Nursing Care Plan Development
Chronic illness - emphysema
9/23/2011
Unit: NURS 8822
Unit co-ordinator: Assistant Professor Olivia Hill
Student: Regan Preston
Student No: 20825201
Table of Contents
Emphysema – a Chronic Obstructive Pulmonary Disease ................................................................. 3 Epidemiology: ........................................................................................................................................ 3 Aetiology: ................................................................................................................................................ 4 Pathophysiology: ................................................................................................................................... 5 Clinical manifestations .......................................................................................................................... 7 Risk Factors ........................................................................................................................................... 8 Diagnosis of emphysema ..................................................................................................................... 9 Problem Identification ............................................................................................................................. 11 Care Planning .......................................................................................................................................... 14 Collaborative care ................................................................................................................................... 23 Conclusion ............................................................................................................................................... 24 References ............................................................................................................................................... 25 2 Emphysema – a Chronic Obstructive Pulmonary Disease
Chronic Obstructive Pulmonary Disease (COPD) is a multi-component respiratory disease that
is progressive, with no known cure.1-3 COPD is defined by the Global Initiative for Chronic
Obstructive Lung Disease (GOLD)4 as a preventable and treatable disease with significant extra
pulmonary effects that may contribute to the severity in the individual patient.4, 5 A mixture of
small airway disease and parenchymal destruction are characteristic of emphysema, and
conditions vary amongst individuals.4
6
COPD has a very variable history and diseased patients do not follow typical symptomatic
patterns, and trends. It is a progressive disease and limiting exposure to harmful agents will
reduce progression of the disease, however once COPD has developed, only treatment can be
given to reduce symptoms and exacerbations, and improve overall quality of patients life.4
Epidemiology:
COPD has a huge burden on our society and health care system, and according to the World
Health Organization (WHO) World Health Report 2000, respiratory diseases account for 17.4%
of all deaths and 13.3% of all Disability Adjusted Life Years (DALYs).2, 7, 8 COPD is projected by
2020 to become the fifth largest in burden of disease, and the third leading cause of death
worldwide.2 9, 10 The Burden of Obstructive Lung Disease (BOLD) study showed that the
worldwide prevalence of COPD was approxiatemelty10%.11 This figure varied by geographic
3 location and by sex. Prevalence among men was 11.8% and among women was 8.5%.11 The
differences in sex can be explained by the prevalence of smoking. Historically incorrect and
inaccurate definitions of COPD have made difficult to quantify the factors such as prevalence,
morbidity and mortality of COPD and emphysema.4 Under recognition and under diagnosis of
COPD are responsible for large variances in underreporting.4 In Australia, COPD is the fourth
major cause of deaths in males, and sixth major cause in females. It is reported that over 80%
of the COPD sufferers are experienced over the age of 45 years.8 In 2003, the Australian
Burden of Disease and Injury Study estimated almost 400,000 people with COPD in Australia,
with 20,000 new cases every year.8 In Australia, The Australian Institute of Health and Welfare
(AIHW) 2008 reported COPD as the leading cause of death 4%, around 4900 deaths per
annum.12 In 2000, COPD had accounted for 4% of all make deaths and 3% of female deaths in
Western Australia.12 History has shown that COPD was more prevalent among men. This was
attributed to the difference in smoking rates in men and women. However the increase in
smoking among women, the difference has declined.12 Furthermore COPD is also associated
with socio-economic status, and high rates of COPD exist in aboriginal populations.12 This was
due to extremely high rates of smoking within these communities.8 Aetiology:
COPD is most often caused by smoking. Most people with COPD are long-term smokers, and
evidence shows that smoking cigarettes increases the risk of getting COPD.4, 8 13 Overwhelming
evidence that lung destruction resulting in emphysema is largely due to enzymatic action on the
pulmonary connective tissues such as elastin. These enzymes are possibly derived from
neutrophil polymorphonulear leucocytes and alveolar macrophages.4 Some research has shown
release of these enzymes related to cigarette smoking. Emphysema can be seen as very
closely related to the fact that individuals smoke, and result of smoking habit. A mixture of small
airway disease and parenchymal destruction are characteristic of emphysema, and conditions
vary amongst individualls.4 Emphysema damages the structure of the alveoli causing the walls
to break down. This means the alveoli are no longer able to hold the bronchioles open, making it
hard for the lungs to expel air. Emphysema makes the lungs resemble an old used sponge with
large holes that lack elastic recoil.14, 15 4 Pathophysiology:
Emphysema is defined as an enlargement and inflammation of air pathways and coupled with
destruction of alveolar walls and septa of lung tissue.16, 17 There is parenchymal destruction
typical of emphysema and develop from long time smokers and exposure to noxious particles or
gas substances.2, 16, 18 This causes limitations and reduction in elastic recoil required in correct
lung function.16 This loss of lung natural elasticity results in lung becoming permanently
inflated.18 Condition is caused by destruction of the pulmonary connective tissue namely elastin
and collagen.14 Gas exchange abnormalities are characteristic and result in hypercarnia and
hypoxemia.4 The severity of emphysema relates to the ventilation –perfusion (V/Q) imbalance,
and disease worsens as this imbalance gets greater. This imbalance and loss of elastic recoil in
alveoli, depicted in figure 1, leads to carbon dioxide retention and hypercapnia state.
