Efusi Pleura

Case Report

PLEURAL EFFUSION

SUPERVISOR : dr. Nelly Rosdiana, Sp. A (K)

PRESENTATOR : Rosa Yulise Putri 110100117

Mageswari Selvarajoo 110100396

DEPARTMENT OF CHILD HEALTH

MEDICAL FACULTY NORTH SUMATRA UNIVERSITY

H. ADAM MALIK GENERAL HOSPITAL

MEDAN

2015

ii

ACKNOWLEDGMENTS

We are greatly indebted to the Almighty One for giving us blessing to finish this case

report,“Pleural effusion”.This case report is a requirement to complete the clinical assistance

program in Department of Child Health in H. Adam Malik General Hospital, Medical Faculty

of North Sumatra University.

We are also indebted to our supervisor and adviser, dr. Nelly Rosdiana, Sp.A (K) for

much spent time to give us guidances, comments, and suggestions. We are grateful because

without Her this case report wouldn’t have taken its present shape.

This case report has gone through series of developments and corrections. There were

critical but constructive comments and relevants suggestions from the reviewers. Hopefully

the content will be useful for everyone in the future.

Medan, th September 2015

Presentator

iii

CONTENT

INTRODUCTION.......................................................................................................1

LITERATURE REVIEW...........................................................................................2

Pleural Effusion

2.1. Definition ..............................................................................................................2

2.2. Etiology..................................................................................................................2

2.3. Clinical manifestation...........................................................................................4

2.4. Staging...................................................................................................................5

2.5.Diagnosis.................................................................................................................6

2.6.Treatment…………………………………………………………………..……...9

2.7.Complication………………………………………………………………..…….11

2.8.Prognosis……………………………………………………………………..…...11

CASE REPORT.........................................................................................................12

DISCUSSION ............................................................................................................25

SUMMARY ...............................................................................................................28

REFERENCES ………………………………………………………………………29

1

INTRODUCTION

1.1 Introduction

Pleural effusions (liquid in the pleural space), which occur less frequently

in children than in adults, can be caused by a variety of infectious and

noninfectious diseases. Causes of pleural effusions in children differ significantly

from those in adults. Among adults, the most frequent cause is congestive heart

failure (transudate), and bacterial pneumonia and malignancy are the most

frequent causes of exudate. Pleural effusions in children most commonly are

infectious (50% to 70% parapneumonic effusion); congestive heart failure is a less

frequent cause (5% to 15%), and malignancy is a rare cause.1

Parapneumonic effusion and empyema have an incidence of 3.3 per 100.000

children. It has been suggested that the incidence of childhood empyema

increased in the UK, although this is not a universal finding. It is not clear

whether this is related to different referral patterns, changes of antibiotic usage in

primary care, or whether it was a genuine increase in disease incidence.2

Parapneumonic effusion is defined as fluid in the pleural space in the

presence of pneumonia, lung abscess, or bronchiectasis. Nontuberculous bacterial

pneumonia constitutes the most frequent origin of pleural effusion in children.

Establishing a specific causative agent depends on the patient’s age, underlying

disease, standard of laboratory culture method, and initiation of antibiotic therapy.

Staphylococcus aureus is the single most common pathogen causing empyema

(29% to 35% of cases), especially among infants younger than 2 years of age.

Streptococcus pneumoniae is the cause in up to 25% of cases of empyema.

Haemophilus influenzae is a less frequent pathogen but still is significant in the

development of parapneumonic effusion in children up to 5 years of age.1

1.2. Objective

The objective of this paper is to report a case of a patient with a diagnosis

of pleural effusion.

2

LITERATURE REVIEW

2.1. Pleural Effusions

2.1.1 Definition

Pleural effusions are accumulations of fluid within the pleural space. They

have multiple causes and usually are classified as transudates or exudates.

Normally, 10 to 20 mL of pleural fluid, similar in composition to plasma but

lower in protein (< 1.5 g/dL), is spread thinly over visceral and parietal pleurae,

facilitating movement between the lungs and chest wall. The fluid enters the

pleural space from systemic capillaries in the parietal pleurae and exits via parietal

pleural stomas and lymphatics. Pleural fluid accumulates when too much fluid

enters or too little exits the pleural space. 3

2.1.2 Etiology

Pleural effusions are usually categorized as transudates or exudates based on

laboratory characteristics of the fluid. Whether unilateral or bilateral, a transudate

can usually be treated without extensive evaluation, whereas the cause of an

exudate requires investigation. There are numerous causes of pleural effusion

seen in the table below. 4

Transudative effusions are caused by some combination of increased

hydrostatic pressure and decreased plasma oncotic pressure. Heart failure is the

most common cause, followed by cirrhosis with ascites and by

hypoalbuminemia, usually due to the nephrotic syndrome. 5

Exudative effusions are caused by local processes leading to increased

capillary permeability resulting in exudation of fluid, protein, cells, and other

