DEXTRA PLEURAL EFFUSION ET CAUSA SUSPECT

PULMONARY TB

Created by
Elvi Yana

1018011057

Farah Bilqistiputri

1018011060

Perceptor:
dr. Dedy Zairus, Sp.P

CLINICAL WORK OF INTERNAL MEDICINE

SMF PULMONOLOGY
PERIOD OCTOBER TO DECEMBER 2014
ABDUL MOELOEK HOSPITAL
BANDAR LAMPUNG
1

I. PATIENT STATUS

PATIENT IDENTITY
Initial Name

: Mss. MS

Sex

: Female

Age

: 19 years old

Nationally

: Indonesia (Lampungnese)

Marital Status

: Single

Religion

: Islam

Occupation

: Cashier

Educational Background

: Junior High School

Address

: Rajabasa, Lampung

ANAMNESIS
Taken from

: Autoanamnesis

Date

: October, 21st, 2014

Time

: 14.00

Chief Complain

: Shortness of breath since a week ago

Additional Complaint :Fever and cough with phlegm; transparant; thick; blood appearance
(-), since 3 weeks ago, loss of apetite and loss of wheight, night chills.
History of The Present Illness :
Three weeks ago, patients felt fever and cough with phlegm heavely in debt, and become a
shortness of breath 2 weeks later. The pleghm was transparant, thick, and has no blood
appearance (-).Another sypmtoms are loss of apetite and loss of wheight (from 50 kg to 45
kg). The patient had a work partner that has a same symptoms. She never felt the severe
shortness of breath before. Patient deny have previous high blood preassure, diabetes melitus,
and asthma. And the Patient was not a smoker. The doctor suggest the patient to examine
agen to the RS. Abdul Moeloek, to get the comperhensive treatment.
2

The History of Illness :

(-)
(-)
(-)
(-)
(-)
(+)
(-)
(-)
(-)
(-)
(-)

Small pox
Chicken pox
Difthery
Pertusis
Measles
Influenza
Tonsilitis
Kholera
Acute Rheumatoid Fever
Pneumonia
Pleuritic

(-)
(-)
(-)
(-)
(-)
(-)
(-)
(-)
(-)
(-)
(-)

Malaria
Disentri
Hepatitis
TifusAbdominalis
Skirofula
Siphilis
Gonore
Hipertension.
Ventrikuli Ulcer
Duodeni Ulcer
Gastritis

(-)
(-)
(-)
(-)
(-)
(-)
(-)
(-)
(-)

Kidney stone
Hernia
Prostat
Melena
Diabetic
Alergy
Tumor
Vaskular Disease
Operation

Familys diseases History :

Father still alive, healthy
Mother still alive, healthy.
Three siblings still alive, healthy.
Is there any family who suffer :
There are no family member who suffer with the same symptoms or had been diagnose with
pleural effusion.
SYSTEM ANAMNESE
Note of Positive Complaints beside the title
Skin
(-) Boil

(-)

Hair

(-) Night sweat

(-) Nail

(-)

Yellow /Werus

(-) Cyanotic
(-) Others

Head
(-) Trauma

(-)

Headache

(-) Syncope

(-)

Pain of the sinus

Ear
(-) Pain

(-) Tinitus

(-) Secret

(-) Ear disorders

3

(-) Deafness
Nose
(-) Trauma

(-) Clogging

(-) Pain
(-) Sekret
(-) Epistaksis

(-) Nose disorders

(-) common cold

Mouth
(-) Lip

(-) Dirty Tongue

(-) Gums
(-) Membrane

(-) Mouth disorders

(-) Stomatitis

Throat
(-) Throat Pain

(-) Voice Change

(-) Protruding

(-) Neck Pain

Neck

Cor/ Lung
(-) Chest pain

(+) Dyspneu

(-) Pulse

(-) Hemoptoe

(-) Ortopneu

(+) Cough, with white thick phlegm

Abdomen (Gaster/ Intestine)

(-) Puffing

(-)

Acites

(-)
(-)
(-)
(-)
(-)

(-)
(-)
(-)
(-)
(-)
(-)

