53
Airway Diseases May 2013 Mekelle

Chronic obstructive pulmonary disease copy

  • Upload
    elijah

  • View
    395

  • Download
    1

Embed Size (px)

Citation preview

Page 1: Chronic obstructive pulmonary disease   copy

Airway DiseasesMay 2013

Mekelle

Page 2: Chronic obstructive pulmonary disease   copy

Chronic Obstructive Pulmonary Disease

Page 3: Chronic obstructive pulmonary disease   copy

COPD

Definition

COPD- a disease state characterized by airflow limitation that is not fully reversible

The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases

Page 4: Chronic obstructive pulmonary disease   copy

COPD includes Chronic bronchitis

Emphysema

Small airway disease

COPD is the fourth leading cause of death in the USA

Page 5: Chronic obstructive pulmonary disease   copy

Risk factors

In the west

Most important is cigarette smoking

In developing countries

Role of household fuels and indoor pollution have important contribution.

Page 6: Chronic obstructive pulmonary disease   copy

Occupational exposure

Air Pollution

Genetic- α-1 Antitrypsin Deficiency

Page 7: Chronic obstructive pulmonary disease   copy

Regarding smoking

The degree of damage to the lung (FEV loss) is proportional to the amount of cigarettes smoked.

Not all smokers develop COPD ( 15%) only; outlining individual susceptibility

Second hand (passive) smokers are also at risk

Page 8: Chronic obstructive pulmonary disease   copy

Regarding asthma and COPD

Dutch hypothesis – asthma and COPD are two diseases in the same spectrum

British hypothesis – different entities

Page 9: Chronic obstructive pulmonary disease   copy
Page 10: Chronic obstructive pulmonary disease   copy

Natural history

Risk of mortality from COPD is closely associated with reduced levels of FEV1

FEV1 is a marker of obstruction

Page 11: Chronic obstructive pulmonary disease   copy

Obstruction leads to hyperinflation.

Hyperinflation leads to impaired diaphragmatic function.

Page 12: Chronic obstructive pulmonary disease   copy

Pathology Cigarette smoke exposure may affect

the large airways, small airways ( 2 mm diameter), and alveolar space

Large airway changes cause cough and

sputum (i.e. the symptoms),

small airways and alveolar changes are responsible for physiologic alterations

Page 13: Chronic obstructive pulmonary disease   copy

Patterns

Emphysema

Defined in anatomic terms

Destruction of the airways

Pan or centri acinar pattern

Chronic bronchitis

Defined in clinical terms

Based on symptoms

Page 14: Chronic obstructive pulmonary disease   copy

Diagnosis Consider COPD in any patient with combination of

these symptoms

Dyspnea

Chronic cough

Chronic sputum production

History of exposure to risk factors

Page 15: Chronic obstructive pulmonary disease   copy

Physical examination is rarely diagnostic in COPD Wheezes here and there

Page 16: Chronic obstructive pulmonary disease   copy

With severe airflow obstruction- use of accessory muscles of respiration- tripod

position

Cyanosis

Systemic wasting Later on

Signs of right sided heart failure

Sometimes Features of systemic inflammation ( ischemic

heart disease osteoporosis ….), poor sleep

Page 17: Chronic obstructive pulmonary disease   copy

Laboratory findings

CXR can be normal or some times shows some hyperinflation. Don’t rule out COPD b/c you have a normal CXR

Pulm Function tests

Low FEV1/FVC

Low peak flow

Some reversibility might be there in the obstruction

Page 18: Chronic obstructive pulmonary disease   copy

Hct – for erythrocytosis

ECG and Echo – for Cor pulmounale

Page 19: Chronic obstructive pulmonary disease   copy

Stage of COPD

We use spirometric parameters

GOLD staging

Page 20: Chronic obstructive pulmonary disease   copy

Management plan has four components

Assess and monitor disease

Reduce risk factors

Manage stable COPD

Manage exacerbations

Page 21: Chronic obstructive pulmonary disease   copy

Assess and monitor

Stage of the disease

Use spirometry and clinical features

Page 22: Chronic obstructive pulmonary disease   copy

Risk factor reduction

Smoking cessation

Page 23: Chronic obstructive pulmonary disease   copy

Stable COPD

Bronchodilators – anticholinergics, beta agonist

Inhaled corticosteroids- for patients with frequent exacerbations

Vaccination- influenza and pnuemococcal

Non pharmacotherapies- pulmonary rehabilitation, lung volume reduction surgery, lung transplantation

Page 24: Chronic obstructive pulmonary disease   copy

Treatment of exacerbations Exacerbations are a prominent feature of

the natural history of COPD The frequency of exacerbations increases

as airflow obstruction increases Exacerbations are commonly considered to

be episodes of increased dyspnea and cough and change in the amount and character of sputum

Infections- bacteria most common cause of exacerbation

Page 25: Chronic obstructive pulmonary disease   copy

Treatment includes-

Bronchodilators

Antibiotics

Glucocorticoids

Oxygen therapy

Mechanical ventilation

Page 26: Chronic obstructive pulmonary disease   copy

Home O2 therapy for resting and nocturnal hypoxemia

Lung volume reduction surgery

Page 27: Chronic obstructive pulmonary disease   copy
Page 28: Chronic obstructive pulmonary disease   copy

Asthma

Page 29: Chronic obstructive pulmonary disease   copy

Asthma

Asthma is a syndrome characterized by airflow obstruction that varies markedly, both spontaneously and with treatment

Narrowing of the airways is usually reversible, but in some patients with chronic asthma there may be an element of irreversible airflow obstruction

Page 30: Chronic obstructive pulmonary disease   copy

Prevalence

~10–12% of adults and 15% of children affected by the disease

can present at any age

peak age is 3 years

Page 31: Chronic obstructive pulmonary disease   copy

Children with asthma – the asthma can subside as they grow older.

