CHRONIC

Document Sample
CHRONIC Powered By Docstoc
					CHRONIC
OBSTRUCTIVE
PULMONARY
DISEASE
                          Contents

                                                   Page

Diagram of the lungs                                2

Chronic Obstructive Pulmonary Disease               3

Changes in the lungs patients with COPD             5

Consequences of the pathological changes in COPD    6

The clinical picture of COPD                        7

COPD is a chronic progressive condition             8

Investigations to confirm COPD                      9

Complications of COPD                               11

Treatment of exacerbations of COPD                  13

Common drugs used in the treatment of COPD          14

Oxygen                                              15

Physiotherapy                                       16

Nutrition and COPD                                  17

Conclusion                                          18

Suggested Reading                                   20


                           2
3
Chronic Obstructive Pulmonary Disease (COPD) is a major cause
of morbidity and mortality, globally. In 2002, COPD is the fifth
most common cause of death. It is estimated by 2020 it will be
the third most common cause of death, and responsible for
around 2.9 million, adult deaths per year, worldwide

In 1998, 26,630 deaths were recorded as attributed to COPD
England and Wales, but this is probably an underestimate.
COPD prevalence in the United Kingdom is estimated to be 2.96
million and is among the highest in Europe

The annual cost of COPD to the NHS is around £500 million
(1995/96 figure). Almost half of this expenditure is in
secondary care, where emergency admissions account for 78%
of costs (174 million). In 1998/1999, COPD accounted for
around 952,495 inpatient bed days, compared with 201,240 for
asthma

The condition predominantly affects people in middle age and
later life, and is often induced through cigarette smoking.
Central Manchester is no exception, and has a higher than
average proportion of smokers and ex smokers.
Chronic obstructive pulmonary disease (COPD) is a lung disease
characterized by obstruction to airflow that does not change
markedly over several months (NICE 2004). Chronic meaning
‘long term’, obstructive meaning ‘blocked’, for the patient who
has COPD this means their airways are narrowed, making it
difficult for air to flow in and out of the lungs. Pulmonary
means ‘affecting the lungs and airways’.


                               4
Most of the lung obstruction is permanent, although in some
patients there may be some reversibility. COPD is a common

clinical condition – it is seen most commonly in cigarette
smokers (only 15% of smokers will develop COPD) but also in
some non-smokers where occupational factors, atmospheric
pollutants or an inherited tendency may be responsible for the
disease.

COPD is not a single disease entity, but a variable mixture of
chronic bronchitis, small airways disease and emphysema.




                              5
Changes in the lungs of patients with COPD

The large airways
In the large airways there is increased mucous gland size and
number and thus increased mucus production – this is called
chronic bronchitis. The increased mucus production seen in
chronic bronchitis does not lead to reduced airflow but does
cause a chronic cough and sputum production.

The medium airways
The airway smooth muscle is thickened and excessively
contracted compared with that in normal individuals. In many
respects, these patients have similar changes to those in
patients’ with asthma.

The small airways
The small airways of patients with COPD are swollen
(oedematous) and are infiltrated with inflammatory cells such
as lymphocytes, neutrophils and macrophages.

The alveoli
Destruction of the alveoli is called emphysema, which is an
irreversible disease of the lungs that is characterised by the
physical destruction of the alveolar walls within the lungs. The
damaged alveoli merge into larger sacs called bullae, which are
relatively inefficient for gas exchange, resulting in
breathlessness. Progression of the disease results in collapse
of small airways making air entry more difficult. However
these patients will have a well preserved respiratory drive even
in the presence of severe airway’s obstruction.




                               6
Consequences of the pathological changes in COPD

Compared with normal individuals the airways of patients with
COPD are narrowed. This starts in the small airways – the
bronchioles – and as the condition progresses the narrowing
becomes more widespread.         Airway narrowing leads to
increased airway resistance and hyperinflation resulting in
reduced airflow the hallmark of COPD.

Loss of alveolar leads to impaired gas exchange and loss of
radial traction, which means the airways are not supported and
tend to close resulting in impaired gas exchange as areas being
perfused are not being ventilated.




                               7
THE CLINICAL PICTURE OF COPD

Symptoms
The typical symptoms of patients with COPD are those of
cough with sputum production, wheeze and breathlessness
(dyspnoea).

