TUBERCULOUS PLEURAL

EFFUSION DISEASE

Created by:

Dessy Eva Dermawaty, S. Ked.

Gita Augesti, S. Ked.

PATIENT STATUS
PATIENT IDENTITY

Initial Name
Sex
Age
Nationality
Marital Status
Religion
Occupation
Educational Background
Address

: Mr. S
: Male
: 42 years old
: Indonesia (Javanese)
: Married
: Islam
: Freelance Workers
: Elementary School
: Kangkung

ANAMNESIS
Taken from
Date
Time

: Autoanamnesis
: June 8th, 2015
: 16.15

Chief Complain
: Dyspnea
Additional Complaint
: Productive cough, chills,
fever, decrease appetite, colic pain.

HISTORY OF THE PRESENT

ILLNESS :

Patient came to hospital and told that he has

gotten a dyspneu since one week ago, and it was
getting worse on the seventh day. Dyspneu felt
worst when the patient was doing his activities
and in lying position. Tightness will be reduced if
the patient is in the down position or sitting
position. Patient also felt difficulty to throw the
greeny mucus when he was coughing up. The
patient also felt colic pain, chills at night, fever,
and decrease apppetite.

Patient felt dyspneu and productive cough since 3 weeks

ago. He said that he has treated in a hospital 3 times.
History of bleeded cough was denied. History of taking
6 months drug package was denied. History of family
disease is hypertention in his father. History of
Asthma was denied. He had been a smoker since 40
years ago (1packs/day). The patient works as a
freelance worker and often affected by dust.

Familys diseases History :

Familys Disease History is hypertention in his
father.

Is there any family who suffer :

Patient didnt know

Weight

Average weight (kg)

: - kg

Height (cm)

: 165cm

Present Weight : 80 kg

(if the patient doesnt know certainly)

(-) steady
(+) down
(-) up

THE HISTORY OF LIFE

Birth place
(+) in home

(-) matrinity

Helped by:
(+) Traditional matrinity

(-) Doctor

Imunitation History (Unknown)

(-) Hepatitis (-) BCG (-) Campak
Food History
Frequency/day
Amount/day
Variation/day
Appetite

(-) matrinity hospital

(-) Nurse

(-) DPT (-) Polio Tetanus

: 3x/day
: 1 place/eat (health)
: Rice, vegetables, fish
: Decrease

(-) Others

Educational
(+) Elementary school
Problem
Financial
Works
Family
Others

(-) SMP (-) SMA

: low
:: Bad Relation
:-

Body Check Up
General Check Up
Height
: 165 cm
Weight
: 80 kg
Blood Pressure: 120/80 mmHg
Pulse
: 88x/minute
Temperature
: 36,60C

(-)SMK (-) Course Academy

Breath (Frequence&type)
Nutrition Condition
Consciousness
Cyanotic
General Edema
The way of walk
Mobility
The age predicyion based on check up

Mentality Aspects

Behavior

: Normal

Nature of Feeling

: Normal

The thinking of process : Normal

: 20x/minute
: Fat, IMT 29,38
: Compos Mentis
: (-)
: (-)
: Normal
: Active
: 42 years old

Skin

Color
: Olive
Keloid
Pigmentasi
Hair Growth
Arteries
Touch temperature
Humid/dry
Sweat
Turgor
Icterus
Fat Layers
Efloresensi
Edema
Others

: (-)
: (-)
: Normal
: Touchable
: Afrebris
: Dry
: Normal
: Normal
: Anicteric
: Enough
: (-)
: (-)
: (-)

Lymphatic Gland
Submandibula
Neck
Supraclavicula
Armpit

: no enlargement
: no enlargement
: no enlargement
: no enlargement

Head
Face Expression
Face Symmetric
Hair
Temporal artery
Eye

: looked moderate illness

: Symmetric
: Black
: Normal

Exopthalmus
Enopthalmus
Palpebra
Lens
Conjunctiva
Visus
Sklera

: (-)
: (-)
: edema (-)/(-)
: Clear/Clear
: Anemis +/+
: Normal
: Anicteric

Ear
Deafnes
Foramen
Membrane tymphani
Obstruction
Serumen
Bleeding
Liquid
Mouth
Lip
Tonsil
Palatal

: (-)
: (-)
: normal
: (-)
: (-)
: (-)
: (-)

: (-)
: (-)
: Normal

Halibsts

: No

Teeth

: (-)

Trismus
Farings
Liquid Layers
Tongue

: (-)
: Unhiperemis
: (-)
: Clean

Neck
JVP
Tiroid Gland
Limfe Gland

: Normal
: no enlargement
: no enlargement

Chest
Shape
Artery
Breast

: Simetric
: Normal
: Normal

Lung

Inspection : Left : simetric, normal

Right: simetric, normal

Palpation : Left : vocal fremitus decreased, pain (-)

Right : vocal fremitus normal,
pain (-)

Percussion : Left : redup

Right: redup

Auscultation

: Left : vesicular decrease

Right: vesicular normal

Cor

Inspection : Ictus cordis invisible.

