Asthma

 Airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.

Pathophysiology:

1. Airway inflammation:

The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present. Some of the principal cells identified in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes. T lymphocytes play an important role in the regulation of airway inflammation through the release of numerous cytokines. Other constituent airway cells, such as fibroblasts, endothelial cells, and epithelial cells, contribute to the chronicity of the disease. Other factors, such as adhesion molecules (eg, selectins, integrins), are critical in directing the inflammatory changes in the airway. Finally, cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway.The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.Chronic inflammation of the airways is associated with increased bronchial hyperresponsiveness, which leads to bronchospasm and typical symptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants, viruses, cold air, or exercise. In some patients with chronic asthma, airflow limitation may be only partially reversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated disease.Airway inflammation in asthma may represent a loss of normal balance between two "opposing" populations of Th lymphocytes. Two types of Th lymphocytes have been characterized: Th1 and Th2. Th1 cells produce interleukin (IL)-2 and IFN-α, which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation. A study by Gauvreau et al found that IL-13 has a role in allergen-induced airway responses.

2. Intermittent airflow obstruction:

Airflow obstruction can be caused by a variety of changes, including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. Acute bronchoconstriction is the consequence of immunoglobulin E-dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response. Chronic mucous plug formation consists of an exudate of serum proteins and cell debris that may take weeks to resolve. Airway remodeling is associated with structural changes due to long-standing inflammation and may profoundly affect the extent of reversibility of airway obstruction. Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changes lead to a decreased ability to expel air and may result in hyperinflation. The resulting overdistention helps maintain airway patency, thereby improving expiratory flow; however, it also alters pulmonary mechanics and increases the work of breathing.

3. Bronchial hyperresponsiveness:

Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolar hypoventilation. Uneven changes in airflow resistance, the resulting uneven distribution of air, and alterations in circulation from increased intra-alveolar pressure due to hyperinflation all lead to ventilation-perfusion mismatch. Vasoconstriction due to alveolar hypoxia also contributes to this mismatch. Vasoconstriction is also considered an adaptive response to ventilation/perfusion mismatch.In the early stages, when ventilation-perfusion mismatch results in hypoxia, hypercarbia is prevented by the ready diffusion of carbon dioxide across alveolar capillary membranes. Thus, patients with asthma who are in the early stages of an acute episode have hypoxemia in the absence of carbon dioxide retention. Hyperventilation triggered by the hypoxic drive also causes a decrease in PaCO2. An increase in alveolar ventilation in the early stages of an acute exacerbation prevents hypercarbia. With worsening obstruction and increasing ventilation-perfusion mismatch, carbon dioxide retention occurs. In the early stages of an acute episode, respiratory alkalosis results from hyperventilation. Later, the increased work of breathing, increased oxygen consumption, and increased cardiac output result in metabolic acidosis. Respiratory failure leads to respiratory acidosis due to retention of carbon dioxide as alveolar ventilation decreases.

Etiology:

Environmental allergens (eg, house dust mites; animal allergens, especially cat and dog; cockroach allergens; and fungi)

Viral respiratory tract infections

Exercise, hyperventilation

Gastroesophageal reflux disease

Chronic sinusitis or rhinitis

Aspirin or nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity, sulfite sensitivity

Use of beta-adrenergic receptor blockers (including ophthalmic preparations)

Obesity

Environmental pollutants, tobacco smoke

Occupational exposure

Irritants (eg, household sprays, paint fumes)

Various high- and low-molecular-weight compounds (eg, insects, plants, latex, gums, diisocyanates, anhydrides, wood dust, and fluxes; associated with occupational asthma)

Emotional factors or stress

Perinatal factors (prematurity and increased maternal age; maternal smoking and prenatal exposure to tobacco smoke; breastfeeding has not been definitely shown to be protective)

Aspirin Induced Asthma:

The triad of asthma, aspirin sensitivity, and nasal polyps affects 5-10% of patients with asthma. Most patients experience symptoms during the third to fourth decade. A single dose can provoke an acute asthma exacerbation, accompanied by rhinorrhea, conjunctival irritation, and flushing of the head and neck. It can also occur with other nonsteroidal anti-inflammatory drugs and is caused by an increase in eosinophils and cysteinyl leukotrienes after exposure. Primary treatment is avoidance of these medications, but leukotriene antagonists have shown promise in treatment, allowing these patients to take daily aspirin for cardiac or rheumatic disease.  Aspirin desensitization has also been reported to decrease sinus symptoms, allowing daily dosing of aspirin.

