MEDICAL AND SURGICAL MANAGEMENT OF COPD (GOLD 2016-2017)

BY DR.YOGENDRA RATHORE

09/01/2017

THERAPEUTIC OPTIONS 1)SMOKING CESSATION 2)PHARMACOLOGICAL THERAPY 3)NON-PHARMACOLOGICAL THERAPY

(1)SMOKING CESSATION Smoking cessation is the intervention. If effective resources and time are

dedicated to smoking cessation,25% long term quit rates can be achieved.

PHARMACOTHERAPIES FOR SMOKING CESSATION1. Nicotine replacement products-nicotine

gum,inhaler,nasal spray,transdermal patch,sublingual tablets or lozenge.

Contraindications-a)unstable CAD b)untreated peptic

ulcer disease c)recent M.I d)recent stroke. acidic beverages(coffee,juices,soft drink)

interfere with the obsorption of nicotine.

Other Pharmacologic drugs –1. varenicline2. Bupropion3. Nortriptyline

Used as supportive intervention quit rate at one year-a)for bupropion

30% b)for bupropion plus nicotine patch 40% c)for counseling(3 min) 5-10% d)nicotine replacement therapy 35%

BRIEF STRATEGIES TO HELP THE PATIENT WILLING TO QUIT1. ASK - Systematically identify all tobacco

users at every visit.2. ADVISE – Strongly urge all tobacco users to

quit in a clear, strong, and personalized manner.

3. ASSESS – Determine willingness to make a quit attempt.

4. ASSIST – Helps the patient in quitting by providing practical counseling,intra treatment social support and extra treatment social support.

5. ARRANGE- Schedule followup contact either in person or via telephone.

(2)PHARMACOLOGIC THERAPY Used to reduce symptoms,reduce the

frequency and severity of exacerbations and improve health status and exercise tolerance.

CLASSES OF MEDICATIONS Βeta2-agonists Anticholinergics Methylxanthines Inhaled corticosteroids Systemic corticosteroids Phosphodiesterase 4 inhibitors others

The choice within each class depends on the availability and cost of medication and patient response.

When treatment is given by the inhaled route,attention to effective drug delivery and training in inhaler technique is essential.

The choice of inhaler device will depend on availability,cost,the prescribing physician and the skill and ability of the patient.

COPD patient may have problems with coordination and find it hard to use a metered dose inhaler(MDI).It is essential to ensure that inhaler technique is correct and re check this at each visit.

Particle deposition from DPI will tend to be more central with the fixed airflow limitation and lower inspiratory flow rates in COPD.

Many drugs are available as nebulizer solutions for patient who are severely overinflated and consequently may have very low inspiratory flow rates.

Nebulized treatment should only be continued if the patient reports clear symptomatic benefit that cannot be achieved by simpler,cheaper and more portable alternatives.

BETA2-AGONIST Mechanism of action-drug act on beta2

receptor(G protein couple receptor) increase adenyl cyclase increase CAMP activate protein kinase A relaxation of smoth musle

Short acting-salbutamol,terbutaline Long acting-salmeterol,formoterol Ultra long acting-indacaterol,olodaterol, tulobuterol

Short acting-T ½ -4 to 6 hours. Doses- Salbutalmol-100/200μg in

MDI/DPI qid ,5mg IN nebulization. terbutaline-400μg DPI,also s.c. Long acting-T ½-12 hours. dose-formoterol-6,12μg in MDI/DPI bd, 15 μg IN nebulization. salmeterol-25,50 μg in MDI/DPI bd.

Ultra long acting-T ½ -24 hours. dose-indacaterol-75-300 μg DPI od.

beta2 agonist significantly improve FEV1 and lung volume,dyspnea

health related quality of life and exacerbation rate.

No effect on mortality and rate of decline of lung function.

ADVERSE EFFECTS.1. Resting sinus tachycardia2. Tremor3. Hypokalemia(especially when treated

with thiazide diuretics)4. Hyperglycemia.

