Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Mahu copd

953 views

Published on

  • Be the first to comment

  • Be the first to like this

Mahu copd

  1. 1. COPD Chronic Obstructive Pulmonary Disease By Mr. Mahadev Prasad KB Msc Nurse
  2. 2. SYNONYMS        Chronic obstructive lung disease (COLD) Chronic obstructive airways disease (COAD) Chronic airflow obstruction (CAO) CHRONIC BRONCHITIS EMPHYSEMA Small airways disease ASTHMA NOT included in COPD
  3. 3. Definition Chronic obstructive pulmonary disease (COPD) is characterised by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. 1 The disease is predominantly caused by smoking. 1. NICE 2004
  4. 4. The Umbrella Disease COPD – an umbrella term covering the “irreversible” aspect of chronic bronchitis, emphysema and asthma Chronic bronchitis Emphysema COPD (shaded area) Airway obstruction Chronic severe asthma
  5. 5. Umbrella Disease  COPD now preferred term for previous diagnosis of bronchitis or emphysema, chronic asthma  Significant airflow obstruction may be present before individual is aware of it  May also be related to occupational exposures e.g. asbestos
  6. 6. Epidemiology  COPD is the fourth leading cause of death in the USA and Europe. The leading cause of death worldwide 1  Mortality in females has more than doubled over the last 20 years. 1  Nearly 900,000 people in England and Wales have a diagnosis of COPD 2  Morbidity data greatly underestimate the total burden of COPD because the disease is usually not diagnosed until it is clinically apparent and moderately advanced. 1  COPD is a more costly disease than asthma and, depending on country, 50–75% of the costs are for services associated with exacerbations. 1 1 COPD Audit Commission 2 BTS Consortium 2005
  7. 7. Characteristic  Changes characteristic of the disease include:         smooth muscle contraction (bronchoconstriction) mucus hypersecretion ciliary dysfunction pulmonary hyperinflation gas exchange abnormalities pulmonary hypertension cor pulmonale These abnormalities contribute to the characteristic symptoms of COPD - chronic cough, sputum production and dyspnoea 1 1 Pauwels et al, 2001
  8. 8. Risk Factors  Tobacco Smoke Cigarettes,  Pipes, cigars – lower rates than cigarette smokers but higher than non-smokers    Occupational dusts and chemicals  Vapors, irritants, fumes   Need sufficiently intense or prolonged exposure Indoor air pollution  Biomass fuel used for cooking and heating in poorly vented dwellings Outdoor air pollution    Minor risk factor Passive cigarette smoke exposure Respiratory infections in early childhood Lower socioeconomic status association with COPD  May be secondary to crowding, poor nutrition, etc. 
  9. 9. WHAT CAUSES COPD? COPD is usually related to a history of tobacco smoking,cigarette smoking,pipe&cigar smoke.  Breathing in air pollution and chemical fumes or dust from the environment or workplace also can contribute to COPD.  In rare cases a genetic condition called alpha1-antitrypsin deficiency may play a role in causing COPD 
  10. 10. Healthy Respiratory Mucosa This electron micrograph shows the respiratory mucosa in a healthy state The cells are fully ciliated The cilia beat in a co-ordinated fashion to move mucus out of the airways (mucociliary transport) Scanning electron micrograph showing a sheet of mucus being moved along by the cilia
  11. 11. Damaged Respiratory Mucosa   This slide shows the result of bacterial infection stripping away the cilia from the mucosa  Scanning electron micrograph showing cilial and epithelial damage induced by bacteria Damage to the cilia and epithelium occur as a result of disease processes in COPD. This can also occur as a result of bacterial damage The damage to the cilia means they are less effective in removing mucus from the airways
  12. 12. Chronic Bronchitis ↑ in mucus glands and goblet cells – Production of sputum on most days for > 3 months on 2 consecutive years – Small airway disease (structural changes in the small airways 2-5mm) > 50% of bronchioles may be effected before any SOB –↑ airway smooth muscle – Inflammatory infiltration resulting in structural narrowing and distortion Collagen deposition / fibrosis / mucous plugging
  13. 13. EMPHYSEMA
  14. 14. Emphysema •Dilation of alveolar wall •↓ alveolar capillary network, loss of guy rope effect •↓ lung tissue elasticity •Caused by smoking » irritation » inflammation » neutrophils and macrophages » release neutrophil elastase (type of proteases) Normal Lung Emphysema
