INTRODUCTION

1.1 Background
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 patients 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.

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

exudatesNormally, 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.
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 seen in the table below.
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.

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 nailsall thought to be the result of impaired lymphatic
drainage.

Table 1 Etiology of pleural effusions

Cause
Transudate
Heart failure

Comments
- Bilateral effusions in 81%; right-sided in 12%; leftsided in 7%
- With left ventricular failure, there is increased
interstitial fluid, which crosses the visceral pleura

Cirrhosis with ascites

(hepatic hydrothorax)

and enters the pleural space

- 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

Hypoalbuminemia

Nephrotic syndrome

clinically apparent ascites

- Uncommon
- Bilateral effusions in > 90%
- Decreased intravascular oncotic pressure causing
transudation into the pleural space
- Associated with edema or anasarca elsewhere
- Usually
bilateral
effusions;
commonly
subpulmonic
- Decreased intravascular oncotic pressure plus
hypervolemia causing transudation into the pleural
space

Exudate
Pneumonia

- May be uncomplicated or loculated and/or purulent

(parapneumonic effusion)

(empyema)
- Thoracentesis necessary to differentiate
- Effusion usually unilateral and ipsilateral to

Tuberculosis

parenchymal infiltrates if present

- Effusion due to hypersensitivity reaction to TB

Cancer

protein
- Pleural fluid TB cultures positive in < 20%
- Most commonly lung cancer, breast cancer, or
lymphoma but possible with any tumor metastatic
to pleurae
- Typically causing dull, aching chest pain

Pulmonary embolism

Uremia

- Effusion present in about 30%:

- Almost always exudative; bloody in < 50%
- Pulmonary embolism suspected when dyspnea is
disproportionate to size of effusion
- 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
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 pericardium.
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 overlap:

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.

2.1.5 Diagnosis
Tests may need to be ordered to rule out immune dysfunction or other
underlying systemic or local pulmonary disorders that cause empyema.
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:

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 useful.
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 result.)
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 titer.
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
be helpful in interpreting results of pleural fluid analysis. If chylous effusion is
suspected, serum cholesterol and triglyceride levels should be obtained.
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.
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 follows:

Pleural fluidtoserum lactate dehydrogenase (LDH) ratio of more than 0.6

Pleural fluidtoserum 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
follows:

Low pleural glucose level (< 60 mg/dL) or pleural fluidtoserum 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 fluidtoserum LDH ratio of 1 and pleural fluidtoserum 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,
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).

*Based on presence of fever, weight loss, history of cancer, or other suggestive

symptoms.

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 3) to cover the most common pathogens for pneumonia for the
childs 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 weeks.
Tabel 2 Common organism causing Parapneumonic effusion in children and
corresponding empiric antibiotic therapy
Age
0 to 6 mon

7 to 12 mon

13 to 24 mon

2 to 5 y

6 to 12 y

13 to 18 y

Predominant pathogens
Gram-negative rods*
Staphylococcus aureus
Streptococcus
Haemophilus influenzae
Pneumococcus
Streptococcus
H. Influenzae
Pneumococcus
S. aureus
H Influenzae
Pneumococcus
S. aureus
Streptococcus
Anaerobes
Pneumococcus
S. aureus
Streptococcus
Anaerobes
Pneumococcus

Therapy
Nafcillin,

gentamicin,

and

ampicilin
Nafcilin and cefuroxime

Cefuroxime, clindamycin

Cefuroxime and clindamycin

or imipenem

Cefuroxime and clindamycin

or imipenem
Nafcilin or cefuroxime plus

S. aureus
Anaerobes

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 following:
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 patients
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 include:
Poor drainage despite an appropriately positioned chest tube
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
thickening.
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.

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 parents medication:
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:

37.8C, 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
Thorax

: Lymph node enlargement (-)

: 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
(-/-)

Abdomen : Supple, normal peristaltic, liver normal

Extremities : Pulse 136 bpm regular, p/v adequate, warm acral, CRT
< 3, clubbing finger(-).

