1. 1 Chronic Obstructive Pulmonary Diseases Prof. Mohamed Awad Tag ElDin Professor of Thoracic Medicine Ain Shams University Chairman of The Egyptian Society of Chest Diseases and Tuberculosis

2. 2 Facts About COPD  Cigarette smoking is the primary cause of COPD.  The WHO estimates 1.3 billion smokers worldwide, increasing to 2 billion by 2025. In low- and middle-income countries, rates are increasing at an alarming rate.  In 2000, the WHO estimated 2.74 million deaths worldwide from COPD.  In 1990, COPD was ranked 12 th as a burden of disease; by 2020 it is projected to rank 5 th.

3. 3 Definition of COPD Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive, associated with an abnormal inflammatory response of the lungs to noxious particles or gases and associated with systemic manifestations.

4. 4 Clinicopathological Definition Chronic bronchitis Cough productive of sputum for at least three month of two consecutive years excluding other cardiopulmonary diseases. Emphysema An enlargement of the terminal air space due to destruction of the alveolar wall without fibrosis.

5. 5 COPD is an umbrella term to cover the “irreversible” aspect of chronic bronchitis, emphysema and asthma What is COPD?

6. 6 New Definitions of chronic bronchitis, emphysema and chronic obstructive pulmonary disease

7. 7 Definitions of chronic bronchitis, emphysema and chronic obstructive pulmonary disease

8. 8 Classification of the severity of chronic obstructive pulmonary disease, based on post-bronchodilator FEV1

9. 9 Burden of COPD  The burden of COPD is underestimated because it is not usually recognized and diagnosed until it is clinically apparent and moderately advanced.  Prevalence, morbidity, and mortality in Egypt are still lacking and have to be estimated, however, COPD is a significant health problem in both men and women.

10. 10  The economic costs of COPD are high and will continue to rise in direct relation to the ever- aging population, the increasing prevalence of the disease, and the cost of new and existing medical and public health interventions. Burden of COPD

11. 11 Etiology and Risk Factors for COPD Host Factor Genes (e.g. Alpha 1-antitrypsin deficiency) Hyper-responsiveness Lung growth Exposure Tobacco smoke Occupational dusts and chemical Infections Socioeconomic status

12. 12 Risk Factors Tobacco Smoking The most important risk factor for COPD is cigarette smoking,a greater annual rate of decline in FEV1and a greater COPD mortality rate in smokers than non smokers are reported, in direct proportion to the quantity of smoking. Shisha and Goza smokers have greater COPD morbidity and mortality rate than cigarette smokers. Not all smokers develop clinically significant COPD which suggests that genetic factors must modify each individual’s risk

13. 13 Passive exposure to cigarette smoke may also contribute to respiratory symptoms and COPD by increasing the lungs’ total burden of inhaled particles and gases. Exposure to particulate matter, irritants, organic dusts and sensitizing agents can cause an increase in airway hyperresponsiveness. High level of urban air pollution are harmful to individuals with existing heart or lung disease.

14. 14 Indoor air pollution from biomass fuel is a risk factors for the development of COPD. Airway hyperresponsiveness caused by infection in children may be considered risk factor for COPD. Low socioeconomic status may be a risk factor for COPD probably due to indoor and outdoor air pollutants, crowding, and poor nutrition.

15. 15 Pathogenesis of COPD  Inflammation  Protease- antiprotease imbalance  Oxidative stress  Mucous hypersecretion

16. 16 Pathogenesis of COPD NOXIOUS AGENT (tobacco smoke, pollutants, occupational agent) COPD Genetic factors Respiratory infection Other

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20. 20 Causes of Airflow Limitation  Irreversible - Fibrosis and narrowing of the airways - Loss of elastic recoil due to alveolar destruction - Destruction of alveolar support that maintains patency of small airways.

21. 21  Reversible - Accumulation of inflammatory cells, mucus, and plasma exudates in bronchi - Smooth muscle contraction in peripheral and central airways - Dynamic hyperinflation during exercise Causes of Airflow Limitation

22. 22  Exposure to inhaled noxious particles and gases causes inflammation of the lungs that can lead to COPD if the normal protective and/or repair mechanisms are overwhelmed or defective.  Exacerbations of COPD are associated with an increase in airway inflammation. Pathogenesis, pathology, and pathophysiology

23. 23  Although inflammation is important in both diseases, the inflammatory response in COPD is markedly different from that in asthma.  In addition to inflammation, two other processes thought to be important in the pathogenesis of COPD are an imbalance of proteinases and antiproteinases in the lung, and oxidative stress.