ANTICHOLINERGICS MECHANISM OF ACTION-blockage of

acetylcholine effect on muscarinic receptors (M2 and M3).

But Tiotropium is M3 and M1antagoinst. The bronchodilating effect of short

acting inhaled anticholinergics last longer than of short acting beta2 agonist.

Short acting –oxitropium bromide ipratropium bromide .

Long acting-tiotropium glycopyrronium bromide.

Short acting-T ½ -6 to 8 hours. ipratropium bromide- dose-20-40μg MDI/DPI QID. 250-500μg Nebulizer. oxitropium bromide- dose-100μg MDI QID. 1500μg Nebulizer.

Long acting-T ½ -24 hours. tiotropium- dose-9-18μg od. glycopyrronium bromide- dose-50μg DPI od.

Long acting anticholinergics reduces exacerbations andhospitalizations,improves symptoms, health status and improves the effectiveness of pulmonary rehabilitation.

No effect on rate of lung function decline.

Some study shows tiotropium is superior to salmeterol in reducingexacerbation.

ADVERSE EFFECTS Dryness of mouth Bitter,metallic taste Acute glaucoma-use of solution with

face mask put direct effect on eye. Urine retention

METHYLXANTHINES Mechanism of action- 1)nonselective phosphodiesterase inhibitors

bronchodilation(ATP CAMP 5AMP) 2)stimulate histone deacetylase enzyme-

antiinflammatory via decrease inflammatory gene expression.

Drug-1)theophylline 2)aminophylline 3)new drug-acebrophylline and doxofylline

Theophylline -T ½variable,upto 24 hours dose-100-600mg oral and iv tds.

Aminophylline- T ½variable,upto 24 hours.

loading dose-5-6mg/kg in 100ml NS over 30 min.

maintance dose-nonsmoker- .7mg/kg/hr smoker-.9mg/kg/hr

FUNCTION Bronchodilation Anti inflammatory Diaphragm activity increase Mild diuretic Central respiratory stimulator

Theophylline is less effective and less well tolerated than inhaled long acting bronchodilators and is not recommended if those drugs are available and affordable.

Low dose theophylline reduces exacerbations but does not improve post bronchodilator lung function.

ADVERSE EFFECTS Narrow therapeutic ratio Most of the benefit occurs only when

near toxic doses are given. Plasma level should be between 5-

10mg/l. If >15mg/l , show zero order reaction accumulation toxicity

A/E when >10mg/l range1.Hypotension2. Reflex tachycardia3.Headache 4.Insomnia5.Nausea and vomiting6.Heart burn >15mg/l-atrial andventricular arrhythmia >20mg/l-grand mal convulsions >30mg/l-respiratory suppression-death

INHALED CORTICOSTEROIDS Mechanism of action-stimulate histone

deactylase enzyme decrease inflammatory gene expression anti inflammatory effect.

eg beclomethasone budesonide fluticasone

Regular treatment with inhaled steroids improves symptoms,lung function,quality of life and reduces the frequency of exacerbations in COPD patients with an FEV1 <60% predicted.

Regular treatment with inhaled steroids does not modify the long term decline of FEV1 nor mortality in patient with COPD.

Budesonide- dose-100/200/400μg DPI BD 250/500μg nebulizer

Beclomethasone- dose-100/200/400μg DPI/MDI BD 200/400μg nebulizer

Fluticasone- dose-250/500 μg DPI/MDI BD 500 μg nebulizer

ADVERSE EFFECTS Oral fungal infection Hoarse voice Skin bruising Increase risk of pneumonia

SYSTEMIC CORTICOSTEROIDS Use in acute exacerbation shows

improve symptoms,lung function,reduce rate of treatment failure and shorten length of hospital stay.

