ASSESSMENT AND MANAGEMENT OF
STABLE COPD
PRESENTOR-DR RASHI VOHRA
MODERATOR- DR JAGDISH RAWAT
GOALS OF ASSESSMENT
In order to eventually guide therapy, goals of assessment
are ascertained as follows :
Determine level of airflow limitation
Impact on patient’s health status
Risk of future events (exacerbations, hospital admissions,
death)
GOALS OF ASSESSMENT
In order to achieve these goals, we have to consider:-
Presence and severity of spirometry abnormalities
Current nature and magnitude of patient’s symptoms
History of moderate and severe exacerbations and future
risk
Presence of co-morbidities
1. CLASSIFICATION OF AIRFLOW LIMITATION
SEVERITY
(BASED ON POST BRONCHODILATOR-FEV1)
2. ASSESSMENT OF SYMPTOMS
mMRC Score : measure of breathlessness
: relates to other measures of health status
: predicts future mortality risk
 Beyond dyspnea, comprehensive assessment is required
 Disease specific health status questionnaires used are:
• Chronic Respiratory Questionnaire (CRQ)
• St. George’s Respiratory Questionnaire (SGRQ)
• COPD Assessment Test (CAT)
• COPD Control Questionnaire (CCQ)
COPD ASSESSMENT TEST (CAT)
CUT OFF VALUE IS
10
CUT OFF VALUE IS 10
SGRQ
• Most widely documented comprehensive score with a
score of 25 as the threshold for considering regular
treatment.
• Score < 25 : uncommon in COPD diagnosed patients
• Score > 25 : uncommon in healthy population
3. ASSESSMENT OF EXACERBATION RISK
 Defined as acute worsening of symptoms that result in
additional therapy
 Classified as
• Mild - treated with Short acting bronchodilators (SABD)
• Moderate ( SABD + antibiotics and/or Oral Corticosteroids)
• Severe ( hospitalization or visits EMR)
 Best predictor of frequent exacerbations ( ≥2 episodes/year)
is history of earlier treated events
Other predictors:
 Deteriorating airflow limitation
 Blood eosinophil count
4. ASSESSMENT OF C0-MORBIDITIES
Assess common co-morbidities
Assess common risk factors ( smoking, alcohol, diet, inactivity)
Assess extra pulmonary effects of COPD ( weight loss, nutritional anomalies,
skeletal muscle dysfunction)
• Skeletal muscle dysfunction is characterized by : Sarcopenia (loss of cells) and
abnormal function of remaining cells
• Causes – inactivity, poor diet, inflammation, hypoxia
• Rectifiable source of exercise intolerance
COMBINED ASSESSMENT (REFINED
ABCD ASSESSMENT TOOL)
ROLE OF SPIROMETRY IN COPD
 Diagnosis
 Assessment of airflow obstruction severity (Prognosis)
 Follow up assessment
• Therapeutic decisions- Pharmacological (discrepancy
between spirometry and level of symptoms)
- Consider alternative diagnosis
- Non-pharmacological (interventional procedures)
• Identification of rapid decline
OTHER INVESTIGATIONS
Alpha-1 antitrypsin deficiency screening in:-
• Early onset emphysema (<45 years)
• Emphysema in a non-smoker
• Panacinar
• Necrotizing panniculitis ( Weber- Christian disease)
• c-ANCA positive vasculitis (e.g- Wegner’s granulomatosis)
• Family h/o early onset/ non smoker’s emphysema
• Bronchiectasis without other etiology
Imaging, Lung volumes, DLCO, ABG, exercise testing capacity and
biomarkers ( CRP, Procalcitonin) should also be assessed during
initial work up.