24. 24  Pathological changes characteristic of COPD are found in the central airways, peripheral air- ways, lung parenchyma, and pulmonary vasculature.  The peripheral airways become the major site of airways obstruction in COPD. The structural changes in the airway wall are the most important cause of the increase in peripheral airways resistance in COPD. Inflammatory changes such as airway edema and mucus hypersecretion also contribute to airway narrowing.

25. 25  Most common in COPD patients is the centrilobular form of emphysema, which involves dilatation and destruction of the respiratory bronchioles.  Physiological changes characteristic of the disease include mucus hypersecretion, ciliary's dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, and cor pulmonale, and they usually develop in this order over the course of the disease.

26. 26  The irreversible component of airflow limitation is primarily due to remodeling of the small air-ways. Parenchymal destruction (emphysema) also contributes but plays a smaller role.  In advanced COPD, peripheral airways obstruction, parenchymal destruction, and pulmonary vascular abnormalities reduce the lung's capacity for gas exchange, producing hypoxemia and, later on, hypercapnia. Inequality in the ventilation/perfusion ratio (V A /Q) is the major mechanism behind hypoxemia in COPD.

27. 27  Pulmonary hypertension develops late in the course of COPD. It is the major cardiovascular complication of COPD and is associated with a poor prognosis.  COPD is associated with systemic inflammation and skeletal muscle dysfunction that may contribute to limitation of exercise capacity and decline of health status.

28. 28 Objectives of COPD Management  Prevent disease progression  Relieve symptoms  Improve exercise tolerance  Improve health status  Prevent and treat exacerbations  Prevent and treat complications  Reduce mortality  Minimize side effects from treatment

29. 29 Four Components of COPD Management I- Assess and monitor disease II- Reduce risk factors III- Manage stable COPD  Education  Pharmacologic  Non-pharmacologic IV- Manage exacerbations

30. 30 I- Assess and Monitor Disease:  Assessment of symptoms and signs & differential diagnosis  Assessment of severity  Additional investigations  Monitor disease progression and complication  Monitor exacerbation history  Monitor Co-morbidities

31. 31 Symptoms Typical of COPD  History of heavy smoking for many years –often > 25 pack/years.  Cough and sputum production for many years  Cough often present only on walking at first, later cough occurs throughout the day  Sputum usually mucoid – becomes purulent with exacerbation of disease but not excessive  Cough and sputum often worse in winter due to infection  Insidious onset of breathlessness on exertion with wheezing or tightness of chest

32. 32  Some develop increasingly sever exacerbation of disease leading to chronic respiratory failure (the blue bloater) type of COPD.  Others have little or no sputum or hypoxia at rest, but breathlessness and wheezing is sever and emphysema is prominent (the pink puffer) type of COPD.  Most patient with COPD present with a mixed pattern.

33. 33 Physical examination  Large barrel shaped chest  Prominent accessory respiratory muscle in neck  Low, flat diaphragm causing costal margin retraction on inspiration  Diminished breath sound, distant heart sound  Prolonged expiration with generalized wheezing  Depressed liver, which is not enlarged

34. 34 The ‘blue bloater’ type of COPD patient may also have:  Cyanosis at rest or mild exertion  Oedema of ankles  Crakles at lung bases  Loud second heart sound in pulmonary area (difficult to hear in COPD)

35. 35 The ‘pink puffer’ type of COPD patient may also have:  Expiratory pursed-lip breathing (auto-PEEP)  Thin body build  Tendency to lean forward over a support to assist breathing Clubbing is not a feature of COPD and suggest either malignancy, bronchiectasis, or some other type of lung disease

36. 36 Differential Diagnosis of COPD 1- Asthma 2- Congestive heart failure 3- Bronchiectasis 4- Pulmonary TB

37. 37  Diagnosis of COPD is based on a history of exposure to risk factors and the presence of airflow limitation that is not fully reversible, with or without the presence of symptoms.  Patients who have chronic cough and sputum production with a history of exposure to risk factors should be tested for airflow limitation, even if they do not have dyspnea.