serum constituents. Causes are numerous; the most common are pneumonia,

cancer, pulmonary embolism, viral infection, and TB. Yellow nail syndrome is

a rare disorder causing chronic exudative pleural effusions, lymphedema, and

dystrophic yellow nails—all thought to be the result of impaired lymphatic

drainage. 5

3

Table 1 Etiology of pleural effusions4

Cause Comments

Transudate

Heart failure - Bilateral effusions in 81%; right-sided in 12%; left-

sided in 7%

- With left ventricular failure, there is increased

interstitial fluid, which crosses the visceral pleura

and enters the pleural space

Cirrhosis with ascites

(hepatic hydrothorax)

- Right-sided effusions in 70%; left-sided in 15%;

bilateral in 15%

- Ascitic fluid migration to the pleural space through

diaphragmatic defects

- Effusion present in about 5% of patients with

clinically apparent ascites

Hypoalbuminemia - Uncommon

- Bilateral effusions in > 90%

- Decreased intravascular oncotic pressure causing

transudation into the pleural space

- Associated with edema or anasarca elsewhere

Nephrotic syndrome - Usually bilateral effusions; commonly

subpulmonic

- Decreased intravascular oncotic pressure plus

hypervolemia causing transudation into the pleural

space

Exudate

Pneumonia

(parapneumonic effusion)

- May be uncomplicated or loculated and/or purulent

(empyema)

- Thoracentesis necessary to differentiate

Tuberculosis - Effusion usually unilateral and ipsilateral to

parenchymal infiltrates if present

- Effusion due to hypersensitivity reaction to TB

4

protein

- Pleural fluid TB cultures positive in < 20%

Cancer - Most commonly lung cancer, breast cancer, or

lymphoma but possible with any tumor metastatic

to pleurae

- Typically causing dull, aching chest pain

Pulmonary embolism - Effusion present in about 30%:

- Almost always exudative; bloody in < 50%

- Pulmonary embolism suspected when dyspnea is

disproportionate to size of effusion

Uremia - Effusion in about 3%

- In > 50%, symptoms secondary to effusion: Most

commonly fever (50%), chest pain (30%), cough

(35%), and dyspnea (20%)

- Diagnosis of exclusion

2.1.3 Clinical manifestation

Respiratory symptoms in the presence of fluid in the pleural space are

common in children. When the underlying cause is pneumonia, the predominant

symptoms are cough, fever, chills, and dyspnea. If the effusion is not associated

with pneumonia, the child may be asymptomatic until the effusion becomes

sufficiently large to cause dyspnea or orthopnea. Children who have neurologic

impairments are more likely to aspirate secretions or gastric content and develop

anaerobic infections, which cause a more insidious onset of pneumonia and

effusion. Older children may complain of a sharp pleuritic pain with inspiration or

cough, which is due to stretching of the parietal pleura. As the effusion increases

and separates the pleural membranes, pleuritic pain becomes a dull ache and

disappears. Specific signs indicating pleural effusion are much more difficult to

elicit in the infant or the young child. Dullness to percussion and decreased

breath sounds over the affected area almost always are present, but they can be

5

difficult to perceive if the effusion is small. In infants, breath sounds from one

lung often are transmitted throughout the chest, making unilateral findings

difficult to appreciate. A pleural rub, due to roughened pleural surfaces, can be

present in the early phase, but it disappears as fluid accumulates. Decreased vocal

fremitus and fullness of the intercostal spaces can be detected. Expectoration of

purulent sputum may herald the onset of bronchopleural fistula and ensuing

pyopneumothorax. Findings of chest wall abscess and costal chondritis indicate

extension of the process (ie, empyema necessitatis). Decreased heart tones and

pericardial rub indicate extension to the pericardium1.

2.1.4 Staging

In children, parapneumonic effusion due to subpleural infectious pneumonia

is the most common cause of pleural effusion. There are three stages associated

with parapneumonic effusion that may overlap6:

Exudative stage: the inflammatory process associated with the underlying

pneumonia leads to the accumulation of clear fluid with a low white cell

count within the pleural cavity (simple parapneumonic effusion).

Fibropurulent stage: there is deposition of fibrin in the pleural space leading

to septation and the formation of loculations. There is an increase in white

cells, with the fluid thickening (complicated parapneumonic effusion) and

eventually becoming overt pus (empyema). The presence of septations

(fibrinous strands within the pleural fluid) does not necessarily mean the fluid

does not flow freely, although separate loculations will not communicate with

each other.

Stage of Organization: fibroblasts infiltrate the pleural cavity, and the thin

intrapleural membranes are reorganised to become thick and non-elastic (the

‘peel’). These solid fibrous pleural peels may prevent lung re-expansion

(trapped lung), impair lung function, and create a persistent pleural space with

ongoing potential for infection. At this stage spontaneous healing may occur

or a chronic empyema may develop.