Hemoroid
Diarrhea
Melena
Pale colour of feses
Black colour of feses
Nodul

(-) Dysuria

(-)

Pyuria

(-) Stranguria
(-) Polyuria
(-) Polakysuria

(-)
(-)
(-)

Kolik
Oliguria
Anuria

Nausea
Emesis
Hematemesis
Disfagi
Colic

Urogenital

(-) Hematuria
(-) Kidney stone
(-) Wet the bed

(-)
(-)
(-)

Urine retention
Drip urine
Prostat

Katamenis
(-)

Leukorhoe

(-)

Other

(-)

Bleeding

Muscle and Neuron

(-)

Anestesi

(-)

Hard to bite

(-)
(-)
(-)
(-)
(-)

Parestesi
Weak muscle
Afasia
Amnesis
Others

(-)
(-)
(-)
(-)
(-)

Ataksia
Hipo/hiper-estesi
Tick
Vertigo
Disartri

(-)

Convultion

(-)

Syncope

Extremities
(-) Edema

(-)

Deformitas

(-) Hinge pain

(-)

Cyanotic

Weight
Average weight (kg) : 50 kg
Height (cm)

: 155 cm

Present Weight

: 45 kg

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

THE HISTORY OF LIFE

Birth place
(+) in home

(-) matrinity

(-) matrinity hospital

Helped by:
(+) Traditional matrinity

(-) Doctor

(-) Nurse

(-) Others

(-) DPT

(-) Polio Tetanus

Imunitation History (Unknown)

(-) Hepatitis

(-) BCG

(-) Campak

Food History
Frequency/day

: 3x/day

Amount/day

: 1 place/eat (health)

Variation/day

: Rice, vegetables, fish

Appetite

: Decrease

Educational
(-) SD

(+) SMP

(-) SMA

(-)SMK

(-) Course Academy

Problem
Financial

: low

Works

:-

Family

: normal

Others

:-

Body Check Up
General Check Up
Height

: 155 cm

Weight

: 45 kg

Blood Pressure

: 120/80mmHg

Pulse

: 100 x/minute, regular, tense and feeling enough

Temperature

: 36.5 0C

Breath (Frequence&type)

:40x/minute, regular, thorako-abdominal

Nutrition Condition

: Normal,
6

Consciousness

: Compos Mentis

Cyanotic

: (-)

General Edema

: normal

The way of walk

: normal

Mobility

: Active

The age predicyion based on check up

: 19 years old

Mentality Aspects
Behavior

: Normal

Nature of Feeling

: Normal

The thinking of process

: Normal

Skin
Color

: Olive

Keloid

: (-)

Pigmentasi

: (-)

Hair Growth

: Normal

Arteries

: Touchable

Touch temperature

: Afrebris

Humid/dry

: Dry

Sweat

: Normal

Turgor

: Normal

Icterus

: Normal

Fat Layers

: Enough

Efloresensi

: (-)

Edema

: (-)

Others

: (-)

Lymphatic Gland
Submandibula

: no enlargement

Neck

: enlargement

Supraclavicula

: enlargement

Armpit

: no enlargement

Head
Face Expression

: Normal

Face Symmetric

: Symmetric

Hair

: Black

Temporal artery

: Normal

Eye
Exopthalmus

: (-)

Enopthalmus

: (-)

Palpebra

: edema (-)/(-)

Lens

: Clear/Clear

Conjunctiva

: Anemis -/-

Visus

: Normal

Sklera

: Icteric -/-

Ear
Deafnes

: (-)

Foramen

: (-)

Membrane tymphani : intact

Obstruction

: (-)

Serumen

: (-)

Bleeding

: (-)

Liquid

: (-)

Mouth
Lip

: (-)

Tonsil

: (-)

Palatal

: Normal

Halibsts

: No

Teeth

: (-)

Trismus

: (-)

Farings

: Unhiperemis

Liquid Layers

: (-)

Tongue

: Normal
8

Neck
JVP

: Normal

Tiroid Gland

: no enlargement

Limfe Gland

: enlargement

Chest
Shape

: Simetric

Artery

: Normal

Breast

: Normal

Lung
Inspection

: Left : asimetric, no lession, normochest

Right : asimetric, no lession, normochest

Palpation

: Left : vokal fremitus normal, pain (-)