Not in stable COPD for maintenance Eg – hydrocortisone- 100mg iv tds prednisone- 10-60mg od methyl prednisolone- 4/8/16mg od dexamethasone- 8/16mg iv bd

ADVERSE EFFECTS Musle weakness Central obesity Osteoporosis and hypocalcemia Thinning of skin Hypertension Psychosis Cataract Increase water retension

PHOSPHODIESTERASE 4 INHIBITORS Mechanism of action-anti inflammatory and

bronchodilator action via inhibiting of the breakdown of intracellular cyclic AMP.

Reduce moderate and severe exacerbations

Use in severe to very severeCOPD and history of exacerbations.

Should always be used in combination with at least one long acting bronchodilator.

Roflumilast and theophylline should not be given together.

Roflumilast Cilomilast Tofimilast

Roflumilast- T ½-24 hr dose-250/500mg od

ADVERSE EFFECTS Nausea Reduced appetite Abdominal pain Diarrhea Sleep disturbances Headache Weight loss(avoid in underweigt

patient ) depression

OTHER PHARMACOLOGY TREATMENTS Vaccines Alpha 1 antitrypsin augmentation

therapy Antibiotics Mucolytic and antioxidant agents Immunoregulators Antitussives Vasodilators Narcotics others

VACCINES1)influenza vaccine-can reduce serious

illness,hospitalization and death in COPD patient.

Vaccines cantaining killed,live and inactivated viruses are recommended.

More effective in elderly patient with COPD and decrease risk of ischemic heart disease.

DOSE-.5ml sc/im,given once each year.

2)Pneumococcal vaccines-a)PCV 13- >65year old b)PPSV 23- <65year old

Recommended for COPD patients 65 years and old and also in younger patients with significant comorbid condition such as cardic disease.

It reduce the incidence of CAP in COPD patient younger than age 65 with FEVI <40%.

Dose-.5ml im/sc age >19 with asthma,bronchiectasis, copd one dose of ppsv

23 followed by one dose of pcv13 at 65 year.

age >65 with copd one dose of pcv13 followed by a dose of ppsv23 after first dose of pcv 13.

NON-PHARMACOLOGY THERAPIES Rehabilitation Oxygen therapy Ventilatory support Surgical treatment

OXYGEN THERAPY The long term oxygen (>15 hr per day)

indicated for1. PaO2 at or below 55mmhg or SpO2at

or below 88% with or without hypercapnia confirmed twice over a three week period.

2. PaO2 between 55 and 60mmhg with evidence of PAH ,peripheral edema,CHF or polycythemia.

Air travel is safe for most patient with chronic respiratory failure who are on LTOT.

Patient should be maintain an in-flight PaO2 of atleast 50mmhg,this can be achieved at 3L/min oxygen by nasal cannulae or 31%by venturi mask.

Those with a resting PaO2 at sea level >70mmhg are likely to be safe to fly with out supplementary oxygen.

VENTILATORY SUPPORT

SURGICAL TREATMENT Lung volume reduction surgery(LVRS) Bronchoscopic lung volume

reduction(BLVR) Bullectomy Lung transplantation

LVRS Parts of lung are resected to reduce hyperinflation,making

respiratory muscles more effective pressure generators by improving their mechanical efficiency.

LVRS increase the elastic recoil pressure of the lung and thus improves expiratory flow rates and reduces exacerbations.

The advantage of surgery in patient with predominantly upper lobe emphysema and low exercise capacity.

LVRS shows higher mortality than medical management in severe emphysema patient with an FEV1 <20% and homogeneous emphysema on HRCT or a Dlco <20% predicted.

BLVR Copd patient with severe airflow

limitation(FEV1<50%),heterogenous emphysema on HRCT and hyperinflation lung(TLC>100%and RV>150%predicted)

EBV,LVRC

Improve lung function,exercise tolerance and reduce symptoms.

Side effect-exacerbation frequency increase,pneumonia and Hemoptysis.

