Bronchitis, Asthma, EIB, and Influenza: Diagnosis & Treatment

Introduction to Respiratory Tract Infections

Respiratory tract infections are highly infectious diseases that involve the respiratory tract. They are divided into upper (URTI or URI) and lower respiratory tract infections (LRTI or LRI). LRIs include pneumonia, bronchitis, and influenza, and they tend to affect patients more seriously than URIs, which include the common cold, tonsillitis, sinusitis, and laryngitis. This paper examines four respiratory conditions — bronchitis, bronchial asthma, exercise-induced bronchospasm, and influenza — and explores their risk factors, etiology, pathology, differential diagnosis, and treatment. Most of these respiratory infections present with similar symptoms and can therefore be easily mistaken for one another, making it important to carefully examine the available evidence regarding each condition.

Bronchitis is an inflammation of the bronchi, which are the main passages of air to the lungs. It may present as either an acute or a chronic inflammation and has a potential for recurring. Acute bronchitis usually follows a viral infection of the respiratory system. The first signs are that it affects the nose, throat, and sinuses before spreading to the lungs. Bronchitis may also lead to a secondary bacterial infection in the airways. The at-risk groups for bronchitis include smokers, people with lung and heart disease, the elderly, and young children. Chronic bronchitis, on the other hand, usually begins with a cough lasting several months accompanied by excessive production of mucus. Chronic bronchitis is one type of COPD (chronic obstructive pulmonary disease) (Salameh, Waked, Baldi, Brochard, & Saleh, 2006). It is worsened by allergies, air pollution, and occupational hazards such as coal mining, grain handling, textile manufacturing, and other respiratory infections.

Bronchitis: Etiology, Pathology, and Treatment

Acute bronchitis usually presents as a single isolated case or as a series of recurring illnesses. There is typically hypertrophy and hyperplasia of mucus-secreting cells in the bronchus, which characterizes chronic bronchitis as observed in rats exposed to a gaseous chemical irritant for 4–6 weeks (Melbostad, Wijnand, & Magnus, 1997). When bacteria colonize the bronchi, the bacteria implicated are normally normal flora of the nasopharynx region. Therefore, the use of antibiotics to treat bronchitis should be done carefully to avoid harming the normal flora bacteria (Gelb, Nix, & Gellman, 1998).

The first changes to occur in patients with bronchitis include congestion and edema of the bronchial mucosa. At this stage, secretions are few and scanty, but they increase over time as mucus-producing cells and goblet cells become more active. These secretions become progressively more purulent depending on the degree and type of infection. Epithelial desquamation also takes place, and in more severe cases, necrotic changes are observed that extend down to the bronchioles, causing obstruction of the terminal air passages and resulting in patchy atelectasis due to associated inflammation of the alveoli (alveolitis). In many cases, there is complete recovery of the mucous membrane, but some episodes of acute bronchitis may heal by scarring, causing permanent damage to the mucosa and the related alveoli. This damage predisposes the patient to further attacks of acute bronchitis that may eventually become chronic (Toro et al., 1997).

Most cases of bronchitis result from an infection in the upper respiratory tract that then descends to the bronchi. Chemical or traumatic bronchitis arises from exposure to certain gases or vapors that irritate the bronchi, or from atmospheric pollutants that produce minor transient damage to the bronchial epithelium. This is accompanied by paralysis of ciliary action, which in turn permits bacterial infection from the upper respiratory tract (Toro et al., 1997).

Some symptoms of both acute and chronic bronchitis include discomfort in the chest, a cough that produces mucus, fatigue, fever, and shortness of breath that is worsened by exertion or mild activity, as well as wheezing. Additional symptoms of chronic bronchitis include ankle, foot, and leg swelling; frequent respiratory system infections; and blue-tinged lips due to low oxygen levels in the body. With acute bronchitis, even after the infection has cleared, patients often experience a dry, lingering cough that persists for several weeks (Toro et al., 1997).

The healthcare provider first listens to the patient's lungs using a stethoscope, checking for abnormal sounds called rales and any other signs of abnormal breathing, including wheezing. Other diagnostic tests include a chest X-ray, lung function tests, and sputum samples to check for bacterial infection or inflammation. Yellow-green mucus typically indicates a bacterial infection. A pulse oximetry test is conducted to determine blood oxygen levels — this test is quick, painless, and performed using a device placed on the patient's fingertip. An arterial blood gas test provides a more accurate measurement of both oxygen and carbon dioxide levels but requires a needle to be inserted into the patient's artery and is more painful (Toro et al., 1997).

