Asthma

Definition and Epidemiology

Asthma is a syndrome characterized by airflow obstruction that varies both spontaneously and with specific treatment. Chronic airway inflammation causes airway hyperresponsiveness to a variety of triggers, leading to airflow obstruction and respiratory symptoms including dyspnea and wheezing. Although asthmatics typically have periods of normal lung function with intermittent airflow obstruction, a subset of pts develop chronic airflow obstruction. The prevalence of asthma has increased markedly over the past 30 years. In developed countries, approximately 10% of adults and 15% of children have asthma. Most asthmatics are atopic, and they often have allergic rhinitis and/or eczema. The majority of asthmatics have childhood-onset disease. Most asthmatics have atopy, and asthmatics often have atopic dermatitis (eczema) and/or allergic rhinitis. A minority of asthmatic pts do not have atopy (negative skin prick tests to common allergens and normal serum total IgE levels). These individuals, occasionally referred to as intrinsic asthmatics, often have adult-onset disease. Occupational asthma can result from a variety of chemicals, including toluene diisocyanate and trimellitic anhydride, and also can have an adult onset. Asthmatics can develop increased airflow obstruction and respiratory symptoms in response to a variety of different triggers. Inhaled allergens can be potent asthma triggers for individuals with specific sensitivity to those agents. Viral upper respiratory infections (URIs) commonly trigger asthma exacerbations. β-Adrenergic blocking medications can markedly worsen asthma symptoms and should typically be avoided in asthmatics. Exercise often triggers increased asthma symptoms, which usually begin after exercise has ended. Other triggers of increased asthma symptoms include air pollution, cold air, occupational exposures, and stress.

Chronic Obstructive Pulmonary Disease

DEFINITION AND EPIDEMIOLOGY 

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by chronic airflow obstruction; thus, pulmonary function testing is central to its diagnosis. The presence of airflow obstruction is determined by a reduced ratio of the forced expiratory volume in 1 s (FEV1) to the forced vital capacity (FVC). Among individuals with a reduced FEV1/ FVC ratio, the severity of airflow obstruction is determined by the level of reduction in FEV1 : ≥80% is stage I, 50–80% is stage II, 30–50% is stage III, and <30% is stage IV. Cigarette smoking is the major environmental risk factor for COPD. The risk of COPD increases with cigarette smoking intensity, which is typically quantified as pack-years. (One pack of cigarettes smoked per day for 1 year equals 1 pack-year.) Individuals with airway hyperresponsiveness and certain occupational exposures (e.g., coal mining, gold mining, and cotton textiles) are likely also at increased risk for COPD. In countries in which biomass combustion with poor ventilation is used for cooking, an increased risk of COPD among women has been reported. COPD is a progressive disorder; however, the rate of loss of lung function often slows markedly if smoking cessation occurs. In normal individuals, FEV1 reaches a lifetime peak at around age 25 years, enters a plateau phase, and subsequently declines gradually and progressively. Subjects can develop COPD by having reduced maximally attained lung function, shortened plateau phase, or accelerated decline in lung function. Symptoms often occur only when COPD is advanced; thus, early detection requires spirometric testing. The Pao2 typically remains near normal until the FEV1 falls to <50% of the predicted value. Hypercarbia and pulmonary hypertension are most common after FEV1 has fallen to <25% of predicted. COPD pts with similar FEV1 values can vary markedly in their respiratory symptoms and functional impairment. COPD often includes periods of increased respiratory symptoms, such as dyspnea, cough, and phlegm production, which are known as exacerbations. Exacerbations are often triggered by bacterial and/or viral respiratory infections. These exacerbations become more common as COPD severity increases, but some individuals are much more susceptible to developing exacerbations than others with similar degrees of airflow obstruction.