Exercise Induced Asthma:

Exercise-induced asthma (EIA), or exercise-induced bronchoconstriction (EIB), is an asthma variant defined as a condition in which exercise or vigorous physical activity triggers acute bronchoconstriction in persons with heightened airway reactivity. It is observed primarily in persons who have asthma (exercise-induced bronchoconstriction in asthmatic persons) but can also be found in patients with normal resting spirometry findings with atopy, allergic rhinitis, or cystic fibrosis and even in healthy persons, many of whom are elite or cold weather athletes (exercise-induced bronchoconstriction in athletes). Exercise-induced bronchoconstriction is often a neglected diagnosis, and the underlying asthma may be silent in as many as 50% of patients, except during exercise.The pathogenesis of exercise-induced bronchoconstriction is controversial. The disease may be mediated by water loss from the airway, heat loss from the airway, or a combination of both. The upper airway is designed to keep inspired air at 100% humidity and body temperature at 37°C (98.6°F). The nose is unable to condition the increased amount of air required for exercise, particularly in athletes who breathe through their mouths. The abnormal heat and water fluxes in the bronchial tree result in bronchoconstriction, occurring within minutes of completing exercise. Results from bronchoalveolar lavage studies have not demonstrated an increase in inflammatory mediators. These patients generally develop a refractory period, during which a second exercise challenge does not cause a significant degree of bronchoconstriction.

Factors that contribute to exercise-induced bronchoconstriction symptoms (in both persons with asthma and athletes) include the following:

Exposure to cold or dry air

Environmental pollutants (eg, sulfur, ozone)

level of bronchial hyperreactivity

Chronicity of asthma and symptomatic control

Duration and intensity of exercise

Allergen exposure in atopic individuals

Coexisting respiratory infection

Clinical Presentation :

History:

Family history may be pertinent for asthma, allergy, sinusitis, rhinitis, eczema, and nasal polyps. The social history may include home characteristics, smoking, workplace or school characteristics, educational level, employment, social support, factors that may contribute to nonadherence of asthma medications, and illicit drug use.

Symptoms:

Wheezing, a musical, high-pitched, whistling sound produced by airflow turbulence, is one of the most common symptoms. In the mildest form, wheezing is only end expiratory. As severity increases, the wheeze lasts throughout expiration. In a more severe asthmatic episode, wheezing is also present during inspiration. During a most severe episode, wheezing may be absent because of the severe limitation of airflow associated with airway narrowing and respiratory muscle fatigue.

Asthma can occur without wheezing when obstruction involves predominantly the small airways. Thus, wheezing is not necessary for the diagnosis of asthma. Furthermore, wheezing can be associated with other causes of airway obstruction, such as cystic fibrosis and heart failure. Patients with vocal cord dysfunction, now referred to as inducible laryngeal obstruction (ILO), have a predominantly inspiratory monophonic wheeze (different from the polyphonic wheeze in asthma), which is heard best over the laryngeal area in the neck. Patients with excessive dynamic airway collapse (EDAC), bronchomalacia, or tracheomalacia also have an expiratory monophonic wheeze heard over the large airways. In exercise-induced bronchoconstriction, wheezing may be present after exercise, and in nocturnal asthma, wheezing is present during the night.

Cough may be the only symptom of asthma, especially in cases of exercise-induced or nocturnal asthma. Usually, the cough is nonproductive and nonparoxysmal. Children with nocturnal asthma tend to cough after midnight and during the early hours of morning. Chest tightness or a history of tightness or pain in the chest may be present with or without other symptoms of asthma, especially in exercise-induced or nocturnal asthma.

Other nonspecific symptoms in infants or young children may be a history of recurrent bronchitis, bronchiolitis, or pneumonia; a persistent cough with colds; and/or recurrent croup or chest rattling. Most children with chronic or recurrent bronchitis have asthma. Asthma is also the most common underlying diagnosis in children with recurrent pneumonia; older children may have a history of chest tightness and/or recurrent chest congestion.

