Lapkas Paru

CHAPTER 1
BACKGROUND
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 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

CHAPTER 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
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 nails—all thought to be the
result of impaired lymphatic drainage.

Cause
Transudate
Heart failure

Comments
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

Cause

Comments
pleural space
Right-sided effusions in 70%; left-sided in 15%; bilateral
in 15%

Cirrhosis with ascites
(hepatic hydrothorax)

Ascitic fluid migration to the pleural space through
diaphragmatic defects
Effusion present in about 5% of patients with clinically
apparent ascites
Uncommon
Bilateral effusions in > 90%

Hypoalbuminemia

Decreased intravascular oncotic pressure causing
transudation into the pleural space
Associated with edema or anasarca elsewhere
Usually bilateral effusions; commonly subpulmonic

Nephrotic syndrome
Hydronephrosis

Decreased intravascular oncotic pressure plus
hypervolemia causing transudation into the pleural space
Retroperitoneal urine dissection into the pleural space,
causing urinothorax
Increases IV hydrostatic pressure

Constrictive pericarditis In some patients, accompanied by massive anasarca and
ascites due to a mechanism similar to that for hepatic
hydrothorax
Atelectasis
Increases negative intrapleural pressure
Mechanism similar to that for hepatic hydrothorax
Peritoneal dialysis
Pleural fluid with characteristics similar to dialysate
Encasement with fibrous peel increasing negative
intrapleural pressure
Trapped lung
Systemic capillary leak
syndrome
Myxedema
Exudate
Pneumonia

May be exudative or borderline effusion
Rare
Accompanied by anasarca and pericardial effusion
Effusion present in about 5%
Usually transudate if pericardial effusion is also present;
either transudate or exudate if pleural effusion is isolated
May be uncomplicated or loculated and/or purulent

Cause
(parapneumonic
effusion)
Cancer

Comments
(empyema)
Thoracentesis necessary to differentiate
Most commonly lung cancer, breast cancer, or lymphoma
but possible with any tumor metastatic to pleurae
Typically causing dull, aching chest pain
Effusion present in about 30%:

Pulmonary embolism

Viral infection

Coronary artery bypass
surgery

Almost always exudative; bloody in < 50%
Pulmonary embolism suspected when dyspnea is
disproportionate to size of effusion
Effusion usually small with or without parenchymal
infiltrate
Predominantly systemic symptoms rather than
pulmonary symptoms
Effusions left-sided or larger on the left in 73%; bilateral
and equal in 20%; right-sided or larger on the right in 7%
> 25% of the hemithorax filled with fluid 30 days
postoperatively in 10% of patients
Bloody effusions related to postoperative bleeding likely
to resolve
Nonbloody effusions likely to recur; etiology unknown
but probably with an immunologic basis
Effusion usually unilateral and ipsilateral to parenchymal
infiltrates if present

TB

Effusion due to hypersensitivity reaction to TB protein
Pleural fluid TB cultures positive in < 20%
Effusion in 1–2%

Sarcoidosis

Uremia

Extensive parenchymal sarcoid and often extrathoracic
sarcoid
Pleural fluid predominantly lymphocytic
Effusion in about 3%
In > 50%, symptoms secondary to effusion: Most

Cause

Comments
commonly fever (50%), chest pain (30%), cough (35%),
and dyspnea (20%)
Diagnosis of exclusion
Causes sympathetic subpulmonic effusion

Infradiaphragmatic
abscess

HIV infection

RA

Neutrophils predominant in pleural fluid
pH and glucose normal
Many possible etiologic factors: Pneumonias
(parapneumonic), including Pneumocystis jirovecii
pneumonia, other opportunistic infections, TB, and
pulmonary Kaposi sarcoma
Effusion typically in elderly men with rheumatoid
nodules and deforming arthritis
Must differentiate from parapneumonic effusion
Effusion possibly first manifestation of SLE

SLE

Drugs

Ovarian hyperstimulation
syndrome

Pancreatitis

Common with drug-induced SLE
Diagnosis established by serologic tests of blood, not of
pleural fluid
Many drugs, most notably bromocriptine, dantrolene,
nitrofurantoin, IL-2 (for treatment of renal cell cancer
and melanoma), and methysergide
Syndrome occurring as a complication of ovulation
induction with human chorionic gonadotropin (hCG) and
occasionally clomiphene
Effusion developing 7–14 days after hCG injection
Effusion right-sided in 52%; bilateral in 27%
Acute: Effusion present in about 50%: Bilateral in 77%;
left-sided in 16%; right-sided in 8%
Effusion due to transdiaphragmatic transfer of the
exudative inflammatory fluid and diaphragmatic
inflammation
Chronic: Effusion due to sinus tract from pancreatic
pseudocyst through diaphragm into pleural space

