Chronic obstructive pulmonary disease is a chronic progressive lung disease caused predominantly by smoking National Institute for Health and Clinical Excellence NICE, 2010. It is characterised by airflow obstruction which is not fully reversible. The airflow obstruction does not change markedly over several months and is usually progressive in the long term (NICE, 2010). COPD is the fourth most common cause of death globally, and incidence of the disease is predicted to rise in the next 20 years (Global Initiative for Chronic Obstructive Lung Disease, (GOLD), 2011). In the United Kingdom (UK), chronic respiratory disease, including COPD, is the third most common cause of death, with 30,000 deaths reported annually (NICE, 2010). There are almost one million people diagnosed with COPD in the UK and it is estimated that a further two million people, referred to as the 'missing millions', remain undiagnosed (Department of Health (DH), 2011). Many patients have mild COPD; women have a 72% chance and men a 78% chance of survival at five years (British Lung Foundation, 2010). However, in patients with severe COPD requiring oxygen therapy and treatment with nebulisers, five-year survival rates are lower at 24% for women and 30% for men (National End of Life Intelligence Network, 2011). COPD is one of the most common causes of hospital admissions, and rates of COPD have increased by 50% in the past ten years (Price et al., 2006, George et al., 2011). Patients with COPD who are treated in acute hospitals have increased mortality rates, particularly in the first three months following admission, and re-admission rates are high (Gruffydd-Jones et al., 2007). Patients with severe COPD and those who are experiencing an exacerbation of the disease can be managed in the community by the primary care team, a specialist respiratory nurse or by a hospital-at-home team to avoid hospital admission. However, patients experiencing an exacerbation of COPD will be hospitalised if their condition continues to deteriorate and many have recurrent admissions to hospital (British Lung Foundation, 2010). Once admitted to hospital, patients are treated with various therapies, ranging from nebuliser therapy with bronchodilators and corticosteroids to mechanical ventilation (NICE, 2010). All active supportive treatment is aimed at palliating symptoms to maintain health, but as the patient's exacerbations of the disease worsen and become more frequent, there is a need to consider incorporating end of life care into the person's care plan. In this context, predicting whether a patient has reached the stage of his or her disease where further treatment will not improve quality of life is particularly difficult (Spathis and Booth, 2008). Although many patients have mild COPD, approximately 25,000 people die at the end stages of the disease each year (British Thoracic Society, 2006). It is the aim of this case study to analyse the holistic care of a patient with severe COPD. This will include: diagnosis, assessment and care planning of the patient, treatment of the disease, prevention of psychosocial complications, the use and benefits of multidisciplinary care teams and an exploration of the legal and moral issues pertaining to the care of a patient with severe COPD. However, it is posited that initially it is important to understand the anatomy and pathophysiology related to the disease as this influences the care given.
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The term COPD encompasses three conditions: emphysema, chronic bronchitis and small airway disease, chronic, severe asthma. Many patients have elements of all three conditions (British Thoracic Society, 2006). The 'obstruction' in COPD involves the diameters of peripheral airways becoming progressively smaller so that it becomes difficult and eventually impossible to breathe. At first this may mean that it is possible to sit comfortably, but it may be necessary to stop to catch one's breath when walking a distance or climbing stairs. As COPD progresses, patients can begin to feel uncomfortable at rest. Indeed, the diameter of the airways may slow airflow to the extent that it may take so long to breathe out that, even during light exercise, there may not be enough time for the lungs to empty before it is time to breathe in again. This leads to exercise-induced air trapping, or dynamic pulmonary hyperinflation. Air can also become trapped in the lungs because of a loss of elasticity in and collapse of smaller airways. When the patient has 'trapped air', the muscles of inspiration, such as the diaphragm and intercostal muscles, become inefficient and tire easily. The effects of COPD affect the whole body, including the heart, kidneys and muscles. The condition also involves cognitive and emotional aspects such as panic and anxiety, which may contribute directly to the sensation of dyspnoea (Kelly, 2007).
COPD is predominantly caused by smoking, although factors such as occupational exposures
may also contribute to its development. Factors that put patients at increased risk include a history of childhood respiratory symptoms, middle and old age, genetic factors and socioeconomic status (NICE, 2010). Smoking irritates the bronchiolar wall, which can result in the development of chronic bronchitis. Smoke can also damage the respiratory bronchioles and the alveoli by attracting neutrophils that release enzymes called proteases and elastase. In susceptible individuals this results in the destruction of the alveoli, as occurs in emphysema.
