k16-Pleural Effusion and Pneumothorax 2010

7/13/2019 k16-Pleural Effusion and Pneumothorax 2010

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PLEURAL EFFUSION

ANDPNEUMOTHORAX

By:

WIDIRAHARDJO

Pulmonary Department, Faculty of Medicine,

Sumatera Utara University/ Adam Malik Hospital

Medan

2011


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ANATOMY OF THE PLEURAI. Pleura is the serous membrane:

1. Visceral pleura: covers the lung parenchyma, untilinterlobar fissures

2. Parietal pleura: covers the mediastinum,

diaphragm and the rib cage.The space between the two layers of pleura call as

pleural space.

II. Pleural space contain a film of fluid: pleural fluid, aslubricant and allows the sliding between the two pleuras

during respiratory movements. No air in the pleural

space and no communication between right and left

pleural space.


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ANATOMY OF THE PLEURA

(contd)

III. Histology: covered by a single layer ofmesothelial cells. Within the pleura are bloodvessels, mainly capillaries, lymphatic lacunas

(only in the parietal pleura), and connectivetissue.

Two important function of the connectivetissue in the visceral pleura:

- contributes to the elastic recoil of the lung

- restricts the volume to which the lung can

be inflated


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(contd)

Elastic and collagen fibers areinterdependent elements.

The mesothelial cells are active cells,sensitive and responsive to various stimuliand very fragile. They may betransformed into macrophage.

Scanning electron microscopy: microvilliare present diffusely over the pleuralsurface:


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(contd)

IV. Pleural fluid: the important in the understanding

are volume, thickness, cellular components, and

physicochemical factors.Normally a small amount of pleural fluid present,

behaves as a continuous system.

The total white cell count of 1,500/mm3,with 70% monocytes (mononuclear cell). The

protein, ionic concentrations are differ significantly

from serum.


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(contd)

V. Blood supply: from the systemic capillaries

VI. Lymphatics: the lymphatic vessels in the parietalpleura are in communication with the pleural

space by stomas.

VII.Innervation: sensory nerve endings are presentin the costal and diaphragmatic parietal pleura.

The visceral pleura contains no pain fibers.


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PHYSIOLOGY OF THE PLEURAL SPACE

I. The pleural space is important in thecardiopulmonary physiology, as a buffer zone for overloading of fluid in the circulatory system of the lung.

The gradient of pressure depend on the threecomponents:

- cardiac rhythm

- respiratory rhythm- elastic recoil of the lung

PLEURODYNAMIC: the capacity of thepleural space to change in the pleural pressurevariability.

The normal pleural pressure ranged from - 8,1 to-11,2 cmH2O (the negative or sub atmospheric

pressure).


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Intrapleural pressure

- 8,1 Cm H2O 0 Cm H2O

inspiration expiration

Negative / sub atmospheric pressure

-11,2 Cm H2O


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(contd)

The pleural pressure changes associated with manypleural diseases. Commonly by the increasing ofpleural pressure.

Pleural fluid formation from:

- pleural capillaries

- interstitial spaces of the lung- intrathoracic lymphatic

- intrathoracic blood vessels

- peritoneal cavity


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(contd)

Pleural fluid absorption:

- Lymphatic clearance: fluid clearance through

the pleural lymphatics is though to explain thelack of fluid accumulation normally.

Stomas in the parietal pleura, as an initial

drainage. There are no stomas in the visceralpleura.

- Capillaries clearance: few for small molecules and

water across both pleural surfaces.


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CLINICAL MANIFESTATIONS

I. Symptoms: mainly dictated by underlying process,

may have no symptom to severe illness.- pleuritic chest pain

- dullness

- non productive cough

- dyspnea

II. Physical examination:

- inspection: sizes of the hemithoraces and the

intercostal space- palpation

- percussion

- auscultation: decreased or absent breath sounds,

pleural rubs


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LABORATORY APPROACH

Separation of exudates from transudates

Appearance of pleural fluid

BronchoscopyThoracoscopy

Needle biopsy of the pleura

Open pleural biopsy


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PLEURAL DISEASES

Pleural effusion

Pneumothorax

Empyema

Hydropneumothorax Pyopneumothorax

Hemothorax

Chylothorax Mesothelioma

Etc


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PLEURAL EFFUSION

Definition: an accumulation of pleural fluid

in the pleural space.

