Assessment and Techniques in Assessment for Patient with Long-Term Medical Condition - Report Example

Assessment and techniques in assessment for patient with long term medical condition. Assessmentand techniques in assessment for patient with long term medical condition. Chronic Obstructive pulmonary disease is an entity that comprises a number of pathological phenomenon involving the respiratory system and also exhibiting the systemic component. COPD is an obstructive disease of the airways and can present either in the form of chronic inflammation of the bronchi and the bronchioles or as emphysema (destruction of the lung). Most patients present with the combination of the two. The disease also has a systemic component affecting metabolism, salt and water excretion and the musculoskeletal system. The net result of these dysfunctions gives rise to the typical clinical picture of a wasted person, with peripheral edema and an increased respiratory effort evident by the hyper-inflated chest and pursed lip breathing along with the use of accessory muscles. COPD is one of the most common respiratory diseases and as it is a chronic progressive condition developing over the span of years, it often passes unrecognized and the patients present at the stage when complications of chronic disease have already developed. COPD is a source of considerable morbidity and mortality around the globe. The prevalence of COPD in UK is 1%, with about 60, 000 people having been diagnosed as cases of COPD. The ratio is thought to be even more as the statistics only take into account definite diagnosis from the people presenting at later stages. Approximately 30, 000 people die due to COPD each year in UK, making it the sixth leading cause of death in that region. COPD is growing concern worldwide. It is estimated that by 2020, COPD will the third leading cause of death worldwide (Bellamy 2011, Boon and Davidson 2006). The major risk factor towards the development and progression of COPD is cigarette smoking. There is a strong correlation between COPD and the number of pack years (where 1 pack year refers to 20 cigarettes smoked per day per year). COPD often develops after 10 pack years of cigarette smoking. In sharp contrast, not all people who smoke develop COPD. COPD develops in only about 20% of smokers (Bellamy & Booker 2011). This leads to the concept that other environmental or genetic factors play important role as well. Alpha 1 antitrypsin deficiency is evident in patients with emphysema. Other factors that put a person at an increased risk for acquiring COPD are biomass fuel fires, exposure in coal mine workers, pollution, infections and low socio economic status. Apart from these, perinatal events (low birth weight babies) and childhood infections also play a role in the development of COPD later in life (Hanania et al 2011) The pathology in COPD is multisystem. In the pulmonary system, chronic inflammation involving the large and the small airways is attributed to inflammatory cell infiltration and an increase in size and number of mucus secreting goblet cells. This leads to production of large amounts of sputum leading to chronic bronchitis. It is defined by the ‘presence of productive cough on most days for 3 months, for 2 consecutive years’, in the absence of any alternative explanation (Philip jevan). Emphysema is due to the deficiency of alpha 1 antitrypsin, which results in unhindered action of proteases causing destruction of the alveolar walls. The alveoli collapse during expiration due to the lack of support and this leads to gas trapping, giving rise to air spaces. Emphysema can be panacinar, centriacinar or periacinar, depending on the location of enlarged air spaces in relation with the airway tree (Hall & Guyton 2011, Ganong 2005). Also in COPD, the lungs and airways lose elasticity. Fibrosis combined with premature airway closure results in airway constraint. This leads to chest hyperinflation and reduced chest wall compliance. The increase in dead space volume gives rise to ventilation/ perfusion mismatch and the work of breathing is increased. This is further worsened by pulmonary vascular remodeling and impaired cardiac performance (Boon and Davidson 2006, Kumar et al 2005). Initially, these changes are reversible, like airway infiltration, smooth muscle contraction, and hyperinflation during exercise only. Later, as the disease progresses, changes like fibrosis, loss of elasticity and emphysema developed mark the irreversible damage to the respiratory system (Hanania et al 2011). The advanced stage of COPD is thus characterized by gas exchange abnormalities, i.e. hypoxia (decreased pressure of oxygen) and then progress to hypercapnia (increased in the pressure of CO2) due to the combination of above mentioned factors eventually leading to the respiratory failure (Champe et al 2005). Persistent cough with sputum, along with breathlessness especially in older people should prompt the diagnosis of COPD. Most often the first clinical manifestation is cough. This is accompanied by production of mucus and may be complicated by hemoptysis. The condition may be aggravated by bacterial super-infection. The symptom that makes the patient seek medical care however, is breathlessness. There is little day to day variability (in contrast to Asthma) (Barnes 2009).This reflects an advanced stage of disease and is assessed through a modified MRC dyspnea scale. Given below is the gradation of breathlessness on the scale of 0 to 4 (Boon and Davidson 2006): 1. No breathlessness except with strenuous exercise. 2. Breathlessness when hurrying on level or walking up a slight hill. 3. Walks slower than a contemporary on level ground because of breathlessness or has to stop for breath when walking at own pace. 4. Stops for breath after walking about 100meters or after a few minutes on level ground. 5. Too breathless to leave the house, or breathless when dressing or undressing. Apart from the respiratory symptoms, a search should be prompted for other systemic components of COPD. These include, muscle weakness due to deconditioning changes in skeletal muscles, peripheral oedema because of disturbed salt and water excretion, weight loss and cachexia due to impaired nutrition and altered fat metabolism, increased rates of osteoporosis and increases in the levels of circulating inflammatory markers (fibrinogen, C reactive protein. The advanced disease is often accompanied by various degrees of chronic heart failure, central and peripheral vascular resistance, metabolic syndrome and type-2 diabetes (Nici & Zuwallack 2012, Hanania et al 2005). COPD patients can either be ‘pink puffers’ (wasted, breathless with normal pressure of CO2 initially) or ‘blue bloaters’ (Rise in the pressure of CO2 right from the initial stages of the disease, patients develop oedema and polycythemia) (Boon and Davidson). As in all respiratory tract problems, a chest x-ray is the initial investigation. It does not diagnose COPD itself but aids in ruling out the differential diagnosis and looking for complications (carcinoma, bullae). The patient is checked for anemia or polycythemia by ordering a blood count. Sputum culture is done for the detection of any bacterial infection. Also, assays for alpha 1 antiproteinase should be carried, especially in young patients with basal disease (Ballinger 2012). Since COPD is an obstructive lung disease, lung function tests are carried out to check for the degree of obstruction and severity of the condition. This is done by spirometry and takes into account various factors to check lung function, which include Forced Expiratory Volume in one second (FEV1), Forced vital capacity (FVC), and the ratio between the two. The obtained values from the patient re compared with the standard predicted values to grade the severity. The forced expiratory volume is assessed after a dose of bronchodilator. A normal response should be increase in the volume. In COPD, the obstructed and narrow airways do not allow sufficient dilatation of the airways and the response to bronchodilators is below the predicted levels. Thus, a person is considered to have COPD when FEV1 after the dose of bronchodilators remains below 80% of predicted along with the FEV1/ FVC ratio below 70% (Lynes 2007, Boon and Davidson 2006). Severity of airflow obstruction is graded in comparison with predicted values as follows: Severity FEV1 Mild >80% predicted Moderate 50-80% predicted Severe 30-49% predicted Very Severe Read More