Case Study: Chronic Obstructive Pulmonary Disorder
Edwige Hyousseu, Katherine Humphrey, Lindsey Jackson,
Katherine McNabb, Laura Moro, Jodie Pelusi, Kathryn Spearman
Johns Hopkins University
I. Overview of Case and Pathophysiology
Pathogenesis
Chronic Obstructive Pulmonary Disease (COPD) is a slow developing medical condition presenting with long term airflow limitation. The obstruction is a result of an adaptive inflammatory immune response to inhaled antigens, or irritants such as particles and gases (McCance and Huether, 2014, p. 1264). “The most common obstructive diseases are asthma, chronic bronchitis, and emphysema. Because many individuals have chronic bronchitis with emphysema, these diseases together are often called COPD” (McCance and Huether, 2014, p. 1263). The initial immune response is an inflammation of the airway epithelium, with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall. During this inflammatory response, cytokines and interleukins cause oxidative stress and progressive damage to the airways and parenchyma of the lungs. In addition to muscle weakness, weight loss, and anemia, the abnormal response to the noxious irritants results in vasodilation, increased capillary permeability, hypersecretion of mucosa, bronchial edema, and bronchospasm (McCance and Huether, 2014, p. 1267-8). These contributing symptoms of COPD are associated with chronic bronchitis. The continual bronchial irritation causes an increase in thick mucus production that cannot be cleared due to damaged cilia (McCance and Huether, 2014, p. 1267). In addition to symptoms of chronic bronchitis, COPD presents with emphysema, which is indicated by reduced elasticity of bronchial walls and destroyed alveoli, due to breakdown of elastin in lung connective tissue (McCance and Huether, 2014, p. 1269). The increased protease and decreased antiprotease activity results in apoptosis of lung cells, leading to decreased surface area for gas exchange and air trapping (McCance and Huether, 2014, p. 1269). The breakdown of elastin in the lungs may also be caused by an inherited lack of alpha-1-antitrypsin. These chronic bronchitis and emphysema events noted above, more often triggered by tobacco smoke or pollution, help define COPD. Ultimately, the disease process leads to dyspnea, cough, hypoxemia, hypoventilation and hypercapnia. COPD is the combination of these small airway diseases (McCance and Huether, 2014, p. 1268).
Clinical Manifestations
The signs and symptoms of chronic obstructive pulmonary disorder are vast due to its complex etiology and the comorbidities often associated with the disease. However, there are classic symptoms that present in most COPD cases, which include dyspnea, chronic cough, and sputum production (King Han, 2017). Other signs of COPD include, shortness of breath, wheezing, chest tightness, cyanotic lips or fingernails, lack of energy, swelling of the ankles and frequent respiratory infections (COPD, 2017). Patients often have a greater frequency of symptoms in the morning, which impact health related quality of life and daily living activities (Miravitlles et al, 2017). Furthermore, patients can present with weight changes, either weight gain due to decreased activity, or in later stages of the disease, weight loss potentially caused by dyspnea occurring during meals (King Han, 2017). As the disease progresses, the patient’s physical exam may reveal decreased breath sounds, use of accessory muscles for breathing, more distant heart sounds, increased resonance on percussion of the lungs and a “barrel shaped chest” (King Han, 2017). These symptoms are closely associated to a patient’s use and duration of tobacco smoking or smoke exposure (Liu et al, 2015).
Epidemiology
Incidence: There is minimal information published on COPD incidence rates in the United States. One multi-country study that included the United States, as well as 11 European countries, found a COPD incidence rate of 2.8 per 1000 per year, but not real conclusion as to the annual incidence of new COPD diagnoses in the U.S can be drawn from this study (De Marco et al., 2007).
Prevalence: COPD is a leading cause of death worldwide with a global prevalence of 11.4% (Adeloye et al., 2015). Within the United States 6.4% of adults, or approximately 15.7 million people, have been diagnosed with COPD and are currently suffering from COPD. It is most prevalent among seniors, with prevalence rates of 11.8% and 12.3% for those aged 65 -74 and 75 or older respectively. For young adults who fall into the 18-34 age range, there is a prevalence rate of only 2.6%. When analyzing the prevalence of COPD by ethnic background, the rate is significantly higher for Americans who identified as Native American or Alaskan Native (Non-Hispanic) and those that identified as multiracial (Non-Hispanic) than for any other race. Those populations had prevalence rates of 10.2 % and 10.7 %, respectively. The prevalence in women (6.6%) is slightly higher than in men (5.4%). Among current smokers, the prevalence rate is 14.3%. These U.S. prevalence rates are based on self-reported responses to the question, “Have you ever been told by a doctor or health professional that you have COPD, emphysema, or chronic bronchitis? (Wheaton, Cunningham, Ford, & Croft, 2015, p. 291)” Maryland has a prevalence rate for COPD of 5.9% (CDC, 2011).