Staging:

The severity of asthma is classified as the following:

Intermittent,

Mild persistent

Moderate persistent

Severe persistent

Patients with asthma of any level of severity may have mild, moderate, or severe exacerbations. Some patients with intermittent asthma have severe and life-threatening exacerbations separated by episodes with almost normal lung function and minimal symptoms; however, they are likely to have other evidence of increased bronchial hyperresponsiveness (BHR; exercise or challenge testing) due to ongoing inflammation.

Investigations:

1. Blood and sputum Eosinophils:

Blood eosinophilia greater than 4% or 300-400/μL supports the diagnosis of asthma, but an absence of this finding is not exclusionary. Eosinophil counts greater than 8% may be observed in patients with concomitant atopic dermatitis. This finding should prompt an evaluation for allergic bronchopulmonary aspergillosis, Churg-Strauss syndrome, or eosinophilic pneumonia.

2. Serum Immunoglobulin E:

Total serum immunoglobulin E levels greater than 100 IU are frequently observed in patients experiencing allergic reactions, but this finding is not specific for asthma and may be observed in patients with other conditions (eg, allergic bronchopulmonary aspergillosis, Churg-Strauss syndrome). A normal total serum immunoglobulin E level does not exclude the diagnosis of asthma. Elevated serum IgE levels are required for chronic asthma patients to be treated with omalizumab (Xolair).

3. Arterial Blood Gas:

Arterial blood gas (ABG) measurement provides important information in acute asthma. This test may reveal dangerous levels of hypoxemia or hypercarbia secondary to hypoventilation and, hence, respiratory acidosis. However, the typical finding in the early stages of an acute episode is respiratory alkalosis. Because of the accuracy and utility of pulse oximetry, only patients whose oxygenation is not restored to over 90% with oxygen therapy require an ABG. The clinical picture usually obviates ABGs for most ED patients with acute asthma.

Venous levels of PCO2 have been tested as a substitute for arterial measurements, and a venous PCO2 greater than 45 mm may serve as a screening test but cannot substitute for the ABG evaluation of respiratory function.

Hypercarbia is of concern in that it reflects inadequate ventilation and may indicate the need for mechanical ventilation if the PCO2 is elevated as a result of patient exhaustion; however, the decision to proceed with endotracheal intubation and mechanical ventilation is a clinical assessment.

4. Pulse oximeter:

Pulse oximetry measurement is desirable in all patients with acute asthma to exclude hypoxemia. The hypoxemia of uncomplicated acute asthma is readily reversible by oxygen administration. Oxygenation decreases 4-10 mm Hg with beta-agonist inhalant therapy due to increases in V/Q mismatch. Therefore, all patients with acute asthma should have oxygen saturation measured by pulse oximetry, or they simply should be placed on oxygen therapy.

5. Chest Radiography:

The chest radiograph remains the initial imaging evaluation in most individuals with symptoms of asthma. The value of chest radiography is in revealing complications or alternative causes of wheezing and the minor importance of wheezing in the diagnosis of asthma and its exacerbations. Chest radiography usually is more useful in the initial diagnosis of bronchial asthma than in the detection of exacerbations, although it is valuable in excluding complications such as pneumonia and asthma mimics, even during exacerbations.

In most patients with asthma, chest radiography findings are normal or may indicate hyperinflation. Findings may help rule out other pulmonary diseases such as allergic bronchopulmonary aspergillosis or sarcoidosis, which can manifest with symptoms of reactive airway disease. Chest radiography should be considered in all patients being evaluated for asthma to exclude other diagnoses.

Because pneumonia is one of the most common complications of asthma, chest radiography is indicated in patients with fever to rule out pneumonia. With new-onset asthma and eosinophilia, a radiograph may be useful in identifying prominent streaky infiltrates persisting less than 1 month, indicating Loeffler pneumonia. The infiltrates of Loeffler pneumonia are peripheral with central sparing of the lung fields. These findings have been described as the radiographic negative of pulmonary edema.

Patients with pleuritic chest pain or those with an acute asthmatic episode that responds poorly to therapy, require a chest film to exclude pneumothorax or pneumomediastinum, particularly if subcutaneous emphysema is present.