PROGNOSIS OF COPD
PREDICTORS OF POOR SURVIVAL
• Low FEV1
• Active smoking status
• Hypoxemia
• Resting tachycardia
• Poor nutrition
• Cor pulmonale
• Low exercise capacity
• Severe dyspnea
• Poor health related quality of life
• Anemia
• Frequent exacerbations
• Co-morbidities
• Low DLCO
• By BODE and ADO
BODE INDEX
• BMI
• Obstructive ventilatory defect
severity
• Dyspnea severity
• Exercise capacity
• >7 : 30% 2 year mortality
• 5-6 : 15% 2 year mortality
• <5 : less than 10% 2 year mortality
ADO INDEX
• Age
• Dyspnea
• Obstructive ventilatory defect
severity
• 0-10
• Each point increased in index is
associated with a 42% increase in
odds of death at 3 years
MANAGEMENT OF STABLE COPD
GOALS
Relieve symptoms
Improve exercise tolerance REDUCE SYMPTOMS
Improve health status
Prevent disease progression
Prevent and treat Exacerbations REDUCE RISK
Reduce mortality
MANAGEMENT OF STABLE COPD
DIAGNOSIS INITIAL
ASSESSMENT
INITIAL
MANAGEMENT
Smoking cessation
Vaccination
Active lifestyle and exercise
Initial pharmacotherapy
Self management
education
: risk factor management
: inhaler technique
: breathlessness
: written action plan
Manage co-morbidities
REVIEW
Symptoms (CAT or mMRC)
Exacerbations
Smoking status
Exposure to other risk factors
Inhaler technique and adherence
Physical activity and exercise
Need for pulmonary rehabilitation
Self management skills ( breathlessness,
written action plan)
Need for oxygen, NIV, lung volume
reduction, palliative approaches
Vaccination
Management of co-morbidities
Spirometry annually
ADJUST
PHARMACOLOGICAL TREATMENT OF STABLE
COPD- INITIATION
BROCHODILATORS-BETA AGONISTS
 Beta 2 adrenergic receptor stimulation  inc cAMP 
relaxes airway smooth muscles
 SABA
• 4-6 hours
• Regular and as needed, improves FEV1 and symptoms
• E.g- Levalbuterol, Salbutamol, Terbutaline
 LABA
• 12-24 hours
• Twice daily ( formoterol, salmetrol) improve FEV1, lung volumes, dyspnea, health status,
exacerbation rate
• Once daily ( indacaterol) improves breathlessness, health status, exacerbation rate
BROCHODILATORS-BETA AGONISTS
 Side Effects:-
• Resting sinus tachycardia
• Exaggerated somatic tremors
• Hypokalemia
• Increased oxygen consumption in patients with CHF
• Tachyphylaxis
• Fall in PaO2
• Cough after inhalation of indacaterol
BROCHODILATORS-ANTIMUSCARINIC
Block bronchoconstrictor effect of Ach on M3 receptors of airway
smooth muscle
SAMA
• Also blocks M2 inhibitory neuronal receptor (causes vagally induced broncho constriction)
• Has small benefit over SABA in terms of lung function, health status and requirement of oral
steroids
• E.g- Ipratropium, Oxitropium
LAMA
• Prolonged binding to M3 with faster dissociation from M2  prolong effect
• Improve symptoms, health status, effectiveness of pulmonary rehabilitation, red
exacerbations
• Eg- Tiotropium, aclidinium, glycopyrronium, umeclidinium
BROCHODILATORS-ANTI MUSCARINIC
Side Effects:-
• Dryness of mouth
• Bitter metallic taste with ipratropium
• Urinary retention, CVS events (Very less events)
BROCHODILATORS-METHYLXANTHINES
Non selective PDE inhibitors
E.g- theophylline
Modest bronchodilator effect with enhanced inspiratory
muscle function
BROCHODILATORS-METHYLXANTHINES
Side Effects:-
ANTI-INFLAMMATORY THERAPY
1.INHALED CORTICOSTEROIDS (ICS)
:- More effective when combined with long term bronchodilator therapy rather than the
individual components given alone
(ICS/LAMA/LABA or ICS/LABA or ICS/LAMA)