Right : vokal fremitus decreased, pain (-)

Percussion

: Left : resonance
Right : flatness

Auscultation : Left : vesiculer normal, wheezing (-), ronkhi (-)

Right : vesiculer decrease, wheezing (-), ronkhi (-)
Cor
Inspection

: Ictus cordis not visible

Palpation

: Ictus Cordis no palpable

Percussion

: top: ICS II linea parasternal 2

Right: ICS IV linea sternalis dekstra
Left: ICS VI linea mid clavicula sinistra

Auscultation : Heart Sound 1 & 2 Regular, murmur (-), gallop (-)

Artery
Temporalic artery

: No aberration

Caritic artery

: No aberration

Brachial artery

: No aberration

Radial artery

: No aberration
9

Femoral artery

: No aberration

Poplitea artery

: No aberration

Posterior tibialis artery

: No aberration

Stomach
Inspection

: convex

Palpation

: Stomach Wall

: undulation (-), pain (-)

Heart

: Hepatomegali (-)

Limfe

: Splenomegali (-)

Kidney

: Ballotement (-)

Percussion

: Shifting Dullness (-)

Auscultation

: Intestine Sounds (+)

Genital (based on indication)

Male

: no indication

Penis

: no indication

Testis

: no indication

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
Varices

: not found
: (-)

Muscle (tones&mass)

: Normal

Joint

: Normal

Movement

: Normal

Strength/Power

: Normal
10

Edema

: (-) (pitting 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
Hematology (21-10-2014)

Normal

Haemoglobin

: 9.6 gr/dl

12-16 gr/dl

Leucocyte

: 8000 /ul

4500-10700 / ul

Basophils

:0%

0-1%

Eusinophils

:2%

1-3%

Bands

:0%

2-6%

Segmens

: 71 %

50-70%

Lymphocytes

: 22 %

20-40%

Monocytes

:5%

2-8%

Trombocyte

: 340.000 /ul

150.000-400.000/ul

Malaria

: (-) not found

Variety count

11

Radiology
5-6-2014 PA chest radiograph: pleural effusion dekstra, suspect TB

12

24-10-2014 Rontgen Thorax PA Post Pleural Punction

FNAB Cytology (21-10-2014)

Chronic Inflamation Cell, usually occurs in TB
RIVALTA TEST (21-10-2014)
Macroscopic

Colour : Yellow

Clearness : Cloudy

Microscopic

Normal

Cell count : 900 sel/ul

0-5 sel /uL

Glucose

: 67 mg/dl

50-80 mg/dL

Protein

: 4,7 gr/dl

3 gr/uL
13

Chloride

:-

PMN

: 8%

MN

: 92%

pH

:8

LDH

: 841 mg/dL

720-750 mg Cl.dL

Result : Rivalta test (+) (Excudate)

Resume
Patient Mss. MS (19th), three weeks ago, patients felt fever and cough with phlegm heavely in
debt, and become a shortness of breath 2 weeks later. The pleghm was transparant, thick, and
has no blood appearance (-).Another sypmtoms are loss of apetite and loss of wheight (from
50 kg to 45 kg). The patient had a work partner that has a same symptoms. She never felt the
severe shortness of breath before. Patient deny have previous high blood preassure, diabetes
melitus, and asthma. And the Patient was not a smoker. The doctor suggest the patient to
examine agen to the RS. Abdul Moeloek, to get the comperhensive treatment.

Working Diagnose
-

Effusion Pleura e.c. Suspect Pulmonary TB

Basic Diagnose

Anamnesa: shortness of breath, cough with phlegm; transparant, thick, blood appearance (-),
chest pain with characteristic worsening when coughing and deep breathing, loss of apetite
and loss of wheight (from 50 kg to 45 kg). Without fever and sweating at night.

Patient was non active smooker. The patient had a work partner that has a same symptoms.

