Cr Dr.dedi Hidropneumothorax Ec Tb Paru

Case Report

Created By :BUNGA LISTIA PARAMITA (110.2006.059)

RIA RIZKY DESLISYAHPUTRI (110.2006.221)RESI TRISMAYENNY (0718011078)

Perceptor:Dr. DEDY ZAIRUS, Sp.P

CLINICAL WORK OF INTERNAL MEDICINE, SMF. PULMONOLOGY

PERIOD 26TH MARCH – 26TH MAY 2012ABDUL MOELOEK HOSPITAL, BANDAR LAMPUNG

1

THE UNIT PULMONOLOGY OF INTERNAL MEDICINE …………………………………………….……

RSUD Dr. Hi. ABDUL MOELOEK…………………………………………….……

BANDARLAMPUNG

PATIENT STATUS

PATIENT IDENTITY

Full Name : NurimanSex : maleAge : 35 years oldNationality : JavaneseMarital status : MarriedReligion : IslamOccupation : Farmer Educational background : Senior High schoolAddress : Rantau Tijang Tanggamus

ANAMNESIS

Taken From : Autoanamnesis Date 12nd April 2012 11.30 WIB

The main complained : Dyspneu

The additional complained : Chest pain, Febris, Purulent cough, Night sweat.

The History of the Illness :

Patients come to RSUDAM with complaints of shortness of breath since 2 months

ago and felt become heavy since one week before entering RSUDAM. Perceived shortness

of breath and intermittent positions are not affected by weather and activity. Patients also

complained of intermittent cough since one year ago. Cough accompanied by a discharge

of pus, in which pus is reduced when the patient entered the hospital. Other than that the

patient also complained of chest pain that arises after the cough. Cough is more severe if

the patient is seated. Patients also felat that he had water on the right chest move the

patient to move position. In addition, patients also complain of fever, sepecially late

afternoon and night sweat. The patient claimed to have anever treated before and patient

also claimed to have never felt this before.

2

Patient admitted to TB treatmen in 2010 for 6 months. Denied a history of TB

medication discontinuation by patients. Positive smoking history as much as 2 packs a day

since the age of 11 years and quit as early as 2 months before hospital admission. History

of hypertension and diabetes is denied.

The History of Illness :

( ) Small pox ( ) Malaria ( ) Kidney stone(√ ) Chicken pox ( ) Disentri ( ) Burut (Hernia)( ) Difthery ( ) Hepatitis ( ) Prostat( ) Pertusis ( ) Tifus Abdominalis ( ) Melena( ) Measles ( ) Skirofula ( ) Diabetic( ) Influenza ( ) Sifilis ( ) Alergyc( ) Tonsilitis ( ) Gonore ( ) T u m o r( ) Kholera ( ) Hipertensi ( ) Vaskular Disease( ) Demam Rematik Akut ( ) Ulkus Ventrikuli( ) Pneumonia ( ) Ulkus Duodeni( ) Pleuritis ( ) Gastritis(√) Tuberkulosis ( ) Stone Gall others : ( ) Operation

( ) Accident

History of Family :

ConnectionAge(th)

Sex Healthy Causa of Death

Grandfather 75 Male DeathGrandmother 60 Female DeathFather 70 Male DeathMother 63 Female Death DMBrother-sister 33 Male HealthyChildren 8 Male Healthy

An any relation who suffer :Illness Yes No Connection

Alergyc √Asthma √Tuberkulosa √Artritis √Rematisme √Hipertensi √Cor √Kidney √Gaster √Diabetes √ Mother

3

ANAMNESIS SISTEMNote Complain Positif beside the title

Skin( ) Boil ( ) Hair (√) Night swet( ) Nail ( ) Yellow / Ikterus ( ) Sianotic

( ) Others

Head( ) Trauma ( ) Headache( ) Sinkop ( ) Pain of the sinus

Eye( ) Pain ( ) Inflammation of night sweat( ) Secret ( ) Eye disorder( ) yellow / Ikterus ( ) Sharpness to see

Ear( ) Pain ( ) Tinitus( ) Secret ( ) Ear disorder

( ) Deaf

Nose( ) Trauma ( ) Clogging( ) Pain ( ) Nose disorder( ) Sekret ( ) Have a cold( ) Epistaksis

Mouth( ) Lip ( ) Tongue ( ) Gums ( ) Mouth disorder( ) Membrane ( ) Stomatitis

Throat( ) Throats pain ( ) Voice (change)

Neck( ) Protruding ( ) Necks pain

Cor / Lung(√) Chest pain (Left) (√) Dyspneu( ) Pulse ( ) Hemoptoe( ) Ortopnoe (√) Cough

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Abdomen (Gaster / intestine)( ) Puffing ( ) Acites( ) Nausea ( ) Hemoroid( ) Emesis ( ) Diarrhea( ) Hematemesis ( ) Melena( ) Disfagi ( ) Pale colour of feses ( ) Kholik ( ) Black colour of feses

( ) Nodul

Urogenital( ) Disuria ( ) Pyuria( ) Stranguri ( ) Kolik( √ ) Poliuria ( ) Oliguria(√ ) Polakisuria ( ) Anuria( ) Hematuria ( ) Urine retention( ) Kidney stone ( ) Drip urine( ) Wet the bed ( ) Prostat

Katamenis( ) Leukore ( ) Bleeding( ) Others ( )

Haid( ) Last menarche ( ) Quantity and

duration( ) Menarche

( ) frequently / no ( ) Pain ( ) Klimakterium symptom( ) Menarche disorder ( ) Post menopause

Muscle and neuro( ) Anestesi ( ) Bite less( ) Parestesi ( ) Ataksia( ) Weak muscle ( ) Hipo/hiper-estesi( ) Convultion ( ) Syncope( ) Afasia ( ) Tick( ) Amnesis ( ) Vertigo( ) Others ( ) Disartri

Ekstremitas( ) Edema ( ) Deformitas( ) Hinge pain ( ) Sianotic

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WeightAverage weight (kg) : 75 kgHeight (cm) : 165 cm Present weight (kg) : 60 kg

(if the patient doesn’t know certainly)Steady ( )Down ( √ )Up ( )

