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Pulmonary week 4: Inhalation lung diseases > Pathophysiology of pleural effusions > Flashcards

Pathophysiology of pleural effusions Flashcards

1. Review pleural anatomy and charateristics of pleural space 2. Understand normal pleural fluid dynamics 3. Understand development of pleural effusions in disease states 4. Develop an approach to the investigation of pleural effusion

1
Q

Anatomy of the pleura

A
  • is a serous membrane that covers the lungs
  • made up of 2 layers: visceral, parietal
    a) viseral: covers lungs and extends into fissures
    b) parietal: lines inside of the thoracic cavity
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2
Q

Pleural space -characteristics/comopsition/function

A
  • 10-20 u thick
  • thin layer of fluid
  • lubricates movement between the lung and chest wall
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3
Q

Visceral pleura -composition

A
  • primarily connective tissue

- covers lung

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4
Q

Parietal pleura -composition

A
  • thin layer of loose connective tissue
  • contains blood vessels and lymphatic lacunae
  • covered by a thin layer of mesothelial cells
  • below it is enothoracic fascia
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5
Q

Lymphatic stroma - where found

A

Only within the parietal pleura

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6
Q

Lymphatic stroma -function

A

Remove fluid from the pleural space

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7
Q

Visceral pleura -function

A

Contributes to the elastic recoil of the lung

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8
Q

Parietal pleura - function

A

Fluid is produced and re-absorbed here

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9
Q

Normal pleural fluid - volume

A
  • 8 ml per side
  • forms at 0.01 ml/kg/hr
  • about 15-20 ml per day in 70 kg adult
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10
Q

Normal steady state of pleural fluid

A

-absorption = production

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11
Q

Visualization of pleural fluid

A
  • not normally visible on chest x-ray or CT scan

- about 150 ml per side are necessary to see pleural effusion on plain chest x-ray

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12
Q

Normal pH of pleural fluid

A

-about 7.6 normally

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13
Q

How does pleural fluid form

A
  • a result of differences in hydrostatic and osmotic pressure between vessels and the pleural space
  • parietal pleura is the most important surface for fluid formation + the synthetic vessels that supply pleural surfaces (not from pulmonary circulation)
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14
Q

Hydrostatic pressure

A
  • pressure exerted by liquid (i.e. column of fluid) at equilibrium
  • in the lungs this reflects the pulmonary venous pressures
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15
Q

Oncotic pressure

A
  • osmotic pressure due to proteins and osmoles in the plasma

- draws fluid into the capillaries

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16
Q

Balance of oncotic and hydrostatic pressures (contributing to net pressure and gradient in the pleural space)

A

Flow = change in hydrostatic pressure (parietal pleura vs. visceral pleura) - change in oncotic pressure (parietal pleura vs. visceral pleura)
i.e. the Starling Equation

Because parietal and visceral pleura exterting opposing forces across the pleural space (for both oncotic and hydrostatic)

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17
Q

2 main causes of accumulation of pleural fluid in disease states

A
  1. Increased formation

2. Impaired absorption

18
Q

Cause of increased fluid entry

A
  1. Increase in permeability due to disruption of endothelial cell layer (changing K constant -capillary filtration coefficient)
  2. Increase in microvascular pressure (i.e CHF)
  3. Decreased pleural pressure (ie in atelectasis)
  4. Decreased plasma oncotic pressure (ie in nephrotic syndrome, hypoalbuminemia)
19
Q

Other causes of increased fluid entry - from outside the thoracic cavity

A
  • diaphragm permeable excess fluid from other sources can enter the pleura (i.e. communication from other organs)
    a) hepatic hydrothorax
  • sucked into chest across diaphragm from abdomen
    b) urinothorax
  • abnormal communication from renal collecting system
    c) chylothorax
  • abnomal communication with thoracic duct
20
Q

Mechanisms of fluid accumulation due to increase permeability i.e. what is source of increased permeability

