CHRONIC OBSTRUCTIVE AIRWAYS DISEASE

COAD - Bronchitis

- Emphysema

AOAD - Asthma

COAD - Excessive mucus secretions

- Chronic infection

- Increased size of air spaces ) emphysema

- Loss of elastic recoil )

- Narrowing of bronchial airways.

AETIOLOGY

Cigarette smoking

Air pollution

Occupational exposure

Allergy

Auto-immunity

Infection

Genetic predisposition

Ageing

PREVENTION OF BRONCHITIS

Avoid respiratory irritants eg., tobacco, bronchitis is a smokers disease.

In prone people immunize against influenza.

Prompt treatment of acute infections.

FEATURES OF BRONCHITIS

Many different pathogens may cause exacerbations.

Many exacerbations occur in winter, cold aid causing bronchospasm.

Secretions must be expelled.

Chronic bronchitis often progresses to emphysema.

RVF or Cor pulmonale.

Insidious development - persistent cough.

Thick gelatinous sputum.

Wheezing and dyspnoea progress.

COAD - NURSING INTERVENTIONS

Eliminate pulmonary irritants

No smoking

Avoid aid pollutants and outside activity in polluted air.

Reduce house dust.

Use of home air humidification.

Control Bronchospasm (To reduce respiratory work)

Bronchodilators - check with peak flow measurements, before and after.

- observations for side effects.

Keep secretions liquid - postural drainage - percussion

- cough - something to spit into.

Physiotherapy - breathing exercises

- diaphragmatic breathing.

General management

Early detection of any infection

Sputum C&S

Antibiotics

Prevent cross infection

Steroids as prescribed to inflammation

Observe level of dyspnoea

Regular small meals pressure on diaphragm

Treat hypoxaemia with low concentrations of O²

Avoid narcotics and sedatives

Keep patients fit

Psychological support

Family social support

Acute Bronchitis

Often begins as a viral infection

Initial unproductive cough later becoming productive

Yellow or green sputum

Discomfort behind the sternum

Tightness in the chest

Wheezing

Shortness of breath

Mild fever

In otherwise healthy adults the condition resolves in 4 - 8 days

Often occurs after childhood infections, eg. measles, whooping cough, typhoid

Children

Chest infections are the most common single cause of death in children

Factors

Nutrition

Concurrent infections

Overcrowding

Poor living conditions/damp

Bronchitis

Often respiratory syncytial virus in young children, usual bacteria over the age of 6 years

Cough usually becomes productive in 2 - 3 days

Usually recover in 5 - 10 days

Treatment

Antibiotics, amoxycillin 250 mg three times a day

Antipyretics

Analgesics

Humidity

Rest

Bronchiolitis

Hand to nose transmission of a virus - possible epidemics

Children usually 2 years or under

Chronic bronchitis and emphysema

COAD/COPD/COLD

Chronic bronchitis and emphysema

Both conditions co-exist in each patient to various degrees

Results in chronic airflow limitation

AOAD Asthma

Bronchitis Productive cough on most days for 3 months of the year for more than one year

Emphysema Abnormal permanent enlargement of the air spaces due to destruction of alveolar walls

Type a - Pink and puffing

Breathless Arterial O₂ and CO₂ relatively normal

No cor- pulmonale Predominantly emphysema with little bronchitis

Type B - Blue and bloated

Cyanosed/oedematous Not breathless

Arterial O₂ low and CO₂ high Predominantly chronic bronchitis with little emphysema

Pathology relates poorly with the clinical picture

Most patients are a combination of the two "classic" types

Prevalence

Men, 17% in 40 - 64 age group Women 8% in 40 - 64 age group

Increasing prevalence in many developing countries

Decreasing in the UK Carries a considerable socio-economic burden

Features of bronchitis

An acute or chronic inflammation of the mucous membrane of the tracheobronchial tree

Insidious development - persistent cough

Wheezing and dysponea progresses - SOB on exertion

Purse string lips on expiration

Thick excessive gelatinous sputum - hypertrophy of mucus gland - increased number of goblet cells ----- impaired cillary movement ------- mucus stasis ------- infection

Mucus plugging of smaller airways

When more severe - inflamed bronchi with pus

Ulceration followed by healing ------- fibrosis ------- narrowed lumen ------- airflow limitation

Loss of cilia

Initial small airway inflammation is reversible if smoking/insults stops

Many exacerbations occur in winter - cold air causes bronchoconstriction

Chronic bronchitis often progresses to emphysema - obstruction of bronchioles may lead to distended alveoli

RVF or Cor pulmonale.

Features of emphysema

Increased size of air spaces - distension and damage of lung tissue

Reduces surface area in lungs - decreased gas transfer

Breathless Wheeze Loss of elastic recoil

Emphysematous spaces occur in 50% of smokers over the age of 60

Use of accessory muscles of respiration Intercostal in-drawing

Aetiology

Cigarette smoking - well related to number of cigarettes smoked - 20 times more likely to die from COAD at 30 per day than non-smokers

Smoking probably causes emphysema directly by increasing the number of granulocytes in the lungs ----- serine elastase ------ proteolysis of elastic tissue

Smoking causes mucous gland hypertrophy as a result of persistent irritation

Air pollution - increased mortality during periods of increased pollution

Occupational exposure Allergy Auto-immunity

Genetic predisposition Ageing

Infections

Cause acute exacerbation of chronic disease Often chronic

Many different pathogens may cause exacerbations

Streptococcus pneumoniae and Haemophilus influenza most common

May have a role in aetiology

Prevention of bronchitis

Identify and avoid respiratory irritants eg., tobacco, (bronchitis is a smokers disease), dust, smoke, infection, occupational exposure

Avoid cold/foggy weather, infected people, crowds in influenza season

Immunise at risk people against influenza.