Adults with asthma-rarely so

The severity of asthma does not vary significantly within a given patient

Page 32: Chronic obstructive pulmonary disease   copy

Etiology

Asthma is a heterogeneous disease with interplay between genetic and environmental factors

Page 33: Chronic obstructive pulmonary disease   copy

Genetic predisposition suggested by- familial association of asthma

high degree of concordance for asthma in identical twins

The severity of asthma is also genetically determined

Environmental factors-in early life determine which atopic individuals become asthmatic

Page 34: Chronic obstructive pulmonary disease   copy

Atopy is the major risk factor for asthma Allergic rhinitis and atopic dermatitis

Allergens House dust mite

Page 35: Chronic obstructive pulmonary disease   copy

Intrinsic Asthma or nonatopic asthma-~10% have negative skin test to common inhalant allergens and normal serum concentrations of IgE

Usual adult onset

Page 36: Chronic obstructive pulmonary disease   copy

Pathogenesis Asthma is associated with a specific

chronic inflammation of the mucosa of the lower airways

The degree of inflammation is poorly related to disease severity and may be found in atopic patients without asthma symptoms

Page 37: Chronic obstructive pulmonary disease   copy

Clinical features

Wheezing,

dyspnea, and

Cough

These are variable, both spontaneously and with therapy

Symptoms may be worse at night

Typical physical signs are inspiratory, and to a great extent expiratory, rhonchi throughout the chest

Page 38: Chronic obstructive pulmonary disease   copy

Physical signs

wheezes

Page 39: Chronic obstructive pulmonary disease   copy

Diagnosis

Simple spirometry confirms airflow limitation with a reduced FEV1,

FEV1/FVC ratio,

PEF

Reversibility is demonstrated by a >12% or 200 mL increase in FEV1 15 min after an inhaled short-acting beta 2-agonist or, in some patients, by a 2- to 4-week trial of oral glucocorticoids

methacholine or histamine challenge –rarely needed to confirm airway hyperresponsiveness

Page 40: Chronic obstructive pulmonary disease   copy

Aims of treatment

For the patient to have

No or minimal symptoms esp. nocturnal

No emergency OPD visits

No frequent use of salbutamol

No limitation of activity

Page 41: Chronic obstructive pulmonary disease   copy

Treatment

Two groups of drugs are used

Bronchodilators beta 2-adrenergic agonists,

anticholinergics, and

theophylline

Controllers Glucocorticoids

Antileukotriens

Cromones

antiIGE

Immunotherapy

Page 42: Chronic obstructive pulmonary disease   copy

Management of chronic asthma

Avoid triggers

Pharmacotherapy –stepwise therapy

Patient education

Goals

Reduce impairment

Reduce risk

no cure but symptoms can be controlled

Page 43: Chronic obstructive pulmonary disease   copy

Treatment of chronic asthma

First try to determine severity.

This can be done by looking at Reported symptoms over the previous two to four weeks

Night symptoms

Current level of lung function (FEV1 and FEV1/FVC values)

Number of exacerbations requiring oral glucocorticoids per year

Emergency visits

Page 44: Chronic obstructive pulmonary disease   copy

Then stratify your patient by the severity to either

Intermittent

Mild persistent

Moderate persistent

Severe persistent

Then institute therapy by the level of severity

Page 45: Chronic obstructive pulmonary disease   copy
Page 46: Chronic obstructive pulmonary disease   copy

Adjusting therapy

Assess the status of the patient after 2-4 weeks of therapy.

If improving step down the treatment

If not step up the ladder.

Page 47: Chronic obstructive pulmonary disease   copy
Page 48: Chronic obstructive pulmonary disease   copy

Management of acute severe asthma

The best strategy for management of acute exacerbations of asthma is early recognition and intervention, before attacks become severe and potentially life threatening

Treatment starts with assessment of severity of attack

Page 49: Chronic obstructive pulmonary disease   copy

Look for simple clinical severity indicators

Degree of dyspnea

Can the patient finish a sentence?

Degree of desaturation?

Paradoxic breathing, accessory muscles

Mental status

Silent chest

Level of V/S derangement

Page 50: Chronic obstructive pulmonary disease   copy

Provide

High flow oxygen therapy to keep oxygen saturation >90%

High dose inhaled short acting beta agonists are the main stay of therapy (nebulized or via metered dose inhaler)

Add inhaled anticholinergics if no adequate response

Page 51: Chronic obstructive pulmonary disease   copy

Start systemic glucocorticoids if there is not an immediate and marked response to the inhaled short-acting beta agonists

Slow infusion of aminophylline may be effective in patients not responding to high dose bronchodilators

Make frequent (every one to two hours) objective assessments of the response to therapy until definite, sustained improvement is documented

Page 52: Chronic obstructive pulmonary disease   copy

For patients with respiratory failure, it is necessary to intubate and institute ventilation

Consider antibiotics if signs of pneumonia

Page 53: Chronic obstructive pulmonary disease   copy

Refractory asthma

A small proportion of patients (~5% of asthmatics) are difficult to control despite maximal inhaled therapy

Some of these patients will require maintenance treatment with oral corticosteroids

The most common reason for poor control of asthma is noncompliance with medication