BULLECTOMY Bullous emphysema

Removal of a large bulla that does not contribute to gas exchange decompresses the adjacent lung parenchyma.

Effective for reduce dyspnea and improving lung function.

LUNG TRANSPLANTATION Criteria –BODE index 7-10 and at least

one of the following;-1. History of exacerbation associated

with acute hypercapnia(>50mmhg)2. PAH3. Cor pulmonales4. FEV1<20% with Dlco <20%5. Homogenous distribution of

emphysema

Improve quality of life and functional capacity.

Complications-1. Acute rejection2. Bronchiolitis obliterans3. Opportunistic infections4. Lymphoproliferative disease5. Post operative mortality

ADAVANCED COPD

Emphsema with severe hyperinfaltion Not candidate for bullectomy,BLVR,LVR

S

bullectom

y

Heterogeneous

emphysema

Homogenous

emphysema

No Collateral ventilation

Collateral ventilation present

LVRSBLVR(EBV,LVRC)

LVRSBLVR

(LVRC)

Lung transplan

t

No collateral ventilatio

n

Collateral ventilation present

BLVR(EBV,LV

RC)BLVR

(LVRC)

Large bulla

No large bulla

MANAGEMENT OF STABLE COPD Non-pharmacologic treatment

pharmacologic treatment

Goal of treatment-1. Reduce symptoms-relieve symptoms, improve exercise tolerance, improve health status

2. Ruduce future risk-prevent disease progression , prevent and treat exacerbations , reduce mortality.

Identification and reduction of exposure to risk factors are important in treatment and prevention of COPD.

Smoking cessation should be encouraged for all individuals who smoke.

Reduction of total personal exposure to occupational dusts,fumes,and gases and to indoor and outdoor air pollutants may be more difficult but should be attempted for reduce the prevalence of COPD.

Efficient ventilation,non polluting cooking stoves,use of flues,and similar interventions are feasible and should be recommended.

In previously,COPD treatment recommendations were based on spirometry only.

FEV1 alone is a poor descriptor of disease status and for this reason the treatment strategy for stable COPD should also consider an individual patients symptoms and future risk of exacerbations.

MODEL OF SYMPTOM/RISK OF EVALUATION OF COPD

NON-PHARMACOLOGIC TREATMENT

gp Essential recommend other

A Smoking cessation phycial activity vaccine

B-D Smoking cessation phycial activity vaccine + Pulmonary rehabi litation

PHARMACOLOGIC MANAGEMENT OF COPD

MANAGEMENT OF EXACERBATION Defination-worsening of the patients

respiratory symptoms(baseline dyspnea,cough,sputum production) that is beyond normal day to day variations and leads to a change in medication.

Mortality rate for a hypercapnic exacerbation with acidosis-

at hospital 10% 1 year after discharge 40% 3 year after discharge 49%

Cause of exacerbation-1. Respiratory tract

infections(viral,bacterial)-m/c cause2. Peak of air pollution.3. Unkown in 1/3rd patient.

Hemophilus influenzae,streptococcus pneumoniae ,moraxella catarrhalis and pseudomonas aeruginosa is most common bacteria involved in an exacerbation.

Condition that mimic exacerbation-1. Pneumonia2. Pulmonary embolism3. CHF4. Pneumothorax5. Large pleural effusion

Sign of severity in assessment of COPD exacerbations-

1. Use of accessory respiratory muscle2. Paradoxical chest wall movements3. Worsening or new onset central

cyanosis4. Development of peripheral edema5. Hemodynamic instability6. Deteriorated mental status

Goal- minimize the impact of current exacerbation and prevent the development of subsequent exacerbations.