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THE HISTORY OF LIFE

Birth place : ( ) in home ( √) matrinity ( ) Matrinity hospital Helped by : ( ) Doctor ( √) nurse ( )Traditional matrinity

( ) Others

Imunitation History ( ) Hepatitis ( ) BCG ( ) Campak ( ) DPT ( ) Polio ( ) Tetanus

Food HistoryFrekuensi/day : 3x/dayAmount /day : 2 plate/eat (health), ½ plate/eat (illness)Variation /day : Rice, vegetables, egg, fishAppetite : Enough

Educational( ) SD ( ) SLTP ( √ ) SLTA ( ) SMK ( ) Academy

( ) Course ( ) UnschoolProblemFinancial : LowWorks : FarmerFamily : Good relationOthers : -

Body Check UpGeneral Check upHeight : 165cmWeight : 60 kgBlood Pressure : 120/80 mmhgPulse : 68 x/minute, regular, volume normalTemp : 36,5 oCBreath (frequence&type) : 23 x / minute Nutrition condition : EnoughConsciousness : Compos mentisCianotic : -General edema : -Habity : PiknikusThe way of walk : NormalMobility (active/pasive) : Active

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The age prediction based on check up : 35

Mentality AspectsBehavior : Normal Nature of feeling : NormalThe thinking process : Normal

SkinColor : BrownEfloresensi : -Keloid : -Pigmentasi : -Hair Growth : NormalArteries : feelTouch temperature : AfebrisHumid/dry : HumidSweat : Night sweat Turgor : NormalIcterus : AnictericFat layers : -Edema : -Others : -

Lymphatic GlandSubmandibula : Untouched enlargementNeck : Untouched enlargementSupraklavikula : Untouched enlargementArmpit : Untouched enlargement

HeadFace expression : NormalFace symmetric : SymmetricHair : Black and uprootedTemporal artery : Normal

EyeExopthalmus : -Enopthalmus : -Palpebra : edeme -Lens : ClearConjungtiva : AnanemisVisus : 6/6Sklera : AnictericEye movement : Good in every side

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Vision scope : NormalEye ball pressure : Normal Perpalpation Deviatio konjungae : -Nystagmus : -

EarDeaf : negative / negativeMembrane tymphani : intac / intacForamen : wide / wideObstruction : -Serumen : -Bleeding : -Liquid : -

Mouthlips : cyanosis -Tonsil : T1 / T1Palatal : NormalHalibsts : NoTeeth : CariesTrismus : -Farings : UnhiperemisLiquid layer : Unhiperemis, cyanosis -Tongue : Not dirty

NeckJVP : NormalTiroid gland : Untouched enlargementLimfe gland : Untouched enlargement

ChestShape : SimetricArtery : NormalBreast : Normal, man

Lung

AnteriorInspeksi Left : Asimetric, massa -, retraction -

Right : Asimetric massa -, retraction -Palpasi Left : tactil fremitus & vocal fremitus normal

Right : tactil fremitus & vocal fremitus decreasePerkusi Left : Sonor

Right : Dim

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Auskultasi Left : Vesiculer , ronchi -, wheezing -Right : Vesiculer ↓, ronchi -, wheezing -

PosteriorInspeksi Left : Asimetric, massa -, retraction -

Right : Asimetric massa -, retraction -Palpasi Left : tactil fremitus & vocal fremitus normal

Right : tactil fremitus & vocal fremitus decreasePerkusi Left : Sonor

Right : DimAuskultasi Left : Vesiculer , ronchi -, wheezing -

Right : Vesiculer ↓, ronchi -, wheezing -

CorInspection : IC unseenPalpation : IC feel in linea midclavicula sinistra ICS VPercutionRight boundary : ICS V linea parasternalis dextraThe left boundary : ICS V linea midclavicula sinsitraUpper limit : ICS III linea parasternalis sinsitraAuskultation : heart voice I and II normal, murmur (-), gallop (-)

ArteryArtery temporalis : No distinctArtery karotis : No distinctArtery brakhialis : No distinctArtery radialis : No distinctArtery femoralis : No distinctArtery poplitea : No distinctArtery tibilias posterior : No distinct

StomachInspection : normal in 4 regionPalpation

Stomach wall : pressure pain (-)Heart : not feelLimfe : not feelKidney : ballotemen (-)

Percution : Timpani, shifting dullness (-)Auscultation : intestine sounds (+), normalRefleks stomach wall : normal

Genital (based on indication)

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Female : no indicationOUE : no indicationFlour albus : no indication

Movement jointArm Right LeftMuscle normal normalTonus normotonus normotonusMassa Eutrofi eutrofiJoint normal normalMovement Active ActiveStrength 5 5Others

Heel and legWond/injury : not foundVarices : (-)Muscle (tonus & mass) : normotonus & eutrofiJoint : normalMovement : ActiveStrength/power : 5Edema : (-)Others : (-)

ReflexsRight Left

Tendon reflex normal normalBisep normal normalTrisep normal normalPatela normal normalAchiles normal normalCremaster not done not doneSkin reflex normal normalPatologic reflex not found not found

LABORATORY (9 April 2012)BloodHb : 13,1 gr/dl (13,5 – 18,0 gr/dl)

ESR : 0 (0 – 20 mm/hour)Leukosit : 5000/µl (4.500 – 10.700/ µl)

Variety countBasofil : 0 % (0 – 1 %)

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Eusinofil : 0 % (1 – 3 %)

Batang : 0 % (2 – 6 %)

Segmen : 73% (50 – 70 %)

Limfosit : 21% (20 – 40 %)Monosit : 6 % (2 – 8 %)

Chemical BloodSGOT : 34 U/L (6 – 30 U/L)

SGPT : 42 U/L (6 – 45 U/L)Ureum : 9 mg/dL (10 – 40 mg/dL)Creatinine : 0,7 mg/dL (0,7 – 1,3 mg/dL)Blood Glucosa During : 372 mg/dL (70 – 200 mg/dL)Nacture Glucosa : 299 mg/dL ( < 120 mg/dL)Post Prandial Glucosa : 409 mg/dL (< 140 mg/dL)

