Pulmonology

Emphysema

폐기종

Irreversible alveolar wall destruction with hyperinflation

How common
Common subtype of COPD
Typical age
Smokers ≥50 yrs

What is it?

Imbalance between elastase and antielastase destroys alveolar walls.

Commonly affected: Alveoli (upper lobes in smokers)

How it develops

  1. Smoke exposureRecruits neutrophils/macrophages
  2. Excess elastaseWorse with α1-antitrypsin deficiency
  3. Alveolar destructionAlveolar coalescence into bullae
  4. Reduced gas exchangeDecreased DLCO and elastic recoil

Symptoms

  • Severe dyspneaEven with minimal activity
  • Pursed-lip breathingIncreases expiratory resistance
  • Weight loss/cachexiaIncreased work of breathing
  • Barrel chestIncreased AP diameter

How it is examined

  • Reduced DLCOHallmark of emphysema
  • SpirometryReduced FEV1, increased RV/TLC

Imaging

Hyperinflation, decreased lung markings, flat diaphragms.

  • Hyperinflation
  • Decreased vascularity

Chest CT distinguishes centrilobular vs panlobular emphysema.

  • Centrilobular emphysema
  • Giant bullae

Non-surgical care

  • Quit smoking + bronchodilatorsLAMA/LABA are standard
  • Pulmonary rehabImproves exercise tolerance
  • LTOTFor PaO2 ≤55 mmHg

Conservative options are generally tried first. Medications listed here can have side effects — discuss them with your prescriber.

When surgery is considered

Severe upper-lobe emphysema, giant bullae

Procedures that may be discussed

  • Lung volume reduction surgery
  • Endobronchial valve placement
  • Lung transplant

Outlook

Quit + treatment slows progression; avg survival 10–15 yrs from diagnosis.

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