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2.1.5 Diagnosis

Analysis of the pleural fluid is the single best method to determine the

cause of a pleural effusion. Thoracentesis should be performed when sufficient

fluid is present to allow a safe procedure, except when the suspected effusion is

clearly secondary to a specific underlying disease (for example, congestive heart

failure, nephrotic syndrome, ascites, or recent initiation of peritoneal dialysis).

Simple observation of the gross appearance of the fluid may provide a clue as to

the cause of the pleural effusion, as follows 7:

Grossly purulent fluid indicates an empyema

A putrid odor suggests an anaerobic empyema

Clear, pale yellow fluid suggests a transudate

Milky fluid is consistent with a chylothorax

Bloody pleural fluid is seen with trauma, malignancy, tuberculosis, uremia, and

empyema due to group A Streptococcus

Aspergillus nigrans infection produces a black pleural fluid

In the appropriate clinical setting, measurement of pleural fluid triglyceride levels

(chylous effusion), amylase (pancreatitis, esophageal rupture), and pleural fluid

hematocrit (hemothorax) may be useful7.

A complete blood count (CBC) with differential, blood cultures, and C-

reactive protein (CRP) may help to establish the presence of infection. The white

blood cell (WBC) count and CRP may be useful in monitoring treatment progress

in infectious effusions. A positive blood culture finding may facilitate the

selection of antibiotics in sterile empyema. (Approximately 10-22% of children

with complicated parapneumonic effusions have a positive blood culture result8.

Measurement of titers may be helpful if specific organisms, such as

Mycoplasma species, Legionella species, or adenovirus, are suspected. However,

the use of these tests in early management of parapneumonic effusions is limited

due to the need for convalescent titer8.

If risk factors for tuberculosis are present, sputum (or gastric aspirates) for

acid fast bacilli and a purified protein derivative (PPD) test should be performed.

Serum protein, LDH, amylase, glucose, and hydrogen ion concentration (pH) may

7

be helpful in interpreting results of pleural fluid analysis. If chylous effusion is

suspected, serum cholesterol and triglyceride levels should be obtained8.

Exudate Versus Transudate

Conventionally, the initial evaluation of pleural fluid is directed at

determining whether the effusion is an exudate or a transudate. The classification

is based on simple biochemical criteria first proposed by Light et al. However, the

Light criteria was developed and tested in adults, and its accuracy in children has

been questioned 1.

According to the Light criteria, the pleural fluid is defined as an exudate if it

fulfils at least one of 3 criteria. If none of the criteria are met, then the fluid is

considered a transudate. The criteria are as follows8:

Pleural fluid–to–serum lactate dehydrogenase (LDH) ratio of more than 0.6

Pleural fluid–to–serum protein ratio of more than 0.5

Pleural fluid LDH level of two thirds the upper limit of the reference range

In general, exudates have protein concentration higher than 2.9 g/dL, with the

pleural fluid cholesterol level more than 45 mg/dL.

Biochemical analysis of the pleural fluid provides further information that

may be useful in narrowing the differential diagnosis of exudative effusion, as

follows6:

Low pleural glucose level (< 60 mg/dL) or pleural fluid–to–serum glucose ratio

of less than 0.5 - Seen in several conditions, such as parapneumonic effusion,

tuberculosis, malignancy, esophageal rupture, and rheumatoid effusions

LDH levels of more than 1000 IU/L - Found in empyema and rheumatoid

effusions

Pleural fluid–to–serum LDH ratio of 1 and pleural fluid–to–serum protein ratio

less than 0.5 -Suggest effusion due to P jiroveci pneumonia

Pleural fluid pH below 7.3 (with normal arterial pH) - Seen in parapneumonic

effusion, tuberculosis, malignancy, esophageal rupture, systemic acidosis,

8

urinothorax, and rheumatoid effusions; most exudative effusions have a pH of

7.3-7.45, whereas transudates have a pleural fluid pH ranging from 7.4-7.55

(the pH of normal pleural fluid is about 7.6)

9

*Based on presence of fever, weight loss, history of cancer, or other suggestive symptoms.(Adapted from www.merckmanuals.com/professional/pulmonary-disorders/mediastinal-and-pleural-disorders/pleural-effusion)

2.1.6 Treatment

Most pediatric patients who have uncomplicated parapneumonic effusion

respond well to appropriate antibiotic therapy and do not require tube

thoracostomy. The treatment of empyema (complicated parapneumonic effusion)

in children begins with conservative therapy. The initial treatment is

administration of antibiotics directed at the underlying infection and drainage of

infected fluid by thoracentesis or by closed thoracostomy tube. Antibiotics should

be selected (Table 2) to cover the most common pathogens for pneumonia for the

child’s age group. Until the condition is diagnosed, broad-spectrum antibiotics are

warranted due to the high morbidity and mortality associated with empyema.