BTA Examination : Negative Fluid WSD : types of discharge are greenish yellow pus from the pleural

cavity as much as 1000 cc, undulations +, bubbles + Culture and Resistance : Sterile

Urine : no examinationFaeces : no examination

RADIOLOGY (10 April 2012)

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Lung: Right pleural effusion Fibrotic in the left lung, superior lobe

Cor: Difficult to assess

RADIOLOGY (14 April 2012)

Lung: Broncovaskular spots on the lower right lungMinimal right pleural effusionRadiolucent in the right inferior pulmonaryFibrotic lug superior lobe of the left

Cor: Difficult to assess

RESUMEPatients come to hospital with complaints of dyspneu. The complain held since 2

months ago and felt become heavy since one week before entering hospital. He also

complained chest pain, febris, purulent cough and night sweat. Cough is more severe if the

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patient is seated. The patient claimed to have anever treated before and patient also

claimed to have never felt this before.

Patient admitted to TB treatment in 2010 for 6 months. Denied a history of TB

medication discontinuation by patients. Positive smoking history as much as 2 packs a day

since the age of 11 years and quit as early as 2 months before hospital admission.

Height : 165 cm

Weight : 60 kg

Blood Pressure : 120/80 mmhg

Pulse : 68 x/minute, regular, volume normal

Touch temperature : 36,5ºC, Afebris

Lung

AnteriorInspeksi Left : Asimetric, massa -, retraction -

Right : Asimetric massa -, retraction -Palpasi Left : tactil fremitus & vocal fremitus normal

Right : tactil fremitus & vocal fremitus decreasePerkusi Left : Sonor

Right : DimAuskultasi Left : Vesiculer , ronchi -, wheezing -

Right : Vesiculer ↓, ronchi -, wheezing -

PosteriorInspeksi Left : Asimetric, massa -, retraction -

Right : Asimetric massa -, retraction -Palpasi Left : tactil fremitus & vocal fremitus normal

Right : tactil fremitus & vocal fremitus decreasePerkusi Left : Sonor

Right : DimAuskultasi Left : Vesiculer , ronchi -, wheezing -

Right : Vesiculer ↓, ronchi -, wheezing -

CorInspection : IC unseenPalpation : IC feel in linea midclavicula sinistra ICS V

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PercutionRight boundary : ICS V linea parasternalis dextraThe left boundary : ICS V linea midclavicula sinsitraUpper limit : ICS III linea parasternalis sinsitraAuskultation : heart voice I and II normal, murmur (-), gallop (-)

LABORATORY (9 April 2012)BloodHb : 13,1 gr/dl (13,5 – 18,0 gr/dl)

ESR : 0 (0 – 20 mm/hour)Leukosit : 5000/µl (4.500 – 10.700/ µl)

Variety countBasofil : 0 % (0 – 1 %)

Eusinofil : 0 % (1 – 3 %)

Batang : 0 % (2 – 6 %)

Segmen : 73% (50 – 70 %)

Limfosit : 21% (20 – 40 %)Monosit : 6 % (2 – 8 %)

Chemical BloodSGOT : 34 U/L (6 – 30 U/L)

SGPT : 42 U/L (6 – 45 U/L)Ureum : 9 mg/dL (10 – 40 mg/dL)Creatinine : 0,7 mg/dL (0,7 – 1,3 mg/dL)Blood Glucosa During : 372 mg/dL (70 – 200 mg/dL)Necture Glucosa : 299 mg/dL ( < 120 mg/dL)Post Prandial Glucosa : 409 mg/dL (< 140 mg/dL)

BTA Examination : Negative Fluid WSD : types of discharge are greenish yellow pus from the pleural

cavity as much as 1000 cc, undulations +, bubbles + Culture and Resistance : Sterile

Working diagnose and basic diagnose 1. Working diagnose

Right Lung Empiema e.c Lung Tuberculosis, old case + DM type II

2. Basic Diagnose Anamnesis :Dyspneu, Sputum cough, Chest pain, Hard breathing, Night sweat,and Weakness

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Has a history of TB treatmentPhysical ExaminationLung:

I :Asimetric, hemithorax dextra laggingP:Tactile and vocal fremitus lagging P: Dim/ ResonantA:Right lung Vesiculer ↓, Ronkhi -, Wheezing -

Support checkup : Chest X-Ray : Lung: (10 April 2012)

Right pleural effusion Fibrotic in the left lung, superior lobe(14 April 2012)Broncovaskular spots on the lower right lungMinimal right pleural effusionRadiolucent in the right inferior pulmonaryFibrotic lug superior lobe of the left

Blood Blood Glucosa During : 372 mg/dLNacture Glucosa : 299 mg/dLPost Prandial Glucosa : 409 mg/dL

Differencial diagnose 1. Differencial diagnose

Right Lung Empiema ec Non Tuberculosis + DM type II2. Differencial basic diagnose

Culture and Resistance of the Pus is SterileBTA Sputum Negative

Plan treatment1. General Treatment

IVFD RL gtt XX/ minMethyl prednisolone 4 mg, 3x1Metformin 500 mg 3 x 1 tabB1, B6, B12 3 x 1 tabRanitidine injection 0f 1 ampoule/ 12 hoursSpooling with 0,9 % NaCl 100 cc per dayObserve the development of WSD if the undulations and Bubble negativeChest X-Ray if the lug re-expands, then off WSDInjection ketorolac drip 1 ampoule/ 12 hours1700 kKal per day diet

2. Prevention - Do not smoke and avoid pollution and cigarette smoke- Diligent exercise and of drinking water

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- Avoid keeping your diet and foods containing sugar- Keep somewhat wounded- Diet to lose weight

PrognoseQuo ad vitam : Dubia ad bonamQuo ad functionam : Dubia ad bonamQuo ad sanationam : Dubia ad bonam

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Follow up

Date 9/ 04 / 2012 10 / 04 / 2012 11 / 04 / 2012

Clinical symptoms :

- Right chest has liquid

- Painful breathing

- Blown

- Cough

- Back flushing such as

burs

- Pain at the site of

puncture WSD

(+)