PA chest radiograph: pleural effusion dekstra

Differential Diagnose

Effusion Pleura e.c. Suspect Pulmonary TB

Parapneumonic effusion
Support Check Up
14

Laboratory
o Ureum Creatinin
o Electrolite
o GDS
o Lipid Profile
o Uric Acid
o Albumin

Rivalta test

Sitology

Treatment Plan
(1) General Treatment
-

Bed Rest

Nutrition (high calory, high protein)

(2) Special Treatment

-

Medicamentosa
o IVFD RL gtt 20X/minute
o Ceftriaxone 2x1 amp
o Ambroxol 3x1
o Dexamethasone 3x1 amp
o Rifampisin 450 mg 1x1 tab
o Isoniazid 300 mg 1x1 tab
o Pirazinamid 1000 mg 1x1 tab
o Etambutol 1000 mg 1x1 tab

Non Medicamentosa
o Therapeutic thoracentesis
o Activity adjustment

Prognose
Quo ad Vitam

: Dubia ad bonam

Quo ad Functonam

: Dubia ad bonam

Quo ad Sanationam

: Dubia ad malam
15

16

II. REVIEW LITERATURE

A. Definition
The pleural space lies between the lung and the chest wall and normally contains a very thin
layer of fluid, which serves as a coupling system. A pleural effusion is present when there is
an excess quantity of fluid in the pleural space.
B. Etiology
Pleural fluid accumulates when pleural fluid formation exceeds pleural fluid absorption.
Normally, fluid enters the pleural space from the capillaries in the parietal pleura and is
removed via the lymphatics in the parietal pleura. Fluid also can enter the pleural space from
the interstitial spaces of the lung via the visceral pleura or from the peritoneal cavity via small
holes in the diaphragm. The lymphatics have the capacity to absorb 20 times more fluid than
is formed normally. Accordingly, a pleural effusion may develop when there is excess pleural
fluid formation (from the interstitial spaces of the lung, the parietal pleura, or the peritoneal
cavity) or when there is decreased fluid removal by the lymphatics.
Diagnostic Approach
When a patient is found to have a pleural effusion, an effort should be made to determine the
cause.

17

The first step is to determine whether the effusion is a transudate or an exudate. A

transudative pleural effusion occurs when systemic factors that influence the formation and
absorption of pleural fluid are altered. The leading causes of transudative pleural effusions in
the United States are left-ventricular failure and cirrhosis. An exudative pleural effusion
occurs when local factors that influence the formation and absorption of pleural fluid are
altered. The leading causes of exudative pleural effusions are bacterial pneumonia,
malignancy, viral infection, and pulmonary embolism. The primary reason for making this
differentiation is that additional diagnostic procedures are indicated with exudative effusions
to define the cause of the local disease.
Transudative and exudative pleural effusions are distinguished by measuring the lactate
dehydrogenase (LDH) and protein levels in the pleural fluid. Exudative pleural effusions
meet at least one of the following criteria, whereas transudative pleural effusions meet none:

18

1. Pleural fluid protein/serum protein >0.5

2. Pleural fluid LDH/serum LDH >0.6
3. Pleural fluid LDH more than two-thirds normal upper limit for serum
These criteria misidentify ~25% of transudates as exudates. If one or more of the exudative
criteria are met and the patient is clinically thought to have a condition producing a
transudative effusion, the difference between the protein levels in the serum and the pleural
fluid should be measured. If this gradient is >31 g/L (3.1 g/dL), the exudative categorization
by these criteria can be ignored because almost all such patients have a transudative pleural
effusion.
If a patient has an exudative pleural effusion, the following tests on the pleural fluid should
be obtained: description of the appearance of the fluid, glucose level, differential cell count,
microbiologic studies, and cytology.