:- More effective in patients with exacerbation risk
:-E.g- Fluticasone, Beclomethasone
:-Withdrawal leads to FEV1 loss and increase in exacerbation frequency
Side Effects:-
• Oral candidiasis
• Hoarse voice
• Skin bruising
• Poor control of diabetes
• Cataract
• Mycobacterial infection
Side Effects:-
Pneumonia - Risk factors for developing pneumonia
• Smoker
• >55 years
• H/o prior exacerbation or pneumonia
• BMI < 25 kg/m²
• Poor MRC dyspnea grade/severe airflow limitation
FACTORS TO CONSIDER WHEN INITIATING ICS
STRONG
SUPPORT
CONSIDER USE AGAINST USE
• H/O hospitalization for
exacerbation of COPD (despite
appropriate long term
bronchodilator therapy)
• ≥2 moderate exacerbations of
COPD per year (despite
appropriate long term
bronchodilator therapy)
• Blood eosinophil > 300 cells/µL
• History of or concomitant
asthma
• 1 moderate exacerbation of
COPD per year (despite
appropriate long term
bronchodilator therapy)
• Blood eosinophil 100-300
cells/µL
• Repeated pneumonia events
• H/o mycobacterial infection
• Blood eosinophil <100 cells/µL
ANTI-INFLAMMATORY THERAPY
• ORAL CORTICOSTEROIDS
:- Less long term effect in stable COPD, more useful in acute exacerbations
:- Numerous side effects including steroid myopathy which contributes to muscle weakness,
decreased functionality and respiratory failure in very severe COPD patients
ANTI-INFLAMMATORY THERAPY
2. PHOSPHODIESTERASE-4-INHIBITORS(PDE-4)
:- Reduces inflammation by inhibiting breakdown of intracellular cAMP
:- Reduces moderate and severe exacerbations in patients with chronic bronchitis,
exacerbations in severe to very severe COPD
:- Effective in patients not controlled on LABA/ICS
:- E.g- Roflumilast (oral OD)
Side Effects:-
• Diarrhea, nausea, reduced appetite, abdominal pain
• Weight loss
• Sleep disturbance
• Headache
• Used cautiously in patients suffering from depression
ANTI-INFLAMMATORY THERAPY
3.ANTIBIOTICS
:- Azithromycin (250 mg/day or 500 mg three times a week)
:- Erythromycin (500 mg/day BD) x 1 year (reduces the risk in patients prone to exacerbation)
:- S/E Azithromycin- bacterial resistance, QTc prolongation, impaired hearing test
ANTI-INFLAMMATORY THERAPY
4.MUCOLYTICS and ANTIOXIDANTS
:- Regular treatment with erdosteine, carbocysteine and N-acetyl cysteine reduces
exacerbations and improves health status
5. OTHER DRUGS
:-Anti IL-5 Monoclonal Ab - Mepolizumab
:- Anti IL-5 Receptor Alpha Ab- Benralizumab
:- Statins (simvastatin) given to patients suffering from cardiac disease with COPD may
show improvement but it is not an indicated therapy.
:- Vitamin D given to patients suffering from Vitamin D deficiency with COPD may
show improvement.
OTHER DRUGS
 During influenza epidemic-
Neuraminidase inhibitors ( oral - zanamavir, oseltamivir,
inj-peramivir) can minimize infection if taken < 48 hours of
onset
 Replacement therapy of alpha 1 antitrypsin ( 60 mg/kg iv
weekly)
EFFECTIVE INHALATION THERAPY
• Inhalational devices include nebulizers,MDI,DPI.
• Particle size >5 um are deposited in oropharynx.
• 2-5 um or < 2um are deposited in lower respiratory tract.
• Importance of education and training for inhaler device technique is very
important.
• Essential to provide instructions and demonstrate proper inhalation
techniques when prescribing the device.
• “Teach back approach” is important.
• Choice of inhaler device has to be individually tailored and depends on access
, cost, prescriber and patient’s ability and preference.