5. Chest CT Scanning:

HRCT findings in bronchial asthma include the following:

Bronchial wall thickening

Bronchial dilatation

Cylindrical and varicose bronchiectasis

Reduced airway luminal area

Mucoid impaction of the bronchi

Centrilobular opacities, or bronchiolar impaction

Linear opacities

Airtrapping, as demonstrated or exacerbated with expiration

Mosaic lung attenuation, or focal and regional areas of decreased perfusions

High-resolution CT scan of the thorax obtained during inspiration demonstrates airtrapping in a patient with asthma. Inspiratory findings are normal.

6. Skin Allergy Test:

Allergy skin testing is a useful adjunct in individuals with atopy. Results help guide indoor allergen mitigation or help diagnose allergic rhinitis symptoms. The allergens that most commonly cause asthma are aeroallergens such as house dust mites, animal danders, pollens, and mold spores. Two methods are available to test for allergic sensitivity to specific allergens in the environment: allergy skin tests and blood radioallergosorbent tests (RASTs). Allergy immunotherapy may be beneficial in controlling allergic rhinitis and asthma symptoms for some patients.

7. Pulmonary Function Test:

Spirometry assessments should be obtained as the primary test to establish the asthma diagnosis. Spirometry should be performed prior to initiating treatment in order to establish the presence and determine the severity of baseline airway obstruction.[62]Optimally, the initial spirometry should also include measurements before and after inhalation of a short-acting bronchodilator in all patients in whom the diagnosis of asthma is considered. Spirometry measures the forced vital capacity (FVC), the maximal amount of air expired from the point of maximal inhalation, and the forced expiratory volume in one second (FEV1). A reduced ratio of FEV1 to FVC, when compared with predicted values, demonstrates the presence of airway obstruction. Reversibility is demonstrated by an increase of 12% and 200 mL after the administration of a short-acting bronchodilator.

Differential Diagnosis:

Allergic and Environmental Asthma

Alpha1-Antitrypsin (AAT) Deficiency

Aspergillosis

Bronchiectasis

Bronchiolitis

Chronic Obstructive Pulmonary Disease (COPD)

Chronic Sinusitis

Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss Syndrome)

Cystic Fibrosis

Exercise-Induced Anaphylaxis

Food-Dependent Exercise-Induced Anaphylaxis (FDEIA)

Foreign Body Aspiration

Gastroesophageal Reflux Disease

Heart Failure

Pediatric Airway Foreign Body

Pediatric Tracheomalacia

Pulmonary Embolism (PE)

Pulmonary Eosinophilia

Sarcoidosis

Upper Respiratory Tract Infection

Vocal Cord Dysfunction

Wheat-Dependent Exercise-Induced Anaphylaxis (WDEIA)

Treatment:

Step 1 for intermittent asthma is as follows:

Controller medication not indicated

Reliever medication is a short-acting beta-agonist (SABA) as needed for symptoms

Step 2 for mild persistent asthma is as follows:

Preferred controller medication is a low-dose inhaled corticosteroid

Alternatives include cromolyn, leukotriene receptor antagonist (LTRA),[110]or theophylline

Step 3 for moderate persistent asthma is as follows:

Preferred controller medication is either a low-dose inhaled corticosteroid (ICS) plus a long-acting beta-agonist (LABA) (combination medication is the preferred choice to improve compliance)or an inhaled medium-dose corticosteroid

Alternatives include a low-dose ICS plus either an LTRA or theophylline

Step 4 for moderate-to-severe persistent asthma is as follows:

Preferred controller medication is an inhaled medium-dose corticosteroid plus a LABA (combination therapy)

Alternatives include an inhaled medium-dose corticosteroid plus either an LTRA or theophylline

Step 5 for severe persistent asthma is as follows:

Preferred controller medication is an inhaled high-dose corticosteroid plus LABA

Step 6 for severe persistent asthma is as follows:

Preferred controller medication is an inhaled high-dose corticosteroid plus LABA plus oral corticosteroid.

Chronic Obstructive Pulmonary Disease (COPD)

 Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characterised by persistent airflow limitation that is usually progressive, and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.

COPD includes:

(1) Chronic Bronchitis (cough and sputum on most days for at least 3 months, in each of 2 consecutive years)

(2) Emphysema ( (abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis).