Cough and sputum production
In most patients with COPD, a productive cough often precedes
the onset of breathlessness and is reversible in most smokers
once they stop smoking. The cough is caused by irritation of
the airway nerves due to the release of compounds from
inflammatory cells or by the presence of increased sputum
production due to increased mucus secretion.

Wheeze
Wheeze is a symptom described by as many as 80% of patients
with COPD. It is caused by the sound generated by turbulent
airflow through the airways due to the increased presence of
sputum.

Dyspnoea
Breathlessness occurs in patients with COPD due to the
increased work of breathing. Increased work of breathing is
due to narrowing of the airways. This can affect distribution
of air within the lungs altering ventilation-to-perfusion
matching, which reduces gas exchange.




                              8
COPD IS A CHRONIC PROGRESSIVE CONDITION

By far the most important information is to ascertain the
patient’s history of respiratory symptoms, focusing on
breathlessness which worsens on exertion, sputum production
and smoking history. An accurate history will suggest the
diagnosis and tests will help to confirm it.

A substantial degree of lung damage can take place before
clinical symptoms become obvious. Indeed, most patients with
COPD will have experienced a 50% decrease in FEV1 before
they present to the doctor. Exertional activities will make
these patients breathless and possibly wheezy, while cough
with or without sputum production will be a normal part of
everyday life. Regular winter visits to the doctor will be
needed for ‘chest infections’.      Some patients may have
abnormal blood gases at this stage. These patients are a
target group for proactive intervention.




                             9
Investigations to confirm COPD are:

Spirometry: An abnormal forced expiratory volume in one
second (FEV1) of less than 80% of a predicted value, which
depends on weight, age and height and FEV1 /FVC ratio of <70%.

Chest X-ray: May reveal over inflation of the lungs in
moderate to severe COPD.

Arterial blood gas analysis: Commonly reveals hypoxaemia (low
oxygen levels) and hypercapnia (high carbon dioxide levels).

 At first, as lung function declines, the level of oxygen in the
circulation falls and the respiratory centre in the brain
triggers an increase in respiratory effort. This ensures that
both arterial oxygen (PaO2) and carbon dioxide (PaCO2) remain
at normal levels. As lung damage worsens, this mechanism
proves inadequate to maintain full oxygenation, in which case
the arterial blood gases become abnormal.

In some patients the PaO2 falls but CO2 is still removed – this
is termed Type I respiratory failure. In other patients the
response to low PaO2 is impaired and they have a dysfunctional
respiratory drive. In this case the patient becomes markedly
cyanosed and PaCO2 rises – this is Type II respiratory failure.

   Type I respiratory failure
    The typical patient is breathless, has a hyperinflated
    chest and pink colouring and is underweight for this reason
    they are commonly referred to as ‘pink puffers’.




                               10
   Type II respiratory failure
    The typical patient is said to be less breathless than the
    ‘pink puffer’ and the chest is not hyperinflated, but the
    patient has peripheral oedema, is cyanosed and overweight.
    The patient appears not to be short of breath and is thus
    not seen to use the accessory muscles to breathe. Type
    II respiratory failure is often associated with heart
    failure. The individual with his pattern of blood gas
    abnormalities is often described as a ‘blue bloater’.



An understanding of these processes is of critical
importance in the management of advanced COPD, especially
when oxygen therapy is considered.

     In MILD disease there are few symptoms, with a
      history of a morning cough, recurrent respiratory
      infections, shortness of breath on vigorous exercise and
      FEV1 is 50 –80% (as per NICE guidelines) of predicted
      normal.

     In MODERATE disease, a wide range of symptoms
      present themselves such as cough, production of
      sputum, acute worsening of symptoms of infection,
      wheeze, over –inflation of the lungs and FEV1 is 30 –
      50% (as per Nice guidelines) of predicted normal.

     In SEVERE disease there is breathlessness on minimal
      exertion, cough, wheeze, loss of weight, central
      cyanosis, peripheral oedema, pulmonary hypertension,
      over-inflation of the lungs and FEV1 is less than 30% (as
      per NICE guidelines) predicted normal.