• Determinants of poor inhaler techniques –
 Lack of education about inhaler techniques
 Older age
 Use of multiple devices
NON-PHARMACOLOGICAL TREATMENT OF
STABLE COPD
PATIENT GROUP ESSENTIAL RECOMMENDED DEPENDING ON
LOCAL GUIDELINES
A SMOKING CESSATION PHYSICAL ACTIVITY VACCINATION
B,C,D SMOKING CESSATION
PULMONARY REHABILITATION
PHYSICAL ACTIVITY VACCINATION
IDENTIFY AND REDUCE EXPOSURE TO RISK
FACTORS
 Tobacco smoke
• Smoking cessation has the greatest capacity to influence the natural history of COPD
• Five step program for intervention provides a strategic framework
1. ASK (Identify smokers)
2. ADVISE (To quit)
3. ASSESS (Willingness to quit)
4. ASSIST (Counseling and pharmacotherapy)
5. ARRANGE (follow up visits)
• Pharmacotherapies for smoking cessation
1. Nicotine Replacement Products
:-Nicotine gum, inhaler, nasal spray, transdermal patch, sublingual tablet, lozenges
:- C/I are recent MI, stroke
:- Should be started 2 weeks after occurrence of a cardiovascular event
:- S/E are nausea
2. Other drugs
:- Varenicline
:- Bupropion
:- Clonidine
:- Nortriptyline
Nicotine withdrawal Symptoms (DSM IV)
 :- Dysphoric or depressed mood
 :- Insomnia
 :- Irritability, frustration or anger
 :- Anxiety
 :- Difficulty concentrating
 :- Restlessness
 :- Decreased heart rate
 :- Increased appetite or weight gain
 Indoor and outdoor air pollution
• Efficient ventilation, non-polluting cooking stoves
 Occupational exposures
• Avoid exposures to potential irritants
VACCINATION
 INFLUENZA
• Reduce LRTI, exacerbations and deaths in COPD
• More effective in elderly
 PNEUMOCOCCAL
• PPSV23 reduces exacerbations, CAP in patients < 65 yrs with FEV1< 40% and
co-morbidities
• PCV 13 is given in > 65 yrs , significant efficacy in reducing bacteremia and
serious invasive pneumococcal disease
EDUCATION
Patient education topics for COPD
• Risk factors
• Smoking cessation
• Reduction of noxious environmental exposures
• Immunization
• Respiratory hygiene
• Nature and prognosis
• Indication, benefits and s/e drugs
• Proper inhaler and nebulizer use
• Strategies to improve adherence to treatment
• Pulmonary rehabilitation programs
SELF MANAGEMENT
• Structured, personalized multi-component map with
goals of motivating, engaging and supporting the
patient and develop skills to better manage the
disease on day to day basis
• Written action plan
PULMONARY REHABILITATION
• Group B,C and D
• Improves health status, dyspnea and exercise
intolerance in patients.
• Leads to reduction in symptoms of anxiety and
depression.
• Reduces hospitalization among patients who had
recent exacerbations.
• Supervised exercise training (twice weekly)
PRESCRIPTION OF SUPPLEMENTAL OXYGEN TO COPD
PATIENTS
• Relieves dyspnea
• Increases survival in
patients with severe
resting hypoxemia
VENTILATORY SUPPORT IN STABLE PATIENT
• NPPV improves survival in recently hospitalized patients
particularly in those who have pronounced day time persistent
hypercapnia ( PaCo2 > 53 mmHg)
• CPAP in patients with COPD with OSA improves survival and risk of
hospital administration
INTERVENTIONAL THERAPY IN STABLE COPD
THERAPY DESCRIPTION
LUNG VOLUME REDUCTION SURGERY ( LVRS) Improves survival in severe emphysema patients with
upper lobe emphysema and low post rehabilitation
exercise capacity
BULLECTOMY Helps to decrease dyspnea, improved lung function
and exercise tolerance in large bullae formation
TRANSPLANTATION Improves quality of life and functional capacity in
appropriately selected patients.
BRONCHOSCOPIC INTERVENTIONS Reduce end expiratory lung volume
Improves exercise tolerance and lung function 6-12
post treatment
Include- endobronchial valves, lung coils, vapor
ablation
PALLIATIVE CARE
• DYSPNEA- Opiates, Neuromuscular electrical stimulation (NMES), Chest
wall vibration and fans blowing air onto the face.
NIV can reduce daytime breathlessness
• NUTRITIONAL SUPPORT- Low BMI and Low fat free mass have poor
outcome . Improve nutrition and add Antioxidants ( Vit C,E, Zn, Se)
• PANIC,ANXIETY, DEPRESSION- CBT and mind body interventions (yoga etc)
• FATIGUE- Self management, pulmonary rehabilitation , physical activity
MANAGEMENT CYCLE
REVIEW:-
SYMPTOMS AND
EXACERBATIONS
ASSESS:-
INHALER TECHNIQUE AND
ADHERENCE
NON-PHARMACOLOGICAL
APPROACHES
ADJUST:-
ESCALATE
SWITCH INHALER DEVICE OR
MOLECULES
DE-ESCALATE
THANK YOU !