Morbidity: In 2010, there were 1.47 million ED visits, 10.3 million physician office visits, and 699,000 hospitalizations for COPD as the first-listed diagnosis (Ford et al., 2013). Elderly patients were responsible for the bulk of these hospitalizations, with 65% of the 2010 hospital discharges being for patients aged 65 or older. In 2010, the direct healthcare costs and indirect morbidity costs resulting from COPD is estimated to be $37.5 billion (American Lung Association, 2013, p. 16).
Mortality: COPD is the third leading cause of death in the United States (National Center for Health Statistics, 2017, p.18). Based on the information reported on certificates of death from all 50 states and Washington D.C. in 2014, COPD (including asthma) was the underlying cause of 46.1 out of every 100,000 deaths, approximately 5.5% of deaths in the United States (Kochanek, Murphy, Xu, & Tejada-Vera, 2016, p.5). Deaths from the specific diseases that contribute the COPD are as follows: 563 deaths from bronchitis, 7,455 deaths from emphysema, and 135,432 from other chronic lower respiratory diseases (Kochanek, et al. , 2016, p. 43).
Risk Factors
To prevent a disease, it is important to know the risks factors of the disease. Part of the process of identifying the risk factors consists of finding out whether the disease is congenital or not. In the case of COPD, there are risks that are congenital while others are the results of a lifestyle. Once the condition has been established, it is vital for the individual to know the factors that could risk or worsen a person’s health.
According to lung.com, “Smoking is the biggest risk factor for chronic obstructive pulmonary disease (COPD); this condition manifests itself either as bronchitis or emphysema” (lung.com, 2017). Another way for people to develop the condition of COPD is by breathing secondhand smoke. This smoke can be the result of tobacco or simply working with chemicals that produce dust and fumes.
In the first category of risk factors, human behavior had a play in the making of the condition. The risk factors of the second category are considered to be beyond the control of an individual. The first one is a history of childhood respiratory infections. The constant infections of the lungs has subjected the lungs to airway obstruction and the inability to cough out mucus.
The second risk factor is “a genetic condition called Alpha-1 deficiency”. “In about 1 percent of people with COPD, the disease results from a genetic disorder that causes low levels of a protein called alpha-1-antitrypsin. Produced in the liver and secreted into the bloodstream to help protect the lungs, Alpha-1-antitrypsin deficiency can affect the liver as well as the lungs”. (Mayoclinic.org, 2017)
For patient with COPD, it is imperative that they know how to manage their condition so they may have a “normal” life. For there are risks factors associated with the deterioration of a COPD patient’s health. Acute exacerbation which is explained as a worsening of symptoms manifests through shortness of breath, and quantity and color of phlegm. As a result of these types of developments, patients with COPD do not tolerate the disease for long. According to the World Health Organization, “the most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of approximately one-third of severe exacerbations cannot be identified” (who.int, 2017).
Natural History of the Disease
Chronic obstructive pulmonary disease is a slowly progressive disease resulting in deterioration of lung function. Its onset is related to an abnormal inflammatory response to chronic irritant exposure to the airways and lungs (Hunter, 2001; McCance and Huether, 2014). However, COPD is typically diagnosed later in the disease process since many patients ignore early symptoms such as coughing and sputum production and modify activity levels to accommodate shortness of breath. Patients typically present with signs and symptoms characteristic of a combination of chronic bronchitis and emphysema, such as dyspnea, coughing, prolonged expiration, and wheezing. Systemic clinical manifestations include muscle weakness, muscle wasting, and weight loss. By the time patients present with these signs and symptoms, significant nonreversible airway damage has already occurred. COPD is a disease with some genetic susceptibilities in addition to lifestyle factors such as smoking and exposure to air pollution and occupational dust and chemicals. Chronic exposure to inhaled irritants induces an inflammatory response that results in “progressive damage from oxidative stress, inflammation, extracellular matrix proteolysis, and apoptotic and autophagic cell death” (McCance and Huether, 2014, p. 1267). As a result of these pathological changes, there is an “increased resistance to airflow in the small conducting airways, increased compliance of the lungs, air trapping, and progressive airflow obstruction—all characteristic features of COPD” (MacNee, 2006).
