Asthma

Contents
Introduction
Pathology
Clinical Features
Investigations
Treatment

Introduction

Asthma is a disease in which there are reversible episodes of brochoconstriction that are caused by bronchial hyperreactivity. The basic underlying pathological mechanism in most cases is a type one hypersensitivity reaction.

Asthma is a common condition and typically presents in childhood. The prevalence in the United Kingdom is around 5%. The global prevalence has been estimated as 300,000,000. The disease may cause 250,000 deaths per year worldwide.

Pathology

The lungs are typically normal in an asthmatic patient between attacks. During an epispode of asthma there is bronchoconstriction and increased mucus production. The mucus can contain eosinophilic bodies known as Curschmann's spirals which are composed of shed epithelial cells and debris from inflammatory cells.

If the asthma attack is fatal the lungs are overinflated due to the trapping of air in them because the bronchoconstriction and excess mucus make it easier for air to enter the lungs than to leave.

In chronic, poorly controlled disease there is hypertrophy of the bronchial smooth muscle and an increase in the number of mucus glands.

The majority of cases of asthma are termed extrinsic and are due to a type one hypersensitivity reaction to external antigens. Exposure to the antigens is often via the inhaled route. Common precipitating antigens include pollen, the faeces of the house dust mite and animal hair, although the list of possible triggers is long and diverse.

A few cases of asthma are classified as intrinsic. In these patients the asthmatic response can be triggered by aspirin, pulmonary infection, exercise, stress or cold.

Clinical Features

During an asthma attack the patient will complain of shortness of breath and/or wheezing; there may also be a cough. The patient may be able to relate the attack to exposure to a precipitant.

On examination the patient will be tachypnoeic. The trachea is central. Expansion of the lungs may be reduced. The percussion note can be normal or hyperresonant (if air trapping has occurred) The breath sounds can be normal or reduced, the latter case being due to decreased air flow; wheezing will be heard all over the chest. Vocal resonance will be normal or reduced.

Between attacks the patient is usually asymptomatic, although may report a nocturnal cough or less commonly a chronic dry cough.

Patients may remark that their symptoms are worse in the early hours of the morning.

Certain clinical features are encountered in a severe attack and indicate that the patient requires admission and aggressive treatment. These features include the following.

• Inability to talk in sentences
• Use of the accessory muscles of respiration
• Limited respiratory effort despite respiratory distress
• Altered consciousness
• Cyanosis
• Tachycardia
• Hypotension
• Very quiet breath sounds (silent chest - very little air flow)
• Peak flow less than 50% of normal for that patient
• Normal or raised PaC0₂

The first, second and penultimate items, plus tachycardia, will be the most frequently encountered because the remainder portend an extremely serious asthma attack and hopefully the patient will have sought medical attention before things are that bad.

Investigations

The diasgnosis of asthma requires few investigations because the clinical picture is usually characteristic. A full blood count can be useful to determine if eosinophilia is present. A chest X-ray is useful to serve as a baseline and also to pursue conditions that may mimic asthma (such as tumours, pulmonary infiltrates, inhaled foreign body).

Lung function tests can be useful if there is uncertainty as to whether the symptoms are actually due to chronic obstructive pulmonary disease.

During an acute asthma attack the main investigations are arterial blood gases and a chest X-ray. The chest X-ray again serves to help to exclude alternative diseases but also to determine if a pneumothorax has occurred as a complication of the asthma attack.

Arterial blood gases are vital in the assessment of any asthma attack of significant severity. A reduced arterial partial pressure of oxygen is worrying, but a rising partial pressure of carbon dioxide is even more serious because this implies very severe respiratory failure on the basis that the lungs can exchange carbon dioxide more effectively than oxygen and carbon dioxide levels therefore require a greater degree of lung dysfunction to deteriorate. In addition, if the patient clearly has a severe asthma attack even a normal carbon dioxide level can be worrying: hyperventilation should normally expel carbon dioxide so efficiently that the patient's partial pressure of carbon dioxide is decreased (an accompanying alkalosis occurs); if this hypocapnia does not develop it implies that the lungs are failing to handle carbon dioxide normally.