38. 38 Diagnosis of COPD EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution SYMPTOMS Cough sputum dyspnea SPIROMETRY

39. 39 Assessment of severity Stage Characteristics 0: At Risk Normal spirometry chronic symptoms (cough, sputum production) I: Mild COPD FEV 1 /FVC 80% predicted with or without chronic symptoms (cough, sputum production) II: Moderate COPD FEV 1 /FVC < 70% 30% < FEV 1 < 80% predicted (IIA: 50% < FEV 1 < 80% predicted, IIB: 30% < FEV 1 < 50% predicted) with or without chronic symptoms (cough, sputum production, dyspnea) III: Severe COPDFEV 1 /FVC < 70% FEV 1 < 30% predicted or FEV 1 < 50% predicted plus respiratory failure or clinical signs of right heart failure

40. 40 Additional Investigations 1.Bronchodilator reversibility testing 2. Chest X 3.Glucocorticoid reversibility testing 4.CT chest 5.Arterial blood gases measurement 6.Alpha -1- antitrypsin deficiency screening

41. 41 Bronchodilator Reversibility Testing Spirometry FEV 1 should be measured before a bronchodilator is given. The bronchodilator should be given by metered dose inhaler through a spacer device or by nebulizer to be certain it has been inhaled. The bronchodilator dose should be selected to be high on the dose/response curve. Suitable dosage protocols are 80 mg anticholinergic, 400 mg ß 2 - agonist, or the two combined. FEV 1 should be measured again 30-45 minutes after the bronchodilator is given. Results An increase in FEV 1 that is both greater than 200 ml and 12% above the pre-bronchodilator FEV 1 is considered significant.

42. 42 Chest X-Ray In mild COPD, the plain chest X-Ray may well be normal but with advanced emphysema changes include:  Large volume lungs  Low flat diaphragm  Rapid tapering of the vascular marking  Thin heart shadow  Enlarged retrosternal air space Chest X- Ray is valuable in excluding alternative diagnosis and/or complication

43. 43 Causes of Chronic Cough with a Normal Chest X-ray  Intrathoracic Chronic obstructive pulmonary disease Bronchial asthma Central bronchial carcinoma Endobronchial tuberculosis Bronchiectasis Left heart failure Interstitial lung disease Cystic fibrosis  Extrathoracic Postnasal drip Gastroesophageal reflux Drug therapy (e.g., ACE inhibitors)

44. 44 Glucocorticoid Reversibility Testing Long-term glucocorticosteroid treatment in COPD can at present only be justified in patients with a consistent, significant FEV 1 response to glucocorticosteroids, or in those with repeated exacerbations. The simplest, and potentially safest, way to identify these patients is by a treatment trial with inhaled glucocorticosteroids for 6 weeks to 3 months, using as criteria for glucocorticosteroid reversibility an FEV 1 increase of 200 ml and 15% above base-line. The response to glucocorticosteroids should be evaluated with respect to the post-bronchodilator FEV 1(i.e., the effect of treatment with inhaled glucocorticosteroids should be in addition to that of regular treatment with a bronchodilator).

45. 45 CT of the lung  Is indicated when there is doubt about the diagnosis of COPD  When surgical procedure such as bullectomy is contemplated  Complication as pulmonary thromboembolism and pulmonary artery thrombosis by spiral CT  Superimposed other disease for example malignancy, TB, etc…

46. 46 Arterial blood gas measurement. In advanced COPD measurement of arterial blood gases is important. This test should be performed in patients with FEV 1 < 40% predicted or with clinical signs suggestive of respiratory failure or right heart failure.

47. 47 Alpha-1 antitrypsin deficiency screening. In patients who develop COPD at a young age (< 45 years) or who have a strong family history of the disease, it may be valuable to identify coexisting alpha-1 antitrypsin deficiency. This could lead to family screening or appropriate counseling. A serum concentration of alpha-1 antitrypsin below 15-20 % of the normal value is highly suggestive of homozygous alpha-1 antitrypsin deficiency.

48. 48 Monitor Disease Progression and Development of Complications A- Pulmonary function A patient’s decline in lung function is best tracked by periodic spirometry measurements, performed more than once a year. Other pulmonary function tests, such as flow-volume loops, diffusing capacity (D LCO) measurements, and measurement of lung volumes are not needed in a routine assessment but can provide information about the overall impact of the disease and can be valuable in resolving diagnostic uncertainties & assessing patients for surgery.

49. 49 B- Arterial blood gas measurement Measurement of arterial blood gas tensions should be performed in all patients with FEV 1 50 mm Hg in arterial blood gas measurements made while breathing air at sea level.