Palpation : Ictus Cordis feel in ICS V left midclavicula

Percussion : difficult to essess

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
Palpation

Percussion
Auscultation

: distended , Symetrics
: Stomach Wall: undulation (-), pain (-)
Heart
: Hepatomegali (-)
Limfe
: Splenomegali (-)
Kidney
: Ballotement (-)
: Shifting Dullness (-)
: Intestine Sounds (+)

Movement Joint
Arm Right Left
Muscle
Normal Normal
Tones Normal Normal
Mass Normal Normal
Joint Normal Normal
Movement
Normal Normal
Strength
Normal Normal
Heel and Leg

Wound/injury

: not found

Varices

Muscle (tones&mass)

Joint : Normal

Movement

Strength/Power

Edema

: (-)

Others

: (-)

: (-)
: Normal

: Normal
: Normal

Reflexs
Right
Tendon Reflex
Normal
Bisep
Normal
Trisep
Normal
Pattela
Normal
Achiles
Normal
Cremaster
Normal
Skin Reflex
Normal
Patologic Reflex Not Found

Left
Normal
Normal
Normal
Normal
Normal
Normal
Normal
Not Found

LABORATORY
Routine Blood
Hb
: 12,8 gr/dl
Leukosit
: 11.080/ mikroliter
LED
: 58 mm/jam
Trombosit : 555.000
Diff. Count
Basofil
: 0%
Eosinofil
: 0%
Stem
: 0%
Segment
: 77%
Limfosit
: 12%
Monosit
: 11%

Blood Chemistry Test.

SGOT
: 48
SGPT
: 108
GDS
: 113
Ureum
: 26 mg/dl
Creatinine : 1 mg/dl
BTA Test
One Time : (-)
Morning
: (-)
One Time : (-)

Pleural Analysis
Macroscopic.
Color
: Yellow and cloudy
Microscopic.
Cell count : >1000 cell/Ul
Glucose
: 138 mg/dl
Protein
: 5,4gr/Ul
PMN
: 16%
MN
: 84%
Rivalta Test: Positive
PH
:7,7

Normal: 0-5 cell/Ul

Normal: 50-80 mg/dL

Anatomic Patology Test

There is no malignancy detected, and the morphology
found was consistent with Tuberculous pathology
anatomy

CHEST X-RAY
PULMO: HIPERLUSENT, INTERCOSTAL SPACE
INCREASE, FLATTER DIAFRAGHM

RESUME
Patient came to hospital and told that he has gotten a dyspneu
since one week ago, and it was getting worse on the seventh day.
Dyspneu felt worst when the patient was doing his activities and
in lying position. Tightness will be reduced if the patient is in the
down position or sitting position. Patient also felt difficulty to
throw the greeny mucus when he was coughing up. The patient
also felt colic pain, chills at night, fever, and decrease apppetite.

Patient felt dyspneu and productive cough since 3 weeks ago. He

said that he has treated in a hospital 3 times. History of bleeded
cough was denied. History of taking 6 months drug package was
denied. History of family disease is hypertention in his father.
History of Asthma was denied. He had been a smoker since 40
years ago (1packs/day). The patient works as a freelance worker
and often affected by dust.

Working Diagnose

Tuberculous Pleural Effusion

Basic Diagnose

a. Anamnesis
Recurrent cough with or without sputum greenist white.
Dyspneu with smooth wet crackles
Chills
Sweat
Fever
Malaise
b. Physics Examination
Vocal Fremitus decrease
Dim percussion
Smooth wet crackles.