Intravenous antibiotics should be continued until the child is afebrile for at least 7

to 10 days, has been weaned from supplemental oxygen, and no longer appears ill.

Oral antibiotics subsequently are administered for 1 to 3 weeks2.

Tabel 2 Common organism causing Parapneumonic effusion in children and corresponding empiric antibiotic therapy2

Age Predominant pathogens Therapy

0 to 6 mon Gram-negative rods*

Staphylococcus aureusStreptococcus

Nafcillin, gentamicin, and

ampicilin

7 to 12 mon Haemophilus influenzaePneumococcusStreptococcus

Nafcilin and cefuroxime

13 to 24 mon H. InfluenzaePneumococcusS. aureus

Cefuroxime, clindamycin

2 to 5 y H InfluenzaePneumococcusS. aureusStreptococcusAnaerobes

Cefuroxime and clindamycin

or imipenem

6 to 12 y Pneumococcus Cefuroxime and clindamycin

http://www.merckmanuals.com/professional/pulmonary-disorders/mediastinal-and-pleural-disorders/pleural-effusion


10

S. aureusStreptococcusAnaerobes

or imipenem

13 to 18 y PneumococcusS. aureusAnaerobes

Nafcilin or cefuroxime plus

clindamycin

* Pseudomonas, Eschericia coli, Proteus, Klebsiella

Prompt drainage of the empyema prevents the development of loculation

and fibrous peel. Further, at the second stage of disease, tube drainage becomes

less effective. Whether all empyemas require drainage remains controversial; no

data in children clearly establish criteria. Generally, immediate closed-tube

thoracostomy should be considered strongly with the following9:

● Pleural fluid pH is less than 7.2 or more than 0.05 units below the arterial pH

● Pleural fluid glucose is less than 40 mg/dL (2.2 mmol/L)

● Pleural fluid LDH is greater than 1,000 U/L

● Presence of frank pus

● Positive Gram stain

● Sepsis due to S. aureus or H. influenzae

When the chest tube drainage reaches less than 30 to 50 mL/d and the patient’s

constitutional symptoms improve, the chest tube may be removed.

Another effective therapy is introduction of streptokinase (SK) or urokinase

(UK) into the empyema cavity, which has been shown to lyse adhesions, enhance

drainage, and resolve the symptoms. SK is a bacteria-derived protein that

indirectly activates the fibrinolytic system. Problems associated with this regimen

include allergic reactions and antibody neutralization of the SK. UK is a direct

plasminogen activator. Unlike SK, there is a one to one relationship of plasmin

production for each molecule of UK, making more efficient use of pre-existing

plasminogen. UK is not antigenic. Studies have documented complete resolution

of fluid collection with persistent loculated fluid following instillation of UK into

the chest tube. No complication occurred in either series. Basic indications for UK

in pleural effusion include7:

● Poor drainage despite an appropriately positioned chest tube

11

● Multiple loculi, as depicted by septation on ultrasonography or CT

● Presumed multi loculi, as indicated by initial drainage of a volume far less than

expected by imaging studies

2.1.7 Complication

Complications are uncommon in properly treated parapneumonic effusions.

Possible complications include respiratory failure caused by massive fluid

accumulation, septicemia, bronchopleural fistula, pneumothorax, and pleural

thickening10.

2.1.8 Prognosis

Children who have uncomplicated parapneumonic effusion respond well to

conservative management with no apparent residual lung damage. Viral and

mycoplasmal pleural disease generally resolve spontaneously. Patients who have

empyema have more prolonged and complicated hospital courses. Virtually no

deaths should occur with prompt therapy. Case fatality rates of 3% to 6% have

been reported in some recent series, with the highest rate occurring among infants

younger than 1 year of age. In contrast to adults, infants and children have a

remarkable ability to resolve pleural thickening with no effect on subsequent lung

growth and lung function 11.

http://emedicine.medscape.com/article/298485-overview

12

CASE REPORT

3.1 Case

A, a 1 years and 3 months boy, with 9 kg of BW and 96 cm of BH, is a

new patient of infection unit in Pediatric Department in Central Public Hospital

Haji Adam Malik Medan on September 6th 2015 at 19.30. His chief complaint was

dyspnea/shortness of breath

.

History of disease:

A, a boy, 1 years and 3 months old, came to Haji Adam Malik Hospital on

September 6th 2015 with dyspnea as the chief complaint. The patient have been

experiencing this for the past 2 days. Dyspnea is not associated with weather or

activity. Patient also experienced cough (+) since 1 weeks ago with the production

of sputum (+) but hard to be expelled. Flu (+) for the past 1 week. Fever (+) since

1 weeks ago, rises and drop and hard to be reduced with fever medication. Perut

kembung (+) is noticed by the mother for the past 2 days. History of contact to

patient with prolonged cough (-). History of allergy (-). Nausea (-), Vomiting (-),

Diahreoa (-). Urine and faeces (+) normal.