A progressive decline in lung function is a hallmark in the disease progression of COPD (Mannino et al, 2006). Forced expiratory volume (FEV1) is the measurement typically used to assess the severity and progression of COPD. COPD can be exacerbated by many factors including bacterial or viral infection, heart failure, noncompliance with medication use, allergens, or inhaled environmental irritants. Moreover, COPD exacerbations can contribute to the progressive decline in lung function and a greater frequency of exacerbations are associated with higher incidents of mortality (Suisa, Dell’Aniello, Ernst, 2012). Important predictive factors of outcomes include comorbidities (such as heart failure), exercise capabilities, body mass index and lifestyle factors (such as the cessation of smoking) (Mannino et al, 2006). The expected clinical course of COPD is a progressive, chronic disability with intermittent acute exacerbations and the progressive loss of lung function that is not fully reversible (Hunter, 2001; McCance and Heuther, 2014).
II. Selected Case Study Questions
Is this patient technically underweight, overweight, obese, or is the patients weight considered healthy?
Patient’s height is given to be 5 feet 10 inches and weight is 120 pounds. Considering the information and the formula to compute the body mass index, the weight 120 pounds divided by height 70 in inches squared and the result multiplied by 703. The result of this equation equals 17.2. Based on the found data, the patient’s weight can be considered underweight for an adult.
Identify all of the patient’s risk factors for chronic obstructive pulmonary disorder and note which of them is the single most significant risk factor.
When reading the patient’s case, the first thing that stands out is the fact that the patient used to be a heavy smoker who has improved his moderation and is willing to cease. Also, patient uses alcohol excessively. Looking at the family history, his father died from lung cancer. His mother also has COPD and is being treated with oxygen. Besides, he had left lateral malleolus and first metatarsal fracture and repair 17 months ago. Of all the risk factors noted, the history of being a heavy smoker contributed for the most part to the current COPD condition of the patient.
Identify all of the clinical manifestations in this patient that are consistent with chronic bronchitis.
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Identify all of the clinical manifestations in this patient that are consistent with emphysema.
J.T. presents to the ED with progressive dysnpea, which is the most common symptom of ephysema (McCance and Huether, 2014, p. 1270). The patient is thin (underweight with a BMI of 17.2, weight loss of 25 pounds in past 7 years) with a barrel chest appearance, both of which are classic clinical manifestations of emphysema. Other clinical manifestations of emphysema demonstrated by the patient on physical examination include tachypnea (respiratory rate of 32) with prolonged expiration, pursed lip breathing, hyperresonant percussion of the chest and lungs, and the use of accessory muscles at rest were also noted. A mild cough with little sputum and diminished breath sounds on auscultation are also additional clinical manifestations of emphysema that J.T. demonstrated.
Identify all of the clinical manifestations in this patient that are consistent with pulmonary hypertension and cor pulmonale.
An increase in vascular resistance, due to lung disorders, can lead to an increase in pulmonary artery hypertension, as it becomes more difficult to pump blood into the lungs. Cor pulmonale, hypertrophy of the right ventricle due to increased work of pumping blood to lungs, occurs secondarily (Weitzenblum, 2003). The clinical manifestations of pulmonary hypertension and cor pulmonale in J.T. are his peripheral edema, enlarged pulmonary vasculature (Klings, 2017), his complaints of dyspnea and exhaustion, and his mild jugular vein distention (JVD) (Rubin, 2017).
Which serious condition is indicated by the patient’s arterial blood gas analysis?
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The patient has a strong history of alcohol abuse which can cause liver dysfunction. Are there any indications that liver function has been compromised?
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Would this patient benefit from home oxygen therapy?
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Is there any reason to believe that an infection caused this patient’s relapse of chronic obstructive pulmonary disease?
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III. Pertinent Diagnostic and Laboratory Tests
A blood test was conducted that provided electrolyte levels, blood cell counts, and other blood protein levels. While a complete blood test (CBC) is not very useful for diagnosis and treatment of COPD, it can show an increase in red blood cells in patients with chronic hypoxia (Tabatabai, 2018). If tested for, brain natriuretic peptide levels (BNP) can be helpful in determining the presence of decompensated heart failure in patients with chronic respiratory difficulty (Tabatabai, 2018). In J.T.’s case, his blood test showed slightly elevated sodium levels (147 mEq/L; normal range 135-145 mEq/L), slightly elevated chloride levels (114 mEq/L; normal range 97-107 mEq/L), an elevated blood urea nitrogen (BUN) (29 mg/dL; normal range 8-21 mg/dL), slightly elevated hemoglobin (19.3; range 11.7-17.3), and a slightly elevated hematocrit (55%; range 40-54%) (Pagana, 2016).