Figure 1: The major mechanism of airflow limitation is loss of elastic recoil.19
19
5 Figure 2: The pathophysiology of emphysema.20
6 Figure 3: The effects of emphysema on the gas exchange units. A Normal lung with many small
alveoli. B Lung tissue affected by emphysema. Notice that the alveoli have merged into larger
air spaces, reducing the surface area for gas exchange.21
21
Clinical manifestations
The clinical manifestations of emphysema are tabulated in table 1. Typically dyspnoea,
productive cough, history of smoking and barrel chest are common clinical manifestations of
emphysema.
Table 1: Clinical manifestations of emphysema: 15 VARIABLES
EMPHYSEMA
Age (years)
50-75
Infections
Occasional
Dyspnoea
Severe, early in course
Productive cough
Late in course with infection
Wheezing
Common
History of smoking
Common
Prolonged expiration
Always present
Cyanosis
Late in course
Chronic hypoventilation
Late in course
Chest x-ray findings
Hyperinflation
General appearance
“pink puffer”
Barrel chest
Classic
7 A classical clinical manifestation is the barrel chest of an emphysema sufferer. This is well
depicted in Figure 4.
22
22
Figure 4: Lateral CXR of a person with emphysema. Not the barrow chest and flap diaphragm Risk Factors
Cigarette smoking is the most common risk factor for COPD and emphysema.4, 23 Identification
of risk factors is an important step in determining strategies for prevention and treatment of
these chronic respiratory diseases. Risk factors do interact and interlink with each other and
with the current overpopulation being experienced around the world, factors like poverty, socioeconomic status, level of nutrition and level of education are all becoming major determinants in
COPD.4 Figure 3-1 lists common risk factors associated with emphysema and COPD6.
6
8 Diagnosis of emphysema
Key indicator in considering a diagnosis for emphysema would be the presence of dyspnoea,
chronic cough, sputum production, and health history of smoking or smoke related risk factors.6
Diagnosis of emphysema is achieved through physical assessment, spirometry tests, arterial
blood gas assessment, chest x-ray, electro cardio graphs (ECG) and microbial testing.2, 16
Although physical examination is an important clinical diagnostic tool, in COPD it is used
conjunctively with other diagnostic assessments such as spirometry, spirometry being the gold
standard in assessment and diagnosis of COPD.4 A physical assessment is made up of an
inspection, palpation, percussion, auscultation of respiratory region. Table 3 compares the
assessment process and diagnostic difference between and normal and a diseased lung.
Physical Assessment
Inspection
Normal Lung
Anteroposterior transverse
diameter, RR 10-18, regular,
no cyanosis or pallor14
Palpation
Symmetric chest expansion.
Tactile fremitus present and
equally bi laterally, diminishes
towards periphery. No
masses, lumps, tenderness.14
Resonant. Diaphragmatic
excursion 3-5 cm14
Vesicular over peripheral
fields. Broncho vesicular
parasternally (ant) and
between scapula (post)
None
Percussion
Auscultation
Adventitious Sounds
Emphysema
Increased anteroposterior
diameter. Barrel chest. Use
accessory muscles to breathe.
Tripod position. Shortness of
breath. Tachypnea.14
Decreased tactile fremitis and
chest expansion.
Hyper resonant. Decreased
diaphragmatic excursion.14
Decreased breath sounds.
Prolonged expiration. Muffled
heart sounds from over
distention of lungs.14
Usually None, occasionally,
wheeze.