History of previous illness:

The patient is referred from RS Pertamina Brandon with dd of URTI,

bronchiolitis, nephrotic syndrome and GNA.

History of medication:

IVFD RL, Inj. Viccilin, Inj.Novalgin, Inj.Gentamicin, Sanmol Syrup,amborox

syrup,nebule ventolin

History of family:

No family history of DM and other diseases

History of parent’s medication:

13

unclear

History of pregnancy:

The gestation age was 36 weeks. No history of complication, neonate and

maternal problem.

History of birth:

Birth assisted by midwife spontaneously. The baby was born pervaginal and she

cried immediately. Bluish was not found. Body weight 3900 gram, body length 50

cm, and head circumference was not measured.

History of feeding:

Breast feeding from born till now, additional food since 2 months old.

History of immunization:

BCG, Polio, Hepatitis B. Immunization is not complete

History of growth and development:

Face down: 4 months old, Sit down: 6 months old, Crawl: 8 months old, Stand up:

10 months old, Walk: 13 months old, Talk: 12 months old.

Physical Examination:

Present status: Level of consciousness: Consious, Body temperature:

37.8°C, BP: 100/90 mmHg, HR: 130 bpm, RR: 40 bpm, BW: 9 kg, BH: 76

cm, anemic (+), icteric (-), dyspnea (+), cyanosis (-), edema (-).

Localized status:

Head : Eyes: Light reflex +/+, isochoric pupil,

pale was found in inferior conjunctiva palpebral.

Ears : Within normal range

Nose : Nostril breathing

Mouth : Within normal range

Neck : Lymph node enlargement (-)

Thorax : Symmetrical fusiform, retraction (+) epigastrial, Cor S1,

S2 reguler, Weak breathing sound on the left lung.

HR: 136 bpm, regular, murmur (-)

RR: 48 bpm, regular, rhonchi (+/+) wheezing (-/-), rales

(-/-)

14

Abdomen : Supple, normal peristaltic, liver normal

Extremities : Pulse 136 bpm regular, p/v adequate, warm acral, CRT

< 3”, clubbing finger(-).

Differential diagnosis :

Working diagnosis : Left pleural effusion + suspect of sepsis

Laboratory finding

Complete blood analysis (September 6th , 2015)

Test Result Unit Referral

Hemoglobin 8.10 g% 12.0-14.4

Erythrocyte 3.43 106/mm3 4.40-4.48

Leucocyte 39.53 103/mm3 4.5-13.5

Thrombocyte 536 103/mm3 150-450

Hematocrite 25.80 % 37-41

Eosinophil 0.30 % 1-6

Basophil 1.300 % 0-1

Neutrophil 66.20 % 37-80

Lymphocyte 23.40 % 20-40

Monocyte 9.20 % 2-8

Neutrophil absolute 11.41 103/µL 2.4-7.3

Lymphocyte absolute 4.99 103/µL 1.7-5.1

Monocyte absolute 1.39 103/µL 0.2-0.6

Eosinophyl absolute 0.18 103/µL 0.10-0.30

Basophyl absolute 0.16 103/µL 0-0.1

MCV 75.20 fL 81-95

MCH 23.60 Pg 25-29

MCHC 31.40 g% 29-31

RDW 15.70 % 11.6-14.8

Morphology: Erythrocyte: anemia hipokrom microcyte

15

Leukocyte: leukocytosis

Trombocyte: trombocytosis

Clinical Chemistry

Test Result Unit Referral

Carbohydrate Metabolism

Blood Glucose 87.10 mg/dL < 200

Albumin 2.3 g/dl

Electrolite

Natrium 132 mEq/L 135-155

Kalium 3.8 mEq/L 3.6-5.5

Chloride 101 mEq/L 96-106

Blood Arterial Gas Analyse

Ph 7.430 7.35-7.45

pCO2 30.0 mmHg 38-42

pO2 193.0 mmHg 85-100

Bicarbonate (HCO3) 19.9 mmol/L 22-26

Total CO2 20.8 mmol/L 19-25

base excess -3.9 mmol/L (-2)– (+4)

O2 Saturation 100.0 mmol/L 95-100

Foto thoraks : (6 september 2015)

16

Hasil pembacaan : Left pleural effusion

Therapy :

1. O2 nasal canule 1 liter/i

2. IVFD D5% Nacl 0,45% 4cc/hour

3. Inj Ceftriaxon 450 mg/12 jam /iv skin test

4. Paracetamol 3x120mg

5. Diet Peadsure 100cc/3hour/NGT

6. Correction of hipoalbuminemia

7. Consul to the respirology division

17

Follow Up:6th September 2015

S O A P

Dyspnea (+), cough (+), fever (+)

Sensorium: CM, T: 38,1 oC, BW: 9 kg BH: 76cm

Head: eye reflect +/+, conj palpebral inferior pale +/+, mouth/nose/ear: normal.

