Respiratory Chronic Obstructive Pulmonary Disease - Essay Example

Case Study One: Respiratory Chronic Obstructive Pulmonary Disease Discuss your priorities of care for Madeleine on her arrival, giving your rationales. 10% (250 Words)   As with other emergency cases, the priorities in managing the patient would be the Airway, Breathing and Circulation. (A,B,C). Stabilization of airway should be done. Breathing of the patient can be treated with 100% oxygen. Acute exacerbations of chronic obstructive pulmonary disease (COPD) are treated with oxygen (in hypoxemic patients), inhaled beta2 agonists, inhaled anticholinergics, antibiotics and systemic corticosteroids. Methylxanthine therapy may be considered in patients who do not respond to other bronchodilators. Since the most common cause of exacerbation would still be infection, antibiotic therapy can be done. Antibiotic therapy is directed at the most common pathogens, including Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Mild to moderate exacerbations of COPD are usually treated with older broad-spectrum antibiotics such as doxycycline, trimethoprim-sulfamethoxazole and amoxicillin-clavulanate potassium. While doing the abovementioned management for the patient, detailed history should be done, if not obtained from the patient, from the companion. Risk factors, medications,measures done should be detailed. The vital signs of the patient should be checked constantly making sure that values are within normal. In-depth physical examination, not only of the respiratory system, but also of other systems should be done. The patient should be hooked on pulse oximeter to check for oxygenation status.   Angela is also extremely distressed on arrival and asks "She is going to be all right isnt she? I know this is my fault - I wanted her to do everything – spend time with me when I knew she was busy!" 2. Discuss the pathophysiology and aetiology of COPD 10% (250 Words) Chronic pulmonary obstructive diseases is characterized by the inflammation of the lungs especially the small airways as a reaction of the body to inhaled toxins, cigarette smoke, dust and other particles due to air pollution or indoor cooking. Chronic productive cough, sputum and bronchoconstriction also result due to chronic bronchitis but ciliary dysfunctions may cause difficulties in expectorating (Devereux, 2006). The inflammation triggers a series of reactions that can lead to destruction of tissues, defense and repair mechanisms. Overworked proteases and antioxidants that fight off oxidative stress created by lung inflammation causes imbalance of these molecules in the lungs. Metalloproteases and other proteases increase due to increased number of macrophages, neutrophils, and T lymphocytes which are also involved in the pathogenesis of emphysema due to injuries in the alveolar wall (MacNee, 2006) Oxidative stress also stimulates mucous production and may amplify inflammation by increased gene expression of pro-inflammatory activators as a result of released transcription factors. An increase in the concentration of inflammatory mediators, such as leucotrienes, chemokines and growth factors occur and may promote fibrosis in the airways as a result of their interaction with other cellular signals present. Inflammation and narrowing of airways create airflow obstruction resulting in difficulties in breathing or exercise capabilities, wheezing and fatigue (Devereux, 2006). COPD patients have high risk of cardiovascular disease, pulmonary hypertension and ventricular enlargement and, eventually, contract muscle fatigue and alveolar hypoventilation. This can lead to hypoxia and respiratory acidosis due to increased concentration of CO2. The latter reacts with water which produces H2CO3 thereby increasing H+ concentration (Franciosi et al., 2006). Madelines vital signs at this stage are: blood pressure: 130/90 mm Hg, respirations 32/min and shallow, pulse 110/min and irregular, temperature 37.5 ° C, Oxygen saturation 86%. 3. How would you deal with Angela and her distress at this point? 5% (125 words) Exacerbations of COPD, particularly of emphysema, are quite frightening for on-lookers, especially those who are not well-oriented about the disease. The sight of patients gasping for air may lead one to think about death. It is very important to reassure Angela that you are doing everything to stabilize her friend. Careful explanation of the pathophysiology of the disease can eliminate some of the doubts in her mind. Educating her that she did not cause the exacerbation of her friend would be of help. Principles to be used in managing the case of Madelaine should be carefully explained to her with the expected results for each step. Angela should also be given updates on Madelaine’s status from time to time. While waiting, she should also be educated on the prevention of future exacerbations, and what to expect from Madelaine in the future.   