Pathogenesis:

= Increased pleural fluid formation

= Decreased pleural fluid absorption

= Both increased formation and decreasedabsorption


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PLEURAL EFFUSION (contd)

Increased pleural fluid formation:

- increased interstitial fluid in the lung

- increased intravascular pressure in pleura

- increased permeability of the capillaries inthe pleura

- decreased pleural pressure

- increased fluid in the peritoneal cavity

- disruption of the thoracic duct

- disruption of the blood vessel in the thorax


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Decreased pleural fluid absorption:

- obstruction of the lymphatics draining

- elevation of systemic vascular pressure


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Clinical manifestations:

= Symptoms: mainly dictated by the underlyingprocess; may be no symptom, pleuritic chest

pain, referred pain, dullness, dry/ non

productive cough, and dyspnea.= Physical examination: change in sizes of

hemithoraces and intercostal spaces. Tactile

fremitus is absent or attenuated, dull inpercussion, decreased or absent breath sounds,

pleural rub during the latter of inspiration and

early expiration (to and fro pattern)



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Separation of transudative or exudative effusion:Light`s criteria for exudative pleural effusion, if

we found one or more of:

= pleural fluid protein divided by serum proteingreater than 0,5

= pleural fluid LDH divided by serum LDH

greater than 0,6= pleural fluid LDH greater than two thirds of

the upper limit


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exudative transudative

Tuberculosis

Tumor

PneumoniaTrauma

Collagen disease

Asbestosis

UremiaRadiation

Sarcoidosis

Emboli

Congestive heart

Nephrotic syndrome

Cirrhosis hepatisMeigs syndrome

Hydronephrosis

Peritoneal dialysis



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TRANSUDATIVE PLEURAL EFFUSION

Occurs when the systemic factors influencing theformation and absorption of pleural fluids are

altered.

The most common cause: congestive heart

failure (CHF);

Pathogenesis: pressure in the pulmonary capillary

elevated fluid enter the interstitial spaces of

the lung across the visceral pleura into the

pleural space.


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(contd)

Clinical manifestation: associated withCHF:

- dyspnea on excertion

- peripheral edema- orthopnea or paroxysmal nocturnal

dyspnea

- distended neck vein- rales

- gallop

- signs of the pleural effusion


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(contd)

Treatment:

- digitalis

- diuretics- afterload reduction

- thoracocentesis

- pleuroperitoneal shunt


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TUBERCULOUS PLEURAL EFFUSION

Pathogenesis:

- sequel to a primary tuberculous infection

(post primary infection)- reactivation

- result from rupture of subpleural caseous

focus in the lung- delayed hypersensitivity


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(contd)

Clinical manifestation:- most common as an acute illness: < 1

week

- cough, usually nonproductive

- chest pain, ussually pleuritic

- fever

- younger than patients with parenchymal

tb

- usually unilateral and can be of any size


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(contd)

Diagnosis:- acid fast bacilli of: sputum, pleural fluid

pleural biopsy specimen

- granulomas in the pleura (on

thoracoscopy)

- elevated of ADA (adenosine deaminase)

- 20% with parenchymal infiltrate

- 39% with hilar adenopathy

- tuberculin skin test


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(contd)

Treatment:

- Chemotherapy

- Corticosteroid- Thoracocentesis

- WSD (water sealed drainage)


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PNEUMOTHORAX

DEFINITION: air in the pleural space.CLASIFICATION:

1. Spontaneous pneumothoraxoccur without antecedent trauma or other obvious cause,

devided into:

Primary spontaneous pneumothorax (PSP): occur in

healthy individuals

Secondary spontaneous Pneumothorax (SSP):occur as a

complication of underlying lung disease, most commonly

COPD (chronic obstructive pulmonary disease).


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PNEUMOTHORAX

2. Traumatic pneumothorax:

occur as a result of direct or indirect trauma to

the chest:3. Iatrogenic pneumothorax: occur as a an

intended or inadvertent consequence of a

diagnostic or therapeutic maneuver.


