CHRONIC OBSTRUCTIVE

PULMONARY DISEASE

Created by:

Muhammad Maulana, S. Ked.

M. Adin Archietobias, S. Ked.

Preceptor:

dr. Dedy Zairus, Sp. P.

SMF PENYAKIT DALAM BAGIAN PULMONOLOGI

RUMAH SAKIT UMUM DAERAH ABDUL MOELOEK

BANDAR LAMPUNG

2014

I. PATIENT STATUS

PATIENT IDENTITY

Initial Name : Mr. T

Sex : Male

Age : 68 years old

Nationally : Indonesia (Javanese)

Marital Status : Married

Religion : Islam

Occupation : Farmer

Educational Background : Elementary School

Address : Giri Mulyo, East Lampung

ANAMNESIS

Taken from : Autoanamnesis & Alloanamnesis

Date : March 18th, 2014

Time : 14.20

Chief Complain : Dyspneu

Additional Complaint : Productive cough, Cough up blood, Bloating, Stomachache,

Arm swollen

History of The Present Illness :

Patient came to hospital and told that he has gotten a dyspneu since six months ago, and

it was getting worse a month ago. Patient also complained about his cough with mucus

when he was coughing up and it was contain blood sometimes and he also complained

about his bloating and stomachache.

Patient felt dyspneu and productive cough since six month ago. History of bleeded

cough was approved. And he has history of taking 6 months drug package and it run the

2

fourth month. He had been a smoker since 50 years ago (1 packs/day). The patient

works as a farmer and often affected by dust.

The History of Illness :

(+) Small pox (+) Malaria (-) Kidney stone(-) Chicken pox (-) Disentri (-) Hernia(-) Difthery (-) Hepatitis (-) Prostat(-) Pertusis (-) TifusAbdominalis (-) Melena(-) Measles (-) Skirofula (-) Diabetic(+) Influenza (-) Siphilis (+) Alergy(-) Tonsilitis (-) Gonore (-) T u m o r

(-) Kholera (-) Hipertension. (-) Vaskular Disease(-) Acute Rheumatoid Fever (-) Ventrikuli Ulcer (-) Operation

(-) Pneumonia (-) Duodeni Ulcer (-) Pleuritic (+) Gastritis

Family’s diseases History :

Patient didn’t know about his Family’s Disease History

Is there any family who suffer :

Patient didn’t know

SYSTEM ANAMNESE

Note of Positive Complaints beside the title

Skin

(-) Boil (-) Hair (+) Night sweat(-) Nail (-) Yellow /Werus (-) Cyanotic

(-) Others

Head

Head

(-) Trauma (-) Headache

(-) Syncope (-) Pain of the sinus

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Ear

(-) Pain (-) Tinitus(-) Secret (-) Ear disorders

(-) Deafness

Nose

(-) Trauma (-) Clogging(-) Pain (-) Nose disorders(-) Sekret (-) common cold(-) Epistaksis

Mouth

Mouth

(-) Lip (-) Tongue(-) Gums (-) Mouth disorders(-) Membrane (-) Stomatitis

Throat

(-) Throat Pain (-) Voice Change

Neck

(-) Protruding (-) Neck Pain

Cor/ Lung

(-) Chest pain (+) Dyspneu(-) Pulse (+) Hemoptoe(-) Ortopneu (+) Cough

Abdomen (Gaster/ Intestine)

(+) Puffing (-) Acites(-) Nausea (-) Hemoroid(-) Emesis (-) Diarrhea(-) Hematemesis (-) Melena(-) Disfagi (-) Pale colour of feses(+) Colic (-) Black colour of feses

(-) Nodul

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Urogenital

(-) Dysuria (-) Pyuria(-) Stranguria (-) Kolik(-) Polyuria (-) Oliguria(-) Polakysuria (-) Anuria(-) Hematuria (-) Urine retention(-) Kidney stone (-) Drip urine(-) Wet the bed (-) Prostat

Katamenis

(-) Leukorhoe (-) Bleeding(-) Other

Muscle and Neuron

(-) Anestesi (-) Hard to bite

(-) Parestesi (-) Ataksia(-) Weak muscle (-) Hipo/hiper-estesi(-) Afasia (-) Tick(-) Amnesis (-) Vertigo(-) Others (-) Disartri

(-) Convultion (-) Syncope

Extremities

(+) Edema (-) Deformitas(-) Hinge pain (-) Cyanotic

Weight

Average weight (kg) : 45kg

Height (cm) : 165cm

Present Weight : 45kg

(if the patient doesn’t know certainly)

(+) steady

(-) down

(-) up

THE HISTORY OF LIFE

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Birth place

(+) in home (-) matrinity (-) matrinity hospital

Helped by:

(+) Traditional matrinity (-) Doctor (-) Nurse (-) Others

Imunitation History (Unknown)

(-) Hepatitis (-) BCG (-) Campak (-) DPT (-) Polio Tetanus

Food History

Frequency/day : 3x/day

Amount/day : 3 times a day (health)

Variation/day : Rice, vegetables, fish

Appetite : Normal

Educational

(+) SD (-) SMP (-) SMA (-)SMK (-) Course Academy

Problem

Financial : -

Works : -

Family : -

Others : -

Body Check Up

General Check Up

Height : 165 cm

Weight : 45 kg

Blood Pressure : 100/80 mmHg

Pulse : 100x/minute

Temperature : 35,80C

Breath (Frequence&type) : 28x/minute

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Nutrition Condition : Normal, IMT 19

Consciousness : Compos Mentis

Cyanotic : (-)

General Edema : pitting oedem

The way of walk : Normal

Mobility : Active

\ The age predicyion based on check up : 70 years old

Mentality Aspects

Behavior : Normal

Nature of Feeling : Normal

The thinking of process : Normal

Skin

Color : Brown

Keloid : (-)

Pigmentasi : (-)

Hair Growth : Normal

Arteries : Touchable

Touch temperature : Afrebris

Humid/dry : Dry

Sweat : Normal

Turgor : Normal

Icterus : Anicteric

Fat Layers : Enough

Efloresensi : (-)

Edema : (+)

Others : Superior Vena Cava Syndrome appearance in the chest &

abdomen

Lymphatic Gland

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Submandibula : no enlargement

Neck : no enlargement

Supraclavicula : no enlargement

Armpit : no enlargement

Head

Face Expression : Mild Sickness appearance

Face Symmetric : Symmetric

Hair : Gray and Black

Temporal artery : Normal

Eye

Exopthalmus : (-)

Enopthalmus : (-)

Palpebra : edema (-)/(-)