Support Examination
Leucocyte increase : 11.080
SGOT and SGPT increase : 48 & 108
Chest X-Ray
: : hiperlusent in left lung
Pathology Anatomi test : Positif (+) Tuberculosa
Rivalta Test : Positif (+)

Differential Diagnose
Destroyed Lung
Pneumonia
Ca Paru
Bronchitis
Cor abnormality

Basic Differential Diagnose

Anamnesis
Chronic Productive Cough
Dyspneu with smooth wet crackles
Chills
Sweat
Fever

Physics Examination
Vocal Fremitus decrease
Dim percussion
Smooth wet crackles.
Support Examination
Leucocyte increase : 11.080
SGOT and SGPT increase : 48 & 108

Support Check Up

Check sputum smear (culture and resistance)

Check smear of pleural fluid (culture and resistance)

Re-check your blood sugar after correction

Laboratory
Ureum Creatinin
Electrolite
GDS
Lipid Profile
Uric Acid
Albumin

TREATMENT PLAN
(1) General Treatment
Bed Rest
Nutrition (high calory, high protein)
(2) Special Treatment
Non Medicamentosa
Stop

Tobacco
Avoid Tobacco Smoke
Activity adjustment
Go to doctor immedietly if appear any symptoms

Medicamentosa

O2 3-4L/minute

IVFD RL gtt XX/minute

Rifampicin 600mg
INH 300 mg
Pirazinamide 1000mg
Etambutol 1000mg
Ceftriaxone inj 1 gram/12 hour
Aminophilin 1 amp/ drip
Salbutamol tab 0,5 mg / GGI / Cetirizine / Metil Prednisolon
2mg 3 caps 1
Paracetamol 3 x 500 mg tab
Ranitidine inj 1amp / 12 hour
Mucogard 3xCII
Metil Prednisolon 3 x 16mg Tapp off
Curcuma 2x1

Prognose
Quo ad Vitam
Quo ad Functonam
Quo ad Sanationam

: Dubia ad bonam
: Dubia ad bonam
: Dubia ad bonam

REFERENCE
Pleural Effusion et cause Tuberculosa
Tuberculous pleural effusions occur in up to 30% of patients with
tuberculosis. Tuberculosis (TB) is a major public health problem in
developing countries. Although the majority of patients with TB
have pulmonary TB, extrapulmonary TB affecting mainly the
lymph nodes and pleura serves as the initial presentation in about
25% of adults. TB is the leading cause of pleural effusions in some
countries. It is important to consider the possibility of tuber- culous
pleuritis in all patients with an undiagnosed pleural effusion. A
pleural effusion as an isolated manifestation of TB has been likened
to a primary chancre as a manifestation of syphilis. Both are selflimited and of little immediate concern, but both may lead to
serious disease many years later. Tuberculous pleuritis is thought
to represent primarily a hypersensitivity reaction to tuberculous
protein and the bacillary burden in the pleural space is low.

INCIDENCE

The percentage of patients with TB who have pleural

effusions has varied markedly from county to country.
In Burundi more than 25% of patient with TB have
tuberculous pleural effusions while in South Africa
20% of TB patients have tuberculous pleural effusions.
In contrast only 35% of patients in the USA are
reported to have tuberculous pleural effusions.The
lower percentage in the USA is probably in part due to
under reporting of the disease in the USA because the
pleural fluid cultures are frequently negative.

PATHOGENESIS

The current hypothesis for the pathogenesis of primary

tuberculous pleural effusion is that a subpleural caseous
focus in the lung ruptures into the pleural space 612
weeks after a primary infection. Mycobacterial antigens
enter the pleural space and interact with T-cells previously
sensitized to mycobacteria resulting in a delayed
hypersensitivity reaction and the accumulation of fluid. It
seems that this reaction of the pleura augments the entry
of fluid into the pleural space by increasing the
permeability of pleural capillaries to serum proteins, and
thereby increasing the oncotic pressure in the pleural fluid.
Involvement of the lymphatic system probably also
contributes to the accumulation of pleural fluid. An
impaired clearance of proteins from the pleural space has
been reported in human tuberculous effusions.

CLINICAL MANIFESTASION

TB was the third leading cause of large or massive pleural

effusion (12%) after malignancy (55%) and pneumonia (22%).
The most frequent symptoms are cough (70%), which is usually
non-productive and chest pain (70%), which is usually pleuritic in
nature. If both cough and pleuritic pain are present, the pain
usually precedes the cough.
Most patients are febrile but approximately 15% will be afebrile.
Patients with tuberculous pleural effusions may be dyspneic if the
effusion is large.
On occasions the onset of tuberculous pleuritis is less acute with
mild chest pain, at most a low grade fever, a non-productive
cough, weight loss and easy fatigability.
The pleural effusions secondary to tuberculous pleuritis are
usually unilateral and can be of any size.