Table 263-1 Differential Diagnoses of Pleural Effusions

Transudative Pleural Effusions
1. Congestive heart failure

5. Peritoneal dialysis

2. Cirrhosis

6. Superior vena cava obstruction

3. Pulmonary embolization

7. Myxedema

4. Nephrotic syndrome

8. Urinothorax

Exudative Pleural Effusions

1. Neoplastic diseases

6. Post-coronary artery bypass surgery

a. Metastatic disease

7. Asbestos exposure

b. Mesothelioma

8. Sarcoidosis

2. Infectious diseases
a. Bacterial infections

9. Uremia
10. Meigs' syndrome

19

b. Tuberculosis

11. Yellow nail syndrome

c. Fungal infections

12. Drug-induced pleural disease

d. Viral infections

a. Nitrofurantoin

e. Parasitic infections

b. Dantrolene

3. Pulmonary embolization

c. Methysergide

4. Gastrointestinal disease

d. Bromocriptine

a. Esophageal perforation

e. Procarbazine

b. Pancreatic disease

f. Amiodarone

c. Intraabdominal abscesses

g. Dasatinib

d. Diaphragmatic hernia

13. Trapped lung

e. After abdominal surgery

14. Radiation therapy

f. Endoscopic variceal sclerotherapy

15. Post-cardiac injury syndrome

g. After liver transplant

16. Hemothorax

5. Collagen vascular diseases

17. Iatrogenic injury

a. Rheumatoid pleuritis

18. Ovarian hyperstimulation syndrome

b. Systemic lupus erythematosus

19. Pericardial disease

c. Drug-induced lupus

20. Chylothorax

d. Immunoblastic lymphadenopathy
e. Sjgren's syndrome
f. Granulomatosis with polyangiitis (Wegener's)
g. Churg-Strauss syndrome

1. Effusion due to heart failure

The most common cause of pleural effusion is left-ventricular failure. The effusion occurs
because the increased amounts of fluid in the lung interstitial spaces exit in part across the

20

visceral pleura; this overwhelms the capacity of the lymphatics in the parietal pleura to
remove fluid. In patients with heart failure, a diagnostic thoracentesis should be performed
if the effusions are not bilateral and comparable in size, if the patient is febrile, or if the
patient has pleuritic chest pain to verify that the patient has a transudative effusion.
Otherwise the patients heart failure is treated. If the effusion persists despite therapy, a
diagnostic thoracentesis should be performed. A pleural fluid N-terminal pro-brain
natriuretic peptide (NT-proBNP) >1500 pg/mL is virtually diagnostic of an effusion
secondary to congestive heart failure.
2. Hepatic hydrothorax
Pleural effusions occur in ~5% of patients with cirrhosis and ascites. The predominant
mechanism is the direct movement of peritoneal fluid through small openings in the
diaphragm into the pleural space. The effusion is usually right-sided and frequently is large
enough to produce severe dyspnea.
3. Parapneumonic effusion
Parapneumonic effusions are associated with bacterial pneumonia, lung abscess, or
bronchiectasis and are probably the most common cause of exudative pleural effusion in
the United States. Empyema refers to a grossly purulent effusion. Patients with aerobic
bacterial pneumonia and pleural effusion present with an acute febrile illness consisting of
chest pain, sputum production, and leukocytosis. Patients with anaerobic infections present
with a subacute illness with weight loss, a brisk leukocytosis, mild anemia, and a history
of some factor that predisposes them to aspiration. The possibility of a parapneumonic
effusion should be considered whenever a patient with bacterial pneumonia is initially
evaluated. The presence of free pleural fluid can be demonstrated with a lateral decubitus
radiograph, computed tomography (CT) of the chest, or ultrasound. If the free fluid
separates the lung from the chest wall by >10 mm, a therapeutic thoracentesis should be
performed. Factors indicating the likely need for a procedure more invasive than a
thoracentesis (in increasing order of importance) include the following:

Loculated pleural fluid

Pleural fluid pH <7.20

Pleural fluid glucose <3.3 mmol/L (<60 mg/dL)