                              11
COMPLICATIONS OF COPD

Cor pulmonale
Right-sided heart failure caused by enlargement of the right
ventricle secondary to primary pulmonary disease. The right
side of the heart must work harder to maintain circulation due
to increased pulmonary resistance caused by narrowing of the
pulmonary capillaries. Over time this leads to hypertrophy and
then failure of the right ventricle causing peripheral oedema,
because right heart failure pushes fluid out of the capillaries
into the tissues.
In the early stages, cor-pulmonale usually presents as ankle
oedema.
As the condition worsens, swelling spreads up the legs and
lower trunk. The presence of peripheral oedema in COPD is
indicative of a poor prognosis.

Pneumothorax
This is the presence of air in the pleural cavity. In COPD this
may occur spontaneously, as a specific result of emphysema. In
advanced emphysema the damaged alveoli, form large air spaces
(bullae) within the lung. If a bullae ruptures into the pleural
space, the result is total deflation of the affected lung. Tends
to present as a sudden onset of pleuritic chest pain,
accompanied by a marked worsening of breathlessness. Chest
X-ray usually confirms the diagnosis.

Polycythaemia
When there are chronically low levels of oxygen in the
circulation, an increase in the number of red blood cells may

                               12
result. This increases the oxygen-carrying capacity of the
blood, but also increases its viscosity and may make the patient
more liable to pulmonary embolism. In this case several units
of blood are usually removed in order to reduce the risk. If
polycythaemia is not corrected, pulmonary emboli may result.




                               13
TREATMENT OF EXACERBATIONS OF COPD

Although COPD is a progressive condition, the deterioration in
respiratory function is generally gradual. From time to time,
however, patients will present with sudden worsening of their
symptoms (exacerbation) this is particularly common in the
wintertime. Typical complaints include:

       Increased breathlessness
       Increased sputum production
       Change in sputum colour and purulence
       Increased wheeze or chest tightness
       Fluid retention (peripheral oedema)

COPD exacerbations have been associated with a number of
aetiological factors, including infection. Exacerbations are
frequently triggered by upper respiratory tract infections and
these are more common in the winter months when there are
more respiratory viral infections in the community.
Exacerbations may also be triggered by secondary factors such
as worsening of pre-existing heart failure.         Alternative
diagnoses such as pneumothorax or pulmonary embolus must
also be considered.
The single most important way of influencing the outcome of
patients at any stage of disease is smoking cessation. Patients
should be offered help by referral to a smoking cessation
specialist nurse.
As disease worsens the patient will experience frequent
infective exacerbations, with increased breathlessness,

                               14
increased sputum production, decreased exercise tolerance.
Some exacerbations may require hospitalisation.

Common drugs used in the treatment of COPD
Bronchodilator drug therapy with beta2 antagonist such as
salbutamol or terbutaline can be used via inhaler device or
nebuliser . Anti-cholinergic, broncho-dilator drugs such as
ipratopium bromide may also be used, or a combination of both.

Xanthines such as aminophylline, a bronchodilator, may be used
orally or may be given intravenously in an exacerbation.

Steroidal drug therapy such as prednisolone may be either
prescribed or if already being taken, the dose maybe increased.

Antibiotics may be prescribed. Generally, standard, first-line,
broad-spectrum agents will be sufficient such as Amoxycillin
and Erythromycin orally. It is suggested that a sputum sample
is sent for culture and sensitivity testing.

Diuretics may be of value where there is associated heart
failure that causes peripheral oedema.

Inhaled steroids - Current management guidelines advise
inhaled steroids only for those who have a positive steroid
trial, or those whose FEV1 is less than 50% of predicted and
who have frequent exacerbations of their condition.

Oxygen
The use of long-term oxygen therapy is the only other
intervention other than smoking cessation said to significantly
alter disease progression in COPD.

                              15
Patients undergoing an exacerbation, already established on
long-term oxygen therapy (LTOT) from an oxygen concentrator
will usually need hospital admission. The dose should not be
adjusted until blood gases are assessed in hospital. Patients
not on LTOT may have their breathlessness helped by up to
28% oxygen. Higher concentrations should not be given unless
arterial blood gases have been assessed.

Patients in Type II respiratory failure are in a state of
precarious balance. They have very low levels of oxygen in the
circulation and very high levels of carbon dioxide.