50. 50 C- Diagnosis of right heart failure or cor-pulmonale Elevation of the jugular venous pressure and the presence of pitting ankle edema are often the most useful findings suggestive of cor-pulmonale in clinical practice. Firm diagnosis of cor-pulmonale can be made through a number of investigations, including radiography, electrocardiography, and echocardiography..

51. 51 D- Hematocrit Polycythemia can develop in the presence of arterial hypoxemia, especially in continuing smokers. Polycythemia can be identified by hematocrit > 55%. E- Sleep studies Sleep studies may be indicated when hypoxemia or right heart failure develops in the presence of relatively mild airflow limitation or when the patient has symptoms suggesting the presence of sleep apnea.

52. 52  Monitor Pharmacotherapy and Other Medical Treatment  Monitor Exacerbation History  Monitor Co-morbidities

53. 53  Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD.  Smoking cessation is the single most effective-and cost-effective- intervention to reduce the risk of developing COPD and stop its progression. II- Reduce risk factors

54. 54 Brief Strategies To Help The Patient Willing To Quit Smoking  ASK Systematically identify all tobacco users at every visit.  ADVISE Strongly urge all tobacco users to quit.  ASSESS Determine willingness to make a quit attempt.  ASSIST Aid the patient in quitting.  ARRANGESchedule follow-up contact.

55. 55  Progression of many occupationally- induced respiratory disorders can be reduced or controlled through a variety of strategies aimed at reducing the burden of inhaled particles and gases.

56. 56  Education  Pharmacologic  Non-pharmacologic III- Manage stable COPD

57. 57  The overall approach to managing stable COPD should be characterized by a stepwise increase in the treatment, depending on the severity of the disease.  For patients with COPD, health education can play a role in improving skills, ability to cope with illness, and health status. It is effective in accomplishing certain goals, including smoking cessation.

58. 58 Topics for Patient Education Stage 0: At Risk - Information and advice about reducing risk factors Stage I: Mild COPD to Stage II: Moderate COPD (Above topic, plus): - Information about the nature of COPD - Instruction on how to use inhalers and other treatments - Recognition and treatment of acute exacerbations - Strategies for minimizing dyspnea. Stage III: Severe COPD (Above topics, plus): - Information about complications - Information about oxygen treatment

59. 59 What is COPD? Neutrophil damage in COPD

60. 60  Bronchodilator medications are central to the symptomatic management of COPD.  The principal bronchodilator treatments are anticholinergics, Beta2-agonists, theophylline, or a combination of these drugs.

61. 61  None of the existing medications for COPD has been shown to modify the long-term decline in lung function that is the hallmark of this disease. Therefore, pharmacotherapy for COPD is used to decrease symptoms and/or complications.

62. 62 Bronchodilators in Stable COPD  Inhaled therapy is preferred.  The choice between Anticholinergic, Beta 2 -agonist, theophylline or combination therapy depends on availability and individual response in terms of symptoms relief and side effects.

63. 63  Theophylline is effective in COPD  Bronchodilators are prescribed on an as- needed or on a regular basis to prevent or reduce symptoms.  Long-acting inhaled bronchodilators are more convenient.  Combining bronchodilators may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator

64. 64 Drug Metered dose (mcg) Nebulizer (mg) Oral (mg) Duration of action (hrs) Anticholinergics Tiotropium bromide 18 (Inhalant Cap) -24 Ipratropium bromide 40 – 800.25 – 0.5-6 – 8 Methylxanthines Theophylline SR --100 - 400 Variable, up to 24 Commonly used formulations of Bronchodilator drugs

65. 65 DrugMetered dose (mcg ) Nebulizer (mg) Oral (mg)Duration of action (hrs) B2 – agonists Fenoterol100 - 2000.5 2.0-4 - 6 Salbutamol (Albuterol) 100 - 2002.5 – 5.02 - 44 - 6 Terbutaline250 - 5005 - 102.5 - 54 - 6 Formoterol12 - 24-12 + Salmeterol50 - 100-12 + Bambuterol2024 Commonly used formulations of Bronchodilator drugs

66. 66  Regular treatment with inhaled glucocorticoid- steroids should only be prescribed for symptomatic COPD patients with a documented spirometric response to glucocorticosteroids or in those with an FEV 1 < 50% predicted and repeated exacerbations requiring treatment with antibiotics and/or oral glucocorticosteroids. Glucocorticosteroids in Stable Asthma

67. 67  Chronic treatment with systemic glucocorticoid- steroids should be avoided because of an unfavorable benefit-to-risk ratio.