Lens : Clear/Clear

Conjunctiva : Anemis -/-

Visus : Normal

Sklera : Anicteric

Ear

Deafnes : (-)

Foramen : (-)

Membrane tymphani : intak

Obstruction : (-)

Serumen : (-)

Bleeding : (-)

Liquid : (-)

Mouth

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Lip : (-)

Tonsil : (-)

Palatal : Normal

Halibsts : No

Teeth : (-)

Trismus : (-)

Farings : Unhiperemis

Liquid Layers : (-)

Tongue : Clean

Neck

JVP : Normal

Tiroid Gland : no enlargement

Limfe Gland : no enlargement

Chest

Shape : Simetric

Artery : Normal

Breast : Normal

Lung

Inspection : Left : simetric

Right : simetric

Palpation : Left : pain (-)

Right : vokal fremitus decreased, pain (-)

Percussion : Left : sonor

Right : dim

Auscultation : Left : vesiculer

Right : decreased vesicular

Cor

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Inspection : Ictus cordis seen in ICS V left midclavicula

Palpation : Ictus Cordis feel in ICS V left midclavicula

Percussion : difficult to assess

Auscultation : Heart Sound 1 & 2 Regular

Artery

Temporalic artery : No aberration

Caritic artery : No aberration

Brachial artery : No aberration

Radial artery : No aberration

Femoral artery : No aberration

Poplitea artery : No aberration

Posterior tibialis artery : No aberration

Stomach

Inspection : Flat , Symetrics

Palpation : Stomach Wall : undulation (-), pain (-)

Heart : Hepatomegali (-)

Limfe : Splenomegali (-)

Kidney : Ballotement (-)

Percussion : Shifting Dullness (-)

Auscultation : Intestine Sounds (+)

Genital (no indication)

Movement Joint

Arm Right Left

Muscle Normal Normal

Tones Normal Normal

Mass Normal Normal

Joint Normal Normal

Movement Normal Normal

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Strength Normal Normal

Heel and Leg

Wound/injury : not found

Varices : (-)

Muscle (tones&mass) : Normal

Joint : Normal

Movement : Normal

Strength/Power : Normal

Edema : (+)

Others : (-)

Reflexs

Right Left

Tendon Reflex Normal Normal

Bisep Normal Normal

Trisep Normal Normal

Pattela Normal Normal

Achiles Normal Normal

Cremaster Normal Normal

Skin Reflex Normal Normal

Patologic Reflex Not Found Not Found

Laboratory

Routine Blood

- Hb : 11,2 gr/dl

- Leukosit : 6500 /ul

- LED : 78 mm/jam

- Trombosit : 270.000

- Diff. Count

o Basofil : 0%

o Eosinofil : 0%

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o Stem : 0%

o Segment : 80%

o Limfosit : 9 %

o Monosit : 11%

Chest X-Ray

Pulmo : radioopaque in pulmo dextra, intercostal space increase

Resume

Patient came to hospital and told that he has gotten a dyspneu since six months ago, and

it was getting worse a month ago. Patient also complained about his cough with mucus

when he was coughing up and it was contain blood sometimes and he also complained

about his bloating and stomachache.

Patient felt dyspneu and productive cough since six month ago. History of bleeded

cough was approved. And he has history of taking 6 months drug package and it run the

fourth month. History of diabetic mellitus and hypertenton were denied. He had been a

smoker since 50 years ago (1 packs/day). The patient works as a farmer and often

affected by dust.

Working Diagnose

- Dextra Pleural Effusion due to Suspect Tubercullosis

Basic Diagnose

Anamnesis

- Recurrent cough with or without sputum

- History of hemaptoe

- Dyspneu

- History of taking Anti Tubecullosa Drugs

Physics Examination

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- Inspection : Simetric, Appearance of Superior Vein Cava Syndrome

- Palpation : Decreased fremitus tactil in the dextra side

- Percution : Dim sound in the dextra side

- Auscultation : Decreased of vesicular sound in the dextra side

Support Examination

LABORATORY

(RSAM March 15th 2014)

Routine blood

- Hb : 11,2 gr % (N : 13,5 – 18 gr% )

- LED : 78 mm/hour (N : 0-10 mm/hour)

- WBC : 6.500 mm³ (N : 4500 – 10.700/ul )

- Diff. Count :

Basofil : 0 % ( 0 - 1 % )Eusinofil : 0% ( 1 - 3 % )Stem : 0 % (2 — 6 %)Begment : 80% (50 — 70 %)Limfosit : 9% (20 — 40 %)Monosit : 11% (2 — 8 %)

Chemical Blood

- SGOT : 16 (6-25 u/l)

- SGPT : 10 (6-35 u/l)

- Total protein : 5,9 (6-8,5 g/dl)

- Albumin : 3 (3,5-5,0 g/dl)

- Globulin : 2,9 (2,3-3,5 g/dl)

- At the time blood glucose : 166 mg/dl (70-200 mg/dl)

- Ureum : 14 mg/dl (10-40 mg/dl)

- Creatinin : 0,6 mg/dl (0,7-1,3 mg/dl)

Roentgen Thorax AP :

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- Pulmo dextra shows radiopaque, trachea deviation and cor to the left side

Dextra Pleural Effusion.

Pre-WSD Rontgen

Post-WSD Rontgen

Differential Diagnose

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- Dextra Pleural Effusion due to malignancy

Basic Differential Diagnose

Anamnesis

- Chronic Productive Cough

- Recurrent Dyspneu

- Nocturnal sweating

- Hemaptoe

Physics Examination

- Inspection : Simetric, Appearance of Superior Vein Cava Syndrome

- Palpation : Decreased fremitus tactil in the dextra side

- Percution : Dim sound in the dextra side

- Auscultation : Decreased of vesicular sound in the dextra side

Support Check Up

- Sputum and pleura fluid culture and resistance test

- Acid-fast Bacillus (AFB) Sputum at the time - at the morning – at the time

- EKG

Treatment Plan

(1) General Treatment

- Bed Rest

- Nutrition (high calory, high protein)

(2) Special Treatment

- Medicamentosa

o O2 2-3 L/minute

o Bed rest

o High calory and protein diet

o IVFD RL 20 gtt/mnt

o Salbutamol 0,5 mg/Metyl Prednisolon 1 mg/Cetirizine ½ tab/GG 1 tab 3 x 1

cap

o Ceftriaxone 1 gr vial/ 12 h

o Ranitidin amp/12 h

o WSD

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o primary category TB therapy planning