Assessment and management of stable copd

  • 1.
    ASSESSMENT AND MANAGEMENTOF STABLE COPD PRESENTOR-DR RASHI VOHRA MODERATOR- DR JAGDISH RAWAT
  • 2.
    GOALS OF ASSESSMENT Inorder to eventually guide therapy, goals of assessment are ascertained as follows : Determine level of airflow limitation Impact on patient’s health status Risk of future events (exacerbations, hospital admissions, death)
  • 3.
    GOALS OF ASSESSMENT Inorder to achieve these goals, we have to consider:- Presence and severity of spirometry abnormalities Current nature and magnitude of patient’s symptoms History of moderate and severe exacerbations and future risk Presence of co-morbidities
  • 4.
    1. CLASSIFICATION OFAIRFLOW LIMITATION SEVERITY (BASED ON POST BRONCHODILATOR-FEV1)
  • 5.
    2. ASSESSMENT OFSYMPTOMS mMRC Score : measure of breathlessness : relates to other measures of health status : predicts future mortality risk
  • 6.
     Beyond dyspnea,comprehensive assessment is required  Disease specific health status questionnaires used are: • Chronic Respiratory Questionnaire (CRQ) • St. George’s Respiratory Questionnaire (SGRQ) • COPD Assessment Test (CAT) • COPD Control Questionnaire (CCQ)
  • 7.
    COPD ASSESSMENT TEST(CAT) CUT OFF VALUE IS 10 CUT OFF VALUE IS 10
  • 9.
    SGRQ • Most widelydocumented comprehensive score with a score of 25 as the threshold for considering regular treatment. • Score < 25 : uncommon in COPD diagnosed patients • Score > 25 : uncommon in healthy population
  • 10.
    3. ASSESSMENT OFEXACERBATION RISK  Defined as acute worsening of symptoms that result in additional therapy  Classified as • Mild - treated with Short acting bronchodilators (SABD) • Moderate ( SABD + antibiotics and/or Oral Corticosteroids) • Severe ( hospitalization or visits EMR)
  • 11.
     Best predictorof frequent exacerbations ( ≥2 episodes/year) is history of earlier treated events Other predictors:  Deteriorating airflow limitation  Blood eosinophil count
  • 12.
    4. ASSESSMENT OFC0-MORBIDITIES Assess common co-morbidities Assess common risk factors ( smoking, alcohol, diet, inactivity) Assess extra pulmonary effects of COPD ( weight loss, nutritional anomalies, skeletal muscle dysfunction) • Skeletal muscle dysfunction is characterized by : Sarcopenia (loss of cells) and abnormal function of remaining cells • Causes – inactivity, poor diet, inflammation, hypoxia • Rectifiable source of exercise intolerance
  • 13.
  • 14.
    ROLE OF SPIROMETRYIN COPD  Diagnosis  Assessment of airflow obstruction severity (Prognosis)  Follow up assessment • Therapeutic decisions- Pharmacological (discrepancy between spirometry and level of symptoms) - Consider alternative diagnosis - Non-pharmacological (interventional procedures) • Identification of rapid decline
  • 15.
    OTHER INVESTIGATIONS Alpha-1 antitrypsindeficiency screening in:- • Early onset emphysema (<45 years) • Emphysema in a non-smoker • Panacinar • Necrotizing panniculitis ( Weber- Christian disease) • c-ANCA positive vasculitis (e.g- Wegner’s granulomatosis) • Family h/o early onset/ non smoker’s emphysema • Bronchiectasis without other etiology Imaging, Lung volumes, DLCO, ABG, exercise testing capacity and biomarkers ( CRP, Procalcitonin) should also be assessed during initial work up.
  • 16.
    PROGNOSIS OF COPD PREDICTORSOF POOR SURVIVAL • Low FEV1 • Active smoking status • Hypoxemia • Resting tachycardia • Poor nutrition • Cor pulmonale • Low exercise capacity • Severe dyspnea • Poor health related quality of life • Anemia • Frequent exacerbations • Co-morbidities • Low DLCO • By BODE and ADO
  • 17.
