Lapkas EP Edit

INTRODUCTION1.1 BackgroundPleural 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.1Parapneumonic 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.2Parapneumonic 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.11.2. 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 arepneumonia, 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

CauseComments

Transudate

Heart failure Bilateral effusions in 81%; right-sided in 12%; left-sided in 7%

With left ventricular failure, there is increased interstitial fluid, which crosses the visceral pleura and enters the pleural space

Cirrhosis with ascites (hepatic hydrothorax) Right-sided effusions in 70%; left-sided in 15%; bilateral in 15%

Ascitic fluid migration to the pleural space through diaphragmatic defects

Effusion present in about 5% of patients with clinically apparent ascites

Hypoalbuminemia Uncommon

Bilateral effusions in > 90%

Decreased intravascular oncotic pressure causing transudation into the pleural space

Associated with edema or anasarca elsewhere

Nephrotic syndrome Usually bilateral effusions; commonly subpulmonic

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

Exudate

Pneumonia (parapneumonic effusion) May be uncomplicated or loculated and/or purulent (empyema)

Thoracentesis necessary to differentiate

Tuberculosis Effusion usually unilateral and ipsilateral to parenchymal infiltrates if present

Effusion due to hypersensitivity reaction to TB protein

Pleural fluid TB cultures positive in < 20%

Cancer Most commonly lung cancer, breast cancer, or lymphoma but possible with any tumor metastatic to pleurae

Typically causing dull, aching chest pain

Pulmonary embolism Effusion present in about 30%:

Almost always exudative; bloody in < 50%

Pulmonary embolism suspected when dyspnea is disproportionate to size of effusion

Uremia Effusion in about 3%

In > 50%, symptoms secondary to effusion: Most commonly fever (50%), chest pain (30%), cough (35%), and dyspnea (20%)

Diagnosis of exclusion

2.1.3 Clinical manifestation

Respiratory symptoms in the presence of fluid in the pleural space are common in children. When the underlying cause is pneumonia, the predominant symptoms are cough, fever, chills, and dyspnea. If the effusion is not associated with pneumonia, the child may be asymptomatic until the effusion becomes sufficiently large to cause dyspnea or orthopnea. Children who have neurologic impairments are more likely to aspirate secretions or gastric content and develop anaerobic infections, which cause a more insidious onset of pneumonia and effusion. Older children may complain of a sharp pleuritic pain with inspiration or cough, which is due to stretching of the parietal pleura. As the effusion increases and separates the pleural membranes, pleuritic pain becomes a dull ache and disappears. Specific signs indicating pleural effusion are much more difficult to elicit in the infant or the young child. Dullness to percussion and decreased breath sounds over the affected area almost always are present, but they can be 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 StagingIn 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

AgePredominant pathogensTherapy

0 to 6 monGram-negative rods*Staphylococcus aureus

StreptococcusNafcillin, gentamicin, and ampicilin

7 to 12 monHaemophilus influenzae

Pneumococcus

StreptococcusNafcilin and cefuroxime

13 to 24 monH. Influenzae

Pneumococcus

S. aureusCefuroxime, clindamycin

2 to 5 yH Influenzae

Pneumococcus

S. aureus

Streptococcus

AnaerobesCefuroxime and clindamycin or imipenem

6 to 12 yPneumococcus

S. aureus

Streptococcus

AnaerobesCefuroxime and clindamycin or imipenem

13 to 18 yPneumococcus

S. aureus

AnaerobesNafcilin or cefuroxime plus clindamycin

* Pseudomonas, Eschericia coli, Proteus, KlebsiellaPrompt 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. influenzaeWhen 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 ComplicationComplications 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 REPORT3.1 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 completeHistory 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: Lymph node enlargement (-) Thorax : Symmetrical fusiform, retraction (+) epigastrial, Cor S1, S2 reguler, Weak breathing sound on the left lung.HR: 136 bpm, regular, murmur (-)

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

(-/-)

Abdomen : Supple, normal peristaltic, liver normal Extremities : Pulse 136 bpm regular, p/v adequate, warm acral, CRT < 3, clubbing finger(-). Differential diagnosis : Working diagnosis: Left pleural effusion + suspect of sepsis Laboratory findingComplete blood analysis (September 6th , 2015)

TestResultUnitReferral

Hemoglobin8.10g%12.0-14.4

Erythrocyte3.43106/mm34.40-4.48

Leucocyte39.53103/mm34.5-13.5

Thrombocyte536103/mm3150-450

Hematocrite25.80%37-41

Eosinophil0.30%1-6

Basophil1.300%0-1

Neutrophil66.20%37-80

Lymphocyte23.40%20-40

Monocyte9.20%2-8

Neutrophil absolute11.41103/L2.4-7.3

Lymphocyte absolute4.99103/L1.7-5.1

Monocyte absolute1.39103/L0.2-0.6

Eosinophyl absolute0.18103/L0.10-0.30

Basophyl absolute0.16103/L0-0.1

MCV75.20fL81-95

MCH23.60Pg25-29

MCHC31.40g%29-31

RDW15.70%11.6-14.8

Morphology:Erythrocyte:anemia hipokrom microcyte

Leukocyte:

leukocytosis

Trombocyte: trombocytosisClinical Chemistry

TestResultUnitReferral

Carbohydrate Metabolism

Blood Glucose87.10mg/dL< 200

Electrolite

Natrium132mEq/L135-155

Kalium3.8mEq/L3.6-5.5

Chloride101mEq/L96-106

Blood Arterial Gas Analyse

Ph7.4307.35-7.45

pCO230.0mmHg38-42

pO2193.0mmHg85-100

Bicarbonate (HCO3)19.9mmol/L22-26

Total CO220.8mmol/L19-25

base excess-3.9mmol/L(-2) (+4)

O2 Saturation100.0mmol/L95-100

Therapy:1. O2 nasal canule 1 liter/i2. IVFD D5% Nacl 0,45% 4cc/hour3. Inj Ceftriaxon 450 mg/12 jam /iv ( skin test4. Paracetamol 3x120mg5. Diet Peadsure 100cc/3hour/NGT6. Correction of hipoalbuminemia7. Consul to the respirology division

Follow Up:

6th September 2015

SOAP

Dyspnea (+), cough (+), fever (+)Sensorium: CM, T: 38,1 oC, BW: 9 kg BH: 76cm

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

Neck: JVP R+2 H2O

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

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

Left pleural effusion + Susp. Sepsis O2 nasal kanul 1l/i

IVFD D5% 4cc/ jam

Inj. Ceftriaxone 450 mg / 12 jam / IV

Paracetamol Syr. 3 x cth I (120 mg)

Diet pediasure 100 cc / 3 jam/ NGT

Hipoalbuminemia correction

Consul respirology division

Dipstick Urine result

7th September 2015- 8th September 2015SOAP


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.



IVFD D5% 4cc/ jam




Hipoalbuminemia correction

9th September 2015 10th SeptemberSOAP


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 -/-.




Threeway




11 September 2015-13 September 2014SOAP



Neck: JVP R+2 H2O




Mantoux result: Induration 0 mmLeft pleural effusion + Susp. Sepsis O2 nasal kanul 1l/i

Threeway




14 September 2015SOAP



Neck: JVP R+2 H2O





Threeway

Inj. Ampicilin 450mg/6jam/IV Inj. Ceftriaxone 450 mg / 12 jam / IV


Diet pediasure 100 cc / 3 jamKeluar hasil kultur : Klebsiella pneumoniaAntibiotik Inj.Ceftiaxon changed to Inj.Meropenem 350 mg/8jam/IV

15 September 2015

SOAP

Dyspnea (+), cough (+), fever (-)Sensorium: CM, T: 37,1oC, BW: 9 kg BH: 76cm


Neck: JVP R+2 H2O

Thorax: symetris fusiformis, retraction (-), weaken breathing sound on left lung, HR: 110x/i, systolic murmur(-), RR: 40x/i, Ronchi -/-.



Left masif pleural effusion + Sepsis ec Klebsiella pneumonia O2 nasal kanul 1l/i

Inj. Meropenem 350 mg / 8 jam / IV


Diet pediasure 100 cc / 3 jam/ NGTDari Respirologi:

-Ambroxol 2x2,5cc

-Salbutamol 3x0,5mg

-Rencana tapping cairan pleura




Neck: JVP R+2 H2O




Left masif pleural effusion + Sepsis ec Klebsiella pneumonia O2 nasal kanul 1l/i



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

-Salbutamol 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


Dyspnea (+), cough (+), fever (+)Sensorium: CM, T: 37,1oC, BW: 9 kg BH: 76cm


Neck: JVP R+2 H2O




Post chest tube insersion a/i efusi pleura massif sinistra + Sepsis ec Klebsiella pneumonia O2 nasal kanul 1l/i



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

20 September 2015-22 September 2015

SOAP

Dyspnea (+), cough (+), fever (+)Sensorium: CM, T: 37,1oC, BW: 9 kg BH: 76cm


Neck: JVP R+2 H2O




Efusi pleura (s) para pneumonia ec Klebsiella pneumonia O2 nasal kanul 1l/i

Inj. Meropenem 350 mg / 8 jam / IV ASI ad libitum ? Paracetamol Syr. 3 x cth I (120 mg)

Diet pediasure 100 cc / 3 jam/ NGT-ambroxol 2x2,5cc

Salbutamol 3x0,5mg

Kultur cairan pleura: Klebsiella pneumoniaLanjut dengan terapi meropenem

23 September 2015-26 September 2015

SOAP



Neck: JVP R+2 H2O




Efusi pleura (s) para pneumonia ec Klebsiella pneumonia O2 nasal kanul 1l/i

Inj. Meropenem 350 mg / 8 jam / IV -Ambroxol 2x2,5cc

Salbutamol 3x0,5mg


DISCUSSIONSUMMARY

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