If the patient is given supplementary oxygen, the respiratory
centre may interpret this as improvement in the overall
condition and actually reduce respiratory drive, which is
dependant on the low oxygen levels. This may worsen acute
respiratory failure, carbon dioxide will accumulate still further
and the patient may die. The use of oxygen in these patients
must therefore be judged very carefully, using measurements
of arterial oxygen and carbon dioxide to determine the exact
concentration that can be tolerated.

PHYSIOTHERAPY
Physiotherapy looks at all aspects of a patient’s lifestyle and
management. It aims to educate patients to understand their
problems and have some control in managing their condition.

Breathlessness
Patients are taught how to control their breathlessness using
breathing control, position, relaxation, anxiety management,
energy conservation and pacing.



                               16
Chest clearance
The importance of chest clearance is taught, as well as
breathing exercises and drainage positions. Other adjuncts
such as the flutter and saline nebulisers can also be used.

Exercise tolerance and functional capacity
Patients are helped to return to their pre-exacerbation level
and educated on the importance of exercise.            Energy
conservation techniques are taught helping to maintain quality
of life and independence.

Oxygen therapy
Oxygen saturations are closely monitored and patients are
advised on how to use their oxygen effectively as requirements
vary with physiotherapy and exercise.

Posture and range of movement
The areas of cervical and thoracic spine and the shoulders are
particularly vulnerable to stiffness due to breathlessness. The
overuse of accessory muscles affects posture. These areas are
assessed and exercises given where necessary to minimize loss
of lung capacity.




                              17
NUTRITION AND COPD

Malnutrition in COPD is clinically important. It has been shown
to be a predictor of mortality in COPD with individuals who had
lost weight having higher morbidity and mortality rate than
those whose weight was within predicted values for age, height
and gender. Malnutrition affects the composition and function
of respiratory muscle and impairs skeletal muscle function.
Malnutrition also increases the impairment and disability of
COPD by affecting exercise performance in these patients.

Nutritional supplements may be used, however there is some
evidence to suggest patients offset calorie supplementation by
reducing normal food intake due to insufficient hunger rather
than insufficient food availability.    Combining an anabolic
stimulus such as exercise or anabolic hormones with nutritional
supplementation may prove useful.

Due to the chronic symptoms of this disease, individuals in the
advanced stages of the disease often suffer from depression
as they slowly loose their independence. Research has shown a
pulmonary rehabilitation program is of benefit to patients with
COPD, helping them to maintain some independence.




                              18
                        CONCLUSION

 COPD is a common condition having a major impact on
  patients, corers and healthcare resources.

 Specialist   assessment     and    advice    are   important.
  Implementation of the British Thoracic Society guidelines
  should ensure that all patients receive optimal therapy.
  Audits should be carried out to ensure this is happening.

 COPD will remain a significant problem so long as tobacco
  smoking is widespread.

 Because mild COPD is largely symptomatic, significant and
  irreversible damage is often already present at the time of
  diagnosis.

 Smoking cessation is the only treatment that has been shown
  to alter disease progression. For the continuing smoker the
  prognosis is one of progressive decline into respiratory
  failure.

 The key aim of therapy is palliative, to ensure maximum
  functional capacity within the limitations of the disease.

 Bronchodilators are the cornerstone of the pharmaceutical
  management of COPD, although steroids may have a part to
  play in a minority of patients.




                              19
 Exercise, education and support are equally important in
  overall management. They confer significant benefits when
  they are part of an integrated pulmonary rehabilitation
  programme.

 Long-term oxygen therapy relieves symptoms and reduces
  mortality when used in patients with severe respiratory
  impairment.

 Recent developments in the care of patients with
  uncomplicated exacerbations of COPD, have demonstrated
  that specialist nurses can offer safe, appropriate, clinical and
  cost-effective care at home.




                                20
                           AIRS

         Acute Intervention Respiratory Service

                 The team comprised of:-
             3 Respiratory Nurses Specialists
         1 Part time Respiratory Physiotherapist

                 The service is covered: -

                     Monday - Friday
                     7.30a.m. – 7pm

           Saturday, Sunday and Bank Holidays
                      9 am - 1 pm

                     365 days a year

Outside these times the patients can telephone the Medical
  Assessment Unit for advice or readmission to hospital

The team is based at Manchester Royal Infirmary and visit
  patients with Chronic Obstructive Pulmonary Disease
             (COPD) in the there own homes

 Patients are assessed for AIRS after arrival at Accident
   and Emergency, Medical Assessment Unit and Medical
                          wards.