68. 68 Management of COPD by Severity of Disease Stage 0: At risk Stage 1: Mild COPD Stage 2: Moderate COPD Stage 3: Severe COPD

69. 69 Management of COPD: In All stages  Avoidance of noxious agents  Smoking cessation  Reduction of indoor pollution  Reduction of occupational exposure  Influenza vaccination

70. 70 Management of COPD Stage 0: At Risk Characteristics Recommended Treatment Chronic symptoms - cough - sputum No spirometric abnormalities

71. 71 Characteristics Recommended Treatment FEV 1 /FVC < 70 % FEV 1 > 80 % predicted With or without symptoms Short-acting bronchodilator as needed Management of COPD Stage 1: Mild COPD

72. 72 Characteristics Recommended Treatment FEV 1 /FVC < 70% 50% < FEV 1 < 80% predicted With or without symptoms Regular treatment with one or more bronchodilators Rehabilitation Inhaled glucocortico- steroids if significant symptoms and lung function response. Management of COPD Stage IIA: Moderate COPD

73. 73 Characteristics Recommended Treatment FEV 1 /FVC < 70% 30% < FEV 1 < 50% predicted With or without symptoms Regular treatment with one or more bronchodilators Rehabilitation Inhaled glucocortico- steroids if significant symptoms and lung function response or if repeated exacerbations Management of COPD Stage IIB: Moderate COPD

74. 74 Characteristics Recommended Treatment FEV 1 /FVC < 70% FEV 1 < 30% predicted or presence of respiratory failure or right heart failure Regular treatment with one or more bronchodilators Inhaled glucocorticosteroids if significant symptoms and lung function response or if repeated exacerbations Treatment of complications Rehabilitation Long-term oxygen therapy if respiratory failure Consider surgical options Management of COPD Stage III: Severe COPD

75. 75 Vaccines Influenza vaccines can reduce serious illness and death in COPD patients by about 50%. Vaccines containing killed or live, inactivated viruses are recommended as they are more effective in elderly patients with COPD. The strains are adjusted each year for appropriate effectiveness and should be given once (in Autumn) or twice (in Autumn and Winter) each year. A pneumococcal vaccine containing 23 virulent serotypes has been used, but sufficient data to support its general use in COPD patients are lacking. Other pharmacological treatment

76. 76  The regular use of antibiotic, mucolytic, immunoregulatives, antitussive, vasodilators (nitric oxide), respiratory stimulants (almitrine) and doxapram are not recommended in stable COPD.  Narcotics are contraindicated in stable COPD.  Antioxidant agents reduce frequency of exacerbation.  Nedocromil, Leukotriene modifiers – herbal medicine, acupuncture, homopathy have not been adequately tested in COPD patients.

77. 77 Rehabilitation  Improves exercise capacity.  Reduces the perceived intensity of breathlessness.  Can improve health-related quality of life.  Reduces the number of hospitalizations and days in the hospital.  Reduces anxiety and depression associated with COPD. Non pharmacological treatment

78. 78 Oxygen therapy Oxygen therapy  Oxygen therapy, one of the principal non- pharmacologic treatments for patients with Stage III: Severe COPD, can be administered in three ways: long-term continuous therapy, during exercise, and to relieve acute dyspnea.  The primary goal of oxygen therapy is to increase the baseline PaO 2 to at least 60 mm Hg at sea level and rest, and/or produce an SaO 2 at least 90%.  The long term administration of continuous humidified oxygen (>15 hours/day) to patients with chronic respiratory failure has been shown to increase survival

79. 79  Long-term oxygen therapy is generally introduced in Stage III: Severe COPD for patients who have: - PaO 2 at or below 55 mm Hg or SaO 2 at or below 88%, with or without hypercapnia - PaO 2 between 55 mm Hg and 60 mm Hg, or SaO 2 of 89%, if there is evidence of pulmonary hypertension, peripheral edema suggesting congestive cardiac failure, or polycythemia - In hypercapnia, low flow continuous humidified oxygen is recommended to avoid CO 2 narcosis

80. 80 Although air travel is safe for most patients with chronic respiratory failure who are on long-term oxygen therapy, patients should be instructed to increase the flow by 1-2 L/min during the flight. Those with a resting PaO 2 at sea level of > 70 mm Hg are likely to be safe to fly without supplementary oxygen Oxygen use in air travel

81. 81 Surgical treatment Bullectomy. Indicated when the bullea occupy 50% or more of the hemithorax and produce definite displacement of the adjacent lung. Lung volume reduction surgery (LVRS) Is indicated when FEV1 200% predicted.