- Non Medicamentosa

o Stop Tobacco

o Avoid Tobacco Smoke

o Activity adjustment

o Go to doctor immedietly if appear any symptoms

Prognose

Quo ad Vitam : Dubia ad bonam

Quo ad Functonam : Dubia ad malam

Quo ad Sanationam : Dubia ad malam

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II. DISCUSSION

1. Is the patient diagnosis has been correct ?

In this case, the patient had been diagnosed as a pleural effusion ec suspect TB based on

history taking, physical examination, and support examination.

a. The anamnesis :

- Breathlessness and productive cough since 6 months ago. He also said that

he had ever been productive cough, sweaty night, fever, bloating.

b. Physical examination

Conjungtiva : anemic (-/-)

Neck : Trachea deviation to the left

Chest : Shape Hemithorax dextra looks convex

Lung

Inspection : Left : hemithorax movement normal, retraction (-)

Right : hemithorax movement normal, retraction (-)

Palpation : tactil fremitus asimetris, dextra weaker than sinistra

Percussion : Dim/Sonor

Auscultation : Vesiculer decreased in dextra , Ronchi (-/-), Wheezing (-/-)

Suspect dextra pleura effusion.

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c. Supporting examination

Routine blood

- LED and segment neutrofil increased commonly on TB.

Roentgen Thorax AP :

- Pulmo dextra shows radioopaque, not look dextra contophrenicus angle, trachea

deviation and cor to the left side Dextra Pleural Effusion.

Thoracosentesis

Serohemoragic DD : TB, Malignancy, Trauma.

Cytology: no malignancy.

2. How the pathogenesis pleura effusion from this patient ?

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19

3. Is the patient treatment has been correct ?

- O2 2-3 L/minute suplly oxygen based on tidal volume.

- Bed rest preventing worse breathlessness.

- High calory and protein diet

- IVFD RL 20 gtt/mnt preventing dehidration.

- Salbutamol 0,5 mg/Metyl Prednisolon 1 mg/Cetirizine ½ tab/GG 1 tab 3 x 1 cap

for reducing breathlessness.and cough.

- Ceftriaxone 1 gr vial/ 12 h for temporary treatment for 1 week for evaluation

whether because of TB or the others bacterial. Beside that, because of thoracosentesis

for preventing infection from it.

- Ranitidin amp/12 h preventing gaster acid due to his complained about bloating

- Continue Primary category TB therapy because relapse TB is the basic of

pleura effusion from this patient.

4. How the prognosis from this patient ?

Quo ad vitam : dubia ad bonam because vital signs are still good.

Quo ad functionam : dubia ad bonam because it would indicate repeated pleura

effusion again because of TB. Of course the function of pulmo is still bad. Pleurodesis

is the definitif treatment of malignant pleural effusion.

Quo ad sanationam : dubia ad malam it can always interfere with daily activities

of the patient.

III. PLEURAL EFFUSION

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A. Overview

A pleural effusion is an abnormal collection of fluid in the pleural space

resulting from excess fluid production or decreased absorption. It is the most

common manifestation of pleural disease, with etiologies ranging from

cardiopulmonary disorders to symptomatic inflammatory or malignant diseases

requiring urgent evaluation and treatment.

A.1. Anatomy

The pleural space is bordered by the parietal and visceral pleurae. The parietal

pleura covers the inner surface of the thoracic cavity, including the mediastinum,

diaphragm, and ribs. The visceral pleura envelops all lung surfaces, including

the interlobar fissures. The right and left pleural spaces are separated by the

mediastinum.

The pleural space plays an important role in respiration by coupling the

movement of the chest wall with that of the lungs in 2 ways. First, a relative

vacuum in the space keeps the visceral and parietal pleurae in close proximity.

Second, the small volume of pleural fluid, which has been calculated at 0.13

mL/kg of body weight under normal circumstances, serves as a lubricant to

facilitate movement of the pleural surfaces against each other in the course of

respirations. This small volume of fluid is maintained through the balance of

hydrostatic and oncotic pressure and lymphatic drainage, a disturbance of which

may lead to pathology.

A.2. Etiology

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The normal pleural space contains approximately 1 mL of fluid, representing the

balance between (1) hydrostatic and oncotic forces in the visceral and parietal

pleural vessels and (2) extensive lymphatic drainage. Pleural effusions result

from disruption of this balance.

Pleural effusion is an indicator of an underlying disease process that may be

pulmonary or nonpulmonary in origin and may be acute or chronic. Although

the etiologic spectrum of pleural effusion is extensive, most pleural effusions are

caused by congestive heart failure, pneumonia, malignancy, or pulmonary

embolism. The following mechanisms play a role in the formation of pleural

effusion:

Altered permeability of the pleural membranes (eg, inflammation,

malignancy,pulmonary embolus)

Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, cirrhosis)

Increased capillary permeability or vascular disruption (eg, trauma,

malignancy, inflammation, infection, pulmonary infarction, drug

hypersensitivity, uremia, pancreatitis)

Increased capillary hydrostatic pressure in the systemic and/or pulmonary

circulation (eg, congestive heart failure, superior vena cava syndrome)

Reduction of pressure in the pleural space, preventing full lung expansion (eg,

extensive atelectasis, mesothelioma)

Decreased lymphatic drainage or complete blockage, including thoracic duct

obstruction or rupture (eg, malignancy, trauma)

Increased peritoneal fluid, with migration across the diaphragm via the

lymphatics or structural defect (eg, cirrhosis, peritoneal dialysis)

Movement of fluid from pulmonary edema across the visceral pleura

Persistent increase in pleural fluid oncotic pressure from an existing pleural

effusion, causing further fluid accumulation

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The net result of effusion formation is a flattening or inversion of the diaphragm,

mechanical dissociation of the visceral and parietal pleura, and a restrictive

ventilatory defect.

Pleural effusions are generally classified as transudates or exudates, based on the

mechanism of fluid formation and pleural fluid chemistry. Transudates result

from an imbalance in oncotic and hydrostatic pressures, whereas exudates are

the result of inflammation of the pleura or decreased lymphatic drainage. In

some cases, the pleural fluid may have a combination of transudative and

exudative characteristics.

A.3 Prognosis

The prognosis in pleural effusion varies in accordance with the condition’s

underlying etiology. However, patients who seek medical care earlier in the

course of their disease and those who obtain prompt diagnosis and treatment

have a substantially lower rate of complications than do patients who do not.

Morbidity and mortality

Morbidity and mortality of pleural effusions are directly related to cause, stage

of disease at the time of presentation, and biochemical findings in the pleural

fluid.