Risk Factors of COPD:

1. Environmenal:

• Tobacco smoke accounts for 95% of cases in UK

• Indoor air pollution; cooking with biomass fuels in confined

areas in developing countries

• Occupational exposures, such as coal dust, silica and

cadmium

• Low birth weight may reduce maximally attained lung

function in young adult life

• Lung growth: childhood infections or maternal smoking may

affect growth of lung during childhood, resulting in a lower

maximally attained lung function in adult life

• Infections: recurrent infection may accelerate decline in FEV1;

persistence of adenovirus in lung tissue may alter local

inflammatory response, predisposing to lung damage; HIV

infection is associated with emphysema

• Low socioeconomic status

• Cannabis smoking

2. Host 

• Genetic factors: α1-antiproteinase deficiency; other COPD

susceptibility genes are likely to be identified

• Airway hyper-reactivity

Clinical Presentation of COPD:

History:

Patients with chronic obstructive pulmonary disease (COPD) present with a combination of signs and symptoms of chronic bronchitis, emphysema, and asthma. Symptoms include worsening dyspnea, progressive exercise intolerance, and alteration in mental status. In addition, some important clinical and historical differences can exist between the types of COPD.

In the Chronic bronchitis group, classic symptoms include the following:

•Productive cough, with progression over time to intermittent dyspnea

•Frequent and recurrent pulmonary infections

•Progressive cardiac/respiratory failure over time, with edema and weight gain

In the Emphysema group, the history is somewhat different and may include the following set of classic symptoms:

•A long history of progressive dyspnea with late onset of nonproductive cough

•Occasional mucopurulent relapses

•Eventual cachexia and respiratory failure

Physical Examination of COPD:

Chronic bronchitis (blue bloaters) findings may be as follows:

•Patients may be obese.

•Frequent cough and expectoration are typical.

•Use of accessory muscles of respiration is common.

•Coarse rhonchi and wheezing may be heard on auscultation.

•Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis.

•Because they share many of the same physical signs, COPD may be difficult to distinguish from congestive heart failure (CHF). One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation.

Emphysema (pink puffers) findings may be as follows:

•Patients may be very thin with a barrel chest.

•They typically have little or no cough or expectoration.

•Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position. In this manner, the patient is trying to maintain a certain amount of positive end-expiratory pressure (PEEP) at the end of expiration, to help keep their lungs open, owing to the loss of lung structure from the disease.

•The chest may be hyperresonant, and wheezing may be heard; heart sounds are very distant.

•Overall appearance is more like classic COPD exacerbation.

Investigations for COPD:

1:Pulmonary Function Test (PFT):

Forced expiratory volume in 1 second (FEV1) is decreased, with concomitant reduction in FEV1/forced vital capacity (FVC) ratio. Patients have poor/absent reversibility with bronchodilators. FVC is normal or reduced. Total lung capacity (TLC) is normal or increased. Residual volume (RV) is increased. Diffusing capacity is normal or reduced.

2:Arterial Blood Gas (ABG's):

Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity. In general, renal compensation occurs even in chronic CO2 retainers (ie, bronchitics); thus, pH usually is near normal. Generally, consider any pH below 7.3 a sign of acute respiratory compromise.

3:CBC 

CBC may reveal polycythemia.

4:Chest Radiology

Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly.

Emphysema is associated with a small heart, hyperinflation, flat hemidiaphragms, and possible bullous changes. Typical findings are shown in the radiographs below.

Chronic obstructive pulmonary disease (COPD). A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on lateral chest radiograph.

Chronic obstructive pulmonary disease (COPD). A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior chest radiograph.

Spirometric classification of COPD severity based on post-bronchodilator FEV1

Stage                  Severity                 FEV1

I                         Mild*                    FEV1/FVC < 0.70

                                                        FEV1 ≥ 80% predicted

II                        Moderate              FEV1/FVC < 0.70

                                                        FEV1 50–79% predicted

III                      Severe                   FEV1/FVC < 0.70

                                                        FEV1 30–49% predicted

IV                     Very severe            FEV1/FVC < 0.70

                                                       FEV1 < 30% predicted or FEV1 < 50%

                                                       predicted if respiratory failure present

Management:

Prevention and maintenance therapy recommendations are as follows:

Smoking cessation is key. Pharmacotherapy and nicotine replacement increase long-term smoking abstinence rates, as do legislative bans on smoking. The effectiveness and safety of e-cigarettes as a smoking cessation aid is uncertain.

