COPD with acute exacerbation

What is COPD?

COPD is a chronic slowly progressive disorder characterized by airflow obstruction (FEV1 < 80% predicted and FEV1/FVC ratio < 70%) which does not change markedly over several months.

It encompasses three clinical entities :EMPHYSEMACHRONIC BRONCHITISSMALL AIRWAYS DISEAES

DEFINITIONS

CHRONIC BRONCHITIS : It is defined as cough with sputum on most days for at least three consecutive months for more than two successive years.

EMPHYSEMA : It is defined as permanent destructive enlargement of the air spaces distal to the terminal bronchioles.

SMALL AIRWAYS DISEASE : A condition in which small bronchioles are narrowed.

RISK FACTORS

SMOKING: studies have shown accelerated decline in FEV1 in a dose response relationship to the intensity of cigarette smoking which is expressed as pack years.

AIR WAY RESPONSIVENESS: Increased air way responsiveness is a significant predictor of subsequent decline in pulmonary function.

RESPIRATORY INFECTIONS: Though respiratory infections are an important cause of exacerbation of COPD , their association to the development and progression of COPD remains to be proven.

RISK FACTORS contd..

OCCUPATIONAL EXPOSURE: Including coal mine , gold mining and cotton textile dust have been suggested as risk factors.

AMBIENT AIR POLLUTION: with high rates of COPD in non smoking women in developing countries indoor air pollution associated with cooking has been suggested as potential contributor.

ALPHA 1 ANTI TRYPSIN DEFICIENCY: Cigarette smokers with alpha 1 anti-trypsin deficiency are more likely to develop COPD at early ages.

CLINICAL PRESENTATION

HISTORY: three most common symptoms of COPD are cough, sputum production and exertional dyspnea.

As disease progresses dyspnea occurs with mild activity and in severe cases at rest.

Hallmark of COPD is frequent exacerbation of illness.

Pneumonia , pulmonary HTN , cor pulmonale and chronic respiratory failure characterize the late stages of the disease.

SIGNS OF COPD

Nicotine staining of finger nails.Pursed lip breathing.Characteristic tripod position.Use of accessory muscles.Barrel shaped chest.Excavation of suprasternal and supraclavicular fossae during respiration.Cyanosis.Weight loss , bitemporal wasting.Hoover’s sign : paradoxical inward movement of rib cage during inspiration.

SIGNS OF COPD contd..

Tracheal tugLoss of cardiac dullnessProlonged expiratory phase with wheezingSigns of hypercapnia i.e bounding pulse, warm extremities and flapping tremors

Signs of cor pulmonale namely elevated JVP , right ventricular heave , loud P2 , S3 , hepatic congestion , ascities . Peripheral edema

Clubbing is not a sign of COPD ; CA lung is the most likely explanation for clubbing in COPD.

INVESTIGATIONS

PFTs: Reduction in FEV1 and FEV1/FVC ratio.

ABGs: Indicated if 1. Hypoxemia or hypercapnia is suspected.2. FEV1 is less than 40% of predicted.3. Clinical signs of heart failure.

SPUTUM EXAMINATION for micro organisms in acute exacerbation

ECG may show sinus tachycardia , signs of RVH and Supraventricular arrythmias.

HAEMATOLOGY may show polycythemia.

INVESTIGATIONS contd..

CXR may show hyperinflation with flattening of diaphragm or peripheral arterial deficiency , parenchymal bullae and enlargement of central pulmonary arteries.

CT SCAN is the current definitive test for the establishing the presence or absence of emphysema.

ALPHA 1 ANTI TRYPSIN LEVEL in patients presenting with age < 50 yrs, strong family history , predominant basilar disease or with minimal smoking history.

ECHO for suspected pulmonary HTN,

GOLD CRITERIA FOR COPD SEVERITY

Gold stage

severity symptoms spirometry

0 At risk Ch cough,sputum production normal

I mild With or without ch cough or sputum production

FEV1/FVC<0.7 AND FEV1>80

%

II moderate As above FEV1/FVC<0.7 AND 50%<FEV1<80%

III severe As above FEV1/FVC<0.7 AND 30%<FEV1<50%

IV Very severe As above FEV1/FVC<0.7 AND FEV1<30%

TREATMENTSTABLE PHASE COPD:

1. Smoking cessation is one of the two interventions that influence the natural history of patients with COPD. Nicotine transdermal patch, nicotine gum and bupropion increase cessation rates in motivated smokers.

2. Oxygen therapy also influence natural history of disease in patients with resting hypoxemia. Survival in hypoxemic patients with COPD is directly proportionate to the no. of hrs / day oxygen is administered.

ABG analysis is prefered over oximetry to guide initial oxygen

therapy. Oxygen by nasal prongs must be given for at least 15 hrs a day.Transtracheal oxygen is alternative method of delivery in pts. who require high flows of oxygen than can be deliverd by nasal prongs.

BRONCHODILATORS

Anticholinergic agents like ipratropium bromide is first line agent because of its longer duration of action and absence of sympathomimetic side effects. Dose 2 puffs every 6 hrs.

Beta agonists 1. Short acting: like salbutamol are less expensive, have

rapid duration of action and have bronchodilator effect equal to ipratropium bromide but may cause tachycardia, tremor and hypokalemia.

2. Long acting: like salmeterol appear to achieve bronchodilation that is equivalent or superior to ipratropium but their role in stable COPD is under research.

THEOPHYLLINE

Theophylline is third line agents in COPD patients who fail to achieve adequate symptoms with anticholinergics and beta 2 agonists.

SR theophylline improve arterial oxygen Hb saturation during sleep in COPD pts and is a first line agent for those with sleep related breathing disorders.