It is important to exclude any primary precipitating disorder from the diagnosis of bronchitis. The buccal mucosa should be examined for the presence of Koplik's spots. In patients with mitral stenosis, acute bronchitis may be confused with the onset of left ventricular failure. In patients with chronic renal disease, bronchitis may be difficult to distinguish from early uraemia, but rapid response to antibiotics can help establish the difference. Failure to respond to antibiotics suggests a drug-resistant organism or a viral cause. Many asthmatic children may experience recurrent episodes of coughing and wheezing — even those without allergic tendencies — so bronchopulmonary changes due to mucoviscidosis must also be excluded (Toro et al., 1997).

Since acute bronchitis is typically caused by a viral infection, antibiotics cannot be used to treat it. The infection usually resolves on its own within about one week. During recovery, patients should avoid smoking and exposure to secondhand smoke, drink plenty of fluids, and rest adequately. In the case of fever, aspirin or acetaminophen (Tylenol) may be taken. The patient should also be advised to use a humidifier to maintain room humidity (Toro et al., 1997).

For chronic bronchitis, antibiotic treatment should be started promptly, with the choice of antibiotic guided by the results of bacteriological examination of the patient's sputum. Options include penicillin, chloramphenicol, streptomycin, erythromycin, and tetracycline. Streptomycin should not be used unless tuberculosis has been excluded. Ampicillin and tetracycline are typically given in 500 mg doses three times daily for 5–6 days, followed by a maintenance dose of 500 mg twice daily for a further 7–10 days (Toro et al., 1997).

Bronchial asthma is a hypersensitivity disorder characterized by reversible obstruction of airflow. It is produced by a combination of edema of the mucus-secreting cells and constriction of the bronchial muscles, together with excessive secretion of viscid mucus that forms a mucus plug. A growing list of environmental agents are recognized as risk factors for bronchial asthma, including wood and metal dust, certain chemicals, allergens such as pollen, dust mites, mold, and pet dander, as well as perfumes and tobacco smoke (Wu & Takaro, 2007). Exercise and excessive anxiety or stress can also trigger bronchial asthma. Aspirin and non-steroidal anti-inflammatory drugs may cause severe bronchial asthma, as may beta-adrenergic blockers such as propranolol, which can induce bronchoconstriction through parasympathetic nerve stimulation. Certain infections such as pneumonia, flu, and the common cold, as well as food additives such as MSG, are also recognized risk factors (Shavit et al., 2007).

Atopic (extrinsic) asthma is thought to result from sensitization of the bronchial mucosa by tissue-specific antibodies. These antibodies stimulate the production of IgE-type immunoglobulins, and total serum IgE concentrations are usually elevated. Upon exposure to inhaled allergens, an antigen-antibody reaction occurs, releasing chemical mediators with vasoactive bronchoconstricting action, which produces the characteristic tissue changes. More recent studies indicate that IgG also plays a role similar to IgE in bronchial asthma (Redd, 2002).

In intrinsic (non-atopic) asthma, the bronchial reaction is triggered by non-immunologic stimuli such as irritating inhalants, exercise, cold air, and emotional upset. Patients with non-atopic asthma do not have elevated serum IgE levels and do not exhibit hypersensitivity to allergens. However, certain immunologic mechanisms in this group have not yet been fully demonstrated (Clark et al., 1999).

Bronchial Asthma: Mechanisms and Management

Risk factors for bronchial asthma generally lead to immunologic mechanisms, causing direct or indirect irritation through protein denaturation. Bronchial asthma can also be occupational in nature and should be suspected when patients repeatedly experience symptoms at work (Chen, Schreier, Strunk, & Brauer, 2008).

Bronchial asthma has a hereditary component. When a susceptible individual is infected or exposed to a trigger, IgE stimulation causes mast cell degranulation, which initiates the asthma attack. This can lead to an altered immunologic response and the release of chemical mediators — including histamine, prostaglandins, SRS-A, bradykinins, and leukotrienes (Unger & Leon, 1954). The resulting increased airway resistance, combined with bronchospasm-driven mucus secretion, produces audible expiratory and inspiratory sounds, use of accessory breathing muscles, nasal flaring, tachypnea, and tachycardia. Bronchial asthma also causes increased lung compliance, leading to hyperinflation of the lungs (Lebowitz, Bronnimann, & Camilli, 1995).

Bronchial asthma can also impair mucociliary function, increasing mucus production and slowing clearance, while the mucus itself becomes increasingly viscous. Symptoms include wheezing and paroxysmal dyspnea. Altered O2 and CO2 exchange increases airway resistance, forcing the respiratory muscles to work harder and eventually causing muscular fatigue, exhaustion, and respiratory alkalosis (Flodin, Ziegler, Jönsson, & Axelson, 1996).