(+)

(+)

(+)

(+)

(-)

(+)

(+)

(+)

(+)

(+)

(-)

(+)

(-)

(+)

(+)

( - )

(+)

General State Of Looks sick is

Awareness Compos mentis

Vital sign

- BP

- Temperature

- RR

- HR

120/80 mm

Hg

36,30 C

20 x / menit

110/70 mmHg

36,70 C

22 x / menit

70 x / menit

120/70 mm Hg

36,5 C

22x / menit

70 x / menit

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68 x / menit

Physical Examination

- Inspection

- Palpation

- Percution

- Auscultation

Asimetric, right chest decrease, massa -, retraction -

Right chest tactil fremitus & vocal fremitus decrease

Dim / Sonor

Vesiculer +/+, ronchi -/-, wheezing-/ -

Asimetric, right chest decrease, massa -, retraction -

Right chest tactil fremitus & vocal fremitus decrease

Dim / Sonor

Vesiculer +/+, ronchi -/-, wheezing-/ -

Asimetric, right chest decrease, massa -, retraction -

Right chest tactil fremitus & vocal fremitus decrease,Crepitation on the neck and axilla

Dim / Sonor

Vesiculer +/+, ronchi -/-, wheezing-/ -

WSDyellow-green pus liqu

id with a amount of

500cc,

undulations and positi

ve bubble

yellow-green pus liq

uid with a amount of

200cc/day,

undulations and posi

tive bubble

RontgenLung: Right pleural effusion, Fibrotic in the left lung, superior lobeCor:Difficult to assess

LaboratoriumBlood glucose during 372 mg/dL

- -

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TherapyIVFD RL gtt XX/ minInj. Ceftriaxone 1 g /12 hourMethyl prednisolone 4 mg, 3x1Metformin 500 mg, 3 x 1 tabB1, B6, B12 3 x 1 tabRanitidine injection 0f 1 ampoule/ 12 hours1700 kKal per day diet

IVFD RL gtt XX/ minInj. Ceftriaxone 1 g / 12 hourMethyl prednisolone 4 mg, 3x1Metformin 500 mg, 3 x 1 tabB1, B6, B12 3 x 1 tabRanitidine injection 0f 1 ampoule/ 12 hoursCiprofloxacin infusion 200mg, 2x1Metronidazol infusion 500 mg, 3x1Spooling with 0,9 % NaCl 100 cc per dayObserve the development of WSD if the undulations and Bubble negativeChest X-Ray if the lug re-expands, then off WSDInjection ketorolac drip 1 ampoule/ 12 hours1700 kKal per day diet

IVFD RL gtt XX/ minInj. Ceftriaxone 1 g / 12 hourMethyl prednisolone 4 mg, 3x1Metformin 500 mg, 3 x 1 tabB1, B6, B12 3 x 1 tabRanitidine injection 0f 1 ampoule/ 12 hoursCiprofloxacin infusion 200mg, 2x1Metronidazol infusion 500 mg, 3x1Spooling with 0,9 % NaCl 100 cc per dayObserve the development of WSD if the undulations and Bubble negativeChest X-Ray if the lug re-expands, then off WSDInjection ketorolac drip 1 ampoule/ 12 hours1700 kKal per day diet

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Date 12/ 04 / 2012 13 / 04 / 2012 14 / 04 / 2012

Clinical symptoms :

- Right chest has liquid

- Painful breathing

- Blown

- Cough

- Back flushing such as

burs

- Pain at the site of

puncture WSD

(-)

(+)

(+)

(-)

(-)

(+)

(-)

(+)

(-)

(-)

(-)

(-)

(-)

(-)

(-)

(-)

(-)

(-)

General State Of Looks sick is

Awareness Compos mentis

Vital sign

- BP

- Temperature

- RR

- HR

120/80 mm Hg

360 C

24 x / menit

68 x / menit

110/70 mmHg

36,30 C

22 x / menit

72 x / menit

110/80 mm Hg

36,6 C

22x / menit

70 x / menit

Physical Examination

- Inspection Asimetric, right Asimetric, right Asimetric, right

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- Palpation

- Percution

- Auscultation

chest decrease, massa -, retraction -

Right chest tactil fremitus & vocal fremitus decrease

Dim / Sonor

Vesiculer +/+, ronchi -/-, wheezing-/ -

chest decrease, massa -, retraction -

Right chest tactil fremitus & vocal fremitus decrease

Dim / Sonor

Vesiculer +/+, ronchi -/-, wheezing-/ -

chest decrease, massa -, retraction -

Right chest tactil fremitus & vocal fremitus decrease,Crepitation on the neck and axilla

Dim / Sonor

Vesiculer +/+, ronchi -/-, wheezing-/ -

WSDyellow-green pus li

quid with a small

of

amount, undulation

s and positive bubb

le

Undulation and

bubble negative

Repotition WSD

Rontgen- Pro Rontgen Lun

g:Broncovaskular spots on the lower right lungMinimal right pleural effusionRadiolucent in the right inferior pulmonaryFibrotic lug superior lobe of the leftCor: Difficult to

assess

TherapyIVFD RL gtt XX/ min

IVFD RL gtt XX/ min

IVFD RL gtt XX/ min

22

Methyl prednisolone 4 mg, 3x1Metformin 500 mg 3 x 1 tabB1, B6, B12 3 x 1 tabRanitidine injection 0f 1 ampoule/ 12 hoursCiprofloxacin infusion 200mg, 2x1Metronidazol infusion 500 mg, 3x1Spooling with 0,9 % NaCl 100 cc per dayObserve the development of WSD if the undulations and Bubble negativeChest X-Ray if the lug re-expands, then off WSDInjection ketorolac drip 1 ampoule/ 12 hours1700 kKal per day diet

Methyl prednisolone 4 mg, 3x1Metformin 500 mg 3 x 1 tabB1, B6, B12 3 x 1 tabRanitidine injection 0f 1 ampoule/ 12 hoursSpooling with 0,9 % NaCl 100 cc per dayObserve the development of WSD if the undulations and Bubble negativeChest X-Ray if the lug re-expands, then off WSD1700 kKal per day diet

Methyl prednisolone 4 mg, 3x1Metformin 500 mg 3 x 1 tabB1, B6, B12 3 x 1 tabRanitidine injection 0f 1 ampoule/ 12 hoursSpooling with 0,9 % NaCl 100 cc per dayObserve the development of WSD if the undulations and Bubble negativeChest X-Ray if the lug re-expands, then off WSD1700 kKal per day diet

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TUBERCULOSIS

TB is a infection disease that caused of mycobacterium tuberculosis. The spots of

TB infection germ are respiratory tracts, absorption tracts and opened injury in skin. Most

of TB infection occur pass through air , by means of droplet inhalation that consist of

basil which come from person who infected. The spreading capacity from a sufferer is

depended on the number of germ that issued from the lung.someone might be infected by

TB from the droplet concentration in the air, and how long they breath that air.