Madelines vital signs at this stage are: blood pressure: 130/90 mm Hg, respirations 32/min and shallow, pulse 110/min and irregular, temperature 37.5 ° C, Oxygen saturation 86%. 4. Discuss the subjective symptoms you would take into account when assessing Madeleines respiratory status. 5% (125 words) Since Madeline’s resting oxygen saturation is very low, it may be necessary to determine the concentration of arterial blood gases in addition to continued oxygen therapy (Currie, 2006). Constant observation and monitoring of symptoms such as blood pressure, pulse oximetry, breathlessness, wheezing and chest pains is important to assess any improvement or worsening of the patient’s conditions (Devereux, 2006). Any history of emphysema must also be determined from the patient, including the medications that have already been taken with corresponding durations. Previous sources of stress that could have triggered the attack should also be determined including any previous episodes which might have been caused by smoking. Anxiety or fear in the patient including any source of irritation or stress in the current environment should be observed and, eventually, eliminated (Freeman and Price, 2006). 5. What other investigations/ observations do you anticipate the medical officer would order at this stage – give rationales. 5% (125 words) Other investigations which may be required include a full blood count which may show signs of secondary polycythaemia as a result of hypoxaemia (Freeman and Price, 2006). Thus, elevated RBC count and eosinophils may be confirmed through CBC. This can also confirm leukocytosis and a probable respiratory tract infection. Sputum culture can also be an additional test to confirm lung infection. Pulmonary capacity, increased residual volume and function tests should also be observed as well as the presence of discomforts and chest pains. Hyperinflation of the lungs and chronic right sided heart strain may be evaluated using electrocardiography and chest x-ray examinations. Echocardiography may also be used to assess pulmonary artery pressure, atrial dilation and right ventricular hypertrophy. Pulse oximetry reveals hypoxaemia, thus, administration of oxygen should be continued (Currie, 2006).   You have notified the medical officer of your concern for this patient and having confirmed your observations and examination, he has ordered nebulised Salbutamol (1ml/ 1ml Saline) and Ipratropium (1ml/ 1ml Saline) to be given half-hourly PRN and an Aminophylline infusion (750 mgs in 500mls of Dextrose to run over 24hours)   A junior RN asks you "Why would the medical officer have ordered three drugs which essentially do the same thing?"   6. Discuss the rationales for these orders in this setting. 10% (250 Words) Administering drugs in combination take advantage of the synergistic effects of the prescribed treatments. They can also be optimized as different persons react differently to these drug combinations. The scheme also provides additive treatment at different modes of delivery because these various types of molecules can act on different pathways and stages of attack. Salbutamol, such as Ventolin ® belong to a diverse family of molecules called bronchodilators which act to open airways by reducing its inflammation. They are quick, short acting 2-agonists that are administered first to treat chronic asthma, chronic bronchitis and emphysema. Ipratropium bromide, on the other hand, is an anticholinergic, atropine derived drug which effectively reduces breathlessness (Flenley, 1983). Both drugs have different mechanisms of molecular attack and they are administered by inhalation. A full breath or one puff delivers only approximately 10% of the dose but it is enough to reduce inflammation. The aerosol technique allows direct action on the lungs where small, controlled doses are given to reduce the development of tolerance to the medicine. They also reduce coughing by decreasing inflammation of airways. Aminophylline is also a bronchodilator which significantly acts in tandem with the other drugs to quickly and efficiently suppress airway constriction. It reduces muscle contraction by paralyzing nerve endings resulting in relaxation and reduced inflammation. Atropine derivatives usually interact with 2-agonists to effectively counter attack bronchoconstriction as combination drugs provide better and faster relief to produce similar outcomes. Because of this, fixed combination inhalers are now commonly prescribed for patients of COPD (Barnes, 2006). Madeleines distress begins to settle after the first nebulised dose of Salbutamol and Ipratropium is completed and so you judge that it is appropriate to start collecting a nursing history from Madeleine.   