Pharmacologic therapy can reduce the symptoms of COPD, can reduce the severity and frequency of exacerbations, and can improve exercise tolerance and health status.

Pharmacologic treatment regimens should be individualized. They should be guided by symptom severity; exacerbation risk; adverse effects; comorbidities; drug availability and cost; and patient response, preference, and ability to utilize the various drug delivery devices.

Inhaler technique should be assessed regularly.

Pneumococcal and influenza vaccinations decrease the incidence of lower respiratory tract infections.

Pulmonary rehabilitation improves symptoms, physical and emotional participation in everyday activities, and quality of life.

Patients with severe resting chronic hypoxemia have improved survival with long-term oxygen therapy.

In patients with stable COPD and resting or exercise-induced moderate desaturation, routine long-term oxygen treatment is not recommended; however, consider individual patient factors regarding the need for supplemental oxygen.

With severe chronic hypercapnia and a history of hospitalization for acute respiratory failure, long-term noninvasive ventilation may prevent rehospitalization and decrease mortality.

Select patients with advanced emphysema refractory to optimized medical care may benefit from surgical or bronchoscopic interventional treatments.

In advanced COPD, palliative approaches are effective in controlling symptoms.

Exacerbation recommendations are as follows:

A COPD exacerbation is defined as acute respiratory symptom worsening with the need for additional therapy. Several factors can lead to an exacerbation, the most common being respiratory tract infections.

The recommended initial bronchodilators to treat an exacerbation are short-acting beta2-agonists, with or without short-acting anticholinergics.

As soon as possible before hospital discharge, initiate maintenance therapy with a long-acting bronchodilator.

Systemic corticosteroids can improve lung function and oxygenation. They also shorten recovery time and hospital duration. The duration of systemic corticosteroid therapy should not exceed 5-7 days.

If indicated, antibiotic therapy can shorten recovery time, reduce the risk of early relapse and treatment failure, and reduce hospitalization duration. The duration of antibiotic therapy should not exceed 5-7 days.

Owing to increased adverse effect profiles, methylxanthines are not recommended.

The first mode of ventilation used in COPD with acute respiratory failure and without contraindications is noninvasive mechanical ventilation. It improves gas exchange, reduces the work of breathing, decreases the need for intubation, decreases hospitalization duration, and improves survival.

GOLD patient grouping:

The GOLD patient group-based management recommendations include the following

Group A-D: Reduction of risk factors (influenza and pneumococcal vaccine); smoking cessation; physical activity; short-acting anticholinergic or short-acting beta-adrenergic agonists as needed

Group B: Long-acting anticholinergics or long-acting beta-adrenergic agonists; cardiopulmonary rehabilitation

Group C: Inhaled corticosteroid and long-acting beta-adrenergic agonists or long-acting anticholinergics; cardiopulmonary rehabilitation

Group D: Inhaled corticosteroid and long-acting beta-adrenergic agonists and/or long-acting anticholinergics; cardiopulmonary rehabilitation; long-term oxygen therapy (if criteria met); consider surgical options such as lung volume reduction surgery (LVRS)

Differential Diagnosis:

Acute Respiratory Distress Syndrome (ARDS)

Aspiration Pneumonitis and Pneumonia

Bacterial Pneumonia

Emergent Management of Pleural Effusion

Empyema and Abscess Pneumonia

Heart Failure

Mycoplasmal Pneumonia

Myocardial Infarction

Panic Disorder

Pneumonia in Immunocompromised Patients

Pneumothorax

Pulmonary Embolism (PE)

Viral Pneumoniae

Complications:

Incidence of pneumothorax due to bleb formation is relatively high; consider pneumothorax in all patients with COPD who have increased shortness of breath.

In patients who require long-term steroid use, the possibility of adrenal crisis is very real; at a minimum, patients with steroid-dependent COPD should receive stress dosing in the event of an exacerbation or any other stressor.

Infection (common)

Cor pulmonale

Secondary polycythemia

Bullous lung disease

Acute or chronic respiratory failure

Pulmonary hypertension

Malnutrition