PNEUMONIA

Pneumonia, an infection of the lung parenchyma, is classified as communityacquired (CAP) or health care–associated (HCAP). The HCAP category is subdivided into hospital-acquired pneumonia (HAP) and ventilatorassociated pneumonia (VAP). HCAP is associated with hospitalization for ≥48 h, hospitalization for ≥2 days in the prior 3 months, residence in a nursing home or extended-care facility, antibiotic therapy in the preceding 3 months, chronic dialysis, home infusion therapy, home wound care, and contact with a family member who has a multidrug-resistant (MDR) infection.

BRONCHIECTASIS

Etiology and Epidemiology

Bronchiectasis is an irreversible airway dilation that involves the lung in either a focal (due to obstruction) or a diffuse (due to a systemic or infectious process) manner. Bronchiectasis can arise from infectious or noninfectious causes.
• The epidemiology varies greatly with the underlying etiology; in general, the incidence of bronchiectasis increases with age and is higher among women than among men.
• 25–50% of pts with bronchiectasis have idiopathic disease.

LUNG ABSCESS

Microbiology

Lung abscess—infection of the lung that results in necrosis of the pulmonary parenchyma—can be caused by a variety of microorganisms. The etiology depends, in part, on the characteristics of the host.
• Previously healthy pts are at risk for infection with bacteria (e.g., S. aureus, Streptococcus milleri, K. pneumoniae, group A Streptococcus) and parasites (e.g., Entamoeba histolytica, Paragonimus westermani, Strongyloides stercoralis).
• Aspiration-prone pts are at risk for infection with anaerobic bacteria; S. aureus, P. aeruginosa, and F. necrophorum (embolic lesions); endemic fungi; and mycobacteria.
• Immunocompromised pts are susceptible to M. tuberculosis, Nocardia asteroides, Rhodococcus equi, Legionella species, Enterobacteriaceae, Aspergillus species, and Cryptococcus species.

Pulmonary Thromboembolism and Deep-Vein Thrombosis

DEFINITION AND NATURAL HISTORY

Venous thromboembolism includes both deep-vein thrombosis (DVT) and pulmonary thromboembolism (PE). DVT results from blood clot formation within large veins, usually in the legs. PE results from DVTs that have broken off and traveled to the pulmonary arterial circulation. About one-half of pts with pelvic vein or proximal leg DVT develop PE, which is often asymptomatic. Isolated calf vein thrombi have much lower risk of PE. Although DVTs are typically related to thrombus formation in the legs and/or pelvis, indwelling venous catheters have increased the occurrence of upper extremity DVT. In the absence of PE, the major complication of DVT is postphlebitic syndrome, which causes chronic leg swelling and discomfort due to damage to the venous valves of the affected leg. In its most severe form, postphlebitic syndrome causes skin ulceration. PE is often fatal, usually due to progressive right ventricular failure. Chronic thromboembolic pulmonary hypertension is another long-term complication of PE. Some genetic risk factors, including factor V Leiden and the prothrombin G20210A mutation, have been identified, but they account for only a minority of venous thromboembolic disease. A variety of other risk factors have been identified, including immobilization during prolonged travel, cancer, obesity, smoking, surgery, trauma, pregnancy, oral contraceptives, and postmenopausal hormone replacement. Medical conditions that increase the risk of venous thromboembolism include cancer and antiphospholipid antibody syndrome.

Interstitial Lung Disease

Interstitial lung diseases (ILDs) are a group of >200 disease entities characterized by diffuse parenchymal abnormalities. ILDs can be classified into two major groups: (1) diseases associated with predominant inflammation and fibrosis, and (2) diseases with predominantly granulomatous reaction in interstitial or vascular areas . ILDs are nonmalignant and noninfectious, and they are typically chronic. The differential diagnosis of ILDs often includes infections (e.g., atypical mycobacteria, fungi) and malignancy (e.g., bronchioloalveolar cell carcinoma, lymphangitic carcinomatosis). One of the most common ILDs associated with a granulomatous reaction, sarcoidosis, is discussed in Chap.. Many ILDs are of unknown etiology; however, some ILDs are known to be associated with specific environmental exposures including asbestos, radiation therapy, and organic dusts.