Positive Gram stain or culture of the pleural fluid

21

Presence of gross pus in the pleural space

If the fluid recurs after the initial therapeutic thoracentesis and if any of these
characteristics are present, a repeat thoracentesis should be performed. If the fluid cannot
be completely removed with the therapeutic thoracentesis, consideration should be given
to inserting a chest tube and instilling a fibrinolytic agent (e.g., tissue plasminogen
activator, 10 mg) or performing a thoracoscopy with the breakdown of adhesions.
Decortication should be considered when these measures are ineffective.
4. Effusion secondary to malignancy
Malignant pleural effusions secondary to metastatic disease are the second most common
type of exudative pleural effusion. The three tumors that cause ~75% of all malignant
pleural effusions are lung carcinoma, breast carcinoma, and lymphoma. Most patients
complain of dyspnea, which is frequently out of proportion to the size of the effusion. The
pleural fluid is an exudate, and its glucose level may be reduced if the tumor burden in the
pleural space is high. The diagnosis usually is made via cytology of the pleural fluid. If the
initial cytologic examination is negative, thoracoscopy is the best next procedure if
malignancy is strongly suspected. At the time of thoracoscopy, a procedure such as pleural
abrasion should be performed to effect a pleurodesis. An alternative to thoracoscopy is CTor ultrasound-guided needle biopsy of pleural thickening or nodules. Patients with a
malignant pleural effusion are treated symptomatically for the most part, since the
presence of the effusion indicates disseminated disease and most malignancies associated
with pleural effusion are not curable with chemotherapy. The only symptom that can be
attributed to the effusion itself is dyspnea. If the patients lifestyle is compromised by
dyspnea and if the dyspnea is relieved with a therapeutic thoracentesis, one of the
following procedures should be considered: (1) insertion of a small indwelling catheter or
(2) tube thoracostomy with the instillation of a sclerosing agent such as doxycycline, 500
mg.

5. Mesothelioma
Malignant mesotheliomas are primary tumors that arise from the mesothelial cells that line
the pleural cavities; most are related to asbestos exposure. Patients with mesothelioma
present with chest pain and shortness of breath. The chest radiograph reveals a pleural
22

effusion, generalized pleural thickening, and a shrunken hemithorax. Thoracoscopy or

open pleural biopsy is usually necessary to establish the diagnosis. Chest pain should be
treated with opiates, and shortness of breath with oxygen and/or opiates.

6. Effusion secondary to pulmonary embolization

The diagnosis most commonly overlooked in the differential diagnosis of a patient with an
undiagnosed pleural effusion is pulmonary embolism. Dyspnea is the most common
symptom. The pleural fluid is almost always an exudate. The diagnosis is established by
spiral CT scan or pulmonary arteriography. Treatment of a patient with a pleural effusion
secondary to pulmonary embolism is the same as it is for any patient with pulmonary
emboli. If the pleural effusion increases in size after anticoagulation, the patient probably
has recurrent emboli or another complication, such as a hemothorax or a pleural infection.

7. Tuberculous pleuritis
In many parts of the world, the most common cause of an exudative pleural effusion is
tuberculosis (TB). Tuberculous pleural effusions usually are associated with primary TB
and are thought to be due primarily to a hypersensitivity reaction to tuberculous protein in
the pleural space. Patients with tuberculous pleuritis present with fever, weight loss,
dyspnea, and/or pleuritic chest pain. The pleural fluid is an exudate with predominantly
small lymphocytes. The diagnosis is established by demonstrating high levels of TB
markers in the pleural fluid (adenosine deaminase >40 IU/L or interferon >140 pg/mL).
Alternatively, the diagnosis can be established by culture of the pleural fluid, needle
biopsy of the pleura, or thoracoscopy. The recommended treatments of pleural and
pulmonary TB are identical.
8. Effusion secondary to viral infection
Viral infections are probably responsible for a sizable percentage of undiagnosed
exudative pleural effusions. In many series, no diagnosis is established for ~20% of
exudative effusions, and these effusions resolve spontaneously with no long-term residua.
The importance of these effusions is that one should not be too aggressive in trying to
establish a diagnosis for the undiagnosed effusion, particularly if the patient is improving
clinically.
23

