Research Paper on "Chronic Lung Disease Care Planning"

Research Paper 14 pages (4687 words) Sources: 14

[EXCERPT] . . . .

The absence of hypoxemia at rest, however, does not preclude a diagnosis of COPD since exercise may reveal impaired oxygen diffusion capacity (Andrianopoulos et al., 2014). The inflammation component in COPD is primarily neutrophilic and CD8 T cell driven, which is consistent with the patient's leukocytosis with a left shift. By comparison, asthma is primarily an inflammatory disease commonly associated with a type 2 T. helper responses and eosinophilia (Akgun, Crothers, & Pisani, 2012). In patients with combined asthma and COPD, smoking will induce neutrophilia and steroid resistance. For the patient under consideration here a diagnosis of COPD is supported by the CXR findings of bilateral hyperinflation, increased AP diameter, leukocytosis, and signs of emphysema ("Emphysema," n.d.). The absence of chronic sputum production argues against a diagnosis of COPD, but this symptom may be absent in older patients with severe disease (Snider, 1985). A lung function test revealing a below normal FEV1 and DLCO/VA for this patient would be sufficient confirmation for a diagnosis of COPD, but given the patient's resistance to lung function testing a less demanding 6-minute walk test for exercise-induced hypoxemia (? 88%) using pulse oximetry might be more feasible (Andrianopoulos et al., 2014).

Not so long ago COPD was defined in part by the inclusion of the terms 'emphysema' and 'chronic bronchitis,' but the most recent definition by the Global Initiative for Chronic Obstructive Lung Disease (GICOPD) has deemphasized the use of these terms (GICOPD, 2013, p. 1). From their perspective, emphysema represents the functional destruction of alveoli and is thus a pathological term, not a clinical one; therefore, the term 'emphysema' describes one of several structural abnormalities that help define COPD. In addition, the hallmark symptoms of chronic bronchitis is cough and sputum production, which can occur in COPD, but chronic bronchitis can also occur independent of COPD and therefore represents a distinct disease. With this distinction in mind, the pathophysiology of emphysema and chronic bronchitis will be reviewed next.

The radiological findings unique to emphysema are bullae and a lack of vascularization in the peripheral third of the lung ("Emphysema," n.d.). The main pathogenic risk factor for emphysema is inhaled tobacco smoke (Snider, 1985) and the patient in this case study has been a heavy smoker for the past 40 years. Over time the pulmonary capillary bed and alveolar septa is destroyed by cigarette smoke, resulting in the loss of elastic lung tissue recoil, the trapping of air in the peripheral lungs, and hyperinflation (MacNee, 2005). The diagnostic indicators are decreased FEV1 / FVC ratio, elevated TLC, and low DLCO/VA (Pelligrino et al., 2005). A bronchodilator challenge will typically reveal little improvement, but this is less true in COPD patients. Typical radiologic findings are hyperinflation of the lungs, increased AP diameter, bullae, and reduced vascularization ("Emphysema," n.d.). The morphological changes are irreversible and in severe disease the loss of elastic recoil inhibits bronchial drainage (Snider, 1985). For this reason, the lower airways are susceptible to the development of chronic bronchitis and inflammation. A definitive diagnosis of emphysema will require a lung function test with bronchodilator challenge.

Chronic cough and sputum production define chronic bronchitis and these symptoms are triggered by an inflammatory response to cigarette smoke (MacNee, 2005). The primary pulmonary structures affected are the central airway epithelium and mucus-producing glands, resulting in excess mucus production, reduced mucus clearance, and increased airway epithelium permeability. The role that excess mucus production plays in COPD is uncertain, but could represent a downstream event triggered by inflammatory cell protease secretion. Chronic bronchitis is defined as 3 or more months of cough and sputum production each year for two years in a row, in the absence of other diseases that can cause a cough (Albertson, Louie, & Chan, 2010). Chronic bronchitis is a common comorbid condition in COPD patients.