Neck: JVP R+2 H2O

Thorax: symetris fusiformis, retraction (+), epigastrial, weaken breathing sound on left lung, HR: 136x/i, systolic murmur(-), RR: 48x/i, Ronchi -/-, Slem (+)Abdomen: Seopel, Normal peristaltic, Hepar unpalpable, Lien: unpalpable.

Extremities: Pulse: 120x/i, regular, adequate pressure and volume, warm, CRT < 3’’

Left pleural effusion + Susp. Sepsis

- O2 nasal kanul 1l/i- IVFD D5% 4cc/

jam- Inj. Ceftriaxone 450

mg / 12 jam / IV- Paracetamol Syr. 3

x cth I (120 mg)- Diet pediasure 100

cc / 3 jam/ NGT- Hipoalbuminemia

correction- Consul respirology

division

7th September 2015- 8th September 2015

S O A P



Head: eye reflect +/+, conj palpebral inferior pale +/+,


- O2 nasal kanul 1l/i- IVFD D5% 4cc/

jam- Inj. Ceftriaxone 450

18

mouth/nose/ear: normal.

Neck: JVP R+2 H2O

Thorax: symetris fusiformis, retraction (+), epigastrial, weaken breathing sound on left lung, HR: 126x/i, systolic murmur(-), RR: 44x/i, Ronchi -/-, Slem (+/+)Abdomen: Seopel, Normal peristaltic, Hepar unpalpable, Lien: unpalpable.


mg / 12 jam / IV- Paracetamol Syr. 3

x cth I (120 mg)- Diet pediasure 100

cc / 3 jam/ NGT- Hipoalbuminemia

correctionFrom Respirology:

-Ambroxol 2x2,5cc-Salbutamol 3x0,5mg

9th September 2015 – 10th September

S O A P



Head: eye reflect +/+, conj palpebral inferior pale -/-, mouth/nose/ear: normal.

Neck: JVP R+2 H2O

Thorax: symetris fusiformis, retraction (+), epigastrial, weaken breathing sound on left lung, HR: 120x/i, systolic murmur(-), RR: 40x/i, Ronchi -/-.Abdomen: Seopel, Normal peristaltic, Hepar unpalpable, Lien: unpalpable.



- O2 nasal kanul 1l/i

- Threeway- Inj. Ceftriaxone

450 mg / 12 jam / IV

- Paracetamol Syr. 3 x cth I (120 mg)

- Diet pediasure 100 cc / 3 jam/ NGT-Ambroxol 2x2,5cc-Salbutamol 3x0,5mg

19

11 September 2015-13 September 2014

S O A P




Neck: JVP R+2 H2O



Mantoux result: Induration 0 mm




450 mg / 12 jam / IV



14 September 2015

S O A P







450 mg / 12

20

Neck: JVP R+2 H2O



jam / IV- Paracetamol Syr.

3 x cth I (120 mg)

- Diet pediasure 100 cc / 3 jamResult of culture (stomach): Klebsiella pneumoniaAntibiotic Inj.Ceftiaxon changed to Inj.Meropenem 350 mg/8jam/IV

15 September 2015

S O A P

Dyspnea (+), cough (+), fever (-)

Sensorium: CM, T: 37,1oC, BW: 9 kg BH: 76cm


Neck: JVP R+2 H2O

Thorax: symetris fusiformis, retraction (-), weaken breathing sound on left lung, HR: 110x/i, systolic murmur(-), RR: 40x/i, Ronchi -/-.Abdomen: Seopel, Normal peristaltic, Hepar unpalpable, Lien: unpalpable.


Left masif pleural effusion + Sepsis ec Klebsiella pneumonia


- Inj. Meropenem 350 mg / 8 jam / IV



-Planning of taping the pleural fluid

21


S O A P




Neck: JVP R+2 H2O



Left masif pleural effusion + Sepsis ec Klebsiella pneumonia




- Diet pediasure 100 cc / 3 jam/ NGT-Ambroxol 2x2,5cc-Salbutamol 3x0,5mg-PRC transfusion-Tapping of pleuran fluid was made and sent to lab to be diagnosed.Consult cardiothoracic surgeonAnswer from Cardiothoracic Surgeon: insersion of chest tube emergency dan consult to anesthesiology Answer from anesthesiology: High risk and planning of thorax procedure Insertion of WSD was made.


