 15 m 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

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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

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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

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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

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Old tuberculin is a concentrated filtrate of broth in which tubercle bacillihave 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 2448 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

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reactions may disappear more rapidly.4 The tuberculin test becomes positive

within 46 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 37 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

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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

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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

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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 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

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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 treatmentfrom 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

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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

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children who are contacts of cases of recently diagnosed pulmonary

tuberculosis.1,2,4,8

Careful monthly monitoring of the clinical and bacteriologicresponses to

therapy is important.3 With DOT, clinical evaluationis 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 canpersist

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 necessaryunless 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 everysituation, 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

interruptionoccurred; and (3) the patients 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 specialistin 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 approximatelymonthly during the first several months of treatment.3,4,6

Otherindications for testing include the following: (1) having concurrentor 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 withoutroutine monitoring of

transaminase concentrations is appropriate follow-up.1,2,4 In all cases, regular

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

an important aspect of management.4,8 Patients should be advised to call a

physicianimmediately 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-Gurin (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

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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 childs 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 ( 2 weeks) to a country with a high prevalence of

tuberculosis? (3) Has the child been exposed to an adult with pulmonary

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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).3Most tuberculosis effusions completely resolve withthe 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 8090% of

expected are considered abnormally low.10

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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

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

515 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

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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

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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

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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 (-).

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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


Abdominal: Soepel, normal peristaltic, liver/ spleen: unpalpable.

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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)

Erytrocytes (RBC)

Leucoytes (WBC)

Hematocrite (Ht)Trombocytes (Plt)

MCV

MCH

MCHC

RDW

MPV

PCT

10,70

4,37x10 6

9,75x10

33,00503x10

75,50

24,50

32,40

14,10

7,90

0,40

11,3-14,1

4,40-4,48

4,5-13,5

37-41150-450

81-95

25-29

29-31

11,6-14,8

7,0-10,2

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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


conjunctiva (+). E/N/T: within normal limit



Chest: asymmetric, seems like right dominant, retraction (+) epigastrial. HR : 98







2. Pulmonary TB


- 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)




- Sputum analysis

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- AFB direct smear

- Montoux Test

- Pleural tapping

- Pleural fluid analysis


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

O: Sens: CM, T: 36,8, BL= 125 cm, BW= 22 kg










(-), with warm extremities.

BP: 100/60 mmHg.


2. Pulmonary TB









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

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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.





2. Pulmonary TB







- Paracetamol 3 x 250 mg


- Sputum analysis

- AFB direct smear

- Pleural tapping


Montoux Test Result: - Positive

- Undulation (+) hyperemis, size 12 mm.

Follow Up December 7th

2010

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2. Pulmonary TB








Advice from Pediatric Pulmonology Departement:

- - Pleural tapping




O: Sens: CM, T: 39,2, BL= 125 cm , BW= 22 kg



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2. Pulmonary TB








Until 22.00 WIB AFB direct smear result is negative.












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2. Pulmonary TB









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






Chest: Asimetric with minimal epigastical retraction.

HR: 100 bpm, regular, mur-mur (-)

RR: 48 rpm, regular




A: Pleural effusion ec: DD: 1. Pulmonary TB + Mild malnutrition

2. Pneumonia




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- Rifampicin 1 x 240 mg

- INH 1 x 240 mg

- Pirazinamid 2 x 40 mg



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,

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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.

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REFERENCES

1. Mayse, Martin L. 2008. Non-Malignan Pleural Effusion. In: Fishmans

Pulmonary Diseasse and Disorders. Fourth Edition. New York: Mc Graw-

Hill. 1487-1504.

2. Assefa, Dagnachew. 2010. Pleural Effusion. Available from:

http://emedicine.medscape.com/article/1003121-print [accessed December

10th 2010].

3. Merino, JM et all. 1999. Tuberculous pleural effusion in children.

Available from: http://www.ncbi.nlm.nih.gov/pubmed/19672657

[accessed December 10th 2010].

4. Starke, Jeffrey R. 2004. Tuberculosis in Children. Available from:

http://www.medscape.com/viewarticle/484123_3 [accessed December 10th

2010].

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http://emedicine.medscape.com/article/1003121-printhttp://www.ncbi.nlm.nih.gov/pubmed/19672657http://www.medscape.com/viewarticle/484123_3http://emedicine.medscape.com/article/1003121-printhttp://www.ncbi.nlm.nih.gov/pubmed/19672657http://www.medscape.com/viewarticle/484123_3


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

Medical Microbiology. 24th Edition. New York: Mc Graw-Hill

6. Berger, HW. Mejia, W. 2006. Tuberculous Pleural Effusion. In: Pleural

Disease. Third Edition. USA: Saunders. 211-221.

7. Rubins, Jeffrey. 2010. Pleural Effusion. Available from:

http://emedicine.medscape.com/article/299959-print[accessed December

10th 2010].

8. Janner, Donald. 2004. Pediatric Tuberculosis: Excerpt from Pediatric

Infectious Disease. In: Pediatric Infectious Disease. Lippincott Williams &

Wilkins.

9. Marais, Ben J. et all. 2006. A Refined Symptom-Based Approach to

Diagnose Pulmonary Tuberculosis in Children. Availabe from:

http://www.pediatrics.org/cgi/content/full/118/5/e1350 [accessed

December 18th 2010].

10. Murray B. 2003. Undernutrition. In Nelson Textbook of Pediatrics. 15th

Edition. New York: Mc Graw-Hill. 909-935.

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http://emedicine.medscape.com/article/299959-printhttp://www.pediatrics.org/cgi/content/full/118/5/e1350http://emedicine.medscape.com/article/299959-printhttp://www.pediatrics.org/cgi/content/full/118/5/e1350

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