A
  • infection
  • malignancy
  • inflammation
21
Q

Mechanism of pleural fluid accumulation due to shift of starling forces

A

1) Things which decrease the oncotic gradient
- hypoalbuminemia
2) Things which increase the hydrostatic gradient
- CHF
- Atelectasis

22
Q

Causes of decreased fluid exit

A
  • factors that impair lymphatic drainage

- in many disease states the accumulation of fluid is multi-factorial

23
Q

Common Hx for patient with pleural effusion

A
  • SOB
  • pleuritic chest pain
  • asymptomatic
24
Q

Physical exam for patient with pleural effusion

A
  • percussion: dullness over area of effusion with decreased tactile fremitus (how does this differ from consolidation in the lung)
  • auscultation: decreased air entry
25
Q

Imaging of pleural effusion -modalities

A
  1. Ultrasound
    - close to 100% sensitive for detecting pleural fluid
    - good to identify loculated fluid vs. free-flowing
  2. CT contrast
    - especially good for visualizing pleural surface (thickening, tumors, etc)
26
Q

Treatment pleural effusion

A

Thoracentesis

27
Q

Thoracentesis -how?

A
  1. Insert needle through chest wall into the pleural space
  2. Drain pleural fluid
  3. Diagnostic and therapeutic
    - can be done with U/S guidance at bedside
28
Q

Analysis of pleural fluid

A 
A) Observation of fluid at bedside
1) Note color
2) Note smell
B) Chemistry (protein, LDH and albumin)
C) WBC count and % differential
D) Cytology (examine for cancer cells)
E) pH and glucose
F) Gram stain and cultures (can include AFB and TB culture if indicated)
29
Q

Classification of pleural effusions

A
  1. Transudates
  2. Exuates
    - based on the mechansm of fluid formation and pleural flui chemistry
30
Q

Transudate -general mechanism

A

-result from an imbalance in oncotic and hydrostatic pressure

31
Q

Exudate - general mechanism

A

-result of inflammation of the pleura or decreased lymphatic drainage

32
Q

Differentiating transudate vs exudate

A

Use light’s criteria (analysis of pleural fluid)

  • is 85% sensitive for exudate
    a) fluid protein/serum protein > 05
    b) fluid LDH/serum LDH > 0.6
    c) Fluid LDH > 2/3 upper limit of normal
33
Q

Cell count and differential for pleural fluid analysis

A 
> 85% lymphocytes
-TB, cancer, rheumatoid
> 10% eosinophils
-pneumothorax, hemothorax
Neutrophils
-very high in infections
34
Q

Characteristics of trasudate

A
  • low protein and LDH in pleural fluid
  • implies intact endothelial membrane
  • fluid accumulation from increased hydrostatic pressure or decreased oncotic pressure
35
Q

Characteristics of exudate

A
  • high protein and LDH in pleural fluid

- implies disruption of endothelial membrane

36
Q

Differential diagnosis Transudate

A 
LUCKI ME
L-liver (hepatic hydrothorax)
U - urinothorax
C- CHF
K- Kidney (low protein state - nephrotic)
I - iatrogenic
M-myxedema
E -embolic
37
Q

Exudate

A

-pretty much everything else (including malignancy, infection, PE, serositis due to connective tissue disease etc)

38
Q

Approach to managing plural effusion

A
  1. Look for underlying cause
  2. Thoracentesis for fluid analysis
  3. Transudate
    - work up for differential diagnosis (i.e. CHF, urinalysis, urea, creatinine, liver function, TSH, etc)
  4. Exudate
    - evaluate for clues to underlying cause
    a) infection
    b) malignant
    c) pulmonary embolism
39
Q

Why would check albumin in pleural effusion

A

Check gradient between pleural fluid and serum

-help to confirm transudate

40
Q

Amylase

A
  • not routinely indicated

- order if suspect esophageal rupture into pleural space or pancreatic diseases (rupture of a pseudocyst)

Pulmonary week 4: Inhalation lung diseases (2 decks)

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