    BODE INDEX • BMI •Obstructive ventilatory defect severity • Dyspnea severity • Exercise capacity • >7 : 30% 2 year mortality • 5-6 : 15% 2 year mortality • <5 : less than 10% 2 year mortality
  • 18.
    ADO INDEX • Age •Dyspnea • Obstructive ventilatory defect severity • 0-10 • Each point increased in index is associated with a 42% increase in odds of death at 3 years
  • 19.
    MANAGEMENT OF STABLECOPD GOALS Relieve symptoms Improve exercise tolerance REDUCE SYMPTOMS Improve health status Prevent disease progression Prevent and treat Exacerbations REDUCE RISK Reduce mortality
  • 20.
    MANAGEMENT OF STABLECOPD DIAGNOSIS INITIAL ASSESSMENT INITIAL MANAGEMENT Smoking cessation Vaccination Active lifestyle and exercise Initial pharmacotherapy Self management education : risk factor management : inhaler technique : breathlessness : written action plan Manage co-morbidities REVIEW Symptoms (CAT or mMRC) Exacerbations Smoking status Exposure to other risk factors Inhaler technique and adherence Physical activity and exercise Need for pulmonary rehabilitation Self management skills ( breathlessness, written action plan) Need for oxygen, NIV, lung volume reduction, palliative approaches Vaccination Management of co-morbidities Spirometry annually ADJUST
  • 21.
    PHARMACOLOGICAL TREATMENT OFSTABLE COPD- INITIATION
  • 22.
    BROCHODILATORS-BETA AGONISTS  Beta2 adrenergic receptor stimulation  inc cAMP  relaxes airway smooth muscles  SABA • 4-6 hours • Regular and as needed, improves FEV1 and symptoms • E.g- Levalbuterol, Salbutamol, Terbutaline  LABA • 12-24 hours • Twice daily ( formoterol, salmetrol) improve FEV1, lung volumes, dyspnea, health status, exacerbation rate • Once daily ( indacaterol) improves breathlessness, health status, exacerbation rate
  • 23.
    BROCHODILATORS-BETA AGONISTS  SideEffects:- • Resting sinus tachycardia • Exaggerated somatic tremors • Hypokalemia • Increased oxygen consumption in patients with CHF • Tachyphylaxis • Fall in PaO2 • Cough after inhalation of indacaterol
  • 24.
    BROCHODILATORS-ANTIMUSCARINIC Block bronchoconstrictor effectof Ach on M3 receptors of airway smooth muscle SAMA • Also blocks M2 inhibitory neuronal receptor (causes vagally induced broncho constriction) • Has small benefit over SABA in terms of lung function, health status and requirement of oral steroids • E.g- Ipratropium, Oxitropium LAMA • Prolonged binding to M3 with faster dissociation from M2  prolong effect • Improve symptoms, health status, effectiveness of pulmonary rehabilitation, red exacerbations • Eg- Tiotropium, aclidinium, glycopyrronium, umeclidinium
  • 25.
    BROCHODILATORS-ANTI MUSCARINIC Side Effects:- •Dryness of mouth • Bitter metallic taste with ipratropium • Urinary retention, CVS events (Very less events)
  • 26.
    BROCHODILATORS-METHYLXANTHINES Non selective PDEinhibitors E.g- theophylline Modest bronchodilator effect with enhanced inspiratory muscle function
  • 27.
  • 28.
    ANTI-INFLAMMATORY THERAPY 1.INHALED CORTICOSTEROIDS(ICS) :- More effective when combined with long term bronchodilator therapy rather than the individual components given alone (ICS/LAMA/LABA or ICS/LABA or ICS/LAMA) :- More effective in patients with exacerbation risk :-E.g- Fluticasone, Beclomethasone :-Withdrawal leads to FEV1 loss and increase in exacerbation frequency
  • 29.
    Side Effects:- • Oralcandidiasis • Hoarse voice • Skin bruising • Poor control of diabetes • Cataract • Mycobacterial infection
  • 30.
    Side Effects:- Pneumonia -Risk factors for developing pneumonia • Smoker • >55 years • H/o prior exacerbation or pneumonia • BMI < 25 kg/m² • Poor MRC dyspnea grade/severe airflow limitation
  • 31.