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Morbidity and mortality rates in patients with pneumonia and pleural effusions

are higher than those in patients with pneumonia alone. Parapneumonic

effusions, when recognized and treated promptly, typically resolve without

significant sequelae. However, untreated or inappropriately treated

parapneumonic effusions may lead to empyema, constrictive fibrosis, and sepsis.

Development of a malignant pleural effusion is associated with a very poor

prognosis, with median survival of 4 months and mean survival of less than 1

year. The most common associated malignancy in men is lung cancer, and the

most common associated malignancy in women is breast cancer. Median

survival ranges from 3-12 months, depending on the malignancy. Effusions from

cancers that are more responsive to chemotherapy, such as lymphoma or breast

cancer, are more likely to be associated with prolonged survival, compared with

those from lung cancer or mesothelioma.

Cellular and biochemical findings in the fluid may also be indicators of

prognosis. For example, a lower pleural fluid pH is often associated with a

higher tumor burden and a worse prognosis.

B. Clinical Presentation

A detailed medical history should be obtained from all patients presenting with a

pleural effusion, as this may help to establish the etiology. For example, a

history of chronic hepatitis or alcoholism with cirrhosis suggests hepatic

hydrothorax or alcohol-induced pancreatitis with effusion. Recent trauma or

surgery to the thoracic spine raises the possibility of a CSF leak. The patient

should be asked about a history of cancer, even remote, as malignant pleural

effusions can develop many years after initial diagnosis.

An occupational history should also be obtained, including potential asbestos

exposure, which could predispose the patient to mesothelioma or asbestos

24

pleural effusion. The patient should also be asked about medications they are

taking.

B.1 Clinical Manifestations

The clinical manifestations of pleural effusion are variable and often are related

to the underlying disease process. The most commonly associated symptoms are

progressive dyspnea, cough, and pleuritic chest pain.

Dyspnea

Dyspnea is the most common symptom associated with pleural effusion and is

related more to distortion of the diaphragm and chest wall during respiration

than to hypoxemia. In many patients, drainage of pleural fluid alleviates

symptoms despite limited improvement in gas exchange. Drainage of pleural

fluid may also allow the underlying disease to be recognized on repeat chest

radiographs. Note that dyspnea may be caused by the condition producing the

pleural effusion, such as underlying intrinsic lung or heart disease, obstructing

endobronchial lesions, or diaphragmatic paralysis, rather than by the effusion

itself.

Cough

Cough in patients with pleural effusion is often mild and nonproductive. More

severe cough or the production of purulent or bloody sputum suggests an

underlying pneumonia or endobronchial lesion.

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Chest pain

The presence of chest pain, which results from pleural irritation, raises the

likelihood of an exudative etiology, such as pleural infection, mesothelioma, or

pulmonary infarction.

Pain may be mild or severe. It is typically described as sharp or stabbing and is

exacerbated with deep inspiration. Pain may be localized to the chest wall or

referred to the ipsilateral shoulder or upper abdomen, usually because of

diaphragmatic involvement. Pain often diminishes in intensity as the pleural

effusion increases in size.

Additional symptoms

Other symptoms in association with pleural effusions may suggest the

underlying disease process. Increasing lower extremity edema, orthopnea, and

paroxysmal nocturnal dyspnea may all occur with congestive heart failure.

Night sweats, fever, hemoptysis, and weight loss should suggest TB.

Hemoptysis also raises the possibility of malignancy, other endotracheal or

endobronchial pathology, or pulmonary infarction. An acute febrile episode,

purulent sputum production, and pleuritic chest pain may occur in patients with

an effusion associated with pneumonia.

B.2 Physical Examinations

Physical findings in pleural effusion are variable and depend on the volume of

the effusion. Generally, there are no physical findings for effusions smaller than

300 mL. With effusions larger than 300 mL, findings may include the following:

Dullness to percussion, decreased tactile fremitus, and asymmetrical chest

expansion, with diminished or delayed expansion on the side of the effusion,

are the most reliable physical findings of pleural effusion.

Mediastinal shift away from the effusion - This is observed with effusions of

greater than 1000 mL; displacement of the trachea and mediastinum toward

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the side of the effusion is an important clue to obstruction of a lobar bronchus

by an endobronchial lesion, which can be due to malignancy or, less

commonly, to a nonmalignant cause, such as a foreign body.

Diminished or inaudible breath sounds

Egophony ("e" to "a" changes) at the most superior aspect of the pleural

effusion

Pleural friction rub

Other physical findings, as follows, may suggest the underlying cause of the

pleural effusion:

Peripheral edema, distended neck veins, and S3 gallop suggest congestive

heart failure. Edema may also be a manifestation of nephrotic syndrome;

pericardial disease; or, combined with yellow nails, the yellow nail syndrome.

Cutaneous changes with ascites suggest liver disease

Lymphadenopathy or a palpable mass suggests malignancy.

C. Workup

C.1 Approach Consideration

Thoracentesis should be performed for new and unexplained pleural effusions

when sufficient fluid is present to allow a safe procedure. Observation of pleural

effusion is reasonable when benign etiologies are likely, as in the setting of overt

congestive heart failure, viral pleurisy, or recent thoracic or abdominal surgery.

Laboratory testing helps to distinguish pleural fluid transudates from exudates;

however, certain types of exudative pleural effusions might be suspected simply

by observing the gross characteristics of the fluid obtained during thoracentesis.

Note the following:

Frankly purulent fluid indicates an empyema

A putrid odor suggests an anaerobic empyema

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A milky, opalescent fluid suggests a chylothorax, resulting most often from

lymphatic obstruction by malignancy or thoracic duct injury by trauma or

surgical procedure

Grossly bloody fluid may result from trauma, malignancy,

postpericardiotomy syndrome, or asbestos-related effusion and indicates the

need for a spun hematocrit test of the sample; a pleural fluid hematocrit level

of more than 50% of the peripheral hematocrit level defines a hemothorax,

which often requires tube thoracostomy.

C.2 Distinguishing Transduates from Exudates

Transudates are usually ultrafiltrates of plasma in the pleura due to imbalance in

hydrostatic and oncotic forces in the chest. However, they can also be caused by

the movement of fluid from peritoneal spaces or by iatrogenic infusion into the

pleural space from misplaced or migrated central venous catheters or nasogastric

feeding tubes.

Exudates are produced by a variety of inflammatory conditions and often require

more extensive evaluation and treatment than transudates. Exudates arise from

pleural or lung inflammation, impaired lymphatic drainage of the pleural space,

transdiaphragmatic movement of inflammatory fluid from the peritoneal space,

altered permeability of pleural membranes, and increased capillary wall

permeability or vascular disruption. Pleural membranes are involved in the

pathogenesis of the fluid formation. Permeability of pleural capillaries to

proteins is high, resulting in an elevated protein content.