TB is a disease that controlled by imunity response insequenced cell. Efector cells

are macrofag and limfosit ( usually T cell ). They are imunoresponsive cells. This type

usually local, involving macrofag which actived in infection spot by limfosit and it’s

limfokin. The response is called as hypersensitivity cellular reaction ( slow reaction )

CLASSIFICATION OF TBC BASE ON THE HISTORY

1. Primary TBC

it’s happen when someone attack primarly by TBC germ. The infection started

when the TBC germ replicated successfully in the lung. That’s cause the inflammation.

Limfe tractus will carry TBC germ into limfe gland around lung hilus and it.s called as

primary complexs.

Time between infection happens until primary complexs form are around 4 – 6 weeks.

The infection cold be proven by by the occur of tuberculin reaction that changes from

negative into positive. The incubation period is time needed from infected till become

sick, approximated for about 6 month.

2. After Primary TBC

Usually happen after several month or year. After primary infection, for example

because of the descent body defense in consequence infected by HIV or malnutrient

status. The main characteristic for after primary TBC is the broadening lung damage in

occurring cavity or pleural effusion.

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Primary Progressive Tuberculosis

Active tuberculosis develops in only 5% to 10% of persons exposed to M

tuberculosis. When a patient progresses to active tuberculosis, early signs and symptoms

are often nonspecific. Manifestations often include progressive fatigue, malaise, weight

loss, and a low-grade fever accompanied by chills and night sweats.22 Wasting, a classic

feature of tuberculosis, is due to the lack of appetite and the altered metabolism associated

with the inflammatory and immune responses. Wasting involves the loss of both fat and

lean tissue; the decreased muscle mass contributes to the fatigue.23 Finger clubbing, a late

sign of poor oxygenation, may occur; however, it does not indicate the extent of

disease.24 A cough eventually develops in most patients. Although the cough may initially

be nonproductive, it advances to a productive cough of purulent sputum. The sputum may

also be streaked with blood. Hemoptysis can be due to destruction of a patent vessel

located in the wall of the cavity, the rupture of a dilated vessel in a cavity, or the formation

of an aspergilloma in an old cavity. The inflamed parenchyma may cause pleuritic chest

pain. Extensive disease may lead to dyspnea or orthopnea because the increased interstitial

volume leads to a decrease in lung diffusion capacity. Although many patients with active

disease have few physical findings, rales may be detected over involved areas during

inspiration, particularly after a cough. Hematologic studies might reveal anemia, which is

the cause of the weakness and fatigue. Leukocytosis may also occur because of the large

increase in the number of leukocytes, or white blood cells, in response to the infection.7

PATOGENENCY

The risk factor are :

1. must have infection sorce

2. the number of bacillus as an infection cause must be sufficient

3. the high virulence of TBC bacillus

4. The descent of body defense make the bacillus reproduce

Clinic illustration :

1. The main symptom

Continous cough with/without sputum during 3 weeks or more

2. Additional symptom

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- Sputum mixed with blood

- Haemoptoe

- Dyspnea and chest pain

- Weakness

- Night sweat

- Decrease weight

- Feverish fever more than 1 month

DIAGNOSIS

Lung TBC diagnosis can be stood at by BTA finding in sputum inspection microscopicly.

The inspection result tangibled positive if at least 2 from 3 SPS specimen must be positive.

If only 1 specimen which positive, so it’s needed a further check up, that is chest x-ray

photo or SPS sputum check up repeated.

a. If the x-ray result supports TBC, so the patient is diagnosed as TBC BTA sufferer

positive

b. If the x-ray result unsupports TBC, so the sputum check up repeated

If three sputum specimen are negative, give an extensive spectrum antibiotic during 1-2

weeks. If the condition still bad, do SPS sputum check up repeated.

a. If the SPS result are positive, diagnosed as infection TBC BTA infected

b. If the SPS result are still negative, do thr chest X-ray check up.

If the X-ray result supports TBC, diagnosed as negative BTA patient but

the X-ray positive

If the X-ray result not supports TBC, the patient is not TBC.

MEDICAL TREATMENT

Purpose :

1. Cure the patient

2. Prevent death

3. Prevent relapse

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4. Decreasing the level of spreading

Category 1 (2HRZE/4H3R3) :

New patient lung TBC positive BTA

Patient lung TBC negative BTA, X-ray positive who got serious illness

Patient heavy extra lung TBC

Intensive stage consist of Isoniasid(H), Rifampicin(R), Pirazinamid(Z), dan Etambutol(E).

Those medicine are given everyday during two (2) month (2HRZE). Then continued by

next stage, that consists of Isoniasid(H), and Rifampicin(R). Given three times a week

during four month (4H3R3).

Category 2 (2HRZES/HRZE/5H3R3E3) :

Relaps patient

Failure patient

After default patient

Intensive stage are given for three month consists of HRZES during 2 month given

everyday (2HRZES), continued by HRZE during 1 month given every day (HRZE). Then

continued by next stage that consists of HRE during 5 month given 3 times a week.

Category 3 (2HRZES/4H3R3) :

New patient BTA negative and X-ray positive, light ill.

Patient extra light lung, it is TBC limfadenitis, pleuritis eksudativa unilateral, skin

TBC, bone TBC (except backbone), joint TBC and adrenal gland.