22

S O A P




Neck: JVP R+2 H2O



Hasil Lab:

Hb: 14,9 mg/dl

Leu: 11.83 mg/dl

Albumin: 3,8 g/dl

Post chest tube insersion a/i efusi pleura massif sinistra + Sepsis ec Klebsiella pneumonia




- Diet pediasure 100 cc / 3 jam/ NGT-Ambroxol 2x2,5cc-Salbutamol 3x0,5mg-PRC transfusionWSD: Fluid from lungs appears reddish.Fluid no more flowing.


S O A P




Neck: JVP R+2 H2O

Thorax: symetris fusiformis, retraction (-), weaken breathing

Efusi pleura (s) para pneumonia ec Klebsiella pneumonia



- ASI ad libitum - Paracetamol Syr.

3 x cth I (120 mg)

- Diet pediasure 100 cc / 3 jam/

23

sound on left lung, HR: 110x/i, systolic murmur(-), RR: 40x/i, Ronchi -/-.Abdomen: Seopel, Normal peristaltic, Hepar unpalpable, Lien: unpalpable.


NGT-ambroxol 2x2,5ccSalbutamol 3x0,5mgResult of pleural fluid culture: Klebsiella pneumoniaContinue treatment with meropenem


S O A P




Neck: JVP R+2 H2O



Efusi pleura (s) para pneumonia ec Klebsiella pneumonia


- Inj. Meropenem 350 mg / 8 jam / IV -Ambroxol 2x2,5ccSalbutamol 3x0,5mg

- Diet pediasure 100 cc / 3 jam/ NGTPlanning of CT scan thoraks non kontras

24

DISCUSSION

Etiology

Pleural effusions are accumulations of fluid within the pleural space.

Normally, 10 to 20 mL of pleural fluid, similar in composition to plasma but

lower in protein (< 1.5 g/dL), is spread thinly over visceral and parietal pleurae,

facilitating movement between the lungs and chest wall3. Causes of pleural

effusions in children differ significantly from those in adults. Pleural effusions in

children most commonly are infectious. Based on a Utine (2006), an experiment

25

was made on 492 pediatrics patient and it is found that the etiological

classification of effusions revealed that parapneumonic effusions predominated

inthe whole group (77.4%). The most frequent organisms encountered in children

are S. aureus, S. pneumoniae, H. Influenzae and S. pyogenes, Pseudomonas

aeruginosa, Mycoplasma pneumoniae and anaerobes. However, the relative

frequencies of the major pathogens responsible for pleural infections have shown

some changes over the years12. On this case, MA, 1 year and 3 months was

diagnosed with pleural effusion caused by paraneumonia infection which is

Klebsiella pneumonia.This matches with the previous study where parapneumonia

is the main cause of pleural effusion in child.

Clinical Manifestation

Respiratory symptoms in the presence of fluid in the pleural space are

common in children. When the underlying cause is pneumonia, the predominant

symptoms are cough, fever, chills, and dyspnea1. They may also present

unwell with a fever but no clear focus, or with chest or abdominal

pain. The clinical features are usually that of pneumonia and

accompanying pleural effusion, i.e. fever, tachypnoea, hypoxia,

respiratory distress, decreased or bronchial breath sounds, and

dullness to percussion. The white cell count (with neutrophilia)

and CRP are typically very high – if these are low,this should

prompt consideration of an alternative cause . If the effusion is not

associated with pneumonia, the child may be asymptomatic until the effusion

becomes sufficiently large to cause dyspnea or orthopnea13.On this case, patient

came with the complaint of shortness of breath which is not related to activity and

weather. Besides that, Os also complaint cough with sputum production. Fever

was also found for the past 1 week where fever is difficult to reduce even with

fever medicine.

Diagnosis

26

Chest radiography in the posteroanterior position is the primary tool for

diagnosing pleural effusion. Obliteration of the costophrenic sinus is the earliest

diagnostic sign of the effusion (in adults, at least 200 mL of fluid must present).

Because the posteroanterior view may be inadequate, a lateral decubitus film may

provide information about the quality and the quantity (as little as 50 mL) of the

effusion, allowing evaluation of the underlying parenchyma. Ultrasonography can

differentiate pleural thickening from effusion, detect the amount of fluid, and

allow distinction between nonaerated lung and pleural fluid. It helps to identify

the best site for thoracentesis or insertion of a thoracostomy tube, detects

loculations, and can determine the quality of the effusion. Multiple echogenic foci

on ultrasonography indicate exudate or empyema. Computed tomography (CT) is

extremely helpful in evaluating the pleura and underlying parenchyma. Pleural

thickening, a mass, or a foreign body is readily apparent. It is also useful for

assessing the location and volume of fluid and lung parenchyma (pneumonia,

bronchiectasis, abscess, or pneumatocele, especially in the chest that has opacified

hemithorax). Magnetic resonance imaging has no advantage over CT in evaluating

pleural disorders1. On this case, chest X-ray and CT scan was made together with

tapping of pleural fluid and its culture. Massive sinister pleural effusion was

found from the chest X-ray.