Arterial blood gas is a measure of the relative concentrations of oxygen and carbon dioxide the give insight into the patient’s acid-base balance and their current state of ventilation (McLachlan, 2017). J.T.’s pH level is 7.32, showing he is acidotic. His PaO2 levels are below normal at 65mmHg, and his PaCO2 levels are elevated at 54 mmHg. This means that he is not getting enough oxygen in, and not getting rid of his CO2. His oxygen saturation is also low, at only 90%. Arterial blood gas measurements can be useful in determining the severity of the respiratory acidosis, and whether or not a patient may be transferred to the ICU or intubated. If J.T.’s PaO2 were less than 60 mmHg, or he had a pH of less than 7.25, he might be considered for ICU transfer (Tabatabai, 2018).
A pulmonary function test was performed that measured the patient’s forced expiratory volume (FEV1) and forced vital capacity (FVC). The ratio of FEV1/FVC is “the proportion of the total vital capacity that can be expelled in the first second of a maximal expiratory effort”. (Scanlon, 2016). Someone with a low FEV1/FVC ratio is likely to have an obstructive lung disease (Scanlon, 2016). J.T.’s FEV1 was 1.67 L, which is 45% of expected, and his FVC was 4.10L (85% of expected), this leads to his FEV1/FVC ratio of 0.41, which is low compared to the normal 0.77.
A chest x-ray is important in monitoring of COPD to determine if there are any co-morbidities such as congestive heart failure, effusions, or tumors (Tabatabai, 2018). During periods of a flare-up, chest x-rays can be used to identify the cause an acute episode that can be treated, such as pneumothorax or atelectasis (Tabatabai, 2018). Outside of acute episodes, routine chest x-rays can be used to monitor changes and disease progression (Tabatabai, 2018). J.T.’s chest x-ray showed hyperinflated lungs, a large anteroposterior diameter, bullae and scarring in the lower lobes, and large pulmonary vasculature (absence of effusions or infiltrates). The hyper-inflated lungs and flattened diaphragm are indicative of advanced disease (King Han, 2017). The large anteroposterior diameter is consistent with the physical examination that revealed a barrel chest, and is due to chronic over-inflation of the lungs with air (Olson, 2016). Bullae are areas of local infection, and may be associated with emphysema (King Han, 2017). Enlarged pulmonary vasculature may indicate pulmonary hypertension secondary to hypoxemia (Klings, 2017)
IV. Patient and Family Education
COPD causes air to be unable to move in and out of the lungs properly due to chronic inflammation. The lung tissue is being constantly irritated and injured from sources such as cigarette smoke, and this leads to the inflammation consistently occurring. The most common conditions that contribute to COPD are chronic bronchitis and emphysema. Chronic bronchitis is when the tubes that carry the oxygen to your lungs are inflamed, this causes you to cough and produce mucus. Emphysema is when the small sacs that transfer the oxygen from the air you breathe into your lungs are destroyed over time due to particle matter, most often found in smoke. These are necessary for your blood to have all of the oxygen it needs to bring around to the rest of your organs (COPD, 2017).
Your willingness to consider completely stopping smoking is a great step. It is important once you are ready, to go over a smoking cessation plan with your doctor, to figure out what is best for you especially to ensure that nothing interacts with any of the medications you are currently on. It may also be beneficial to talk to a nutritionist, this person can help you find more nutrient rich foods to incorporate into your diet, although your weight loss has been gradual, having nutrient rich foods can help your body maintain a healthy weight, and they can help you figure out the best way for you initiate these additions if you would like. In regards to alcohol use, although you have decreased your intake, it is important to be aware that drinking does decrease your body’s ability to fight off infections if they arise, and because of your COPD, respiratory infection can be more frequent. Including your family on the journey to decreased alcohol intake is a great step, because they can support you with alternative options at social events and partake in the decreased consumption as well.
It is also important to stay compliant with your medications when you have COPD, in order to prevent flare ups and hospitalizations. If the ipratropium inhaler is negatively affecting you, we can look for an alternative medication that does not have these side effects so that you can receive the full benefits of your medications and be fully compliant. Like we talked about COPD is most commonly caused by smoking, but there is a small, rare genetic component to COPD that if you have not been tested for before might be something to consider, due to yourself and your mother having the disease. If this is the case it could be important to have the rest of your family tested as well, even if they are not smokers (O’Neil, 2016).
We would like to continue to talk about creating a smoking cessation program for you because this will be a large contributor to increased well being if you choose to go down this path. We encourage you once you have recovered to stay as active as you can, and to continue to take your medications as prescribed. If you have any questions at all, please feel free to ask, or contact your primary care provider.