When chronic bronchitis exacerbations occur the most common symptoms are increased volume of sputum production, altered sputum color (darker), and worse dyspnea (Albertson, Louie, & Chan, 2010). When all three are present the disease severity is considered Type I, but when only two out of three are present the exacerbation is Type II. If only one symptom is present, in addition to wheezing, worse cough, fever, increased heart rate, or increased respiration rate, then disease severity is Type III. The exacerbation risk factors are age, malnutrition, cardiac disease, smoking, recent viral infections, chronic lung disease, and alcoholism. The main triggers for exacerbations are pathogens (80%), including bacteria, viruses, and atypical pathogens; however, tobacco smoke, poor patient self-efficacy/compliance, and congestive heart failure will also trigger exacerbations. Antibiotic therapy has been shown to be effective for reducing adverse outcomes for patients experiencing a chronic bronchitis exacerbation. The pathogen(s) responsible can sometimes be predicted by the baseline FEV1. Gram-positive cocci infections for example, especially by S. pneumoniae, tend to be associated with a minimal change in FEV1, whereas H. influenzae and M. catarrhalis are most often found in patients with a greater reduction in FEV1. A still greater reduction in FEV1 can be caused by enterobacteria species and Pseudomonas. The patient under consideration here would be classified as experiencing a Type III chronic bronchitis exacerbation because of the worsening dyspnea, fever, and tachypnea, but a definitive diagnosis of the pathogen(s) responsible will have to await sputum cultures.

Diagnosis

The history of heavy smoking, childhood asthma, dyspnea with physical activity, and signs of emphysema on CXR is consistent with a diagnosis of COPD. Although the chronic cough is only two weeks old, sputum production is absent, and the patient is not hypoxemic, the dyspnea, wheeze, and radiological findings support a preliminary diagnosis of COPD. The absence of sputum does occur in patients with severe lung disease due to impaired airway clearance (Snider, 1985) and hypoxemia may only be evident with physical activity (Andrianopoulos et al., 2014). A definitive diagnosis of COPD should be obtained with a lung function test, if the patient is willing. A lung function test would also help differentiate between asthma and COPD. In addition, a 6-minute walk test with pulse oximetry could be used to evaluate the patient for exercise-induced hypoxemia (Andrianopoulos et al., 2014).

The most immediate concern is the fever and absence of sputum production. The fever, together with leukocytosis, supports a diagnosis of lower airway infection; however, the absence of CXR signs for pneumonia is more consistent with a diagnosis of chronic bronchitis with an acute exacerbation due to infection. The recurrent exacerbations in the patient's history also support this diagnosis. The severity of the acute exacerbation of chronic bronchitis is Type III based on worsening dyspnea, wheezing, fever, tachypnea, and tachycardia. Given the likely diagnosis of COPD, the absence of sputum production is worrying because it may be a symptom of impaired airway clearance.

To summarize, a preliminary diagnosis of COPD and emphysema seems appropriate pending a lung function test, together with a diagnosis of acute exacerbation of chronic bronchitis due to an airway infection. Asthma could also be a contributing factor and the findings of a bronchodilator challenge could be definitive.

Diagnostic Tests

Sputum, pharyngeal swabs, blood, and urine should be collected for culture and other diagnostics tests used to detect and characterize common airway pathogens. A lung function test with bronchodilator challenge should be performed, if the patient is willing and capable. FEV1, FVC, TLC, FRC, RV, and DLCOA should be determined. A lung biopsy may be indicated depending on the lung function test results. The patient should also be encouraged to take a 6-minute walk test for exercise-induced hypoxemia. Arterial blood gases should be analyzed for hypoxemia and pH, since hyperventilation tends to increase pH. In light of the patient's obesity and sedentary lifestyle a metabolic panel should be run to check for metabolic syndrome. Sedentariness and metabolic syndrome has been associated with systemic inflammation, which could be contributing to pulmonary inflammation (Yawn, 2012).

Care Plan: Integrated Disease Management

Despite the patient's past resistance to diagnostic testing the symptoms were severe enough to cause her to seek medical help, which implies that the patient is probably very sick and anxious about her health. The worsening of a non-productive cough, morning sore throat, fever, and mild anorexia over the past two days should be cause for concern; however, psychogenic dyspnea and COPD exacerbations can occur secondary to generalized anxiety disorder and depression, respectively (Wahls, 2012). The patient has expressed concerns that she might have heart disease or cancer, which may be a sign of generalized anxiety disorder; however, the fever and leukocytosis supports a diagnosis of acute exacerbation of chronic bronchitis due to a lower airway infection.

The patient should be immediately admitted and empirically administered an antibiotic cocktail containing a macrolide and ? lactam to combat the suspected airway infection (Drancourt, Gaydos, Summersgill, & Raoult, 2013) and neutrophilic inflammation (Simpson, Phipps, & Gibson, 2009). Systemic glucocorticoids and a short-acting bronchodilator will also be administered to control the inflammation caused by the acute exacerbation (Nakawah, Hawkins, & Barbandi, 2013). Blood oxygen saturation levels will be monitored using pulse oximetry… READ MORE

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