CHRONIC OBSTRUCTIVE PULMONARY DISEASE

1. CHRONIC OBSTRUCTIVEPULMONARYDISEASE

2. AIMS OF THIS SESSION To • Understand the definition • Discuss causes • Discuss diagnosis • Discuss Management/Medication • Discuss Oxygen Therapy and enjoy!

5. DEFINITION • COPD is characterised by airflow obstruction. • air flow obstruction is usually progressive • It is not fully reversible • does not change markedly over several months . • The disease is pre-dominantly caused by smoking.

6. COPDis an umbrella term for • Emphysema • Chronic Bronchitis • Severe Chronic Asthma NICE (2010)

7. CHRONIC BRONCHITIS • Continuous inflammation of the cells lining the bronchi • Mucous hypersecretion • Destruction of the cilia, impairing mucous clearance leading to increased risk of infection Diagnosed by the production of sputum and cough on most days for three months in two consecutive years

8. EMPHYSEMA • Destructive of the alveoli and terminal bronchioles • Loss of elasticity of smaller airways • Loss of patency of bronchioles

9. CAUSES OF COPD SMOKING: • 90 % of cases,are caused by smoking • 15% are susceptible. • Lung function decline is 3 times faster • If smoking stops, at one year FEV1 decline is age related (Morgan & Britton 2003) ALPHA 1 ANTITRIPSIN DEFICIENCY:GENETIC • Found in only 1% of cases. OCCUPATIONAL EXPOSURE TO RESPIRATORY POLLUTANTS: Chemicals, dust, atmospheric pollutants, inherited tendency

10. Nearly 30,000 deaths a year-accounting for 5% of all deaths, one death every 20 mins 850,000 diagnosed – only 33% Probably 2 million undiagnosed “Missing Millions”(BLF 2009) COPD is the fourth most common cause of death after heart disease, lung disease and cerebrovascular disease

11. COPD is the only leading cause of death that is increasing in prevalence with a total cost £850 million/yr- 24 million working days lost- Cigarette smoking is the major cause of COPD 90% Mortality from COPD is increasing in women while reaching a plateau in men Unless current trends are reversed, COPD may become the biggest public health problem. Death rate one of worst in Europe

13. DIAGNOSIS • Over 35 • Smoker or ex smoker • no clinical features of asthma • Have any of these symptoms? exertional breathlessness chronic cough regular sputum production frequent winter “bronchitis” Wheeze (NICE 2010)

14. COPD OR ASTHMA ?

15. SPIROMETRY Spirometry measures the volume of air expired from the lungs during a single maximal forced expiration. The key measurements are:- Forced Vital capacity (FVC) Forced Expiratory Volume in one second (FEV1) FVC/FEV1 Ratio

16. CLASSIFICATION OF COPD MILD FEV1 >80% MODERATE FEV1 50-80% SEVERE FEV1 30-50% VERY SEVERE FEV1,30% NICE GUIDELINE (2010))

17. SYMPTOMS ASSOCIATED WITH AN EXACERBATION • DYSPNOEA • More breathless than normal • Reduced exercise tolerance • SPUTUM PRODUCTION • Increase in purulence • SPUTUM VOLUME • Increase in normal amount • COUGH

18. INVESTIGATIONS • Chest X ray • Arterial blood gas – can aid medical diagnosis • ECG • FBC, Urea and Electrolytes • Theophylline levels if appropriate • Sputum microscopy/culture if purulent

19. OBSERVATIONS/MONITORING • RESPIRATORY rate/rhythm/workload/equal • O2 Sats – 90-92% • Colour skin, lips, nails(clubbing) • Patient able to speak in sentences/words or not at all • Temp/Pulse/BP • Confusion • urine output • Peripheral oedema • Depression/lethargy • Assess need for NIV/IV • Not needed- PEFR

20. TREATMENT • Regular bronchodilator therapy (consider IV aminophylline if poor response to nebs) • Continue/start Oral antibiotics • Continue/start oral Prednisolone (continue inhaled steroids also as takes 7 – 10 days to kick in) • Oxygen therapy asprescribed (dependant on blood gas result and Sats O2) • Non invasive Ventilation