  15. 15. The COPD Patient  Generally over 40 years  A smoker or ex-smoker  Presentation with: cough  excessive sputum production  shortness of breath   Dyspnoea is the reason most patients seek medical attention 3 1. BTS, 1997; 3. GOLD, 2003 1
  16. 16. Pathophysiology Mucus hypersecretion Ciliary dysfunction Airflow limitation Pulmonary hyperinflation Gas exchange abnormalities Pulmonary hypertension Cor pulmonale  Mucus hyperserection & ciliary dysfunction → cough, sputum production
  17. 17. Diagnosis >35 years  Smoker or ex-smoker  Spirometry (obstructive pattern)  Any symptoms :        Exertional breathlessness Chronic cough Regular sputum production Frequent “winter bronchitis” Wheeze + no clinical features of asthma
  18. 18. Assessment of Severity of COPD Severity of airflow obstruction FEV1 % predicted Mild Moderate Severe 50-80% 30-49% <30% GOLD state that spirometry is the gold standard for diagnosing COPD, severity is measured by FEV1(Forced expiratory volume). 1 NICE Guidelines 2004 1
  19. 19. Management of COPD (Stable)    Use short acting bronchodilator PRN (beta2-agonist or anti-cholinergic) If still symptomatic try combined therapy with a short acting beta2 agonist and a short acting anti-cholinergic. If still symptomatic use a long acting bronch-dilator (beta2 agonist or anticholinergic)
  20. 20. Management In moderate or severe COPD  If still symptomatic consider a trial of a combination of a long acting beta2 agonist and inhaled corticosteroid. (Discontinue if no benefit after 4 – 6 weeks)  If still symptomatic consider adding theophylline.  Offer pulmonary rehab to all patients who consider themselves functionally disabled (usually MRC 3 and above)  Consider referral for surgery.  End of Life Care (need to start these conversations ,what the future will hold, discuss issues, worries and concerns with patients at an earlier stage. Palliative care being part of end of life care)
  21. 21. Acute exacerbation of COPD   Sustained worsening of patients symptoms from their usual stable state, which is beyond normal day-to-day variations and is acute in onset. 1 Symptoms :        1 NICE Guidelines 2004 Increased shortness of breath Increased sputum production and/or change in colour Increased cough Increased wheeze/tightness Decreased exercise tolerance Increased fatigue Confusion
  22. 22. Annual Review – Primary Care             Smoking cessation Spirometry Need for Oxygen Assessment Pharmacological Therapy - inhaler technique Pulmonary Rehabilitation LVRS / Transplantation BMI – Need for Dietician Input Referral to other Services MRC Scale Need for Specialist Referral Chronic NIV End of Life Care
  23. 23. Severe COPD         Smoking cessation Oxygen Pharmacological Therapy Pulmonary Rehabilitation Dyspnoea Clinic LVRS / Transplantation Chronic NIV End of Life Care - Palliation
  24. 24. Look magazine ad from 1951
  25. 25. Oxygen Therapy  Long Term Oxygen Therapy (LTOT)  Short Burst Oxygen Therapy  Ambulatory Oxygen Therapy
  26. 26. Benefits of LTOT          Improved survival Prevention of deterioration of pulmonary haemodynamics Reduction in secondary polycythaemia Neuropsychological benefit improved sleep quality Increased renal blood flow reduction in cardiac arrhythmias Reduction in dyspnoea, improved exercise tolerance Should be worn for 15 hrs or more a day to gain these benefits
  27. 27. Short Burst Oxygen Therapy     Further research is required Episodic dyspnoea not relieved by other treatments Palliative therapy or in emergency situations If improvement in dyspnoea or exercise tolerance can be documented
  28. 28. Ambulatory Oxygen Therapy    Improved exercise tolerance Reduced dyspnoea Improved quality of life
  29. 29. Medicines Management  Flu and Pneumonia vaccination  Bronchodilators  Coticosteroids  Mucolytics Pharmacotherapy does not modify long-term decline, but is used to –prevent and control symptoms / improve exercise tolerance –reduce the frequency and severity of exacerbations –improve health status
  30. 30. Long – Acting Inhaled bronchodilators e.g. Salmeterol / Tiotropium  Significant improvement in lung function  1-3 better sustained improvement in lung function over 12 hours than ipratropium bromide 1  Improve shortness of breath day and night  Reduce risk of exacerbations vs. placebo  Clinically significant improvements in quality of life 4,5  unlike ipratropium bromide, Salmeterol significantly increased the percentage of patients showing a clinically relevant improvement in health status compared with placebo 5 1,3 1 1. Mahler et al, 1999, 2. Mahler et al, 2001, 3. Boyd et al, 1997, 4. Jones et al, 1997, 5. Cox et al, 2000