INDICATIONS FOR HOSPITAL ADMISSION Sudden development of resting dyspnea Severe underlying COPD Cynosis and peripheral edema Failure of an exacerbation to respond to

initial medical management Presence of serious comorbidities Frequent exacerbations Older age Insufficient home support

Factors associated with poor outcome(high five year mortality rate)-

1. Old age2. Low BMI3. Comorbidities4. Frequent exacerbation5. Need for LTOT6. Very severe respiratory symptom7. Poor quality of life8. Worse lung function9. Lower exercise capacity10. Lower lung density11. Thickened bronchial wall on ct scan

THERAPEUTIC COMPONENTS OF HOSPITAL MANAGEMENT Pharmacologic treatment1. Bronchodilator2. Corticosteroids3. Antibiotics4. Adjuent therapy

Respiratory support1. Oxygen thrapy2. Ventilatory support NIV Invasive

PHARMACOLOGIC TREATMENT SHORT ACTING BRONCHODILATORS-1. Short acting inhaled beta2 agoinsts

with or without short acting anticholinergics are preferred bronchodilators.

2. Iv methylxanthines are second line therapy,only to be used in selected cases when there is insufficient response to SAB.

CORTICOSTEROIDS Shorts recovery time Improve lung function Improve hypoxemia Reduce risk of early relapse,treatment failure

and length of hospital stay. Oral prednisolone (40mg od for5 day) is

preferable. Nebulised budesonide alone may be an

alternative to oral corticosteroids in treatment of exacerbation.

Nebulised magnesium as an ajuvent to salbutamol treatment in setting of A/E COPD has no effect on FEV1.

ANTIBIOTICS Antibiotics should be given to patient

with A/E COPD who have three cardinal symptoms

1. Increase in dyspnea2. Increase in sputum volume3. Increase in Sputum purulence

Require mechanical ventilation

ADJUENT THERAPIES Appropriate fluid balance Diuretics Anticoagulant Treatment of comorbidities

GOLD 2017 UPDATE The refined ABCD assessment tool now adopts a 3-Step Approach as compared with the previous ABCD assessment tool.

Treatment recommendations are tailored to patient needs based on symptoms and exacerbation history.

The GOLD 2017 recommends the choice of long acting bronchodilators to depend on patient’s perception of symptom control

LABA/LAMA therapy identified as an important option for people with moderate to very severe COPD patients.

Triple Therapy: The step up treatment to ICS/LABA/LAMA can occur by various pathways. Adding LAMA to LABA/ICS might improves lung function and patient

related outcomes, exacerbation risk in particular.

ICS/LABA might be the first choice, in patients with history of Asthma COPD Overlap (ACO)

There has been a major change in the assessment of COPD. The ABCD assessment tool has been refined to only utilize respiratory symptoms and exacerbations to assign ABCD. A three step approach which includes:

1. Diagnosis (Based on FEV1/FVC <0.7)

2. Assessment of airflow limitation (Based on predicted FEV1)

3. Assessment of Symptoms and Risk of Exacerbations

diagnosisAssesment of

symptom/risk of exacerbation

Assesment of airflow

limitation

FEVI/FVC<0.7

FEVI

GRADE

BASE ON HISTORY OF

EXACERBATION/HOSPITILIZATION,M

MRC AND CAT SCORE

Airflow limitation is not a component of the ABCD system. Spirometry remains important mainly for diagnosis and prognosis. 

Exacerbations are now classified as: a. Mild [Treated only with Short Acting

Bronchodilators (SABD)] b. Moderate (Treated with SABD, plus

antibiotics and /or oral corticosteroids) c. Severe (Patient requires

hospitalization or has an emergency room visit)

Oxygen Not Recommended for Most COPD Patients in GOLD 2017

The 2017 GOLD guidelines generally advise against the routine practice of prescribing supplemental oxygen to stable COPD patients without severe resting hypoxemia. stable COPD patients with moderate hypoxemia, supplemental oxygen did not improve clinical outcomes or quality of life during the followup period.

COPD patients with severe resting hypoxemia (oxygen saturation ≤88% and certain other patients with COPD) should all receive supplemental oxygen to be worn continuously.

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