7. Outline the strategy/ies you would use to gather this data from Madeleine while causing her least stress and the data you would be seeking. 10% (250 Words) A reassuring and positive approach to conversation must be used to extract data to avoid causing Madeline stress. If available, old records can minimize the questions that will be asked to the patient. Starting with familiar topics such as asking about her family can be a great way to start a discussion. Medical history can then be determined. Diagnosis and severity of COPD must be addressed by determining the date of her first attack and when diagnosis was confirmed. It would also be vital to determine Madeline’s smoking status, the date when she stopped smoking and the frequency of her intakes are some questions which might be asked. If, however, Madeline has not yet stopped smoking, advice must be given carefully to facilitate smoking cessation. Risks should also be stressed. For long term patients of COPD like Madeline, exacerbations in the past twelve months should also be discussed. Among questions to be asked are antibiotics and corticosteroids that she has taken and hospital admissions during the mentioned period (Freeman and Price, 2006). A review of her vaccinations, previous therapies and her self-management routine will also help. Lastly, causes of her recent attacks need to discussed, while carefully watching out for symptoms of depression, fear or anxiety (Currie and Legge, 2006). Informing her that she was able to surpass the peak of the attack and will continue to do so if she remains calm will reassure her of continued improvement in her condition. During the conversation, an overall assessment of Madeline’s case can be made which will help in designing the care and services she needs. Madeleine is transferred to the close observation ward of the emergency department for 24hours observation with the following medical orders: • Continue the Aminophylline infusion as ordered • Salbutamol 1ml/1ml N/saline nebulised 4/24 • Ipratropium 1ml/1ml N/saline nebulised 8/24 • Hydrocortisone Sodium 200 mgs IV 6/24   8. How is Hydrocortisone likely to assist in Madeleines recovery? 5% (125 words) Hydrocortisone is a hormone belonging to a family of glucocorticoids that promote carbohydrate, fat and protein metabolism. This molecule stimulates body processes to return to normal as it triggers an increase in gluconeogenesis, lipolysis, and amino acid uptake by the liver. Thus, administration of hydrocortisone can improve symptoms of COPD and exercise tolerance in the patient because of increased energy as well as prevent exacerbations in the patient. They regulate ion concentration and retain balance of Na+ and K+ ions. It also prevents dehydration, hypoglycaemia and low blood pressure to occur. Hydrocortisone is also used when asthma is a characteristic of COPD. Oral corticosteroids, such as prednisone, are used initially. Positive responses may require lower doses daily or every other day. Uptake by inhaler is also preferred to minimise side effects. You are aware that despite its deleterious side-effects, the prescribed Aminophylline infusion will be necessary to help correct the respiratory acidosis Madeleine has developed.   9. Discuss the possible side-effects of Aminophylline that you would be assessing Madeleine for during her stay in your care. 5% (125 words) Aminophylline is a bronchodilator composed of 80% theophylline. Low doses of 400-500 mg can cause nausea, vomiting, headaches, insomnia and agitation but cannot effect bronchodilation at these levels. As a result administration must be slowly increased to prevent CNS or cardiovascular toxicity. Overstimulation of the nervous system causes nervousness, epigatric distress, tachycardia, seizures and ventricular dysrhythmias. Severe hypotension, fainting, palpitations, syncope, precordial pain, flushing and profound bradycardia are signs of rapid increase in its dosage. This should be avoided as cardiac arrest may result. For patients with cirrhosis, congestive heart failure, chronic obstructive lung disease, and cor pulmonale, the half life of the drug is increased and constant nausea and vomiting results (Flenley, 1983). Beveridge et al. (1996) also note that to achieve significant bronchodilation 2-agonists provide additive effects when administered with it. 10. Briefly describe the pathophysiological process of respiratory acidosis. 