Chronic obstructive pulmonary disea...

Chronic obstructive pulmonary disease (COPD) is the fifth leading cause of death in the United States.(1) The majority of patients with COPD have protracted histories of tobacco smoking. This relationship is especially conformable to fact for two subcategories of COPD -- chronic bronchitis and chronic pulmonary emphysema (CPE) In many patients,"chronic bronchitis and CPE be met with together, however, emphysematous symptoms usually predominate.

CHRONIC PULMONARY EMPHYSEMA

Patients who effluvium tobacco products are diagnosed with chronic bronchitis first, because inhaled exhalation produces excessive mucus in their airways, which leads to persistent, productive cough Chronic bronchitis also causes the large and small airways to narrow, making it more difficult to stir air in and out of the lung An estimated 121 million Americans have been diagnosed with chronic bronchitis.(2)

Patients diagnosed with CPE however, have permanent damage to the alveolar walls in their lung This appears because exposure to tobacco sooty vapor causes irreversible destruction of a protein called elastin, which maintains the solidity of the alveolar walls. The los of elastin also causes further narrowing of the bronchioles. This rigorously limits airflow out of the lung and causes air to be trapped in the alveoli. Air entrapment consequence s in alveolar overdistension, loss of elasticity, and impaired gas exchange. The pulmonary capillaries overstretch and tear, resulting in ventilation and perfusion imbalances. The number of patients diagnosed with CPE in the United States is estimated to be pair million.(3)

Quality-of-life issues. Until newly patients diagnosed with CPE have had little confidence of leading normal, productive lives. Completely unable to exist without on medication and supplemental oxygen ([Osub2]) to accomplish the simplest activities of daily living (ADLs), these patients are disabled from chronic dyspnea and live in constant fear of not being able to breathe. Chronic dyspnea interferes with their application prospects, necessitates frequent health care visits, and disrupts family life for decades before death occurs(4)

Medical treatments. Historically, CPE has been treated with supplemental [Osub2] therapy, smoking cessation classes, and prescribed medications (eg bronchodilators, corticosteroids, antibiotics, expectorants, diuretics). The drawbacks of continueed pharmacological therapy include limited medication benefits, side consequences unpredictability of synergistic reactions, and difficulty in regulating therapeutic dosages.

In many cases, physicians are unable to predict which medications will have a desired force for a particular patient and, therefore, prescribe medications based onward trial-and error experimentation and experience.

Surgical treatments. In the past, any patients with CPE have been propounded lung transplantation as a surgical treatment option. The shortage of suitable donor organs, however, has made this surgical option prohibitive for the majority of patients with CPE

Previous surgical attempts to take out large emphysematous bullae (ie, visible air spaces 1 cm or larger in diameter have met with disfavor because of point to be solved [i]or[/i] settleds related to postoperative air leaks. Lung tome reduction surgery (LVRS) using bovine pericardium strips to buttres staple lines and attenuate air leaks offers a technological advantage to other surgical approaches for treatment of patients with CPE The expression LVRS also may be referr to as lung contortion reduction pneumoplasty or pneumectomy.

PATIENT SELECTION CRITERIA

Patient selection criteria for LVR are based upon results of

* health histories and physical examinations,

* exercise dynamics,

* pulmonary function studies,

* chest x-rays and comput tomography (CT) scans,

* quantitative lung perfusion and ventilation scans, and

* cardiac function evaluations.

Health histories. Patients 75 years of age or older or patients who weigh les than 80% of their ideal corpse weight may not be considered for LVR transactions however, these are not absolute criteria for exclusion. Candidates for LVR proceedings must have progressive and methodical dyspnea that is secondary to pulmonary dysfunction from CPE Patients with [alpha.sub.1]-antitrypsin deficiencies (ie, familial enzymatic deficiency that leads to premature alveolar breakdown and bullae formation in the lung bases) also are included as candidates for LVR proceedings The majority of candidates, however, have nonfamilial forms of CPE that watch to destroy the lungs' apexes (ie, the tip or top of the lungs)

Patients with small airway disease (eg asthma, chronic bronchitis, bronchorrhea) or significant systemic diseases (eg diabetes, renal failure) are not eligible for LVR conducts Finally, patients resistant to intensive preoperative pulmonary rehabilitation (ie, reliable participation in a supervised, mandatory exercise program, three to five times by week) also are excluded as candidates.

Physical examinations. upon physical examination, candidates for LVR deeds must exhibit hyperexpanded chests (ie, barrel chests); elevated shoulders; immobile diaphragms, and uncoordinated, thoracoabdominal breathing patterns. Patients with other significant abnormalities (eg kyphoscoliosis, muscular dystrophy) that affect diaphragmatic excursions and patients who exhibit normal diaphragmatic excursions (ie, 4 cm to 6 cm) are not eligible for LVR procedures