A full blood count may disclose a raised white cell count that could in turn be caused by an infection and that infection could have precipitated or exacerbated the asthma.

Treatment

A full descrition of the treatment of asthma is beyond the scope of a discussion of asthma for the purposes of BMS cut up but there are several basic concepts.

Patients should be given a peak flow meter and should document their peak flow several times per day during the first few weeks after diagnosis. This establishes their normal peak flow and this baseline is central to assisting management.

Pharmacological treatment centres around reliever drugs and preventer drugs, both of which are given by the inhaled route if possible. The reliever drugs are usually beta-2 adrenoreceptor agonists such as salbutamol. These relax smooth muscle and thus are bronchodilators. In mild disease a patient may just require an inhaled bronchodilator to be taken as necessary.

The preventer inhalers are corticosteroids. These aim to suppress the type one hypersensitivity reaction in the airways. The use of the inhaled route of administration prevents the systemic features which can result from chronic corticosteroid use.

If a bronchodilator alone, taken to relieve symptoms, is unsuccessful in controlling the disease, the bronchodilator can be taken regularly. If this is not successful then a regular corticosteroid inhaler is added.

If the regular bronchodilator-corticosteroid inhaler approach still fails to prevent attacks a long acting bronchodilator inhaler may be added. These drugs are often derived from xanthine derivatives (an example is aminophylline).

Should the bronchodilator-corticosteroid-xanthine derivate combination not deliver the desired results, oral steroids can be added.

Other inhaled agents include sodium cromoglycate which stabilises mast cells; cromoglycate is introduced early in the escalating pathway of treatment.

Drugs which interfere with the metabolism of leukotrienes can be used.

In addition to the various drugs prevention by avoiding precipitants is beneficial.

Patients who have asthma tend not to be given beta-blockers or non-steroidal anti-inflammatory drugs. Beta-blockers can precipitate asthma, possibly by interfering with beta-adrenoreceptor mediated bronchodilatation. NSAIDs disrupt the arachidonic acid cascade and may bias it towards the production of bronchoconstriction-inducing leukotrienes.

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In an acute asthma attack inhaled oxygen can start the ball rolling but bronchodilator nebulisers are also given. The nebulised drugs are usually salbutamol and ipratropium bromide. The latter is a muscarinic antagonist which blocks the parasympathetic bronchoconstrictor innervation to the airways. Salbutamol and iptratropium bromide often work well as a team.

If a round of nebulisers fails to resolve the situation or features are present which indicate a severe attack, high dose corticosteroids are given. The initial dose may be intravenous; the remainder of the course is given orally if possible.

If the attack is particularly severe or fails to resolve, intravenous bronchodilators are given. Both salbutamol and aminophylline can be used; the latter is likely to have more side effects. Should the attack be of a degree whether intravenous therapy is even being considered it is prudent to alert the ITU team to the presence of the patient because if the intravenous therapy fails it is very likely that the patient will require intubation and mechanical ventilation and it is better if the ITU team are forewarned in advance rather than having to spring into action when the patient is in severe respiratory distress that is resistant to other treatment.

In terms of discharging the patient they should have returned to their normal preadmission medication, have restored a peak flow of at least 80% of normal and have spent one night without an attack (asthma tends to flare up at night so failure to observe this precaution and discharging the patient prematurely may result in a readmission the same night with a resurgence of the acute attack).

Management of asthma in the community by the patient can be guided by the peak flow. If the PEFR drops below 80% of normal the patient should double the dose of their inhalers (bronchodilator and steroid). If it drops to 60% they should take the first dose of the course of oral corticosteroids they will have been prescribed for such an situation and seek medical advice. If the PEFR falls to 50% the patient should take the steroids and go to accident and emergency.