5% (125 words) Inflammation, arterial dilation, bronchoconstriction and very low oxygen saturation, indicative of moderate hypoxaemia, causes dyspnoea and hypoventilation which in turn causes an increase in the CO2 pressure and concentration in the lungs. With the progression of the disease, PaO2 also decreases as CO2 continues to be retained in the lungs. This results in the disruption of the acid and base balance in the system. Carbonate and bicarbonate ion balance maintains the acidity levels in the lungs through buffering reactions. The equilibrium is upset by a sudden increase in CO2 and fluid retention. These two couple and undergo a reaction that produces carbonic acid. The latter is a weak acid that dissociates in water to form bicarbonate and H+ ions thereby causing a decrease in pH characteristically at 45 mmHg, has important implications for treatment. In contrast to its utility in the management of exacerbations of asthma, measurement of pulmonary function has not been demonstrated to be helpful in the diagnosis or management of exacerbations of COPD. There are no definitive guidelines concerning the need for inpatient treatment of exacerbations. Patients with respiratory acidosis and hypercarbia, significant hypoxemia, or severe underlying disease or those whose living situation is not conducive to careful observation and the delivery of prescribed treatment should be admitted to the hospital.  The use of supportive oxygen for Madeleine is very important in this case. Her lungs are currently not working to their fullest and supplemental oxygen will aid not only in supplying the Oxygen demand but will also help in letting her lungs “rest” for a while. Supplemental Oxygen should be supplied to keep arterial saturations =90%. Hypoxic respiratory drive plays a small role in patients with COPD1. Studies have demonstrated that in patients with both acute and chronic hypercarbia, the administration of supplemental O2 does not reduce minute ventilation. It does, in some patients, result in modest increases in arterial PCO2, chiefly by altering ventilation-perfusion relationships within the lung. This should not deter practitioners from providing the oxygen needed to correct hypoxemia. Typically, patients are treated with an inhaled ß agonist, often with the addition of an anticholinergic agent. These may be administered separately or together, and the frequency of administration depends on the severity of the exacerbation. Patients are often treated initially with nebulized therapy, as such treatment is often easier to administer in older patients or to those in respiratory distress. It has been shown, however, that conversion to metered-dose inhalers is effective when accompanied by education and training of patients and staff. This approach has significant economic benefits and also allows an easier transition to outpatient care. The addition of methylxanthines (such as theophylline) to this regimen can be considered, although convincing proof of its efficacy is lacking. If added, serum levels should be monitored in an attempt to minimize toxicity. Patients with COPD are frequently colonized with potential respiratory pathogens and it is often difficult to identify conclusively a specific species of bacteria responsible for a particular clinical event. Bacteria frequently implicated in COPD exacerbations include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. In addition, Mycoplasma pneumoniae or Chlamydia pneumoniae are found in 5 to 10% of exacerbations. The choice of antibiotic should be based on local patterns of antibiotic susceptibility of the above pathogens, as well as the patients clinical condition. Most practitioners treat patients with moderate or severe exacerbations with antibiotics, even in the absence of data implicating a specific pathogen. Among patients admitted to hospital, the use of glucocorticoids has been demonstrated to reduce the length of stay, hasten recovery, and reduce the chance of subsequent exacerbation or relapse for a period of up to 6 months. A recent study demonstrated that 2 weeks of glucocorticoid therapy produced benefit indistinguishable from 8 weeks of therapy. The GOLD2 guidelines recommend 30 to 40 mg of oral prednisolone or its equivalent for a period of 10 to 14 days. Hyperglycemia, particularly in patients with preexisting diagnosis of diabetes, is the most frequently reported acute complication of glucocorticoid treatment. Madeleine improves and stabilises over the next 24 hours and the medical officer is happy to discharge her home. He asks you to organise this. You are concerned about the factors precipitating this admission and prepare an education package for Madeleine before she leaves the ward.     12. Outline the factors/ issues you would include in this package, the media/ resources you might use to deliver it and the individuals you would include. 