Spirometry is a simple and painless test which measures the capacity of your lungs.24
9 24
Emphysema can be diagnosed by using the gold standard spirometric classification of stages of
COPD, and GOLD guidelines.2, 17, 25 The presence of a post bronchodilator FEV1/FVC<0.70 and
FEV1 <80% predicted confirms the presence of airflow limitation that is no fully reversible.4
Table 2: Spirometric classifications of COPD26
Arterial blood gas measurement is performed on patients with FEV<50%. Development of
respiratory failure is indicated by a PaO2<6.7kPa (60mmHg) with or without PaCO2>6.7 kPa
(50mmHg) in arterial blood gas measurements made while breathing air at sea level.4, 23 Low
10 pH, High PaCO2, normal or high normal bicarbonate, are indicators of lung disease like COPD. Chest X-ray can determine densities in lung fields that are produced by fluids, tumors and other
pathological conditions and also used in excluding alternative diagnoses and establishing the
presence of other co morbidities such as cardiac failure.23 Chest x-rays on CPOD patients show
signs of hyperinflation, flattened diaphragm, and increase in the volume of the retrosternal air
space. In addition chest CT scans also useful in showing the actual distribution of the
emphysema, for patients that may undergo lung volume reduction surgery. Genetic diagnostic
screen testing can also be undertaken, checking for Alpha-1 antitrypsin deficiency. A serum
concentration of below 15-20% of the normal value is a predictive sign of alpha-1 antitrypsin
deficiency and COPD.6 Presence of purulent sputum during exacerbation of symptoms is
sufficient indication for starting empirical antibiotic treatment, with common COPD pathogens
being namely Streptococcus pneumonia, Hemophilus influenzae and Moraxella catarrahalis.6
Problem Identification
COPD is a chronic and disabling respiratory disease, studies cited by Blinderman et al 20099
have shown that the most prevalent symptoms experienced by COPD sufferers were dyspnoea
(94%), fatigue (71%), coughing (56%) and anxiety (51%).9 Other symptoms with high
prevalence were drowsiness, nervousness and wheezing.9 Studies by Silbeck et al 1998 as
cited by Wilson27 showed breathlessness (95%), pain (68%), fatigue (68%), sleeping difficulty
(55%) and thirst were common clinical manifestations.27 Edmonds et al 2001 as cited by Wilson,
collect evidence to show that breathlessness was experienced more often, and became
extremely distress by this excacerbation.27 Evidence shows dyspnoea as the main standout
symptom of COPD patients who seek medical attention, and major cause of disability and
anxiety associated with the disease.4 Studies conducted by a British team Elkington 2004, as
cited by Wilson27, found that breathless was the main symptom experienced by COPD sufferers,
and anxiety and depression were common.27 Feelings of anxiety and depression are also
common in patients with chronic COPD and emphysema, mainly dyspnoea inducing factor of
fear and anxiety.28
The increase in breathlessness will result in the increase in the fear of exercise and this in itself
becoming a major reason for avoidance of physical activities.29 Breathlessness could trigger
11 panic attacks, which in turn exacerbate the symptom of dyspnoea. This avoidance is shown to
cause further disability through physical deconditioning and hence avoidance in social and
physical activities.18 Kunik et al 2005 as cited by Addy29, showed that a very high percentage of
COPD suffers would develop negative beliefs about self image as the disease progressed.29
The onset of increased anxiety and depression would develop and become major comorbid
symptom. Feelings of anxiety and depression are common place in COPD sufferers due to the
impact of the increase in dyspnoea, altered sleep patterns and the feelings of loss and grief
associated with disability of COPD.28, 29 The element of fear is aroused when breathlessness is
experienced in large majority of sufferers. The psychosocial problems experienced by
emphysema patients range from depression, loneliness, helplessness and hopelessness.30, 31
Intense loneliness can be brought about by lack of self worth feelings and overall lack in
personal confidence. Loneliness has been associated with depression.30
Psychological states such as depression and anxiety in COPD have important repercussions.32
Physical deterioration, becoming further housebound and reflection on what was once a
previously active body, produce negative depressive emotions.1 Patients become withdrawn,
lonely, isolated, anxious and in worse cases, lose the ability to show or display any emotion
such as anger, or even sadness.18, 32 Without a clinical intervention from mental health
specialists, symptoms like fatigue, weight loss and ability to cope and tolerate symptoms of
emphysema will not alleviated.1 Attitudes such us wanting to “give up” have also been observed
in chronic suffers, due to the fact that not much more could be done with respect to a cure for
disease.1, 29 Sleep pattern alterations and difficulties due to COPD symptoms further enhanced
feelings of anxiety and depression.18 Sleep anxiety is also prevalent in oxygen therapy patients
with fear of one dying in ones sleep.25 Angel et al 2007 as cited by Rabe2 study showed that a
serious element of depression in COPD patients was there lack of desire and willingness to
participate in rehabilitation programs for the disease. These programs have been proven to
increase patients self esteem, decrease fear of dyspnoea and physical activity and overall
depression.2
Therefore, from the above evidence reviewed, the following patient problem statements have
been prioritized:
12 Patient problem statements:
1. Ineffective airway clearance related to bronchoconstriction, increased mucous
production, ineffective cough and sputum expectoration, manifested by acute episodes
of dyspnoea and breathlessness.
2. Impaired gas exchange related to the imbalance and loss of elastic recoil in alveoli,
secondary to parenchymal lung tissue destruction, manifested by pursed lip breathing
and inability to speak.
3. Fatigue and activity intolerance related to imbalance between oxygen supply and
demand, manifested by verbalizations of lack of energy, lethargy and increased need for
rest.
4. Anxiety related to the fear of episodes of breathlessness, threat of death, and
hopelessness to a chronic illness, manifested by lack of self care and depressive mood
states.
13