Lung Diseases

Lung Diseases

• Interstitial Pneumonia
• – Reticulonodular pattern
• – Peribronchial thickening
• Viruses, Mycoplasma pneumoniae, Pneumocystis carinii
• Bronchopneumonia 
• – Patchy inhomogeneous consolidation
• – Several lobes involved
• Common organisms:
• S. aureus, E coli, Pseudomonas aeruginosa, Anaerobes, Hemophilus influenzae
• Lobar Pneumonia
• – Predominately one lobe
• – Consolidation crosses segmental boundaries
• Common organisms:
• S. Pneumoniae, Klebsiella pneumoniae, Legionella Pneumophila
• Nodular Pneumonia
• Chronic Pneumonia/Recurrent
• Etiology of Chronic Pneumonia
• Mycobacteria
• Tuberculosis and non-tuberculous
• Fungus
• Chronic aspiration pneumonia
• Post-obstructive pneumonia
• Foreign body
• Tumor
• Not pneumonia

Anatomical Sites of TB Infection

• Lung 80-85%  (nl route of infection)
• Extrapulmonary
• – Lymph nodes
• – Pleura
• – Bones and joints
• – GU system
• – Central nervous system

Tx

long duration = only kill during organisms reproductive cycle

Fungal Infection = Mycoses

• Coccidioidomycosis
• Valley fever (central California)
• CXR - lots of calcified little spots
• 
  
• Histoplasmosis
• Ohio river valley
• CXR - same as Cocci
• more virulent than Cocci
• complication = fibrosing mediastinum
• Blastomycosis
• muddy bogs - Southeast Southcentral
• clinically same as other mycoses

Pleural Effusions

Pleural Diseases

• Pleural fluid 
• Originates from systemic (mainly bronchial) vessels of pleural membranes
• Approximately 15 ml per hemithorax is formed every 24 hours
• Usually has a low protein and low wbc with predominance of macrophages
• Makeup is markedly altered in disease states
• Increased fluid entry
• Increase in permeability of membrane
• Increase in microvascular pressure outside the membrane
• Decrease in intra-pleural pressure
• Atelectasis of the lung
• Decrease in plasma oncotic pressure
• Decreased fluid exit
• Inflammation due to infection, tumor or pulmonary infarct
• Direct infiltration of lymphatics by tumor or infection

Pleural fluid studies

• All effusions: Total protein, LDH, glucose, cell count and differential
• If infection is in differential: cultures and stains (bacterial, mycobacterial and fungal).
• If infection or malignancy is suspected: pH which should be collected in a blood gas syringe (heparinized) on ice and run as soon as possible.
• Cytology if malignancy is in the differential

Transudate vs. exudate

pressure/oncotic imbalance vs inflammation

transudative pleural effusions

• Result from imbalances in hydrostatic and oncotic pressures in the chest rather than local inflammation
• As they result from systemic processes, they are frequently bilateral
• Are rarely the result of primary pulmonary pathology

Causes of transudative effusions

• Increased venous hydrostatic pressure
• – Congestive heart failure; right or left sided  
• Pericardial disease
• Hypoalbuminemia (nephrotic syndrome, liver disease)
• – Decreased intravascular oncotic pressure
• Leakage of ascites or peritoneal dialysate through the diaphragm into the pleural space.
• Treatment of hepatic hydrothorax is aimed at ascites management rather than drainage of pleural fluid
• Hypothyroidism
• Endobronchial obstruction with atelectasis
• Decreased intrapleural pressure
• ? Pulmonary embolism

Exudative pleural effusions = inflammation

• Result from inflammatory processes of the lung or pleural space.
• Present more of a diagnostic dilemma
• – 30% may remain undiagnosed despite repeated studies
• Causes of exudative effusions
• • Infection
• • Pulmonary embolism
• • Malignancy
• • Collagen vascular disease
• – Systemic Lupus, Rheumatoid Arthritis
• Subdiaphragmatic inflammation
• – Pancreatitis
• – Liver abscess
• – Spontaneous bacterial peritonitis
• • Drug reactions
• • Hypothyroidism
• • Prior asbestos exposure

Parapneumonic effusions

• Occur frequently in patients with bacterial pneumonia

if cultures are positive or frank pus is present, an “empyema”

– Pneumococcus most common organism

– Anaerobes and staphylococci also occur frequently

Tuberculous pleural effusions

• Usually not a direct infection of the pleural space, 

but an immunologic reaction to new tuberculous infection

– Exudative effusion with lymphocytic predominance and moderately low glucose

Malignant pleural effusions

• As prognosis is generally poor, management is aimed at palliation

Pulmonary embolism

• Small exudative pleural effusions occur frequently with PE

Pleural Fibrosis

• Usually results from large amounts of 
  • undrained infection or blood in pleural 
  • space
• May also occur with tumor
• May result from asbestos exposure
• Heals with progressive thickening of 
  • pleura
• Some cases are idiopathic
• May result in “trapped lung”

Pulmonary Edema

It is less confusing to think of the colloid osmotic pressure as a positive number with a minimum value of zero (NO PROTEIN).

When the rate of fluid filtration from the capillary 

into the interstitium is the rate of lymphatic 

removal and evaporation - no net fluid 

accumulation.

• However, when the rate of fluid filtration from the 

capillary into the interstitium is > the rate of 

lymphatic removal and evaporation - there is net 

fluid accumulation PULMONARY EDEMA.

Cardiogenic Pulmonary Edema

In a normal lung, the driving force for fluid filtration is 

~1 mmHg

• If in CHF the pulmonary capillary pressure increases 

to ~25 mmHg

• Assuming that at least initially Pi ~ 8 mmHg, plasma 

protein osmotic pressure is ~28 mmHg, interstitial 

fluid protein osmotic pressure is ~14 mmHg, and 

remains 0.98

• Then [(25 8) 0.98(28 14)] = ~ 19 mmHg

Treatment for pulmonary edema

• Decrease Preload: diuretics, sit patient up in bed, n
  • itrates, morphine, dialysis.
• Improve Cardiac Performance: Nitrates, Inotropes, 
  • Digoxin.
• Decrease Afterload: ACE inhibitors, nitroprusside
• Increase Pi: Continuous positive airway pressure, 
  • mechanical ventilation
• Decreasing LpA, or osmotic pressure has not been 
  • attempted.

Non-cardiogenic Pulmonary Edema

If there is endothelial damage Lp

increases and Jv increases

Capillary endothelium loses barrier function

– Does not require change in hemodynamics

– Forces that oppose Pc decrease

– LpA increases

– leaky capillaries and increased fluid filtration!

Treatment of non-cardiogenic pulmonary edema

Treatment / Removal of offending source (infection , aspiration , inhalation)
• Mechanical Ventilation if necessary (with low tidal volumes)
• Many experimental therapies (antiinflammatory among others)


DDx Cardiogenic versus Non-cardiogenic


Underlying condition: Myocardial infarction vs. severe infection
• X-ray appearance
• Estimates of Pc (central venous pressure, BNP peptide)
• Measurement of Pc (Swann-Ganz Catheter)
• Measurement of Alveolar protein concentration (estimate of πi)


Hanta virus = both cardiogenic and non-cardiogenic pulmonary edema

High altitude pulmonary edema (HAPE)

• cardiogenic = pulm venoconstriction
• non-cardiogenic = protein in alveolar fluid