Without medical intervention, the patient may compensate without an increase in respiration rate, leading to respiratory alkalosis and mild hypoxemia. If untreated, this may progress to severe hypoventilation causing respiratory acidosis, severe hypoxemia, and potentially death. With medical intervention — including oxygen therapy and medications such as inhaled steroids, beta-2 adrenergic agents, and bronchodilators (salbutamol) — the airway opens, allowing deep breathing and coughing exercises. Adequate rest and increased fluid intake promote further recovery (Flodin et al., 1996).

Prevention of bronchial asthma involves elevating the head of the bed, limiting exposure to allergens, minimizing strenuous activities, and increasing fluid intake (Flodin et al., 1996).

Bronchial asthma is typically characterized by attacks of coughing, dyspnea, and expectoration of tenacious, mucous sputum, often accompanied by wheezing. Symptoms are usually mild and may occur in association with other respiratory infections. Classic atopic bronchial asthma generally begins in childhood and progresses in severity with age. Hay fever frequently accompanies atopic bronchial asthma (Flodin et al., 1996).

Acute bronchial asthma is often characterized by dyspnea associated with wheezing that can be heard without a stethoscope. Cough may be present but is often not the predominant symptom, though a small group of patients may present with paroxysmal cough as the main symptom. Prolonged bronchial asthma may present as severe, intractable wheezing — a condition known as status asthmaticus (Flodin et al., 1996).

The most important differential diagnosis for asthma is COPD, because COPD can coexist with asthma or arise as a complication of chronic asthma. By age 65, most patients with obstructive airway disease will have both asthma and COPD. COPD can be differentiated by increased neutrophils in the airway, abnormally increased wall thickness, and increased bronchial smooth muscle. It resembles asthma in terms of symptom triggers such as smoke exposure and advanced age, and overlapping management strategies including long-acting beta agonists, corticosteroids, and smoking cessation (Cerveri et al., 1987).

Other differential diagnoses in children include allergic rhinitis, allergic sinusitis, bronchopulmonary dysplasia, cystic fibrosis, and viral bronchiolitis. In adults, they include COPD, congestive heart failure, pulmonary embolism, pulmonary infiltration with eosinophilia, and vocal cord dysfunction. Bronchial asthma is identified in part by an increase in eosinophils in the peripheral blood (Cerveri et al., 1987).

The most effective approach to controlling bronchial asthma is to identify and eliminate triggers, which may include cigarette smoke, aspirin, and pets. When trigger avoidance is insufficient, medical treatment is given based on the severity and frequency of symptoms. Asthma medication is divided into long-acting and fast-acting categories. Bronchodilators provide short-term relief. For mild persistent disease — approximately two attacks per week — low-dose inhaled glucocorticoids, a mast cell stabilizer, or a leukotriene antagonist is given. For frequent daily attacks, high-dose inhaled glucocorticoids are prescribed. Oral glucocorticoids are reserved for severe asthma exacerbations (Unger & Leon, 1954).

Fast-acting medications include SABA (short-acting beta2-adrenoceptor agonists) such as salbutamol, anticholinergics such as ipratropium bromide, and less selective adrenergic agonists such as inhaled epinephrine. Long-term medications include glucocorticoids, LABA (long-acting beta-adrenoceptor agonists, with approximately 12-hour effect), leukotriene antagonists such as zafirlukast, and mast cell stabilizers such as cromolyn sodium (Unger & Leon, 1954).

Asthma medication is primarily delivered via metered-dose inhalers (MDIs) with asthma spacers or as dry powder inhalers; nebulizers may also be used. Complementary approaches include air filtration, mattress and bedding encasement to reduce dust mite exposure, and washing laundry in hot water. One experimental technique, the Buteyko breathing method, aims to control hyperventilation, though evidence for its efficacy remains insufficient to recommend it broadly (Unger & Leon, 1954).

Exercise-induced bronchospasm (EIB) is a disorder that causes breathing problems during or after exercise. Its exact cause is not fully established, but several theories have been proposed. One theory holds that rapid breathing dries the airways, making them easily irritated, which causes them to tighten and narrow — a process called bronchoconstriction. A second theory suggests that injury to the airway cell layer caused by the high flow of air during exercise is responsible. Research indicates that both theories may be on the right path toward explaining EIB. The primary risk factor for EIB is heavy or sustained exercise.