Intensive stage consist of HRZ, given everyday during 2 month(2HRZ), continued by

sequel stage that consist of HR during 4 month given 3 times a week(4H3R3). One packet

of Combipac 3rd category contents of 114 daily blister that consist of 60 blister HRZ for

the intensive stage and 54 blister HR for the sequel stage each packed in a small doss and

bounded in a big doss.

Implied OAT (HRZE)

If the end of intensive treatment of new patient BTA positive in 1st category or patient

BTA positive retreatment by category 2nd, sputum check up result still BTA positive

(positive BTA), given medical implied (HRZE) everyday during 1 month.

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COMPLICATION OF TUBERCULOSIS

Without treatment, tuberculosis can be fatal. Untreated active disease typically affects

your lungs, but it can spread to other parts of the body through your bloodstream.

Examples include:

Bones. Spinal pain and joint destruction may result from TB that infects your bones. In

many cases, the ribs are affected.

Brain. Tuberculosis in your brain can cause meningitis, a sometimes fatal swelling of

the membranes that cover your brain and spinal cord.

Liver or kidneys. Your liver and kidneys help filter waste and impurities from your

bloodstream. These functions become impaired if the liver or kidneys are affected by

tuberculosis.

Heart. Tuberculosis can infect the tissues that surround your heart, causing

inflammation and fluid collections that may interfere with your heart's ability to pump

effectively. This condition, called cardiac tamponade, can be fatal.

PLEURAL EFFUSION IS CAUSED BY TUBERCULOSIS

DEFINITION

A pleural effusion is a collection of fluid in the space between the two linings (pleura) of

the lung.

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Pleural effusion is excess fluid that accumulates between the two pleural layers, the fluid-

filled space that surrounds the lungs. Excessive amounts of such fluid can impair breathing

by limiting the expansion of the lungs during ventilation.

When we breathe, it is like a bellows. We inhale air into our lungs and the ribs move out

and the diaphragm moves down. For the lung to expand, its lining has to slide along with

the chest wall movement. For this to happen, both the lungs and the ribs are covered with a

slippery lining called the pleura. A small amount of fluid acts as a lubricant for these two

surfaces to slide easily against each other.

Too much fluid impairs the ability of the lung to expand and move.

Pleural fluid is secreted by the parietal layer of the pleura and reabsorbed by the visceral

layer of the pleura.

Types of fluids

Four types of fluids can accumulate in the pleural space:

Serous fluid  (hydrothorax)

Blood  (haemothorax)

Chyle  (chylothorax)

Pus  (pyothorax or empyema)

ETIOLOGI

A pleural effusion is not normal. It is not a disease but rather a complication of an

underlying illness. Extra fluid (effusion) can occur for a variety of reasons. Common

classification systems divide pleural effusions based on the chemistry composition of the

fluid and what causes the effusion to be formed. Two classifications are 1) transudate

pleural effusions; and 2) exudate pleural effusions. Sometimes the pleural effusion can

have characteristics of both a transudate and an exudate.

1. Transudate pleural effusions are formed when fluid leaks from blood vessels into the

pleural space. Chemically, transudate pleural effusions contain less protein and LDH

(lactate dehydrogenase) than exudate pleural effusions. If both the pleural fluid–to–serum

total protein ratio is less than or equal to 0.50 and the pleural fluid–to–serum LDH ratios

are less than or equal to 0.67, the fluid is usually considered to be a transudate while

exudates ratios are above 0.50 and above 0.67.

Examples of transudate pleural effusions include:

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congestive heart failure ,

liver failure or cirrhosis,

kidney failure  or nephritic syndrome, and 

peritoneal dialysis .

2. Exudate pleural effusions are caused by inflammation of the pleura itself and are often

due to disease of the lung.

Examples of exudate causes include:

lung  or breast cancer,

lymphoma,

pneumonia ,

tuberculosis , 

post pericardotomy syndrome,

systemic lupus erythematosus ,

uremia or kidney failure,

Meigs syndrome,

pancreatic pseudocyst , 

ascites ,

intra abdominal abscess, and

asbestosis  and mesothelioma.

Most pleural effusions are caused by congestive heart failure, pneumonia, pulmonary

embolism and malignancy.

Transudate Exudate

Main causes

Increased hydrostatic

pressure,

Decreased colloid

osmotic pressure

Inflammation

Appearance Clear[5] Cloudy[5]

Specific gravity < 1.012 > 1.020

Protein content < 25 g/L > 35 g/L[6]

  fluid protein  

serum protein< 0.5 > 0.5[7]

Difference of > 1.2 g/dL < 1.2 g/dL[8]

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albumin content

with blood albumin

        fluid   LDH          

upper limit for serum< 0.6 or < ⅔ > 0.6[6] or > ⅔[7]

Cholesterol content < 45 mg/dL > 45 mg/dL[6]

See also: Rivalta test

SIGN AND SYMPTOM

Shortness of breath is the most common symptom of a pleural effusion. As the effusion

grows larger with more fluid, the harder it is for the lung to expand and the more difficult

it is for the patient to breathe.

Chest pain occurs because the pleural lining of the lung is irritated. The pain is usually

described as pleuritic, defined as a sharp pain, worsening with a deep breath. While the

pain may be localized to the chest, if the effusion causes inflammation of the diaphragm

(the muscle that divides the chest from the abdominal cavity) the pain may be referred to

the shoulder or the upper abdomen. As the pleural effusion increases in size, the pain may

increase.

Other associated symptoms are due to the underlying disease. For example, individuals

with:

congestive heart failure may complain of swelling of their feet and shortness of breath

when laying flat, (orthopnea) or wakening them in the middle of the night (paroxysmal

nocturnal dyspnea); 

tuberculosis may be have night sweats, cough up blood (hemoptysis), and loose weight;

hemoptysis may have associated infection and lung cancer;

pneumonia may complain of fever, shaking chills, cough producing colored sputum

and pleuritic pain.

Many patients with pleural effusions are asymptomatic. However, when symptoms arise,

they do so because of pleural inflammation or the effusion's effects on mechanics. The

most common symptoms of pleural effusion are dyspnea, nonproductive cough, and

pleuritic chest pain.

