Pleural Diseases Flashcards
Parietal vs. Visceral Pleura
Parietal pleura:
• Thin membrane lining inside of chest wall and diaphragm
• Blood from intercostal arteries (left heart)
• Drains blood into RA (right heart)
Visceral pleura:
• Thin membrane lining lung surfaces
• Blood from bronchial circulation (left heart)
• Drains blood with pulmonary veins into LA (left heart)
Describe the mechanisms and pathways by which pleural fluid is formed and absorbed under normal conditions.
Sterling’s Law
o Net fluid movement = [capillary hydrostatic P – interstitial hydrostatic P] – [capillary oncotic P – interstitial oncotic P]
- Pleural space = negative pressure of -5 at FRC (from opposite recoil of lungs and chest wall)
- Pleural space fluid = oncotic pressure of +5 (from small amount of protein)
• Net inward hydrostatic forces:
o Between parietal pleura and pleural space: (30- (-5)) = 35
o Between visceral pleura and pleural space: (24- (-5)) = 29
• Net outward oncotic forces:
o Between parietal pleura and pleural space: (24- (-5)) = 29
o Between visceral pleura and pleural space: (34- (+5)) = 29
• Net Parietal pleura pressure: 6 cm H2O
o Favors movement from parietal capillaries to pleural space
• Net Visceral pleura pressure: 0 cm H2O
o No gradient
o Balance because blood supply comes from bronchial circulation = low pressure system
o Result: pleural fluid is formed at the parietal pleura
• Normal fluid absorption:
o Lymphatic vessels and stomas in parietal pleura
Describe the mechanisms and pathways by which excessive amounts of pleural fluid accumulate in different diseases and conditions.
o Increased microvascular pressure
• CHF (left heart failure is main cause of increased pleural fluid from visceral pleura)
o Increased capillary permeability
o Decreased oncotic pressure gradient
o Lymphatic obstruction
o Peritoneal fluid traveling through diaphragm gaps
o Increased negative pleural pressure secondary to a collapsed lung
Explain how a pleural effusion can affect respiratory mechanics and gas exchange.
• Restrictive defect on PFTs (decreased TLC)
• Improve dyspnea by removing fluid BUT:
• PFTs improve less than expected when remove pleural fluid:
1) Pleural fluid expands chest wall (not just decrease lung volume)
2) Atelectatic lung slow to expand
3) Underlying lung disease
Analyze the changes in gross appearance of pleural fluids under different conditions and diseases.
Most transudate fluid and many exudates = clear, straw colored, non-viscous, odorless
o Bloody
• Hct < 50% peripheral Hct = cancer, pulmonary embolism, trauma
• Hct > 50% peripheral Hct = hemothorax
o Cloudy (cells, debris, or lipids) • Cloudy supernatant on centrifugation = due to lipids → chylothorax • Clear supernatant on centrifugation = due to cells and debris → related to pleural infection or malignancy
o Viscid:
• Empyema = if thick, purulent pleural fluid
• Likely foul smelling too
Analyze the changes in total and differential cell count of pleural fluids under different conditions and diseases.
Total WBC count of pleural fluid o Most transudates: WBC < 1000 mm^3 o Most exudates: WBC > 1000 mm^3 Differential for effusions with WBC > 10, 000 mm^3: • Parapneumonic (50%) • Malignancy (7%) • Pulmonary embolism (37%) • TB (14%) • Post-cardiac injury syndrome (33%) Can occasionally be low in grossly purulent fluid
• Different cell types in pleural fluid: Neutrophil predominance (>50%) • Parapneumonic • Pancreatitis • Pulmonary embolism • Subphrenic abcess • Early TB
Lymphocyte predominance (>50%)
• Malignancy
• TB pleuritis
• Post-cardiac injury syndrome (late)
o Eosinophilia (>10 %): • Air or blood in pleural space • Asbestos-related effusion (50%) • Eosinophilic pneumonia • Drug-induced • Parasitic • Churg-Strauss syndrome
NOTE: in transudates = pleural fluid neutrophilia and lymphocytosis are not clinically significant
Analyze the changes in glucose, TAGs, and amylase of pleural fluids under different conditions and diseases.
Glucose < 60 mg/dL or low pH ( 110 mg/dL o Chylothorax (acculmulation of lymph in pleural space)
Amylase
o Pancreatic disease
o Esophageal perforation
o Malignancy (salivary isoenzyme)
Pleural fluid cytology
o Initial pleural fluid sample positive in 60% of patients with pleural malignancies
o Three samples positive in nearly 80% (higher sensitivity)
o Larger pleural tumor burden = more likely to be positive
History of a pleural effusion
- Small effusions = may be asymptomatic
- Moderate to large effusions → dyspnea
- Pleuritic chest pain (increases with inspiration or cough) if inflamed pleural surfaces
- Dry non- productive cough
- Symptoms related to underlying disease
History of a pneumothorax
- Primary spontaneous:
- Acute chest pain and/or dyspnea
- Chest pain may improve over 24 hours
- Secondary spontaneous:
- More severe manifestations
- Depend on underlying disease
Etiology of a pneumothorax
Primary Spontaneous Pneumothorax
o In people with no known underlying lung disease
o Rupture or leakage from subpleural blebs related to high mechanical stress in apex of lungs
o Congenital bronchial abnoramlities or respiratory bronchiolitis frequently present
o Associated with smoking, being tall and thin
o Peak age of occurrence in early 20’s
Secondary spontaneous pneumothorax
o In people with underlying lung disease
o Blebs, bullae, and cysts develop and predispose to rupture into pleural space
o Associated with COPD, CF, penumocystis jiroveci pneumonia, sarcoidosis TB, lymphangiomyomatosis, and Langerhans cell histiocytosis
Iatrogenic pneumothorax
o Caused by physicians
Traumatic (non-iatrogenic) pneumothorax
o Penetrating or non-penetrating chest trauma
Tension pneumothorax
o One-way valve mechanism = air can’t exit pleural space → increased pleural pressure
o Increased pleural pressures → Displaces mediastinal structures to contralateral side
o → Decreased venous return → will significantly impair hemodynamics, decrease CO
Explain the pathophysiology of pneumothorax.
