Emphysema (IPA2: ˌɛmfəˈzimə) is a chronic obstructive pulmonary disease (COPD, as it is otherwise known, formerly termed a chronic obstructive lung disease). It is often caused by exposure to toxic chemicals, including long-term exposure to tobacco smoke.

Presentation

Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli, owing to the action of alpha 1 antitrypsin deficiency. This causes the small airways to collapse during exhalation, as alveolar collapsibility has increased. As a result airflow is impeded and air becomes trapped in the lungs, in the same way as other obstructive lung diseases. Symptoms include shortness of breath on exertion ]], and an expanded chest. However, the constriction of air passages isn't always immediately deadly, and treatment is available.

Signs of emphysema include pursed-lipped breathing, central cyanosis and finger clubbing. The chest has hyper resonant percussion notes, particularly just above the liver, and a difficult to palpate apex beat, both due to hyperinflation. There may be decreased breath sounds and audible expiratory wheeze. In advanced disease, there are signs of fluid overload such as pitting peripheral edema. The face has a ruddy complexion if there is a secondary polycythemia. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist.

Classification

Emphysema can be classified into two types: Primary and Secondary. However, it is more commonly classified by location.

Emphysema can be subdivided into panacinary and centroacinary (or panacinar and centriacinar, or centrilobular and panlobular).

• Panacinary (or panlobular) emphysema is related to the destruction of alveoli, because of an inflammation or deficiency of alpha 1-antitrypsin. It is found more in young adults who do not have chronic bronchitis.
• Centroacinary (or centrilobular) emphysema is due to destruction of terminal bronchioli muchosis, due to chronic bronchitis. This is found mostly in elderly people with a long history of smoking or extreme cases of passive smoking.

Other types include distal acinar and irregular.

Pathophysiology

[[image:Centrilobular emphysema 865 lores.jpg|left|250px|thumb|Pathology of lung showing centrilobular emphysema characteristic of smoking. Closeup of fixed, cut surface shows multiple cavities lined by heavy black carbon deposits. (CDC/Dr. Edwin P. Ewing, Jr., 1973)]] In normal breathing, air is drawn in through the bronchi and into the alveoli, which are tiny sacs surrounded by capillaries. Alveoli absorb oxygen and then transfer it into the blood. When toxicants, such as cigarette smoke, are breathed into the lungs, the harmful particles become trapped in the alveoli, causing a localized inflammatory response. Chemicals released during the inflammatory response (e.g., elastase) can eventually cause the alveolar septum to disintegrate. This condition, known as septal rupture, leads to significant deformation of the lung architecture. These deformations result in a large decrease of alveoli surface area used for gas exchange. To accomodate the decreased surface area, thoracic cage expansion (barrel chest) and diaphragm contraction (flattening) take place. Expiration increasingly depends on the thoracic cage and abdominal muscle action, particularly in the end expiratory phase. Due to decreased ventilation, the ability to exude carbon dioxide is significantly impaired. In the more serious cases, oxygen uptake is also impaired.