The mechanisms by which dyspnea occurs are not well understood, but they do not appear

to correlate with blood oxygen levels or the size of the pleural effusion. Dyspnea is

probably related to increased thoracic cage size, which affects respiratory muscle function.

31

Nonproductive cough may occur secondary to lung compression and resultant bronchial

irritation.

Pleuritic chest pain is associated with inflammation of the parietal pleura. Pain is

occasionally referred to the abdomen. If the central portion of diaphragmatic pleura is

involved, patients experience pain in the lower chest and ipsilateral shoulder

simultaneously. Historical features, including underlying disease processes, drug use, and

radiation therapy, can alert you to the possibility of pleural effusion in a patient with less

common symptoms.

Several physical findings suggest the presence of pleural effusion. Tactile fremitus is lost

over the area of effusion because voice-induced vibrations are attenuated by the fluid

adjacent to aerated lung. This finding is more sensitive than the use of percussion for

detecting pleural fluid collections.

Absent or diminished breath sounds over the area of effusion are characteristic. Pleural

friction rubs are occasionally noted in the initial stages or as the effusion resolves and are

caused by roughened pleural surfaces moving across one another.

DIAGNOSTIC AND TEST

Pleural effusion is usually diagnosed on the basis of medical history and physical exam,

and confirmed by chest x-ray. Once accumulated fluid is more than 300 ml, there are

usually detectable clinical signs in the patient, such as decreased movement of the chest on

the affected side, stony dullness to percussion over the fluid, diminished breath sounds on

the affected side, decreased vocal resonance and fremitus (though this is an inconsistent

and unreliable sign), and pleural friction rub. Above the effusion, where the lung is

compressed, there may be bronchial breathing and egophony. In large effusion there may

be tracheal deviation away from the effusion. A systematic review (2009) published as

part of the Rational Clinical Examination Series in the Journal of the American Medical

Association (JAMA) showed that dullness to conventional percussion was most accurate

for diagnosing pleural effusion (summary positive likelihood ratio, 8.7; 95% confidence

interval, 2.2–33.8), while the absence of reduced tactile vocal fremitus made pleural

effusion less likely (negative likelihood ratio, 0.21; 95% confidence interval, 0.12–0.37).[2]

Pleural effusions are often discovered by doctors attempting to determine the source of a

patient's symptoms. For example, a doctor examining a patient with a stethoscope may

notice soft breathing or a dull sound when tapping the patient's chest.

32

If a doctor suspects the existence of a pleural effusion, he or she may order X-rays to

confirm the diagnosis and determine how much fluid is present in the pleural space. If

congestive heart failure has been ruled out, the doctor may then perform a procedure

called thoracentesis to extract a small sample of the pleural fluid for analysis. Also known

as pleural fluid aspiration, this relatively painless procedure is done by inserting a needle

between the ribs to access the pleural space. The fluid is then extracted and examined

under a microscope to look for cancerous cells, bacteria and a protein called mesothelin.

New research suggests that high levels of mesothelin may indicate mesothelioma.

Ultrasound and/or a thoracic CT scan (CT scan of the chest) may also be ordered to

diagnose pleural effusions.

MECHANISME PLEURAL EFFUSION IN TUBERCULOSIS

The pleural space is 10 to 20 µm in width and normally contains about 0.1 mL/kg of fluid.

A volume greater than 7 to 14 mL is abnormal. Many mechanisms can result in abnormal

amounts of pleural fluid, including:

Increased hydrostatic pressures in the microvascular circulation.

Decreased oncotic pressures in the microvascular circulation.

Decreased pleural space pressure (resulting from lung collapse).

Increased permeability of the microvascular circulation.

Obstruction of lymphatic drainage

Generally, transudative effusions are formed in response to increased hydrostatic pressure,

while exudative effusions form when pleural inflammation or disrupted lymphatic

drainage results in increased protein leak or decreased protein removal from the pleural

space. In CHF, pleural effusions are secondary to pulmonary venous hypertension.

Neoplasms can cause pleural effusions by direct involvement of the pleura, by lymphatic

obstruction, or in association with a post-obstructive pneumonia. Pleural effusions

associated with pulmonary embolism are secondary to increased capillary permeability,

pleuropulmonary hemorrhage, and increased hydrostatic pressure.

Many different things can cause pleural effusion. Heart failure or other heart and lung

problems may cause pleural effusion. Infections (in-FECK-shuns) such as pneumonia

(noo-MOH-nyah) or tuberculosis (TB) may cause pleural effusion. Inflammation of the

pleura, called pleurisy (PLOOR-i-see), may cause pleural effusion. Other causes may

include cancer, injury, or problems with other organs in your chest or abdomen (belly).

33

Pleural effusion is a secondary disease being related to tuberculosis or other lung disease

such as TB, pneumonia etc. because there is irritation on the lining of pleural cavity, thus

altering the permeability of the membrane and decreasing the oncotic pressure needed to

drain the excess fluid in the pleural space. normally there is a small amount of pleural fluid

in the pleural space that lubricates the parietal and visceral pleura during expiring and

inspiring.

Primary pulmonary tuberculosis is often asymptomatic, so that the results of diagnostic

tests are the only evidence of the disease. Although primary disease essentially exists

subclinically, some self-limiting findings might be noticed in an assessment. Associated

paratracheal lymphadenopathy may occur because the bacilli spread from the lungs

through the lymphatic system. If the primary lesion enlarges, pleural effusion is a

distinguishing finding. This effusion develops because the bacilli infiltrate the pleural

space from an adjacent area. The effusion may remain small and resolve spontaneously, or

it may become large enough to induce symptoms such as fever, pleuritic chest pain, and

dyspnea. Dyspnea is due to poor gas exchange in the areas of affected lung tissue.

Dullness to percussion and a lack of breath sounds are physical findings indicative of a

pleural effusion because excess fluid has entered the pleural space.

COMPLICATION

Complications of pleural effusions include collapse of the lung; pneumothorax, or air in

the chest cavity, which is a common side effect of the thoracentesis procedure; and

empyemas (abscesses) caused by infection of the pleural fluid, which require drainage of

the fluid.