The initial diagnostic consideration is distinguishing transudates from exudates.

Although a number of chemical tests have been proposed to differentiate pleural

fluid transudates from exudates, the tests first proposed by Light et al have

become the criterion standards.

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The fluid is considered an exudate if any of the following applies:

Ratio of pleural fluid to serum protein greater than 0.5

Ratio of pleural fluid to serum LDH greater than 0.6

Pleural fluid LDH greater than two thirds of the upper limits of normal serum

value

These criteria require simultaneous measurement of pleural fluid and serum

protein and LDH. However, a meta-analysis of 1448 patients suggested that the

following combined pleural fluid measurements might have sensitivity and

specificity comparable to the criteria from Light et al for distinguishing

transudates from exudates :

Pleural fluid LDH value greater than 0.45 of the upper limit of normal serum

values

Pleural fluid cholesterol level greater than 45 mg/dL

Pleural fluid protein level greater than 2.9 g/dL

Clinical judgment is required when pleural fluid test results fall near the cutoff

points. The criteria from Light et al and these alternative criteria identify nearly

all exudates correctly, but they misclassify approximately 20-25% of transudates

as exudates, usually in patients on long-term diuretic therapy for congestive

heart failure (because of the concentration of protein and LDH within the pleural

space due to diuresis).

Using the criterion of serum minus pleural protein concentration level of less

than 3.1 g/dL, rather than a serum/pleural fluid ratio of greater than 0.5, more

correctly identifies exudates in these patients.

Although pleural fluid albumin is not typically measured, a gradient of serum

albumin to pleural fluid albumin of less than 1.2 g/dL also identifies an exudate

in such patients.

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In addition, studies suggest that pleural fluid levels of N-terminal pro-brain

natriuretic peptide (NT-proBNP) are elevated in effusions due to congestive

heart failure. Moreover, elevated pleural NT-proBNP was shown to out-perform

pleural fluid BNP as a marker of heart failure–related effusion.  Thus, at

institutions where this test is available, high pleural levels of NT-proBNP

(defined in different studies as >1300-4000 ng/L) may help to confirm heart

failure as the cause of an otherwise idiopathic chronic effusion.

Transudates are caused by a small, defined group of etiologies, including the

following:

Congestive heart failure

Cirrhosis (hepatic hydrothorax)

Atelectasis - Which may be due to malignancy or pulmonary embolism

Hypoalbuminemia

Nephrotic syndrome

Peritoneal dialysis

Myxedema

Constrictive pericarditis

Urinothorax - Usually due to obstructive uropathy

Cerebrospinal fluid (CSF) leaks to the pleura - Generally in the setting of

ventriculopleural shunting or of trauma or surgery to the thoracic spine

Duropleural fistula - Rare, but may be a complication of spinal cord surgery

Extravascular migration of central venous catheter

Glycinothorax - A rare complication of bladder irrigation with 1.5% glycine

solution following urologic surgery

The more common causes of exudates include the following:

Parapneumonic causes

Malignancy (most commonly, lung or breast cancer, lymphoma, leukemia;

less commonly, ovarian carcinoma, stomach cancer, sarcomas, melanoma)[9]

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Pulmonary embolism

Collagen-vascular conditions (rheumatoid arthritis, systemic lupus

erythematosus )

Tuberculosis (TB)

Pancreatitis

Trauma

Postcardiac injury syndrome

Esophageal perforation

Radiation pleuritis

Sarcoidosis

Fungal infection

Pancreatic pseudocyst

Intra-abdominal abscess

Status-post coronary artery bypass graft surgery

Pericardial disease

Meigs syndrome (benign pelvic neoplasm with associated ascites and pleural

effusion)

Ovarian hyperstimulation syndrome

Drug-induced pleural disease (see Pneumotox On Line for an extensive list of

drugs that can cause pleural effusion)

Asbestos-related pleural disease

Yellow nail syndrome (yellow nails, lymphedema, pleural effusions)

Uremia

Trapped lung (localized pleural scarring with the formation of a fibrin peel

prevents incomplete lung expansion, at times leading to pleural effusion)

Chylothorax (acute illness with elevated triglycerides in pleural fluid)

Pseudochylothorax (chronic condition with elevated cholesterol in pleural

fluid)

Fistula (ventriculopleural, biliopleural, gastropleural)

C.3 Radiography

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Effusions of more than 175 mL are usually apparent as blunting of the

costophrenic angle on upright posteroanterior chest radiographs. On supine chest

radiographs, which are commonly used in the intensive care setting, moderate to

large pleural effusions may appear as a homogenous increase in density spread

over the lower lung fields. Apparent elevation of the hemidiaphragm, lateral

displacement of the dome of the diaphragm, or increased distance between the

apparent left hemidiaphragm and the gastric air bubble suggests subpulmonic

effusions. (See the images below.)

Left lateral decubitus film showing freely layering pleural effusion.

C.4. CT Scanning and Ultrasonography

A study by Gurung et al involving 41 consecutive patients with hepatic

hydrothorax indicated that hepatic hydrothorax virtually always presents with

ascites that can be revealed by ultrasonography or computed tomography (CT)

scanning.

Chest CT scanning with contrast should be performed in all patients with an

undiagnosed pleural effusion, if it has not previously been performed, to detect

thickened pleura or signs of invasion of underlying or adjacent structures. The 2

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diagnostic imperatives in this situation are pulmonary embolism and

tuberculouspleuritis. In both cases, the pleural effusion is a harbinger of

potential future morbidity. In contrast, a short delay in diagnosing metastatic

malignancy to the pleural space has less impact on future clinical outcomes. CT

angiography should be ordered if pulmonary embolism is strongly suggested.

C.5. Diagnostic Thoracentesis

Perform diagnostic thoracentesis if the etiology of the effusion is unclear or if

the presumed cause of the effusion does not respond to therapy as expected.

Pleural effusions do not require thoracentesis if they are too small to safely

aspirate or, in clinically stable patients, if their presence can be explained by

underlying congestive heart failure (especially bilateral effusions) or by recent

thoracic or abdominal surgery.

Depending on the clinician’s experience, a pulmonologist can be consulted for

assistance with high-risk diagnostic thoracentesis.

