Download doc - Lapkas Paru

Transcript
Page 1: 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

Page 2: Lapkas Paru

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

Page 3: Lapkas Paru

Cause Commentsin 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 syndromeUsually bilateral effusions; commonly subpulmonic

Decreased intravascular oncotic pressure plus hypervolemia causing transudation into the pleural space

Hydronephrosis Retroperitoneal urine dissection into the pleural space, causing urinothorax

Constrictive pericarditis

Increases IV hydrostatic pressure

In some patients, accompanied by massive anasarca and ascites due to a mechanism similar to that for hepatic hydrothorax

Atelectasis Increases negative intrapleural pressure

Peritoneal dialysisMechanism similar to that for hepatic hydrothorax

Pleural fluid with characteristics similar to dialysate

Trapped lungEncasement with fibrous peel increasing negative intrapleural pressure

May be exudative or borderline effusion

Systemic capillary leak syndrome

Rare

Accompanied by anasarca and pericardial effusionMyxedema Effusion present in about 5%

Page 4: Lapkas Paru

Cause CommentsUsually transudate if pericardial effusion is also present; either transudate or exudate if pleural effusion is isolated

Exudate

Pneumonia (parapneumonic effusion)

May be uncomplicated or loculated and/or purulent (empyema)

Thoracentesis necessary to differentiate

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

Viral infection

Effusion usually small with or without parenchymal infiltrate

Predominantly systemic symptoms rather than pulmonary symptoms

Coronary artery bypass surgery

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

TB

Effusion usually unilateral and ipsilateral to parenchymal infiltrates if present

Effusion due to hypersensitivity reaction to TB protein

Pleural fluid TB cultures positive in < 20%Sarcoidosis Effusion in 1–2%

Extensive parenchymal sarcoid and often extrathoracic

Page 5: Lapkas Paru

Cause Comments

sarcoid

Pleural fluid predominantly lymphocytic

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

Infradiaphragmatic abscess

Causes sympathetic subpulmonic effusion

Neutrophils predominant in pleural fluid

pH and glucose normal

HIV infection

Many possible etiologic factors: Pneumonias (parapneumonic), including Pneumocystis jirovecii pneumonia, other opportunistic infections, TB, and pulmonary Kaposi sarcoma

RAEffusion typically in elderly men with rheumatoid nodules and deforming arthritis

Must differentiate from parapneumonic effusion

SLE

Effusion possibly first manifestation of SLE

Common with drug-induced SLE

Diagnosis established by serologic tests of blood, not of pleural fluid

DrugsMany drugs, most notably bromocriptine, dantrolene, nitrofurantoin, IL-2 (for treatment of renal cell cancer and melanoma), and methysergide

Ovarian hyperstimulation syndrome

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%Pancreatitis Acute: Effusion present in about 50%: Bilateral in 77%;

left-sided in 16%; right-sided in 8%

Effusion due to transdiaphragmatic transfer of the

Page 6: Lapkas Paru

Cause Comments

exudative inflammatory fluid and diaphragmatic inflammation

Chronic: Effusion due to sinus tract from pancreatic pseudocyst through diaphragm into pleural space

Predominantly chest symptoms rather than abdominal symptoms

Patients presenting with cachexia that resembles cancer

Superior vena cava syndrome

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

Esophageal rupture

Patients extremely sick

Medical emergency

Morbidity and mortality due to infection of the mediastinum and pleural space

Benign asbestos pleural effusion

Effusion occurring > 30 yr after initial exposure

Frequently asymptomatic

Tends to come and go

Must rule out mesothelioma

Benign ovarian tumor (Meigs syndrome)

Mechanism similar to that for hepatic hydrothorax

Surgery sometimes indicated for patients with ovarian mass, ascites, and pleural effusion

For diagnosis, disappearance of ascites and effusion postoperatively required

Yellow nail syndrome

Triad of pleural effusion, lymphedema, and yellow nails, sometimes appearing decades apart

Pleural fluid with relatively high protein but low LDH

Tendency for effusion to recur

No pleuritic chest pain

Page 7: Lapkas Paru

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).

Page 8: Lapkas Paru

- 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

Page 9: Lapkas Paru

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:

Page 10: Lapkas Paru

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).

Page 11: Lapkas Paru

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

Page 12: Lapkas Paru

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 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 PneumococcusS. aureusStreptococcusAnaerobes

Cefuroxime and clindamycin

or imipenem

Page 13: Lapkas Paru

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 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

Page 14: Lapkas Paru

● 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.

Page 15: Lapkas Paru

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

Page 16: Lapkas Paru

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,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

Page 17: Lapkas Paru

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

Page 18: Lapkas Paru

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

Carbohydrate Metabolism

Blood Glucose 87.10 mg/dL < 200

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)

Page 19: Lapkas Paru

O2 Saturation 100.0 mmol/L 95-100

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

Page 20: Lapkas Paru

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

divisionDipstick Urine result

7th September 2015

S O A P

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

Sensorium: CM, T: 38,3 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: 126x/i, systolic

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

Page 21: Lapkas Paru

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’’

8th September 2015

S O A P

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

Sensorium: CM, T: 39,8 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: 120x/i, systolic murmur(-), RR: 42x/i, Ronchi -/-.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

Page 22: Lapkas Paru

9th September 2015 – 10th September

S O A P

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

Sensorium: CM, T: 37,6 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: 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’’

Left pleural effusion + Susp. Sepsis

- 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

11 September 2015

S O A P

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

Sensorium: CM, T: 37,8 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: 110x/i, systolic

Left pleural effusion + Susp. Sepsis

- 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

Page 23: Lapkas Paru

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 O A P

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

Sensorium: CM, T: 38,6 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 (-),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’’

Left pleural effusion + Susp. Sepsis

- 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

Page 24: Lapkas Paru

14 September 2015

S O A P

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

Sensorium: CM, T: 38,3 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: 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’’

Left pleural effusion + Susp. Sepsis

- 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 jamKeluar hasil kultur : Klebsiella pneumoniaAntibiotik 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

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,

Left masif pleural effusion + 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

Page 25: Lapkas Paru

Ronchi -/-.Abdomen: Seopel, Normal peristaltic, Hepar unpalpable, Lien: unpalpable.

Extremities: Pulse: 116x/i, regular, adequate pressure and volume, warm, CRT < 3’’