  31. 31. Xanthines - e.g. theophylline Less commonly used than other bronchodilators  Only modest bronchodilators  Side effects within therapeutic range  Many drug interactions  Smoking can affect the metabolism of theophylline
  32. 32. Inhaled Corticosteroids  Inhaled steroids now limited to moderate symptomatic disease with ≥2 exacerbations per year to reduce admission rates 1  Emerging evidence of enhanced effect of xanthines when combined with corticosteroid 1 NICE (2004)
  33. 33. Mycolytics Carbocisteine    Reduces sputum viscosity to aid expectoration Reduces exacerbations of COPD in those with chronic productive cough (caution in peptic ulceration / can cause gastrointestinal irritation) Erdotin - Short course during acute exacerbation GOLD guidelines (2007) suggest there is not enough evidence to support there use. However, there are a group of patients in which it works well in
  34. 34. Lung Reduction In Emphysema ↑ ↑ ↓ ↓ ↑ ↓ ↑ ↓ ↑ ↑ ↓ ↓ Remove hyperinflated areas of lung: Improve V/Q matching Reduce resting length of respiratory muscles Reduce Dynamic Hyperinflation
  35. 35. Pulmonary Rehabilitation  The goal of PR are to reduce the symptoms, disability and handicap to improve functional independence in COPD 5  Programme incorporates a programme of physical training, disease education, nutritional, psychological, social and behaviour intervention 5  Provided by a inter professional team, with attention to individual goals and needs.  Improves exercise tolerance and function / reduces dyspnoea / improves QOL 1,2  Empowerment for patients to manage their own condition recognition of exacerbations. 1 Ries et al. 1995, 2 De Paepe et al. 2000 3, Griffiths at al.2000, 4, Troosters et al, 2000 5 BTS 2001
  36. 36. Pulmonary Rehabilitation        Introduction Benefits of exercising Anatomy, Physiology and Pathology Medication Chest Clearance techniques Dyspnoea management OT pacing/aids        Age Concern Benefits system Exacerbation Nutrition Psychosocial factors Coping/Anxiety/Panic Breath easy Expert patient What next? – Health improvement team
  37. 37. PREVENTION
  38. 38. IF NOT PREVENTED
  39. 39. Chronic Non-Invasive Ventilation  Domiciliary NIV for a highly selected group of COPD patients with recurrent admissions requiring assisted ventilation is effective at reducing admissions and minimizes costs from the perspective of the acute hospital 1  1 Tuggey JM, Plant PK, Elliott MW. Thorax. 2003
  40. 40. When does COPD become Palliative? (1 of 2)       Primary clinical indicators FEV1 < 30% pred History of >2 acute exacerbations in last 12 months Frequent admissions to hospital Progressive shortening of of the intervals between admissions Limited improvement following admission 1
  41. 41. When does COPD become Palliative? (2 of 2)       Supporting clinical Indicators On maximum therapy- no other intervention is likely to alter the conditions progression Dependence on oxygen therapy Severe unremitting dyspnoea (MRC Dyspnoea Scale grade 5) Severe co morbidities e.g. heart failure, diabetes Housebound – unable to carry out normal ADL
  42. 42. Dyspnoea  Symptomatic Treatment Opioids Mechanism unclear   respiratory drive,  sensation of respiratory muscle fatigue, cognitive changes, central effect, cough suppressant 2 – Oral morphine 2.5 4 hourly (dose maybe escalated if well tolerated) No evidence to support nebulised morphine 1 Watson et al 2006 2 Jenner 1991 1
  43. 43. Dyspnoea related to Anxiety  Benzodiazepines Examples include - Diazepam 2 – 5mgs BD and PRN - Lorazepam 1 – 2 mgs p.r.n 1 Watson et al 2006 1
  44. 44. Oxygen Therapy  Some patients do derive good benefit if not already on LTOT  But: Beware the CO2 retainers  Also:      Risk of psychological dependence Paradoxical restriction to activity Dry mouth / nose Isolation and communication problems Consider open window, fan, cool flannel, heliox
  45. 45. Intractable Cough  Steam inhalation  Nebulisation -  Oral morphine 2.5 - 5mg, 4 hourly (0.9% sodium chloride. Consider nebulised bronchodilation and steroid) 1 Watson et al 2006 1
  46. 46. Terminal Breathlessness  Non-pharmacological management Touch  Relaxation  Environment  Modelling of behaviour   Subcutaneous Route may be necessary
  47. 47. Thank – You Any Questions?

×