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INCIDENCE

Males: 7,4/100.000 per year

Females: 1,2/100.000 per year

Relative risk in smoker 7-102 times higher

Usually taller and thinner, associate with genetical

predisposed to bleb formation Peak age of the occurrence is in the early 20s

Rare after age 40

PRIMARY SPONTANEOUS PNEUMOTHORAX

(PSP)


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PATHOPHYSIOLOGY The negative/ sub atmospheric

pressure of the pleural space and

The positive pressure of the alveolarpressure always positive

Develop of communication between

alveolus and pleural space Air flow from alveolus into pleural

space



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CLINICAL MANIFESTATION

The main symptom: chest pain and dyspnea

Usually develop at rest

PD: moderate tachycardia. If HR > 140 or if

hypotension, cyanosis is present, a tension

pneumothorax should be suspected

Larger of the chest, move less, absent of

fremitus tactile, hyper resonant in percussion

note and reduced or absent the breath soundon the affected side.

The trachea may be sifted toward the contra

lateral side



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PRIMARY SPONTANEOUS PNEUMOTHORA

DIAGNOSIS:= Clinical history

= Physical diagnostic

= Chest x-ray: is a definitive diagnostic,

showed the visceral pleural line. Expiratory

films are more sensitive than are inspiratory

films.


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QUANTITATION:
http://thorax.bmjjournals.com/content/vol58/issue90002/images/large/tx02516e.f3.jpeg


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RECURENCE RATE:

= Without thoracotomy: 52%, 62% and 83% in

patient had first, second and third

pneumothoraces respectively

= Chest CT may predict the recurrence, where

the individual with numerous and the largest

bullae would be most likely had recurrence

TREATMENT


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TREATMENT

A. Observation

= Resorbed of the air in the pleural space about

1,25% per day, if the communication between

the alveoli and pleural space is eliminate

= Bed rest

B. Supplemental Oxygen

= Supplemental oxygen: increased the rate of air

absorption until 6 time

= As a routine treatment for all type of

pneumothorax


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TREATMENTC. Aspiration

= As a initial treatment for psp > 15%

= By G-16 needle with internal

polyethylene catheter, inserted into

anterior 2ndICS at mid clavicle line after

local anesthesia, a three way stopcock

and 60ml syringe

= 64% successful

= Tube thoracostomy for unexpanded lung


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TREATMENT

D. Tube thoracostomy= Permits the air to be evacuated effectively

and rapidly

= Connected to underwater seal (WSD), low

pressure continuous suction (up to

100cmH2O), or to a Heimlich valve.

E. Pleurodesis= Instilation of any sclerosing agent to the pleural

space or by abrasion of the pleuras to create

obliteration of the pleural space.


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TREATMENT

F. Thoracoscopy= Direct view to the entire thoracic cavity

= To treat the bullous disease responsible

for the pneumothorax= To create a pleurodesis

G. Thoracotomy

= For patient who fail to previous

treatment


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SECONDARY SPONTANEOUS

PNEUMOTHORAX (SSP) SSP are more serious than PSP, because

decreased the lung function of patient withalready compromised lung function.

INCIDENS: 6,3/100.000/year (US) ETIOLOGIC FACTORS:

= COPD

= TB= Asthma

= Pneumonia

= Lung cancer

S C S T S


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PNEUMOTHORAX CLINICAL MANIFESTATIONS:

= More severe than PSP

= Mostly: dyspnea, chest pain, cyanosis,

and hypotension

= Mortality: 16%, is associated with

respiratory failure

= Recurrent rate: 44%

= PD: similar to PSP, but less helpful,

especially for patient with COPD



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PNEUMOTHORAX

DIAGNOSIS: established by chest x-ray, show of a

visceral pleural line. Must differentiation from

large bulla, if any doubt, CT thorax may be done.

TREATMENT:

The goals are to rid the pleural space of air

and to decreased a recurrence; treatment are

the same as PSP, except the aspiration is a limited

role in SSP.


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MADE IN ENGLAND

PUMP

CC

WSC

PCC

SAFETY TUBE

25


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PUMP

CC

WSC

PCC

25


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MADE IN INDONESIA

PUMP

CC

WSC

PCC

25


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PUMP

CC

WSC

PCC

25


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MADE IN INDONESIA

PUMP

CC

WSC

SAFETY TUBE

50

PCC


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k16-Pleural Effusion and Pneumothorax 2010