Contraindications

Relative contraindications to diagnostic thoracentesis include a small volume of

fluid (< 1 cm thickness on a lateral decubitus film), bleeding diathesis or

systemic anticoagulation, mechanical ventilation, and cutaneous disease over the

proposed puncture site. Mechanical ventilation with positive end-expiratory

pressure does not increase the risk of pneumothorax after thoracentesis, but it

increases the likelihood of severe complications (tension pneumothorax or

persistent bronchopleural fistula) if the lung is punctured.

C.6. Pleural Fluid examinations

Normal pleural fluid

Normal pleural fluid has the following characteristics:

Clear ultrafiltrate of plasma that originates from the parietal pleura

A pH of 7.60-7.64

Protein content of less than 2% (1-2 g/dL)

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Fewer than 1000 white blood cells (WBCs) per cubic millimeter

Glucose content similar to that of plasma

Lactate dehydrogenase (LDH) less than 50% of plasma

Pleural fluid LDH

Pleural fluid LDH levels greater than 1000 IU/L suggest empyema, malignant

effusion, rheumatoid effusion, or pleural paragonimiasis. Pleural fluid LDH

levels are also increased in effusions from Pneumocystis jiroveci (formerly, P

carinii) pneumonia; the diagnosis is suggested by a pleural fluid/serum LDH

ratio of greater than 1, with a pleural fluid/serum protein ratio of less than 0.5.

Pleural fluid glucose and pH

In addition to the previously discussed tests, glucose and pleural fluid pH should

be measured during the initial thoracentesis in most situations.

A low pleural glucose concentration (30-50 mg/dL) suggests malignant effusion,

tuberculouspleuritis, esophageal rupture, or lupus pleuritis. A very low pleural

glucose concentration (ie, < 30 mg/dL) further restricts diagnostic possibilities,

to rheumatoid pleurisy or empyema.

Pleural fluid pH is highly correlated with pleural fluid glucose levels. A pleural

fluid pH of less than 7.30 with a normal arterial blood pH level is caused by the

same diagnoses as listed above for low pleural fluid glucose. However, for

parapneumonic effusions, a low pleural fluid pH level is more predictive of

complicated effusions (that require drainage) than is a low pleural fluid glucose

level. In such cases, a pleural fluid pH of less than 7.1-7.2 indicates the need for

urgent drainage of the effusion, while a pleural fluid pH of more than 7.3

suggests that the effusion may be managed with systemic antibiotics alone.

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In malignant effusions, a pleural fluid pH of less than 7.3 has been associated in

some reports with more extensive pleural involvement, higher yield on cytology,

decreased success of pleurodesis, and shorter survival times.

Handle pleural fluid samples as carefully as arterial samples for pH

measurements, with fluid collected in heparinized syringes and ideally

transported on ice for measurement within 6 hours. However, studies have

shown that when collected in heparinized syringes, pleural fluid pH does not

change significantly even over several hours at room temperature. Consequently,

if appropriately collected samples can be processed quickly, pH measurements

should not be canceled simply because the sample was not transported on ice.

Pleural Fluid Culture and Cytology

Culture of infected pleural fluid yields positive results in approximately 60% of

cases; this occurs even less often for anaerobic organisms. Diagnostic yields,

particularly for anaerobic pathogens, may be increased by directly culturing

pleural fluid into blood culture bottles.

Malignancy is suspected in patients with known cancer or with lymphocytic,

exudative effusions, especially when bloody. Direct tumor involvement of the

pleura is diagnosed most easily by performing pleural fluid cytology.

Heparinize samples (1 mL of 1:1000 heparin per 50 mL of pleural fluid) if

bloody, and refrigerate if samples will not be processed within 1 hour.

The reported diagnostic yields in cytology vary from 60-90%, depending on the

extent of pleural involvement and the type of primary malignancy. Cytology

findings are positive in 58% of effusions related to mesothelioma.

The sensitivity of cytology is not highly related to the volume of pleural fluid

tested; sending more than 50-60 mL of pleural fluid for cytology does not

increase the yield of direct cytospin analysis, and volumes of approximately 150

mL are sufficient when both cytospin and cell block preparations are analyzed.

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Tumor markers, such as carcinoembryonic antigen, Leu-1, and mucin, are

suggestive of malignant effusions (especially adenocarcinoma) when pleural

fluid values are very high. However, because of low sensitivity, they are not

helpful if the values are normal or only modestly increased.

Tuberculous pleuritis

Suspect tuberculouspleuritis in patients with a history of exposure or a positive

PPD finding and in patients with lymphocytic exudative effusions, especially if

less than 5% mesothelial cells are detected on differential blood cell counts.

Because most tuberculous pleural effusions probably result from a

hypersensitivity reaction to the Mycobacterium rather than from microbial

invasion of the pleura, acid-fast bacillus stains of pleural fluid are rarely

diagnostic (< 10% of cases), and pleural fluid cultures grow M tuberculosis in

less than 65% of cases.

In contrast, the combination of histology and culture of pleural tissue obtained

by pleural biopsy increases the diagnostic yield to 90%.

ADA activity of greater than 43 U/mL in pleural fluid supports the diagnosis of

tuberculouspleuritis. However, the test has a sensitivity of only 78%; therefore,

pleural ADA values of less than 43-50 U/mL do not exclude the diagnosis of TB

pleuritis. Interferon-gamma concentrations of greater than 140 pg/mL in pleural

fluid also support the diagnosis of tuberculouspleuritis, but this test is not

routinely available.

C.7. Additional Laboratory Test

Additional specialized tests are warranted when specific etiologies are

suspected. Measure pleural fluid amylase levels if a pancreatic origin or ruptured

esophagus is suspected or if a unilateral, left-sided pleural effusion remains

undiagnosed after initial testing. Of note, increased pleural fluid amylase can

also be seen with malignancy. An additional assay of amylase isoenzymes can

36

help distinguish a pancreatic source (diagnosed by elevated pleural fluid

pancreatic isoenzymes) from other etiologies.

Measure triglyceride and cholesterol levels in milky pleural fluids when

chylothorax or pseudochylothorax is suspected.

Consider immunologic studies, including pleural fluid antinuclear antibody and

rheumatoid factor, when collagen-vascular diseases are suspected.

D. Differential Diagnoses

Sjögren syndrome, liver or lung transplantation, upper genitourinary trauma, and

abdominal trauma are among the conditions to consider in the differential

diagnosis of pleural effusion, but note they are rare.