Air into pleural space = decouples chest wall from lung
o Chest wall recoils outward = expands total volume of chest wall
o Lung recoils inward = decreases volume of air in lung
• Atelectatic lung tissue → Decrease in VC and PaO2; increased P(A-a)O2 gradient
• In healthy people = usually well-tolerated
• In people with impaired lung function = may lead to respiratory insufficiency
• Small or modest pneumothorax = little effect on lung function
Physical exam findings with pleural effusion
- Absent or decreased tactile fremitus (vibration) on side of effusion
- Dull or flat percussion (most dull over bases)
- Decreased or absent breath sounds on auscultation
Physical exam findings with pneumothorax
- Primary spontaneous:
- Less movement of ipsilateral hemithorax
- Decreased tactile fremitus
- Hyperresonant percussion note
- Absent or reduced breath sounds
- Secondary spontaneous:
- More severe manifestations
- In hyperinflated COPD patients = may be difficult to detect new pneumothorax
Radiologic findings with pleural effusion
- Decreased costophrenic angle
- Meniscus of fluid line (artifact of chest x-ray)
- Compare: straight upper border with hydropneumothorax (no meniscus effect when lung is collapsed
Radiologic findings with pneumothorax
- Abnormal pleural line
- Larger rib spaces from expanded chest wall
- Absence of lung lines/markings
- Deep Sulcus sign – costophrenic angle extends past edge of film
Leading causes of pleural effusion
- CHF
- Pneumonia
- Cancer
- Pulmonary embolus
- Viral disease
- Coronary artery bypass surgery
- Cirrhosis with ascites
Diagnosis of pleural effusion
• Thoracentesis if >10 mm of fluid on chest x-ray or atypical features (pleuritic chest pain, fever, aymmetry in size) in CHF patient
Treatment of pleural effusion
- Treat underlying condition
- Remove accumulated fluid
- Recurrent effusions:
- Serial drainage with tunneled pleural catheter
- Eliminate pleural space (pleurodesis) = fuse layers together with sclerosing agents like talc or doxygcycline
Treatment of pneumothorax
Small primary spontaneous or iatrogenic:
• Observation
• Use of supplemental O2 (speeds recovery because lowers capillary N2 concentration → establishes gradient for N2 rich atmospheric air in pneumothorax to diffuse out of pleural space into capillaries)
Secondary spontaneous, large, or traumatic:
• Drain pleural air by manual aspiration or using a chest tube (tube thoracostomy)
Tension pneumothorax = tube thoracostomy
Recurrent spontaneous penumothoraces:
• Pleurodesis
• Video assisted thoracoscopic surgery (VATS) to staple or remove blebs
Identify the distinction between exudative and transudative pleural effusions
Exudate:
o Protein rich (> 3 g/dl)
o Fluid formed by increased permeability of pleural capillaries or lymphatic blockage
Defined by Light’s Criteria:
• An exudate if any one of three criteria are met:
• 1) ratio of pleural fluid protein to serum protein > 0.5
• 2) ration of pleural fluid LDH to serum LDH > 0.6
• 3) pleural fluid LDH >2/3 the upper limit of normal for serum LDH
For an exudate:
• Sensitivity 99%
• Specificity 65-98%
• Most common misclassified transudate as exudate is in pleural effusion in CHF patient treated with diuretics (concentrates/dries out fluid)
Transudate:
o Protein poor (<3 g/dl)
o Fluid formed by increased hydrostatic pressures or decreased oncotic pressures
Possible causes of an exudate
- Parapneumonic effusion
- Pleural malignancies
- Pulmonary embolism
- Viral pleruitis
- Asbestos exposure
- Drugs: nitrofurantoin, dantrolene, bromocriptine (other ergot alkaloids like pergolide, methysergide), amiodarone, many other drugs
- More
Possible causes of a transudate
- CHF
- Cirrhosis (hepatic hydrothorax)
- Hypoalbuminemia
- Constrictive pericarditis
- Nephritic syndrome
Describe how broken ribs may affect chest wall mechanics.
• With non-penetrating/blunt trauma:
o Fractured ribs may puncture lung tissue → pneumothorax
o Sudden chest compression → increased alveolar pressure → rupture → air dissects towards pleura and ruptures it