Differential diagnosis
Working diagnosis

Laboratory finding

:
: Left pleural effusion + suspect of sepsis

Complete blood analysis (September 6th , 2015)

Test
Hemoglobin
Erythrocyte
Leucocyte
Thrombocyte
Hematocrite
Eosinophil
Basophil
Neutrophil
Lymphocyte
Monocyte
Neutrophil absolute
Lymphocyte absolute
Monocyte absolute
Eosinophyl absolute
Basophyl absolute
MCV
MCH
MCHC
RDW
Morphology:

Result
8.10
3.43
39.53
536
25.80
0.30
1.300
66.20
23.40
9.20
11.41
4.99
1.39
0.18
0.16
75.20
23.60
31.40
15.70

Unit
g%
106/mm3
103/mm3
103/mm3
%
%
%
%
%
%
103/L
103/L
103/L
103/L
103/L
fL
Pg
g%
%

Referral
12.0-14.4
4.40-4.48
4.5-13.5
150-450
37-41
1-6
0-1
37-80
20-40
2-8
2.4-7.3
1.7-5.1
0.2-0.6
0.10-0.30
0-0.1
81-95
25-29
29-31
11.6-14.8

Erythrocyte: anemia hipokrom microcyte

Leukocyte:

leukocytosis

Trombocyte: trombocytosis

Clinical Chemistry
Test

Result

Unit

Referral

87.10

mg/dL

< 200

132

mEq/L

135-155

Kalium
3.8
Chloride
101
Blood Arterial Gas Analyse

mEq/L
mEq/L

3.6-5.5
96-106

Carbohydrate Metabolism
Blood Glucose
Electrolite
Natrium

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

Therapy
1.
2.
3.
4.
5.
6.
7.

O2 nasal canule 1 liter/i

IVFD D5% Nacl 0,45% 4cc/hour
Inj Ceftriaxon 450 mg/12 jam /iv skin test
Paracetamol 3x120mg
Diet Peadsure 100cc/3hour/NGT
Correction of hipoalbuminemia
Consul to the respirology division

Follow Up:
6th September 2015
S

Dyspnea (+), Sensorium: CM, T: 38,1 oC, Left

pleural
cough
(+), BW: 9 kg BH: 76cm
effusion + Susp.
fever (+)
Sepsis
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

P
- 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

-/-, Slem (+)

Dipstick
result

Abdomen: Seopel, Normal

peristaltic, Hepar unpalpable,
Lien: unpalpable.

Urine

Extremities: Pulse: 120x/i,

regular, adequate pressure and
volume, warm, CRT < 3

7th September 2015- 8th September 2015

S

Dyspnea (+), Sensorium: CM, T: 38,3 oC, Left

pleural
cough
(+), BW: 9 kg BH: 76cm
effusion + Susp.
fever (+)
Sepsis
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: 126x/i, systolic
murmur(-), RR: 44x/i, Ronchi
-/-, Slem (+/+)
Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 120x/i,
regular, adequate pressure and
volume, warm, CRT < 3

9th September 2015 10th September

P
- 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

S
Dyspnea
cough
fever (+)

(+), Sensorium: CM, T: 37,6 oC, Left

pleural - O2 nasal kanul
(+), BW: 9 kg BH: 76cm
effusion + Susp.
1l/i
Sepsis
- Threeway
Head: eye reflect +/+, conj
- Inj. Ceftriaxone
palpebral inferior pale -/-,
450 mg / 12
mouth/nose/ear: normal.
jam / IV
- Paracetamol Syr.
Neck: JVP R+2 H2O
3 x cth I (120
mg)
Thorax: symetris fusiformis,
- Diet
pediasure
retraction
(+), epigastrial,
100
cc
/ 3 jam/
weaken breathing sound on left
NGT
lung, HR: 120x/i, systolic
murmur(-), RR: 40x/i, Ronchi
-/-.
Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 120x/i,
regular, adequate pressure and
volume, warm, CRT < 3