Pleural effusion can place patients with asbestosis or mesothelioma at even more risk than

other patients — if it leads to difficulty breathing. This is because patients with these

conditions so often suffer from pleural scarring, which itself makes it extremely difficult

to breathe. Pleural effusion can exacerbate this problem, and ultimately the inability to

breathe properly can contribute significantly to the patient's downward spiral.

Risks:

A pleural effusion may cause or worsen a lung infection, such as pneumonia. The extra

fluid may get infected and form a pocket of pus, which is called empyema (em-peye-EE-

ma). You may have other problems, such as a collapsed lung. The problems you may have

depend on what is causing your pleural effusion. Talk to your caregiver about any

concerns you may have about your illness or treatment.

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TREATMENT

In some cases, no treatment is required for pleural effusions. However, when doctors link

the fluid build-up to a patient's discomfort or pain — or to other, more serious side effects

— they often take measures to address the cause and/or effects of the effusion. As

previously mentioned, a patient suffering from asbestosis or mesothelioma may experience

more than one condition that makes it difficult to breathe. To address this, doctors do

whatever they can to treat the root causes.

For patients with pleural-effusion-related breathing problems, this may include the

following:

Thoracentesis. Further extraction of pleural fluid can alleviate pressure in the chest,

making it easier to breathe.

Once a pleural effusion is diagnosed, the cause must be determined. Pleural fluid is drawn

out of the pleural space in a process called thoracentesis. A needle is inserted through the

back of the chest wall in the sixth, seventh, or eighth intercostal space on the midaxillary

line, into the pleural space. The fluid may then be evaluated for the following:

1. Chemical composition including protein, lactate

dehydrogenase (LDH), albumin, amylase, pH, and glucose

2. Gram stain  and culture to identify possible bacterial infections

3. Cell  count and differential

4. Cytopathology  to identify cancer cells, but may also identify some infective

organisms

5. Other tests as suggested by the clinical situation – lipids, fungal culture, viral

culture, specific immunoglobulins

Chemical pleurodesis. This procedure involves the insertion of agents such as talc or

bleomycin to eliminate the pleural space altogether, so that fluid can no longer build up.

Therapeutic aspiration may be sufficient; larger effusions may require insertion of

an intercostal drain (either pigtail or surgical). When managing these chest tubes, it is

important to make sure the chest tubes do not become occluded or clogged. A clogged

chest tube in the setting of continued production of fluid will result in residual fluid left

behind when the chest tube is removed. This fluid can lead to complications such as

hypoxia due to lung collapse from the fluid, or fibrothorax, later, when the space scars

down. Repeated effusions may require chemical

35

(talc, bleomycin, tetracycline/doxycycline), or surgical pleurodesis, in which the two

pleural surfaces are scarred to each other so that no fluid can accumulate between them.

This is a surgical procedure that involves inserting a chest tube, then either mechanically

abrading the pleura or inserting the chemicals to induce a scar. This requires the chest tube

to stay in until the fluid drainage stops. This can take days to weeks and can require

prolonged hospitalizations. If the chest tube becomes clogged, fluid will be left behind and

the pleurodesis will fail.

Pleurodesis fails in as many as 30% of cases. An alternative is to place a PleurX Pleural

Catheter or Aspira Drainage Catheter. This is a 15Fr chest tube with a one-way valve.

Each day the patient or care givers connect it to a simple vacuum tube and remove from

600 cc to 1000 cc of fluid. This can be repeated daily. When not in use, the tube is capped.

This allows patients to be outside the hospital. For patients with malignant pleural

effusions, it allows them to continue chemotherapy, if indicated. Generally the tube is in

for about 30 days and then it is removed when the space undergoes a spontaneous

pleurodesis.

Pleural decortication. Also called pleurectomy, this surgery removes the pleura; like

chemical pleurodesis, pleural decortication eliminates the pleural space, thereby

preventing pleural fluid from building up.

Mesothelioma Lawyers

For more information on mesothelioma symptoms and other issues related to asbestos

exposure, asbestosis and malignant mesothelioma, please refer to other articles on our site.

If you or a family member has been diagnosed with an asbestos-related disease, contact a

mesothelioma attorney as soon as possible.

The treatment you receive may depend on what is causing your pleural effusion and how

bad your symptoms are. You may need medicines such as antibiotics (an-ti-bi-AH-tiks) to

prevent or treat a bacterial (bak-TEE-ree-al) infection. Steroids and other kinds of

medicines may be given to decrease inflammation. You may need medicines for pain.

Diuretic (deye-yoo-RET-ik) medicine may help you lose extra fluid caused by heart

failure or other problems. You may need to have the extra pleural fluid removed by having

a thoracentesis (thohr-ah-sen-TEE-sis) or a chest tube. During a thoracentesis, a needle is

used to remove the extra pleural fluid from around a lung. This fluid may be sent to the lab

for tests. A thoracentesis may help you breathe easier, and help your caregiver find the

36

best way to treat you. A chest tube is a tube that stays in your chest for days or weeks.

This lets the extra fluid around your lung drain out over time. You may need medicines

put directly into your chest if the fluid does not drain out easily.

Some people have pleural effusions that come back over and over. For example, a tumor

(growth) may cause extra fluid to keep collecting around a lung. If your pleural effusion

keeps coming back or if it increases your risk for other problems, you may need surgery or

other treatments. Ask your caregiver for more information about other treatments that you

may need.

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BIBLIOGRAPHY

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.

http://ccn.aacnjournals.org/content/29/2/34.full

http://www.allaboutmalignantmesothelioma.com/pleural-effusion.htm

http://www.consultantlive.com/display/article/10162/36884

http://www.medicinenet.com/pleural_effusion/page2.htm#risk

W, Aru. Sudoyo, et all. 2006. Ilmu Peyakit Dalam Ed IV Jilid I. Departemen Ilmu

Penyakit Dalam FKUI, Jakarta.

Yoga, Tjandra Aditama. 2006. TUBERKULOSIS PEDOMAN DAN PENATALAKSANAAN

DI INDONESIA. Perhimpunan Dokter Paru Indonesia, Jakarta.

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