9. Chylothorax
A chylothorax occurs when the thoracic duct is disrupted and chyle accumulates in the
pleural space. The most common cause of chylothorax is trauma (most frequently thoracic
surgery), but it also may result from tumors in the mediastinum. Patients with chylothorax
present with dyspnea, and a large pleural effusion is present on the chest radiograph.
Thoracentesis reveals milky fluid, and biochemical analysis reveals a triglyceride level that
exceeds 1.2 mmol/L (110 mg/dL). Patients with chylothorax and no obvious trauma should
have a lymphangiogram and a mediastinal CT scan to assess the mediastinum for lymph
nodes. The treatment of choice for most chylothoraxes is insertion of a chest tube plus the
administration of octreotide. If these modalities fail, a pleuroperitoneal shunt should be
placed unless the patient has chylous ascites. An alternative treatment is ligation of the
thoracic duct. Patients with chylothoraxes should not undergo prolonged tube
thoracostomy with chest tube drainage because this will lead to malnutrition and
immunologic incompetence.
10. Hemothorax
When a diagnostic thoracentesis reveals bloody pleural fluid, a hematocrit should be
obtained on the pleural fluid. If the hematocrit is more than one-half of that in the
peripheral blood, the patient is considered to have a hemothorax. Most hemothoraxes are
the result of trauma; other causes include rupture of a blood vessel or tumor. Most
patients with hemothorax should be treated with tube thoracostomy, which allows
continuous quantification of bleeding. If the bleeding emanates from a laceration of the
pleura, apposition of the two pleural surfaces is likely to stop the bleeding. If the pleural
hemorrhage exceeds 200 mL/h, consideration should be given to thoracoscopy or
thoracotomy.
11. Miscellaneous causes of pleural effusion.
There are many other causes of pleural effusion. Key features of some of these conditions
are as follows: If the pleural fluid amylase level is elevated, the diagnosis of esophageal
rupture or pancreatic disease is likely. If the patient is febrile, has predominantly
polymorphonuclear cells in the pleural fluid, and has no pulmonary parenchymal
abnormalities, an intraabdominal abscess should be considered. The diagnosis of an
asbestos pleural effusion is one of exclusion. Benign ovarian tumors can produce ascites
24

and a pleural effusion (Meigs syndrome), as can the ovarian hyperstimulation syndrome.
Several drugs can cause pleural effusion; the associated fluid is usually eosinophilic.
Pleural effusions commonly occur after coronary artery bypass surgery. Effusions
occurring within the first weeks are typically left-sided and bloody, with large numbers of
eosinophils, and respond to one or two therapeutic thoracenteses. Effusions occurring
after the first few weeks are typically left-sided and clear yellow, with predominantly
small lymphocytes, and tend to recur. Other medical manipulations that induce pleural
effusions include abdominal surgery; radiation therapy; liver, lung, or heart
transplantation; and the intravascular insertion of central lines.
C. Therapy
1. Medicamentosa
Pharmacologic management of pleural effusion depends on the conditions etiology. For
example, medical management includes nitrates and diuretics for congestive heart failure
and pulmonary edema, antibiotics for parapneumonic effusion and empyema, and
anticoagulation for pulmonary embolism. In patients with parapneumonic effusions,
empyemas, and effusions associated with esophageal perforation and intra-abdominal
abscesses, antibiotics should be administered early when these conditions are suspected.
Antibiotic selection should be based on the suspected causative microorganisms and the
overall clinical picture. Considerations include the patient's age, comorbidities, duration of
the illness, setting (community vs nursing home), and local organism sensitivities. Various
effective single agents and combination antimicrobial therapies exist. Coverage should
generally include anaerobic organisms. Options may include clindamycin, extendedspectrum penicillins, and imipenem. Depending on the patient's clinical condition,
infectious disease consultation may be appropriate. Particular attention must be given to
potential drug interactions, adverse effects, and preexisting conditions.
2. Therapeutic Thoracentesis
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 diagnostic thoracentesis, note 3 additional
considerations when performing therapeutic thoracentesis.

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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.
3. 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.

REFERENCE
Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, and Loscalzo J. 2012. Harrisons
Principles of Internal Medicine 18th Edition. United States : McGraw-Hill eBooks.
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Maskell NA and Butland RJA.2011. BTS guidelines for the investigation of a unilateral
pleural effusion in adults. thorax.bmj.com on July 16, 2011.
Rahman NM and Munawar M. 2009. Investigation of the patient with pleural effusion. Clin
Med 2009;9:1748.

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