Transudative pleural effusion

Considerations in the differential diagnosis of transudative pleural effusion

include the following:

Congestive heart failure (most common)

Cirrhosis with hepatic hydrothorax

Nephrotic syndrome

Peritoneal dialysis/continuous ambulatory peritoneal dialysis

Hypoproteinemia

Glomerulonephritis

Superior vena cava obstruction

Fontan procedure

Urinothorax

CSF leak to the pleural space

Exudative pleural effusion

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Conditions to consider in the differential diagnosis of exudative pleural effusion

include the following:

Malignancy

Pneumonia

Tuberculosis

Pulmonary embolism

Fungal infection

Pancreatic pseudocyst

Intra-abdominal abscess

After coronary artery bypass graft surgery

Postcardiac injury syndrome

Pericardial disease

Meigs syndrome

Ovarian hyperstimulation syndrome

Rheumatoid pleuritis

Lupus erythematosus

Drug-induced pleural disease

Asbestos pleural effusion

Yellow nail syndrome

Uremia

Trapped lung

Chylothorax

Pseudochylothorax

Acute respiratory distress syndrome

Chronic pleural thickening

Malignant mesothelioma

E. Treatment and Management

Transudative effusions are usually managed by treating the underlying medical

disorder. However, whether transudates or exudates, large, refractory pleural

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effusions causing severe respiratory symptoms, even if the cause is understood

and disease-specific treatment is available, can be drained to provide relief.

The management of exudative effusions depends on the underlying etiology of

the effusion. Pneumonia, malignancy, or TB causes most diagnosed exudative

pleural effusions, with the remainder typically deemed idiopathic. Complicated

parapneumonic effusions and empyemas should be drained to prevent

development of fibrosingpleuritis. Malignant effusions are usually drained to

palliate symptoms and may require pleurodesis to prevent recurrence.

Medications cause only a small proportion of all pleural effusions and are

associated with exudative pleural effusions. However, early recognition of these

iatrogenic causes of pleural effusion avoids unnecessary additional diagnostic

procedures and leads to definitive therapy, which is discontinuation of the

medication. Implicated drugs include medications that cause drug-induced lupus

syndrome (eg, procainamide, hydralazine, quinidine), nitrofurantoin, dantrolene,

methysergide, procarbazine, and methotrexate.

Tuberculouspleuritis

Tuberculouspleuritis typically is self-limited. However, because 65% of patients

with primary tuberculouspleuritis reactivate their disease within 5 years, empiric

anti-TB treatment is usually begun pending culture results when sufficient

clinical suspicion is present, such as an unexplained exudative or lymphocytic

effusion in a patient with a positive PPD finding.

Chylous effusions

Chylous effusions are usually managed by dietary and surgical modalities.

However, studies suggest that somatostatin analogues also may help in reducing

the efflux of chyle into the pleural space.

Surgical treatment

39

Surgical intervention is most often required for parapneumonic effusions that

cannot be drained adequately by needle or small-bore catheters. Surgery may

also be required for the diagnosis and sclerosis of exudative effusions.

Video-assisted thoracoscopy with the patient under local or general anesthesia

allows direct visualization and biopsy of the pleura for diagnosis of exudative

effusions.

Pleurodesis by insufflating talc directly onto the pleural surface using video-

assisted thoracoscopy is an alternative to using talc slurries.

Decortication is usually needed for trapped lungs to remove a thick, inelastic

pleural peel that restricts ventilation and produces progressive or refractory

dyspnea. In patients with chronic, organizing parapneumonic pleural effusions,

technically demanding operations may be required to drain loculated pleural

fluid and to obliterate the pleural space.

Surgically implanted pleuroperitoneal shunts are another treatment option for

recurrent, symptomatic effusions, most often in the setting of malignancy, but

they are also used for management of chylous effusions. However, the shunts are

prone to malfunction over time, are poorly tolerated by patients, and can require

surgical revision.

In unusual cases, surgery might be required to close diaphragmatic defects

(thereby preventing recurrent accumulation of pleural effusions in patients with

ascites) and to ligate the thoracic duct to prevent reaccumulation of chylous

effusions.

E.1. TherapeuaticThoracentesis

Therapeutic thoracentesis to remove larger amounts of pleural fluid is used to

alleviate dyspnea and to prevent ongoing inflammation and fibrosis in

parapneumonic effusions. In addition to the precautions listed previously for

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diagnostic thoracentesis, note 3 additional considerations when performing

therapeutic thoracentesis.

First, to avoid producing a pneumothorax during the removal of large quantities

of fluid, remove fluid during therapeutic thoracentesis with a catheter, rather

than with a sharp needle, introduced into the pleural space. Various specially

designed thoracentesis trays are available for introducing small catheters into the

pleural space. Alternatively, newer systems using spring-loaded, blunt-tip

needles that avoid lung puncture are also available.

Second, monitor oxygenation closely during and after thoracentesis because

arterial oxygen tension paradoxically might worsen after pleural fluid drainage

due to shifts in perfusion and ventilation in the reexpanding lung. Consider use

of empiric supplemental oxygen during the procedure.

Third, remove only moderate amounts of pleural fluid to avoid reexpansion

pulmonary edema and to avoid causing a pneumothorax. Removal of 400-500

mL of pleural fluid is often sufficient to alleviate shortness of breath. The

recommended limit is 1000-1500 mL in a single thoracentesis procedure.

Larger amounts of pleural fluid can be removed if pleural pressure is monitored

by pleural manometry and is maintained above -20 cm water. However, this

monitoring is rarely used by most proceduralists.

The onset of chest pressure or pain during the removal of fluid indicates a lung

that is not freely expanding, and the procedure should be stopped immediately to

avoid reexpansion pulmonary edema.   In contrast, cough frequently occurs

during removal of fluid, and this is not an indication to stop the procedure,

unless the cough is causing the patient discomfort.

Mediastinal position and lung entrapment

The position of the mediastinum on the chest radiograph may predict whether a

patient is likely to benefit from the procedure. A mediastinal shift away from the

41

pleural effusion indicates a positive pleural pressure and compression of the

underlying lung that can be relieved by thoracentesis. (See the images below.)

Massive right pleural effusion with shift of mediastinum towards left

In contrast, a mediastinal shift towards the side of the effusion indicates lung

entrapment by extensive pleural involvement or endobronchial obstruction that

prevents reexpansion of the lung when the pleural fluid is removed, or it

indicates a lung trapped by encasement by chronic pleural thickening. Lung

entrapment with malignant effusions is most common with mesothelioma or

primary lung cancer.

Attempts at therapeutic thoracentesis usually do not improve dyspnea in patients

with lung entrapment, due to the inability of the lung to reexpand. In fact,

attempts at drainage of fluid in these patients usually results in a

hydropneumothorax being visualized on postprocedure imaging studies. (See the

image below.)