11 September 2015-13 September 2014

S
Dyspnea
cough
fever (+)

(+), Sensorium: CM, T: 37,8 oC, Left

pleural - O2 nasal kanul
(+), BW: 9 kg BH: 76cm
effusion + Susp.
1l/i
Sepsis
- Threeway
Head: eye reflect +/+, conj
- Inj. Ceftriaxone
palpebral inferior pale -/-,
450 mg / 12
mouth/nose/ear: normal.
jam / IV
- Paracetamol Syr.
Neck: JVP R+2 H2O
3 x cth I (120
mg)
Thorax: symetris fusiformis,
Diet
pediasure
retraction
(+), epigastrial,
100 cc / 3 jam/
weaken breathing sound on left
lung, HR: 110x/i, systolic

murmur(-), RR: 40x/i, Ronchi

-/-.

NGT

Abdomen: Seopel, Normal

peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 116x/i,
regular, adequate pressure and
volume, warm, CRT < 3
Mantoux result: Induration 0
mm

14 September 2015
S
Dyspnea
cough
fever (+)

(+), Sensorium: CM, T: 38,3 oC, Left

pleural
(+), BW: 9 kg BH: 76cm
effusion + Susp.
Sepsis
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: 110x/i, systolic
murmur(-), RR: 40x/i, Ronchi
-/-.
Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 116x/i,
regular, adequate pressure and
volume, warm, CRT < 3

15 September 2015

P
- O2 nasal kanul
1l/i
- Threeway
- Inj.
Ampicilin
450mg/6jam/IV
- Inj. Ceftriaxone
450 mg / 12
jam / IV
- Paracetamol Syr.
3 x cth I (120
mg)
- Diet
pediasure
100 cc / 3 jam
Keluar
hasil
kultur
:
Klebsiella
pneumonia
Antibiotik
Inj.Ceftiaxon
changed
to
Inj.Meropenem
350 mg/8jam/IV

S
Dyspnea
cough
fever (-)

(+), Sensorium: CM, T: 37,1oC, Left masif pleural - O2 nasal kanul

(+), BW: 9 kg BH: 76cm
effusion + Sepsis
1l/i
ec
Klebsiella - Inj. Meropenem
Head: eye reflect +/+, conj pneumonia
350 mg / 8 jam /
palpebral inferior pale -/-,
IV
mouth/nose/ear: normal.
- Paracetamol Syr.
3 x cth I (120
Neck: JVP R+2 H2O
mg)
Diet
pediasure
Thorax: symetris fusiformis,
100 cc / 3 jam/
retraction (-), weaken breathing
NGT
sound on left lung, HR: 110x/i,
systolic murmur(-), RR: 40x/i,
Dari Respirologi:
Ronchi -/-.
-Ambroxol
Abdomen: Seopel, Normal
2x2,5cc
peristaltic, Hepar unpalpable,
-Salbutamol
Lien: unpalpable.
3x0,5mg
Extremities: Pulse: 116x/i,
regular, adequate pressure and
volume, warm, CRT < 3

-Rencana tapping
cairan pleura

16 September 2015-17 September 2015

S
Dyspnea
cough
fever (-)

(+), Sensorium: CM, T: 37,1oC, Left masif pleural - O2 nasal kanul

(+), BW: 9 kg BH: 76cm
effusion + Sepsis
1l/i
ec
Klebsiella - Inj. Meropenem
Head: eye reflect +/+, conj pneumonia
350 mg / 8 jam /
palpebral inferior pale -/-,
IV
mouth/nose/ear: normal.
- Paracetamol Syr.
3 x cth I (120
Neck: JVP R+2 H2O
mg)
- Diet
pediasure
Thorax: symetris fusiformis,
100
cc
/ 3 jam/
retraction (-), weaken breathing
NGT
sound on left lung, HR: 110x/i,
-Ambroxol
systolic murmur(-), RR: 40x/i,
2x2,5cc
Ronchi -/-.
-Salbutamol
Abdomen: Seopel, Normal

peristaltic, Hepar unpalpable,

Lien: unpalpable.