82. 82  Criteria for referral for lung transplantation include: - FEV1 < 35% predicted, PaO 2 55-60 mmHg - PaCO 2 > 50 mmHg and secondary pulmonary hypertension Lung Transplantation

83. 83  Increases breathlessness, the main symptom of an exacerbation, is often accompanied by wheezing & chest tightness, increase cough & sputum, change of the color and/or tenacity of sputum & fever  Exacerbations of respiratory symptoms requiring medical intervention are important clinical events in COPD.  The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified. IV- Manage Exacerbations

84. 84  Inhaled bronchodilators (Beta 2 -agonists and/or anticholinergics), theophylline, and systemic, preferably oral, glucocortico-steroids are effective for the treatment of COPD exacerbations.

85. 85  Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased volume and change of color of sputum, and/or fever) may benefit from antibiotic treatment.

86. 86  Noninvasive intermittent positive pressure ventilation (NIIPPV) in acute exacerbations improves blood gases and pH, reduces in- hospital mortality, decreases the need for invasive mechanical ventilation and intubations, and decreases the length of hospital stay.

87. 87 Common causes of Acute exacerbation of COPD Primary Tracheo-bronchial infection. Air pollution. Secondary Pneumonia. Pulmonary embolism. Rib fractures/ chest trauma. Inappropriate use of sedatives, narcotics, beta-blocking agents. Right and/ or left heart failure or arrhythmias.

88. 88 Medical History  Duration of worsening or new symptoms  Number of previous episodes (exacerbations /hospitalizations)  Present of treatment regimen Medical history and signs of severity of acute exacerbations of COPD

89. 89 Signs of severity  Use of accessory respiratory muscles.  Paradoxical chest wall movements.  Worsening or new onset central cyanosis.  Development of peripheral edema.  Hemodynamic instability.  Signs of right heart failure.  Reduced alertness. Medical history and signs of severity of acute exacerbations of COPD

90. 90 Initiate or increase bronchodilator therapy Consider antibiotics Consider antibiotics Reassess within hours Resolution or improvement of signs and symptoms Continue management Step down when possible Review long-term management No resolution or improvement Add oral corticosteroids Reassess within hours Worsening of signs/symptoms Refer to hospital Algorithm for the management of an acute exacerbation of COPD at home

91. 91  Marked increase in intensity of symptoms, such as sudden development of resting dyspnea.  Severe background COPD.  Onset of new physical signs (e.g., cyanosis, peripheral edema).  Failure of exacerbation to respond to initial medical management.  Significant co-morbidities.  Newly occurring arrhythmias.  Diagnostic uncertainty.  Older age.  Insufficient home support. Indications for hospital assessment or admission for acute exacerbations of COPD

92. 92  Severe dyspnea that responds inadequately to initial emergency therapy.  Confusion, lethargy, coma.  Persistent or worsening hypoxemia (PaO 2 9.3 kPa, 70 mmHg), and/or severe/worsening respiratory acidosis (pH < 7.30) despite supplement oxygen and NIPPV. Indications for hospital assessment or admission for acute exacerbations of COPD

93. 93 Management of Severe but Not Life-Threatening Exacerbations of COPD in the Emergency Department or the Hospital  Assess severity of symptoms, blood gases, chest X-ray.  Administer controlled low flow humidified continuous 1-2 lit/min oxygen therapy and repeat arterial blood gas measurement after 30 minutes.  Bronchodilators: - Increase doses or frequency. - Combine β 2 - agonists and anticholinergics. - Use spacers or air-driven nebulizers. - Consider adding intra-venous aminophylline, if needed.

94. 94  Add oral or intravenous glucocorticoids.  Consider antibiotics: - When signs of bacterial infection, oral or occasionally intravenous.  Consider noninvasive mechanical ventilation.  At all times: - Monitor fluid balance and nutrition. - Consider subcutaneous heparin. - Identify and treat associated conditions (e.g., heart failure, arrhythmias). - Closely monitor condition of the patient. Management of Severe but Not Life-Threatening Exacerbations of COPD in the Emergency Department or the Hospital

95. 95 Thank You mohamedawadtag@yahoo.com