In emphysema the alveolar walls become damaged and may coalesce. This means that some
of the smaller alveolar sacs merge to become larger, inelastic sacs. This reduces the surface area of alveolar membrane and results in impaired gaseous exchange. Emphysema may damage the airways in another way. The smaller airways have microscopically thin walls and their patency is maintained by attachments that act like 'guy ropes' applying radial traction. Emphysema causes a reduction in this radial traction, leading to the collapse of the small airways, especially during expiration. This results in air trapping. If alveoli continue to merge they may form sacs larger than 1cm in diameter. These larger sacs are called bullae. Some smokers will not develop emphysema, which is probably because they have an efficient protective mechanism against the enzymes that are released by neutrophils (Zieliñski et al, 2001). One example of this is provided by alpha1-antitrypsin. This is an 'antiprotease' that protects the lungs from proteases released by the neutrophils. Deficiency in alpha1-antitrypsin can result in the early development of COPD, and may even lead to the development of COPD in a non-smoker. Alpha1- antitrypsin deficiency is a rare genetic condition that is probably responsible for about 1% of cases of COPD (Dirksen et al, 1999).
Unlike asthma, once COPD is established the changes are irreversible and it continues to progress so long as the patient continues to smoke. Those smokers who develop COPD will experience a faster decline in their forced expiratory volume in one second (FEV1) (Fletcher and Peto, 1977). A substantial degree of lung damage may take place before clinical symptoms become apparent. Indeed, many patients with COPD may have a 50% reduction
in FEV1 before they present to a doctor (Zieliñski et al, 2001). With increased disease severity, the alveoli become hypoventilated and the patient becomes hypoxic. The lungs gradually lose their ability to oxygenate blood, and the patient develops respiratory failure. If the patient is significantly hypoxic he or she will need long-term oxygen therapy, which can prolong life (Nocturnal Oxygen Therapy Trial Group, 1980; Medical Research Council, 1981). As the patient's lung function deteriorates he or she may experience exacerbations of the condition with increasing frequency, presenting with a sudden and severe worsening of symptoms such as breathlessness, sputum production and cough. Exacerbations are frightening, distressing and disruptive for patients (Brownrigg, 2007).
One condition that occurs secondary to primary pulmonary disease is cor pulmonale. Cor pulmonale occurs when the alveoli are not ventilated; they become hypoxic and the blood
capillaries constrict. Subsequently the right side of the heart must work harder to maintain
circulation, which can cause right-sided heart failure and pulmonary artery hypertension. There is currently no cure for COPD. Treatment is aimed at managing symptoms, improving quality of life and reducing exacerbations. However, early detection, smoking cessation and correct management of complications such as exacerbation and cor pulmonale can significantly prolong the patient's life and improve its quality (Brownrigg, 2007).
With regard to the case study, it will specifically focus on the holistic assessment and care of one patient who suffered from a severe infective exacerbation of COPD.
As mentioned, COPD has considerable morbidity and mortality, which affects patients, their families and carers, and healthcare provision (Gruffydd-Jones et al., 2007; Spathis and Booth, 2008). Therefore, it is important to consider the place of palliative and end of life care in the management of people with end-stage COPD. Palliative care has traditionally focused on patients with a cancer diagnosis, through National Health Service (NHS) and hospice provision. It is an approach to care that purports to improve the quality of life for patients and their families when they are faced with incurable disease and professes to do this by preventing and treating suffering (National Council for Palliative Care (NCPC), 2003). However, there is growing emphasis on end of life decisions to be addressed for all patients who may require them, not just those with cancer (DH, 2008). Although COPD the symptoms of COPD are treatable, the disease is incurable and the condition is chronic and progressive (NICE, 2010). It is reasonable to assume therefore, that patients with COPD
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would benefit from many palliative care principles and practices. In fact, the NICE (2010) clinical guidelines on COPD state that 'people with advanced COPD, and their carers, are identified and offered palliative care that addresses physical, social and emotional needs'(NICE, 2010, p.7).
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