Its benefits may result from anti inflammatory properties and extra pulmonary effects on diaphragm strength , myocardial activity and renal function.

CORTICOSTEROIDS

Apart from acute exacerbation , COPD is not generally steroid responsive disease.

A trial of inhaled glucocorticoids should be considered in pts with frequent exacerbations defined as 2 or more per year, and in pts who demonstrate a significant amount of acute reversibility in response to inhaled bronchodilators.

Chronic use of oral glucocorticoids for treatment of COPD is not recommended.

OTHER AGENTS

N ACETYL CYSTEINE: has been used in pts of COPD for its mucolytic and anti oxidant properties.

ALPHA 1 ANTI TRYPSIN THERAPY for severe anti trypsin deficiency.

Pts over 18 years of age with air flow obstruction on spirometry and level less than 11 umol/l are candidates for replacement therapy.

NON PHARMACOLOGICAL THERAPIES

General medical care : influenza vaccine annually. Pneumococcal vaccine is also recommended.

Pulmonary rehabilitation: graded aerobic physical exercise programs

walking 20 mins at least thrice weekly, bicycling are helpful for preventing deterioration of physical condition and to improve patient’s ability to carry out daily activities. Pursed lip respiration to slow the rate of breathing and abdominal breathing exercises to relieve fatigue of accessory muscles of respiration may reduce dyspnea in some pts. Adequate systemic hydration and cough training methods for mobilization of secretions in pts with ch bronchitis.

SURGICAL TREATMENT

1. LUNG TRANSPLANTATION: for pts with FEV1 less than 25% and severe limitation in quality of life esp with hypercapnia and hypoxemia.It is not an option for elderly pts.

2. BULLECTOMY: Is considered in pts with COPD and dyspnea in whom a bulla or bullae occupy 50% of hemithorax.

3. LUNG VOLUME REDUCTION SURGERY: In highly selected pts with severe COPD due to emphysema.

ACUTE EXACERBATION

Exacerbations are commonly considered to be episodes of increased dyspnea and cough and change in amount and character of sputum.

It may or may not be accompanied by fever, myalgias and sore throat.

Approach to the pt includes assesment of severity , identification of the precipitating factor and institution of therapy.

PRECIPITATING CAUSES

Bacterial infections play a role in many episodes. (H.influenzae,S.pneomoniae,M.catarrhalis and Mycoplasma)

Viral infections are involved in 1/3 rd of cases. (Influenza and Adenovirus)

In 20 – 35% no specific precipitant can be identified.

PATIENT ASSESMENT

History include degree of dyspnea , by asking about breathlessness during activities , ask about fever , change in character of sputum and associated symptoms as nausea , vomiting , diarrhea , myalgias and chills.

Inquire about frequency and severity of previous exacerbations.

Physical examination : process degree of distress.

CXR and ABGs

INSTITUTION OF THERAPY

OXYGEN to achieve and maintain PaO2 > 55-60 mm Hg and to keep arterial saturation > 90%. Hypoxic respiratory drive plays a small role in pts of COPD.

INHALED BRONCHODILATORS

1. Short acting beta agonists are first line agents as albuterol has reduced duration of action in acute exacerbation allowing a treatment frequency of every 30 – 60 mins as tolerated. Subsequent treatment can be reduced to 2- 4 puffs every 4 hrs.

2. Anticholinergic agents are equally effective to short acting beta 2 agonists. Dose : 2 puffs QID can be increased to 4-6 puffs every 4-6 hrs.

3. Combination therapy has synergistic bronchodilation , rapid onset of action and fewer S/E.

Contd..

GLUCOCORTICOIDS: GOLD guidelines recommend 30 – 40 mg of oral prednisolone over 10 – 14 days. They reduce hospital stay , hasten recovery and reduce the chance of subsequent exacerbation or relapse for a period upto 6 mths.

ANTIBIOTICS: First line antibiotic regimes are Septran (160/800 mg every 12 hrs) , Amoxycillin ( 500mg tds) Doxycycline (100mg bd) for 7-10 days.

For severe exacerbation recommended antibiotics include Azithromycin , Clarithromycin , Levofloxacin and Gatifloxacin.

Contd..

PSYCHOACTIVE DRUGS :low dose anxiolytics may reduce anxiety . Buspirone 5-10 mg tds is usually tolerated well.

INDICATIONS FOR ICU ADMISSION

SEVER DYSPNEA

MENTAL STATUS CHANGES

PERSISTENT WORSENING HYPOXEMIA

HYPERCAPNIA

RESPIRATORY ACIDOSIS ALL DESPITE MEDICAL THERAPY.

MECHANICAL VENTILATORY SUPPORT

Non Invasive positive pressure pressure ventilation (NIPPV) in pts with respiratory failure , defined as Pco2 > 45 mm Hg results in significant reduction in mortality, need for intubation , complication of therapy and duration of hospital stay.

IPPV with ETT is indicated for pts with severe respiratory distress despite initial therapy , life threatening hypoxemia , severe hypercapnia and/or acidosis , impaired mental status , respiratory arrest and hemodynamic instability.

DISCHARGE CRITERIA

Use of inhaled bronchodilators less frequently than every 4 hrs.

Clinical and ABG stability for at least 12 – 24 hrs and

Acceptable ability to eat , sleep and ambulate.

THANK YOU !

SCENARIO

50 years oil male presented in emergency department with history of severe shortness of breath associated with productive cough with yellow color sputum and fever.He has past history of cigarette smoking 2 pack year for last 35 years.

What physical signs you can suspect in this case ?

SCENARIO

BP 100/60mmHg

Pulse 110 beats/min

R/R 34/min

Temp 101 F

Pt is cyanosed a

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