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Lung entrapment with right hydropneumothorax and pleural drain in place

E.2. Tube Thoracostomy

Although small, freely flowing parapneumonic effusions can be drained by

therapeutic thoracentesis, most larger effusions and complicated parapneumonic

effusions or empyemas require drainage by tube thoracostomy.

Traditionally, large-bore chest tubes (20-36F) have been used to drain thick

pleural fluid and to break up loculations in empyemas. However, such tubes are

not always well tolerated by patients and are difficult to direct correctly into the

pleural space. However, small-bore tubes (7-14F) inserted at the bedside or

under radiographic guidance have been shown to provide adequate drainage,

even when empyema is present. These tubes cause less discomfort and are more

likely to be placed successfully within a pocket of pleural fluid. Using 20-cm

water suction and flushing the tube with normal saline every 6-8 hours may

prevent occlusion of small-bore catheters.

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Insertion of additional pleural catheters, usually under radiographic guidance, or

instilling fibrinolytics (eg, streptokinase, urokinase, or alteplase) through the

pleural catheter can help to drain multiloculated pleural effusions.

A randomized trial of 210 participants with pleural infection showed that

instillation of alteplase and DNase produced significantly greater drainage of

pleural effusion, less need for surgical referral or surgical intervention, shorter

hospital stays, and a decrease in pleural fluid inflammatory markers compared

with placebo.

E.4. Pleurodesis

Pleurodesis (also known as pleural sclerosis) involves instilling an irritant into

the pleural space to cause inflammatory changes that result in bridging fibrosis

between the visceral and parietal pleural surfaces, effectively obliterating the

potential pleural space. Pleurodesis is most often used for recurrent malignant

effusions, such as in patients with lung cancer or metastatic breast or ovarian

cancer. Given the limited life expectancy of these patients, the goal of therapy is

to palliate symptoms while minimizing patient discomfort, hospital length of

stay, and overall costs.

Patients with poor performance status (Karnofsky score < 70) and a life

expectancy of less than 3 months can be treated with repeated outpatient

thoracentesis as needed to palliate symptoms. Unfortunately, pleural effusions

can reaccumulate rapidly, and the risk of complications increases with repeated

drainage.

In addition, patients with lung entrapment from malignant effusions are not

candidates for repeated thoracentesis, which does not relieve dyspnea in such

patients, nor for pleurodesis, as the visceral and parietal pleural surfaces cannot

44

stay apposed to allow the bridging fibrosis. The best treatment for effusions in

such patients is the insertion of an indwelling tunneled catheter, which allows

patients to remove pleural fluid as needed at home.

A 2006 systematic review found that in pleurodesis, rotating the patient through

different positions did not appear necessary to ensure distribution of soluble

sclerosing agents throughout the pleural space. In addition, neither protracted

drainage after instillation of sclerotics nor the use of larger-bore chest tubes

increased the effectiveness of pleurodesis.

Pleurodesis is likely to be successful only if the pleural space is drained

completely before pleurodesis and if the lung is fully reexpanded to appose the

visceral and parietal pleura after sclerosis. Animal studies suggest that systemic

corticosteroids can reduce inflammation during sclerosis and can cause

pleurodesis failures.

Sclerosing agents

Various agents, including talc, doxycycline, bleomycin sulfate (Blenoxane), zinc

sulfate, and quinacrine hydrochloride, can sclerose the pleural space and

effectively prevent recurrence of the malignant pleural effusion.

Talc is the most effective sclerosing agent and can be administered as slurry

through chest tubes or pleural catheters. Although a systematic review suggested

that direct insufflation of talc via thoracoscopy was more effective than talc

slurry, both were equally effective in a 2005 prospective trial of malignant

effusions. Importantly, talc particles tend to occlude the small drainage holes in

small pleural catheters. Therefore, pleural catheters should be at least 10-12F if

intended for talc pleurodesis.

45

Doxycycline and bleomycin are also effective in most patients and can be

administered more easily through small-bore catheters, although they are

somewhat less effective and substantially more expensive than talc.

All sclerosing agents can produce fever, chest pain, and nausea. Talc rarely

causes more serious adverse effects, such as empyema and acute lung injury.

The latter appears to be related to the particle size and the amount of talc

injected for pleurodesis.

Injection of 50 mL of 1% lidocaine hydrochloride prior to instillation of the

sclerosing agent may help to alleviate pain. Additional analgesia might be

required in some cases. Clamp chest tubes for approximately 2 hours after

instillation of the sclerosing agent.

E.2. Monitoring Pleuaral Drainage

Record the amount and quality of fluid drained and monitor for an air leak

(bubbling through the water seal) at each shift. Large air leaks (steady streams of

air throughout the respiratory cycle) may be indications of loose connectors or

of a drainage port on the catheter that has migrated out to the skin. Alternatively,

they may indicate large bronchopleural fistulae. Consequently, dressings should

be taken down and the position of the catheter inspected at the puncture site.

Briefly clamping the catheter at the skin helps to determine whether the air leak

is originating from within the pleural cavity (in which case, it stops when the

tube is clamped) or from outside the chest (in which case, the leak persists).

Repeat the chest radiographs when drainage decreases to less than 100 mL/day

to evaluate whether the effusion has been fully drained. If a large effusion

persists radiographically, reevaluate the position of the chest catheter using chest

CT scanning to ensure that the drainage ports are still positioned within the

pleural collection. If the catheter is positioned appropriately, consider injecting

46

lytics through the chest tube to break up clots that may be obstructing drainage.

Alternatively, chest CT scanning may reveal lung entrapment/trapped lung,

which is unlikely to respond to further drainage in the hospital.

IV. CONCLUSION

Treating the underlying disease is the definitif treatment of pleura effusion. So,

it must be found the etiology.

Massive pleura effusion can be removed through the thoracosentesis, WSD, or

pleurodesis.

REFERENCE

W, Aru. Sudoyo, et all. 2006. Ilmu Peyakit Dalam Ed IV Jilid I. Department of Internal

Medicine Medical Faculty of Indonesian University. Jakarta.

Arun Gopi, Sethu M. Madhavan, Surendra K. Sharma and Steven A.Sahn. 2007.

Diagnosis and Treatment of Tuberculous Pleural Effusion in 2006. American College of

Chest Physicians.

Halim, Hadi. 2007. Penyaki-Penyakit Pleura dalam Buku Ajar Ilmu Penyakit Dalam,

Jilid II, Edisi IV. Department of Internal Medicine Medical Faculty of Indonesian

University. Jakarta.

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