    FACTORS TO CONSIDERWHEN INITIATING ICS STRONG SUPPORT CONSIDER USE AGAINST USE • H/O hospitalization for exacerbation of COPD (despite appropriate long term bronchodilator therapy) • ≥2 moderate exacerbations of COPD per year (despite appropriate long term bronchodilator therapy) • Blood eosinophil > 300 cells/µL • History of or concomitant asthma • 1 moderate exacerbation of COPD per year (despite appropriate long term bronchodilator therapy) • Blood eosinophil 100-300 cells/µL • Repeated pneumonia events • H/o mycobacterial infection • Blood eosinophil <100 cells/µL
  • 32.
    ANTI-INFLAMMATORY THERAPY • ORALCORTICOSTEROIDS :- Less long term effect in stable COPD, more useful in acute exacerbations :- Numerous side effects including steroid myopathy which contributes to muscle weakness, decreased functionality and respiratory failure in very severe COPD patients
  • 33.
    ANTI-INFLAMMATORY THERAPY 2. PHOSPHODIESTERASE-4-INHIBITORS(PDE-4) :-Reduces inflammation by inhibiting breakdown of intracellular cAMP :- Reduces moderate and severe exacerbations in patients with chronic bronchitis, exacerbations in severe to very severe COPD :- Effective in patients not controlled on LABA/ICS :- E.g- Roflumilast (oral OD)
  • 34.
    Side Effects:- • Diarrhea,nausea, reduced appetite, abdominal pain • Weight loss • Sleep disturbance • Headache • Used cautiously in patients suffering from depression
  • 35.
    ANTI-INFLAMMATORY THERAPY 3.ANTIBIOTICS :- Azithromycin(250 mg/day or 500 mg three times a week) :- Erythromycin (500 mg/day BD) x 1 year (reduces the risk in patients prone to exacerbation) :- S/E Azithromycin- bacterial resistance, QTc prolongation, impaired hearing test
  • 36.
    ANTI-INFLAMMATORY THERAPY 4.MUCOLYTICS andANTIOXIDANTS :- Regular treatment with erdosteine, carbocysteine and N-acetyl cysteine reduces exacerbations and improves health status 5. OTHER DRUGS :-Anti IL-5 Monoclonal Ab - Mepolizumab :- Anti IL-5 Receptor Alpha Ab- Benralizumab :- Statins (simvastatin) given to patients suffering from cardiac disease with COPD may show improvement but it is not an indicated therapy. :- Vitamin D given to patients suffering from Vitamin D deficiency with COPD may show improvement.
  • 37.
    OTHER DRUGS  Duringinfluenza epidemic- Neuraminidase inhibitors ( oral - zanamavir, oseltamivir, inj-peramivir) can minimize infection if taken < 48 hours of onset  Replacement therapy of alpha 1 antitrypsin ( 60 mg/kg iv weekly)
  • 38.
    EFFECTIVE INHALATION THERAPY •Inhalational devices include nebulizers,MDI,DPI. • Particle size >5 um are deposited in oropharynx. • 2-5 um or < 2um are deposited in lower respiratory tract. • Importance of education and training for inhaler device technique is very important. • Essential to provide instructions and demonstrate proper inhalation techniques when prescribing the device. • “Teach back approach” is important. • Choice of inhaler device has to be individually tailored and depends on access , cost, prescriber and patient’s ability and preference. • Determinants of poor inhaler techniques –  Lack of education about inhaler techniques  Older age  Use of multiple devices
  • 40.
    NON-PHARMACOLOGICAL TREATMENT OF STABLECOPD PATIENT GROUP ESSENTIAL RECOMMENDED DEPENDING ON LOCAL GUIDELINES A SMOKING CESSATION PHYSICAL ACTIVITY VACCINATION B,C,D SMOKING CESSATION PULMONARY REHABILITATION PHYSICAL ACTIVITY VACCINATION
  • 41.
    IDENTIFY AND REDUCEEXPOSURE TO RISK FACTORS  Tobacco smoke • Smoking cessation has the greatest capacity to influence the natural history of COPD • Five step program for intervention provides a strategic framework 1. ASK (Identify smokers) 2. ADVISE (To quit) 3. ASSESS (Willingness to quit) 4. ASSIST (Counseling and pharmacotherapy) 5. ARRANGE (follow up visits)
  • 42.
