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
Anatomy of the pleura
- 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
Pleural space -characteristics/comopsition/function
- 10-20 u thick
- thin layer of fluid
- lubricates movement between the lung and chest wall
Visceral pleura -composition
- primarily connective tissue
- covers lung
Parietal pleura -composition
- 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
Lymphatic stroma - where found
Only within the parietal pleura
Lymphatic stroma -function
Remove fluid from the pleural space
Visceral pleura -function
Contributes to the elastic recoil of the lung
Parietal pleura - function
Fluid is produced and re-absorbed here
Normal pleural fluid - volume
- 8 ml per side
- forms at 0.01 ml/kg/hr
- about 15-20 ml per day in 70 kg adult
Normal steady state of pleural fluid
-absorption = production
Visualization of pleural fluid
- 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
Normal pH of pleural fluid
-about 7.6 normally
How does pleural fluid form
- 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)
Hydrostatic pressure
- pressure exerted by liquid (i.e. column of fluid) at equilibrium
- in the lungs this reflects the pulmonary venous pressures
Oncotic pressure
- osmotic pressure due to proteins and osmoles in the plasma
- draws fluid into the capillaries
Balance of oncotic and hydrostatic pressures (contributing to net pressure and gradient in the pleural space)
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)
2 main causes of accumulation of pleural fluid in disease states
- Increased formation
2. Impaired absorption
Cause of increased fluid entry
- Increase in permeability due to disruption of endothelial cell layer (changing K constant -capillary filtration coefficient)
- Increase in microvascular pressure (i.e CHF)
- Decreased pleural pressure (ie in atelectasis)
- Decreased plasma oncotic pressure (ie in nephrotic syndrome, hypoalbuminemia)
Other causes of increased fluid entry - from outside the thoracic cavity
- 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
Mechanisms of fluid accumulation due to increase permeability i.e. what is source of increased permeability
- infection
- malignancy
- inflammation
Mechanism of pleural fluid accumulation due to shift of starling forces
1) Things which decrease the oncotic gradient
- hypoalbuminemia
2) Things which increase the hydrostatic gradient
- CHF
- Atelectasis
Causes of decreased fluid exit
- factors that impair lymphatic drainage
- in many disease states the accumulation of fluid is multi-factorial
Common Hx for patient with pleural effusion
- SOB
- pleuritic chest pain
- asymptomatic
Physical exam for patient with pleural effusion
- percussion: dullness over area of effusion with decreased tactile fremitus (how does this differ from consolidation in the lung)
- auscultation: decreased air entry
Imaging of pleural effusion -modalities
- Ultrasound
- close to 100% sensitive for detecting pleural fluid
- good to identify loculated fluid vs. free-flowing - CT contrast
- especially good for visualizing pleural surface (thickening, tumors, etc)
Treatment pleural effusion
Thoracentesis
Thoracentesis -how?
- Insert needle through chest wall into the pleural space
- Drain pleural fluid
- Diagnostic and therapeutic
- can be done with U/S guidance at bedside
Analysis of pleural fluid
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)
Classification of pleural effusions
- Transudates
- Exuates
- based on the mechansm of fluid formation and pleural flui chemistry
Transudate -general mechanism
-result from an imbalance in oncotic and hydrostatic pressure
Exudate - general mechanism
-result of inflammation of the pleura or decreased lymphatic drainage
Differentiating transudate vs exudate
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
Cell count and differential for pleural fluid analysis
> 85% lymphocytes -TB, cancer, rheumatoid > 10% eosinophils -pneumothorax, hemothorax Neutrophils -very high in infections
Characteristics of trasudate
- low protein and LDH in pleural fluid
- implies intact endothelial membrane
- fluid accumulation from increased hydrostatic pressure or decreased oncotic pressure
Characteristics of exudate
- high protein and LDH in pleural fluid
- implies disruption of endothelial membrane
Differential diagnosis Transudate
LUCKI ME L-liver (hepatic hydrothorax) U - urinothorax C- CHF K- Kidney (low protein state - nephrotic) I - iatrogenic M-myxedema E -embolic
Exudate
-pretty much everything else (including malignancy, infection, PE, serositis due to connective tissue disease etc)
Approach to managing plural effusion
- Look for underlying cause
- Thoracentesis for fluid analysis
- Transudate
- work up for differential diagnosis (i.e. CHF, urinalysis, urea, creatinine, liver function, TSH, etc) - Exudate
- evaluate for clues to underlying cause
a) infection
b) malignant
c) pulmonary embolism
Why would check albumin in pleural effusion
Check gradient between pleural fluid and serum
-help to confirm transudate
Amylase
- not routinely indicated
- order if suspect esophageal rupture into pleural space or pancreatic diseases (rupture of a pseudocyst)