Cause

Comments
Predominantly chest symptoms rather than abdominal
symptoms

Superior vena cava
syndrome

Patients presenting with cachexia that resembles cancer
Effusion usually caused by blockage of intrathoracic
venous and lymphatic flow by cancer or thrombosis in a
central catheter
May be an exudate or a chylothorax
Patients extremely sick

Esophageal rupture

Medical emergency
Morbidity and mortality due to infection of the
mediastinum and pleural space
Effusion occurring > 30 yr after initial exposure

Benign asbestos pleural
effusion

Frequently asymptomatic
Tends to come and go
Must rule out mesothelioma
Mechanism similar to that for hepatic hydrothorax

Benign ovarian tumor
(Meigs syndrome)

Surgery sometimes indicated for patients with ovarian
mass, ascites, and pleural effusion
For diagnosis, disappearance of ascites and effusion
postoperatively required
Triad of pleural effusion, lymphedema, and yellow nails,
sometimes appearing decades apart

Yellow nail syndrome

Pleural fluid with relatively high protein but low LDH
Tendency for effusion to recur
No pleuritic chest pain

Effusions with no obvious cause are often due to occult pulmonary emboli, TB,
or cancer. Etiology is unknown for about 15% of effusions even after extensive
study; many of these effusions are thought to be due to viral infection.

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 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 follows:


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, 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
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 weeks.
Tabel 1 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 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 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.

CHAPTER III
CASE REPORT

3.1 Objective
The objective of this paper is to report a case of 1 years and 3 months old
boy with a diagnosis of pleural effusion.
3.2 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: 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
Thorax

:Lymph node enlargement (-)
: Symmetrical fusiform, retraction (+) epigastrial, Cor

S1,S2reguler, 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(-).
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
Leukocyte:

leukocytosis

Trombocyte: trombocytosis
Clinical Chemistry
Test

Result

Unit

Referral

87.10

mg/dL

< 200

Carbohydrate Metabolism
Blood Glucose

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

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.

7.35-7.45

:

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

O

A

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
-/-, Slem (+/+)
Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 120x/i,
regular, adequate pressure and
volume, warm, CRT < 3’’

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
Dipstick
Urine
result

7th September 2015
S

O

A

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 (+/+)

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

Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 120x/i,
regular, adequate pressure and
volume, warm, CRT < 3’’

8th September 2015
S
Dyspnea
cough
fever (+)

O

A

P

(+), Sensorium: CM, T: 39,8 oC, Left
pleural - O2 nasal kanul
(+), BW: 9 kg BH: 76cm
effusion + Susp.
1l/i
Sepsis
- IVFD D5% 4cc/
Head: eye reflect +/+, conj
jam
palpebral inferior pale -/-,
- Inj. Ceftriaxone
mouth/nose/ear: normal.
450 mg / 12
jam / IV
Neck: JVP R+2 H2O
- Paracetamol Syr.
3 x cth I (120
Thorax: symetris fusiformis,
mg)
retraction
(+), epigastrial,
- Diet
pediasure
weaken breathing sound on left
100
cc
/ 3 jam/
lung, HR: 120x/i, systolic

murmur(-), RR: 42x/i, Ronchi
-/-.

NGT

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
S
Dyspnea
cough
fever (+)

O

A

P

(+), 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
S
Dyspnea
cough
fever (+)

O

A

P

(+), 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
NGT
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’’
Mantoux result: Induration 0
mm

12 September 2015 – 13 September 2014
S
Dyspnea
cough

O

A

P

(+), Sensorium: CM, T: 38,6 oC, Left
pleural - O2 nasal kanul
(+), BW: 9 kg BH: 76cm
effusion + Susp.
1l/i

fever (+)

Head: eye reflect +/+, conj Sepsis
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 -/-.

- Threeway
- Inj. Ceftriaxone
450 mg / 12
jam / IV
- Paracetamol Syr.
3 x cth I (120
mg)
- Diet
pediasure
100 cc / 3 jam/
NGT

Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 116x/i,
regular, adequate pressure and
volume, warm, CRT < 3’’

14 September 2015
S
Dyspnea
cough
fever (+)

O

A

(+), 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,

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

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

changed
to
Inj.Meropenem
350 mg/8jam/IV

15 September 2015
S
Dyspnea
cough
fever (-)

O

A

P

(+), 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,
Ronchi -/-.
Abdomen: Seopel, Normal
peristaltic, Hepar unpalpable,
Lien: unpalpable.
Extremities: Pulse: 116x/i,
regular, adequate pressure and
volume, warm, CRT < 3’’