                            21
What do the AIRS Team do?

The team manages patients with COPD in their own
homes instead of being in hospital.

Aims:
To reduce hospital acquired infections
Reduce length of hospital stay
To educate patients on COPD in their own environment
Improved quality of service, patients are seen are a 1:1
nurse patient ratio
Smoking cessation advice (where necessary) by AIRS
Team nurses (qualified smoking cessation advisors)

After discharge, by the AIRS Team patients are seen in
6-8 weeks nurse led follow up clinic.




                            22
Typical AIRS visit:

Full set of observations including:
respiratory rate, temperature, blood pressure, oxygen
saturation, pulse, assessment of sputum production,
BORG score

Review of present condition including arrangements for
readmission if required

Medication Review, including inhaler technique
assessment.

Education:

Smoking cessation
Diet
When to call your GP
Energy Conservation
Exercise tolerance
Exercises
Inhaler Technique




                           23
                           Suggested Reading


British Thoracic Society (1997)
Guidelines for the management of chronic obstructive pulmonary
disease.
Thorax 52; S1-S28

Callaghan, S. (1998)
The rite stuff.
Nursing Times Vol 94. No 49. Pg 42-43

Callaghan, S. (1999)
ACTRITE: Acute Chest Triage Rapid Intervention Team.
Accident & Emergency Nursing. 7. Pg 42-46

Coakley, AL. (2001)
Helping patients to master correct inhaler techniques: nursing role
British Journal of Nursing, 2001, Vol 10, No 7. Pg 424-432

Coakley, AL. (2001)
Pulmonary disease and smoking: a case for health promotion
British Journal of Nursing, 2001, Vol 10, No 1. Pg 20-24

Conway, A. (1998)
Breathing life into an idea.
Nursing Times Vol 94. No 39 .Pg 72-74

Dunn, L.& Chisolme, H. (1998)
Oxygen Therapy
Nursing Times. Vol 13. No 7. Pg 57-64

Esmond G (1998)
Nebuliser Therapy
Professional Nurse Vol 14. No1. Pg 39-43

                                     24
Flanigan, U. Irwin, A. & Dagg, K.
An Acute Respiratory Assessment Service
Professional Nurse. Vol 14. No 12 Pg 839-842

Gravil, J.H. Al-Rowans, O.A. Cotton, M.M. Flanigan, U. Irwin, A
& Stevenson R.D. (1998)
Home treatment of exacerbations of Chronic Obstructive
Pulmonary Disease by an acute respiratory assessment service.
The Lancet Vol 351. June issue. Pg 1853-1855.

Lynes D. 2003
An introduction to blood gas analysis
Nursing Times Supplement Resp[iratory Care
Vol 99. No 11
National Institute for Clinical Excellence (2004)
National Clinical Guidelines on Management of Chronic Obstructive
Pulmonary disease in Adults in Primary & Secondary Care.(12)

McAllister, J. (2002)
Chronic Obstructive Pulmonary Disease: Foundation
Epidemiology & Disease Process
Anatomy & Physiology
Signs & Symptoms
Nursing Times. Vol 98. No 35. Pg 41-44

McAllister, J. (2002)
Chronic Obstructive Pulmonary Disease: Diagnosis and
Assessment, Investigations and Treatments
Nursing Times . Vol 98. No 36. Pg 27-30

McAllister, J. (2002)
Chronic Obstructive Pulmonary Disease: Nursing care & implications for
nursing
Nursing Times . Vol 98. No 37. Pg 43-45

Percival, J. (2002)
Smoking strategies for smoking cessation
Nursing Times Plus. Vol 98. No 40.
                                   25
Porter-Jones. G, (2002)
Short-term oxygen therapy
Nursing Times Plus. Vol 98. No 40

Reilly, J. Holt, K. Houghton, I & Eccleston, I. (2002)
Keeping Patients out of Hospital.
The Asthma Journal September Pages 136-139

Skwarska E, Cohen G, Skwarski KM et al (2000).
Randomised controlled trial of supported discharge in patients with
exacerbations of chronic obstructive pulmonary disease.
Thorax 55; 907-12

West R. et al (2000)
Smoking cessation guidelines for healthcare professionals: an
update. Thorax 55; 12,98




                                    26
27