22. NURSING MANAGEMENT Liase with multi disciplinary team members to provide specialised care. • Disease process/progression • Inhalers/medication • Smoking cessation • Nutrition

23. Pulmonary rehab/Community Matron/Breathlessness clinic/Support group • Vaccinations • Physiotherapist-Breathing exercises, expectoration, coping mechanisms, energy conservation • Benefits • Further exacerbations- Exacerbation self management plan and standby antibiotics and steroids

24. PRE DISCHARGE MANAGEMENT • Spirometry • Blood gas • Full knowledge of treatment – correct inhaler technique • Self management plan re antibiotics and steroids at home • FU appt-with Respiratory Nurses if O2 indicated • Refer to Pulmonary rehab • Check smoking status

25. END of LIFE? Palliative care register Advanced directives/PPC/Assessment of concerns Hospice/day hospital

27. COMPLICATIONS OF COPD. • RESPIRATORY FAILURE • COR PULMONALE • POLYCYTHAEMIA • PULMONARY EMBOLI • DEPRESSION / ANXIETY

28. RESPIRATORY FAILURE TYPE 1 Respiratory Failure PaO2 below 8Kpa(60.80mmHg) with normal/low PaCO2 TYPE 2 Respiratory Failure: PaO2, below 8kpa(60.8mmHg) and increased PaCO2 above 6.5kPa( 49.4mmHg)

29. AIMS OF THERAPY • Prevent further disease progression • Relieve symptoms • Improve exercise capacity • Maintain best quality of life • Prevent exacerbations

30. MEDICATIONS Bronchodilators should be the initial treatment Assess effectiveness by • improvement in symptoms • ADL • exercise capacity • rapidity of relief of symptoms Note - FEV1 will not reflect any significant improvement

31. MEDICATIONS If symptoms persist add • Long acting anticholinergic. • Long-acting B2 agonist

32. MEDICATIONS • Inhaled steroids - for all COPD pts? • Methylxanthines • Antidepressants • Mucolytics

33. TREATMENT FACTORS AFFECTING CONCORDANCE OF INHALED MEDICATIONS • Drug regime - Too complex - Frequency of dosing - Unsuitable inhaler ie rheumatic, elderly • Lack of noticeable immediate benefit eg inhaled steroids and long acting bronchodilators • Multiple prescription charges

34. NON TREATMENT FACTORS • Lack of understanding of treatment inc lack of clear instructions • Fear of side effects • Dislike/distrust of health service • Reluctance to accept diagnosis • Preference for alternative therapies • Lack of social support/family circumstances • Language, reading or eyesight difficulties

36. LONG TERM OXYGEN THERAPY LTOT is considered in patients with • PaO2 of 7.3kPa when stable or • PaO2 of 7.3 – 8kPa with one of the following : • secondary polycytheamia • nocturnal hypoxaemia, • peripheral oedema or pulmonary hypertension • Severe airflow obstruction – FEV1<30%

37. ASSESSMENT • Performed in secondary care • Initial - 6 weeks post exacerbation, clinically stable • Second assessment – 3-4 weeks later with trial of oxygen • LTOT should be used for at least 15hrs/day via a concentrator installed by company

38. SHORT BURST OXYGEN No evidence to support its use in COPD . Used more for symptom relief in fibrosis /palliative care • for short bursts only • by cylinder • Can be prescribed by GP

39. AMBULATORY OXYGEN • Evidence of desaturation on exercise • 6 min walk test monitored by saturations. • Lightweight cylinders +/- conserver device

40. CHRONIC OBSTRUCTIVEPULMONARYDISEASEEnd

41. RESPIRATORY NURSES ALISON CALVERT RLI/WGH EXT 3608/5611 MOBILE 07917240710 SARAH JEWELL FGH PAGER VIA SWITCH EXT 1502 HELEN BOOTH RLI BLEEP 767 EXT 3608