PLEURAL FLUID CHARACTERISTICS

The pleural fluid with tuberculous pleuritis is
invariably an exudate. Indeed, the pleural fluid protein
level frequently exceeds 5 g/dL and this finding
suggests tuberculous pleuritis.
The pleural fluid glucose level with tuberculous pleural
effusions may be reduced but it usually is similar to
the serum level.
The pleural fluid pH is usually above 7.30, but it also
may be reduced.

DIAGNOSIS

Mycobacterial stain and culture

One test that is frequently overlooked in the diagnostic work-up of
patients with an undiagnosed pleural effusion is examination of
the sputum for mycobacteria. Conde and associated prospectively
evaluated the diagnostic yield of mycobacterial smears and
cultures in 84 patients with tuberculous pleuritis. They induced
sputum in those unable to spontaneously expectorate. They
reported that the sputum studies were positive in 44 of the 84
patients (52%). In 10 of the 44 patients, sputum smears were
positive, whereas cultures were positive in all. The sputum was
positive in 35 of 64 patients (55%) who had a normal chest
radiograph except for the effusion and in whom the sputum was
induced. Probably sputum examination is underutilized in the
diagnosis of tuberculous pleuritis.

Adenosine deaminase
Testing for pleural fluid ADA levels is an easy and
inexpensive method for establishing the diagnosis of
TB pleuritis.
Sensitivity and specificity of ADA in the diagnosis of
pleural TB were 92% and 90%, respectively.
The most widely accepted cut-off value for pleural fluid
ADA is 40 U/L. The higher the level, the greater the
chance of the patient having TB while the lower the
level the lesser the chance of the patient having TB.

Pleural Biopsy
The most common way to make the diagnosis of
tuberculous pleuritis over the past 50 years has been
with a blind needle biopsy of the pleura.

TREATMENT
The treatment of tuberculous pleuritis has three
goals:
to prevent the subsequent development of active
TB,
to relieve the symptoms of the patient, and
to prevent the development of a fibrothorax.

CHEMOTHERAPY
The recommendation for the treatment all of
pulmonary and ekstrapulmonary TB are as follow.
The initial phase of a 6-month regimen should consist
of a 2-month period of isoniazid (INH), rifampicin and
pyrazinamide. Ethambutol should be included in the
initial regimen until the results of drug susceptibility
studies are available, unless there is little possibility of
drug resistance.
The second phase of the treatment should be INH and
rifampin given for 4 months. Directly observed therapy
(DOT) is recommended. Nine-month regimens using
INH and rifampicin are also effective when the
organisms are fully susceptible to the drug.

With treatment, the patients symptoms and radiological

abnormalities gradually abate. The typical patient
becomes afebrile within 2 weeks, but temperature
elevations may persist as long as 2 months.
The mean time for the complete resorption of pleural
fluid is approximately 6 weeks, but it can be as long as
12 weeks.

CORTICOSTEROIDS
The role of corticosteroids in the treatment of
tuber- culous pleurisy is controversial. In two
controlled studies in which therapeutical
thoracentesis was performed there were no
benefits. In a third study in which no
therapeutical thoracentesis was performed, the
duration of fever and the time required for fluid
resorption were decreased. The administration of
corticosteroids did not decrease the degree of
residual pleural thickening and 6 or 12 months
after therapy was initiated in any of the three
studies.

The recommended approach to the patient with

tuberculous pleuritis is as follows. If the
patient is more than mildly symptomatic, a
therapeutical thoracentesis is recommended. If
the patient continues to have severe systemic
symptoms (fever, malaise, pleuritic chest pain)
after the therapeutical thoracentesis, the
administration of 80 mg of prednisone every
other day until the acute symptoms have
subsided is recommended. Thereafter the
corticosteroids are rapidly tapered.

REFERENCE
Buku

Ajar Ilmu Penyakit Dalam Jilid III

Edisi V (2009)
Buku Interna Harrison
Konsensus PDPI (Tuberculosis Pedoman
Diagnosis dan Penatalaksanaan di Indonesia
2003)
Yew, Wing.W, Migliori, Giovanni.B, Lange,C.
2010. Update on Tuberculous Effusion
Pleura. Respirology J. 15 : 451458.
H. Hamm and R.W. Light. 1997. Pleural
tuberculosis. Eur Respir J, 10: 942947.

THANK YOU
:^)