3x0,5mg
Dilakukan
tapping
cairan
pleura
dan
diperiksakan ke
lab
Dikonsul
ke
bedah thorax
Jawapan Konsul:
insersion of chest
tube emergency
dan konsul ke
anastesi
Jawapan
anastesi: resiko
tinggi
dan
penjadwalan
untuk tindakan
thoraks
Dilakukan
pemasangan
WSD

Extremities: Pulse: 116x/i,

regular, adequate pressure and
volume, warm, CRT < 3

18 September 2015-19 September 2015

S

Dyspnea (+), Sensorium: CM, T: 37,1oC,

cough
(+), BW: 9 kg BH: 76cm
fever (+)
Head: eye reflect +/+, conj
palpebral inferior pale -/-,
mouth/nose/ear: normal.
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

Post chest tube

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

- O2 nasal kanul 1l/i

- Inj. Meropenem 350 mg
/ 8 jam / IV
- Paracetamol Syr. 3 x cth
I (120 mg)
- Diet pediasure 100 cc /
3 jam/ NGT
-ambroxol 2x2,5cc
Salbutamol 3x0,5mg
Transfusi
Cairan dari paru tampak
warna
kemerahan.Kesan:cairan
tidak mengalir lagi
Rencana
CT
scan
thoraks non kontras

peristaltic,
unpalpable,
unpalpable.

Hepar
Lien:

Extremities: Pulse: 116x/i,

regular, adequate pressure
and volume, warm, CRT <
3

20 September 2015-22 September 2015

S
Dyspnea
cough
fever (+)

(+), Sensorium: CM, T: 37,1oC, Efusi pleura (s) - O2 nasal kanul

(+), BW: 9 kg BH: 76cm
para pneumonia ec
1l/i
Klebsiella
- Inj. Meropenem
Head: eye reflect +/+, conj pneumonia
350 mg / 8 jam /
palpebral inferior pale -/-,
IV
mouth/nose/ear: normal.
- ASI ad libitum ?
- Paracetamol Syr.
Neck: JVP R+2 H2O
3 x cth I (120
mg)
Thorax: symetris fusiformis,
- Diet
pediasure
retraction (-), weaken breathing
100
cc
/ 3 jam/
sound on left lung, HR: 110x/i,
NGT
systolic murmur(-), RR: 40x/i,
-ambroxol
Ronchi -/-.
2x2,5cc
Abdomen: Seopel, Normal
Salbutamol
peristaltic, Hepar unpalpable,
3x0,5mg
Lien: unpalpable.
Kultur
cairan
pleura:
Extremities: Pulse: 116x/i,
Klebsiella
regular, adequate pressure and
pneumonia
volume, warm, CRT < 3
Lanjut
dengan
terapi
meropenem

23 September 2015-26 September 2015

S

Dyspnea
cough
fever (-)

(+), Sensorium: CM, T: 37,1oC, Efusi pleura (s) - O2 nasal kanul

(+), BW: 9 kg BH: 76cm
para pneumonia ec
1l/i
Klebsiella
- Inj. Meropenem
Head: eye reflect +/+, conj pneumonia
350 mg / 8 jam /
palpebral inferior pale -/-,
IV
mouth/nose/ear: normal.
-Ambroxol
2x2,5cc
Neck: JVP R+2 H2O
Salbutamol
3x0,5mg
Thorax: symetris fusiformis,
- Diet
pediasure
retraction (-), weaken breathing
100
cc
/ 3 jam/
sound on left lung, HR: 110x/i,
NGT
systolic murmur(-), RR: 40x/i,
Ronchi -/-.
Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 116x/i,
regular, adequate pressure and
volume, warm, CRT < 3

DISCUSSION

SUMMARY

REFERENCE