    • Pharmacotherapies forsmoking cessation 1. Nicotine Replacement Products :-Nicotine gum, inhaler, nasal spray, transdermal patch, sublingual tablet, lozenges :- C/I are recent MI, stroke :- Should be started 2 weeks after occurrence of a cardiovascular event :- S/E are nausea 2. Other drugs :- Varenicline :- Bupropion :- Clonidine :- Nortriptyline
  • 43.
    Nicotine withdrawal Symptoms(DSM IV)  :- Dysphoric or depressed mood  :- Insomnia  :- Irritability, frustration or anger  :- Anxiety  :- Difficulty concentrating  :- Restlessness  :- Decreased heart rate  :- Increased appetite or weight gain
  • 44.
     Indoor andoutdoor air pollution • Efficient ventilation, non-polluting cooking stoves  Occupational exposures • Avoid exposures to potential irritants
  • 45.
    VACCINATION  INFLUENZA • ReduceLRTI, exacerbations and deaths in COPD • More effective in elderly  PNEUMOCOCCAL • PPSV23 reduces exacerbations, CAP in patients < 65 yrs with FEV1< 40% and co-morbidities • PCV 13 is given in > 65 yrs , significant efficacy in reducing bacteremia and serious invasive pneumococcal disease
  • 46.
    EDUCATION Patient education topicsfor COPD • Risk factors • Smoking cessation • Reduction of noxious environmental exposures • Immunization • Respiratory hygiene • Nature and prognosis • Indication, benefits and s/e drugs • Proper inhaler and nebulizer use • Strategies to improve adherence to treatment • Pulmonary rehabilitation programs
  • 47.
    SELF MANAGEMENT • Structured,personalized multi-component map with goals of motivating, engaging and supporting the patient and develop skills to better manage the disease on day to day basis • Written action plan
  • 49.
    PULMONARY REHABILITATION • GroupB,C and D • Improves health status, dyspnea and exercise intolerance in patients. • Leads to reduction in symptoms of anxiety and depression. • Reduces hospitalization among patients who had recent exacerbations. • Supervised exercise training (twice weekly)
  • 50.
    PRESCRIPTION OF SUPPLEMENTALOXYGEN TO COPD PATIENTS • Relieves dyspnea • Increases survival in patients with severe resting hypoxemia
  • 51.
    VENTILATORY SUPPORT INSTABLE PATIENT • NPPV improves survival in recently hospitalized patients particularly in those who have pronounced day time persistent hypercapnia ( PaCo2 > 53 mmHg) • CPAP in patients with COPD with OSA improves survival and risk of hospital administration
  • 52.
    INTERVENTIONAL THERAPY INSTABLE COPD THERAPY DESCRIPTION LUNG VOLUME REDUCTION SURGERY ( LVRS) Improves survival in severe emphysema patients with upper lobe emphysema and low post rehabilitation exercise capacity BULLECTOMY Helps to decrease dyspnea, improved lung function and exercise tolerance in large bullae formation TRANSPLANTATION Improves quality of life and functional capacity in appropriately selected patients. BRONCHOSCOPIC INTERVENTIONS Reduce end expiratory lung volume Improves exercise tolerance and lung function 6-12 post treatment Include- endobronchial valves, lung coils, vapor ablation
  • 53.
    PALLIATIVE CARE • DYSPNEA-Opiates, Neuromuscular electrical stimulation (NMES), Chest wall vibration and fans blowing air onto the face. NIV can reduce daytime breathlessness • NUTRITIONAL SUPPORT- Low BMI and Low fat free mass have poor outcome . Improve nutrition and add Antioxidants ( Vit C,E, Zn, Se) • PANIC,ANXIETY, DEPRESSION- CBT and mind body interventions (yoga etc) • FATIGUE- Self management, pulmonary rehabilitation , physical activity
  • 54.
    MANAGEMENT CYCLE REVIEW:- SYMPTOMS AND EXACERBATIONS ASSESS:- INHALERTECHNIQUE AND ADHERENCE NON-PHARMACOLOGICAL APPROACHES ADJUST:- ESCALATE SWITCH INHALER DEVICE OR MOLECULES DE-ESCALATE
  • 55.