Prompt treatment of acute infections

Early disease seems to predominantly effect the smaller airways and may be reversible

Complications

Respiratory failure Low pO₂ high pCO₂

Cor - pulmonale

Normal pulmonary arterial pressure about 25/8

Reduced O₂ in air spaces

Results in localised pulmonary arterial vasoconstriction through poorly oxygenated areas

Therefore blood left over for better oxygenated areas of the lung

Therefore blood flow matched alveoli oxygenation

However if low O₂ is global all over the lung pulmonary arterial pressure will increase ------ cor-pulmonale Blue - polycythemia Bloated -- RHF - systemic oedema

Heart disease secondary to disease of the lung

Tricuspid incompetence may develop - raised JVP and ascites

Discomfort due to liver congestion

Investigations

Lung function tests CXR Blood tests - possible rise in Hb and PCV

Blood gases Sputum ECG

Antitrypsin

Nursing interventions

Eliminate pulmonary irritants

No smoking Avoid air pollutants and outside activity in polluted air.

Reduce house dust Use of home air humidification

Management

Observations Observe level of dyspnoea/cyanosis/mental state TPR Regular weight

Treat blood gas abnormality Treat hypoxaemia with low concentrations of humidified O_² - 24 %, this can be of significant benefit Avoid narcotics and sedatives Nurse sitting up

Encourage expectoration

Secretions must be expelled Encourage deep breathing

Keep secretions liquid, avoid dehydration, use steam inhalation

Postural drainage - percussion Cough - something to spit into.

Physiotherapy

Prevent/treat infection Early detection of any infection Sputum C&S Prevent cross infection

General measures

ADL support and mouth care Nutrition Counter obesity

Regular small meals - reduce pressure on diaphragm

Rest periods - constant coughing can be exhausting Keep patients fit

Psychological support

Breathlessness may be very frightening - possible panic reactions

Need to come to terms with chronic nature of condition

Possible anger or depression

Family social support - patient may see condition as socially unacceptable

Counter rationalisations for continued smoking Employment problems - possible inability to work

Drugs

Antibiotics

As soon as sputum turns yellow or green Amoxycillin or Cefaclor, 250 mg eight hourly

Possible use in prophalaxis

Bronchodilators

To reduce respiratory work

Check with peak flow measurements, before and after, observations for side effects.

Anticholinergics give better and more prolonged benefit, eg. ipatropium

Corticosteroids

Should be tried as they may have an unsuspected reversible element, eg. prednisolone 30 mg/day for 2 weeks

Possible maintenance with inhaled corticosteroids

Diuretic therapy For all oedematous patients

Respiratory stimulants May arouse patient and stimulate coughing, eg. doxapram

Management at home

Continuous O₂ at 2 litres per minute via nasal cannula Keep O₂ saturation above 90%

Nebulizer At 15 hours per day - fall in pulmonary artery pressure

At 19 hours per day - substantial improvement in mortality Oxygen concentrators

Exercise training - may reduce feelings of breathlessness and improve general well being

Educate to optimise compliance

Prognosis In severe breathlessness 50% die within 5 years

Even in the severe group stopping smoking improves the prognosis

Chronic bronchitis

Aetiology

Tobacco smoke

Smoke

Pollution

Mucosal inflammation

Pathophysiology

Increased mucus

Mucous gland hypertrophy and hyperplasia

More mucous glands in submucosa

Reduced lumen

Inflammation – metaplasia

Ciliated columnar – squamous

Early disease reversible

Loss of cilia

Mucociliary clearance system

Stasis

Exacerbations

Superimposed infection

Fibrosis in smaller airways

Features

Cough for 3 months over 2 years

Morning cough

Deoxyhaemoglobin – cyanosis

Reduced levels of O₂ with increased CO₂ in lungs

Pulmonary heart disease

Cor pulmonale

Right heart failure – systemic oedema

Hypercarbia

Loss of hypercarbic drive

Non fighters but SOBE

Emphysema

Define

Loss of elasticity in the alveoli with permanent enlargement of the air spaces

Pathophysiology

Smoke particles in alveoli

Inflammation

Neutrophils and monocytes x 6

Phagocyctosis

Proteases, collagenase and elastase

Cell in wall of alveoli are partly digested

Loss of elastic recoil of alveoli

Pressure from adjacent alveoli

Collapse of bronchioles

Airway obstruction

Hyperinflation

Loss of respiratory surface area

Alpha antitrypsin deficiency

Features

Fighters – pink and puffing

Dyspnoea

Normal levels of O₂ and CO₂ in lungs

Preserved hypercarbia drive

No pulmonary heart disease

Barrel chest