Treatment

The treatment of empyema (complicated parapneumonic effusion) in

children begins with conservative therapy. The initial treatment is administration

of antibiotics directed at the underlying infection and drainage of infected fluid by

thoracentesis or by closed thoracostomy tube. Until the condition is diagnosed,

broad-spectrum antibiotics are warranted due to the high morbidity and mortality

associated with empyema. All cases should be treated with intravenous antibiotics

and must include cover for Streptococcus pneumoniae. Where possible, antibiotic

choice should be guided by microbiology results. If a child has significant pleural

infection, a drain should be inserted at the outset and repeated taps are not

recommended2. On this case, patient was given ceftriaxone antibiotics at the early

27

of administration but then the antibiotic was changed to meropenem when the

result of culture came out. Besides that, water sealed drainage (WSD) insertion

was made to remove the pleural fluid.

SUMMARY

MA, a 1 year and 3 months old boy, with a BW 9 Kg and BH 76 cm, was

admitted to emergency room in Haji Adam Malik Hospital on September 6th 2015

with a complain of dyspnea that have been experiencing this for the past 2 days.

Patient also experienced cough (+) since 1 weeks ago with the production of

28

sputum (+), fever (+) since 1 weeks ago, rises and drop and hard to be reduced

with fever medication. Patient treated with O2 nasal canule, pracetamol,

ceftriaxone, meropenem, ambroxol, salbutamol and chest tube insertion (WSD).

REFERENCE

1. Ori Efrati and Asher Barak. Pleural Effusions in the Pediatric Population. The American Academy of Pediatrics. 2002, December 2012. http://pedsinreview.aappublications.org/content/23/12/417.full

http://pedsinreview.aappublications.org/content/23/12/417.full

http://pedsinreview.aappublications.org/search?author1=Asher+Barak&sortspec=date&submit=Submit

http://pedsinreview.aappublications.org/search?author1=Ori+Efrati&sortspec=date&submit=Submit

29

2. BTS guidelines for the management of pleural infection in Children I M Balfour-Lynn, E Abrahamson, G Cohen, J Hartley, S King, D Parikh, D Spencer, A H Thomson, D Urquhart, on behalf of the Paediatric Pleural Diseases Subcommittee of the BTS Standards of Care Committee Thorax 2005;60(Suppl I):i1–i21. doi: 10.1136/thx.2004.030676

3. Najib M. Rahman and Stephen J. Chapman. Oxford Pleural Diseases Unit, Oxford Centre for Respiratory Medicine, Churchill Hospital Oxford, UK. 2005, January 7.

4. Light RW. Pulmonary Disorders. 2014 September. Available from http://www.merckmanuals.com/professional/pulmonary-disorders/mediastinal-and-pleural-disorders/pleural-effusion.

5. Alkrinawi S, Chernick V. Pleural fluid in hospitalized pediatric patients. American Academy of Pediatrics. Clin Pediatr.1996;35 :5– 9 ;2002. Available from: http://pedsinreview.aappublications.org/content/23/12/417.full

6. Light RW. Pleural Diseases. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.

7. Jaime Ferrer Sancho. Diagnosis and Treatment of Pleural Effusion. Spanish Society Of Pulmonology And Thoracic Surgery (Separ). Arch Bronconeumol. 2006;42(7):349-72.

8. Emmet E. McGrath and Paul B. Anderson. Diagnosis Of Pleural Effusion: A Systematic Approach. American Journal Of Critical Care, 2011 March. Available from: www.ajcconline.org

9. Light RW, Lee YCG, editors. Textbook of pleural diseases. London: Arnold; 2003.

10. Benjamin Wedro. Pleural effusion. Emedicine Health. 2014, April. Available from http://www.emedicinehealth.com/pleural_effusion/page8_em.htm

11. Dagnachew (Dagne) Assefa. Pediatric Pleural Effusion. 2013, August 14. Available from: http://emedicine.medscape.com/article/1003121

http://emedicine.medscape.com/article/1003121-overview

http://www.emedicinehealth.com/pleural_effusion/page8_em.htm

http://pedsinreview.aappublications.org/content/23/12/417.full



http://bmb.oxfordjournals.org/search?author1=Stephen+J.+Chapman&sortspec=date&submit=Submit

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12. Utine GE. Pediatric pleural effusions : etiological evaluation in 492 patients. The Turkish Journal of Pediatrics. 2009 ; 51: 214-219.

13. Jane Heraghty and Tom Hilliard. Guidelines for Pleural Infection in Children. Respiratory Medicine, Bristol Children’s Hospital. 2009.

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