10% (250 Words)   An Outline of the Patient Education Kit: Chronic Obstructive Pulmonary Disease (COPD) • COPD Overview • COPD Causes • COPD Symptoms • When to Seek Medical Care • Exams and Tests • COPD Treatment • Self-Care at Home • Medical Treatment • Medications • Surgery • Next Steps • Follow-up • Prevention • Outlook • Support Groups and Counseling Pulmonary rehabilitation Many patients with COPD are unable to enjoy life to the fullest because of shortness of breath, physical limitations, and inactivity. Pulmonary rehabilitation encompasses an array of therapeutic modalities designed to improve the patients quality of life by decreasing airflow limitation, preventing secondary medical complications, and alleviating respiratory symptoms. The 3 major goals of the comprehensive management of COPD are the following: 1. Lessen airflow limitation 2. Prevent and treat secondary medical complications (eg, hypoxemia, infection) 3. Decrease respiratory symptoms and improve quality of life Pulmonary rehabilitation, a multidisciplinary team approach Successful implementation of a pulmonary rehabilitation program usually requires a team approach, with individual components provided by health care professionals who have experience in managing COPD (eg, physician, dietitian, nurse, respiratory therapist, exercise physiologist, physical therapist, occupational therapist, recreational therapist, cardiorespiratory technician, pharmacist, psychosocial professionals). This multidisciplinary approach emphasizes patient and family education, smoking cessation, medical management (eg, oxygen, immunization), respiratory and chest physiotherapy, physical therapy with bronchopulmonary hygiene, exercise, vocational rehabilitation, and psychosocial support. Benefits of pulmonary rehabilitation: As a result of rehabilitation, improvements occur in the objective measures of quality of life, well being, and health status, including a reduction in respiratory symptoms and an increase in exercise tolerance and functional activities (eg, walking, less anxiety and depression, increased feelings of control, self-esteem). Pulmonary rehabilitation also results in substantial savings in healthcare costs by reducing use of hospital and medical resources. Components of pulmonary rehabilitation Pulmonary rehabilitation programs usually are conducted in an outpatient setting. A rehabilitation program may include a number of components and should be tailored to the needs of the individual patient. Provide all patients who complete the program with guidelines for continuing at home. Education is key to comprehensive pulmonary rehabilitation. The educational component prepares the patient and families to be actively involved in providing care. This reliance on patients to assume charge of their care is known as collaborative self-management. Exercise training is a mandatory component of pulmonary rehabilitation. Patients with COPD should perform aerobic lower extremity endurance exercises regularly to enhance performance of daily activities and reduce dyspnea. Upper extremity exercise training improves dyspnea and allows increased activities of daily living requiring the use of upper extremities. Breathing retraining techniques (eg, diaphragmatic, pursed lip breathing) may improve the ventilatory pattern and prevent dynamic airway compression. References Alsaeedi A, Sin DD, McAlister FA: The effects of inhaled corticosteroids in chronic obstructive pulmonary disease: a systematic review of randomized placebo-controlled trials. Am J Med 2002 Jul; 113(1): 59-65[Medline]. Barnes, PJ. (2006). ABC of chronic pulmonary obstructive disease: future treatments. BRITISH Medical Journal, 333;246-248 Beveridge, RC; Grunfeld, AF; Hodder, RV; Verbeek, PR. (1996). Guidelines for the emergency management of asthma in adults. Can. Med. Assoc. 155 (1): 25-37. Braunwald. Chronic Obstructive Pulmonary Disease.Harrison’s Internal Medicine.2674-2676. Currie, GP and Legge, JS. Diagnosis. British Medical Journal. 332;1261-1263 Della Pasqua, OE. (2006). Markers of exacerbation severity in chronic obstructive pulmonary. Disease. Resp. Res. 7:74. Devereux, G. (2006). Definition, epidemiology, and risk factors. British Medical Journal, 332;1142-1144. Fabbri LM, Luppi F, Beghe B: Update in chronic obstructive pulmonary disease 2005. Am J Respir Crit Care Med 2006 May 15; 173(10): 1056-65[Medline]. Flenley, D.C. (1983). New drugs in respiratory disorders I. British Medical Journal, 286: 871-5. Franciosi, LG; Page, CP; Celli, BR; Cazzola, M; Walker, MJ; Danhof, M; Rabe, KF; Freeman, D. and Price, D. (2006). Primary care and palliative care. British Medical Journal, 333;188-190 MacNee, W. (2006). Pathology, pathogenesis, and pathophysiology. British Medical Journal, 332;1202-1204 William, AJ. (1998). Assessing and interpreting arterial blood gases and acid­base balance. British Medical Journal, 317:1213­6. www.emedicine.com www.goldcopd.com Read More