Extrinsic, intrinsic, occupational, stable bronchial asthma: causes, symptoms, treatment
Bronchial asthma is an obstructive lung disease characterised by the presence of diffuse bronchospasm that, in many cases, appears in response to numerous types of stimuli
The typical finding of bronchial asthma is the reversibility of airway obstruction. Indeed, in the interval between bronchospastic episodes, the patient is often asymptomatic and may even present normal respiratory function.
When the patient presents with an asthmatic attack resistant to conventional therapy, this pathological condition is referred to as an asthmatic state.
Although there is considerable overlap in clinical symptomatology, it may be useful to classify bronchial asthma into two categories, extrinsic bronchial asthma and intrinsic bronchial asthma:
- extrinsic bronchial asthma: is characterised by the presence of bronchospasm that appears in atopic patients (individuals who show an allergic reaction to exposure to allergens) when they are exposed to environmental irritants;
- intrinsic bronchial asthma: it occurs in patients who suffer asthmatic attacks without any evidence of atopy.
Intrinsic bronchial asthma most frequently appears in childhood, while intrinsic bronchial asthma often begins in adult life.
Occupational asthma
The term ‘occupational asthma’ is used to describe a bronchospasm that develops in response to an irritant agent present in the workplace.
Typically, the sufferer becomes asymptomatic during periods away from work, such as weekends or holidays.
Stable asthma
Stable asthma, on the other hand, is that form of asthma that is present with equal intensity for more than four weeks, during which time the patient predisposed to this clinical picture shows no tendency to an increase in symptoms or the need for medication.
Conversely, unstable asthma is defined as asthma in which the patient shows worsening symptoms compared to the previous 4 weeks.
Causes and risk factors of extrinsic bronchial asthma
In some cases of extrinsic bronchial asthma, it is possible to link the onset of asthmatic symptoms to a specific triggering factor; therefore, the terms stress bronchial asthma or pollen bronchial asthma are frequently used.
A large proportion of patients with extrinsic bronchial asthma may show asthmatic attacks triggered by different allergens such as house dust, animal dander and certain foods or food additives such as sulphites.
Besides allergens, asthmatic attacks can be triggered by pharmacological agents such as beta-blockers and aspirin, environmental pollutants such as sulphur dioxide, oxidants, physical exertion, cigarette smoke and respiratory infections.
Pathophysiology of brochial asthma
In addition to the presence of bronchospasm, the airways of a patient with bronchial asthma may be obstructed by oedema and excessive secretions.
Frequently, the asthmatic patient has thick and tenacious mucous secretions that cause clogging of the more distal airways.
The lack of uniform lung ventilation then causes an imbalance between ventilation and perfusion (V/Q), which in turn is responsible for the onset of hypoxaemia.
Initially, airway obstruction hinders the exhalation phase, causing air entrapment and progressive hyperinflation of the lungs.
Due to air entrapment, residual volume increases at the expense of vital capacity.
The combination of increased airway resistance and lung hyperinflation eventually leads to increased work of breathing in patients with bronchial asthma.
Symptoms and signs
Asthma presents in the form of two different stages (asthmatic attack and stationary phase) each characterised by different symptoms and signs.
Symptoms commonly experienced in the stationary phase (i.e. between attacks) are:
- coughing, especially at night
- dyspnoea (shortness of breath and difficulty breathing);
- sense of constriction in the chest;
- easy fatigability.
During an asthmatic attack, the symptoms and signs are:
- severe dyspnoea (severe shortness of breath and difficulty breathing);
- wheezing;
- very intense sense of constriction in the chest;
- coughing;
- inability to speak (shortness of breath);
- tachypnoea (increased respiratory rate);
- tachycardia (increased heart rate);
- drowsiness;
- confusion;
- dizziness;
- asthenia (lack of strength);
- cyanosis (blue lips and/or fingers);
- fainting.
Asthmatic attacks
- occur relatively often;
- do not appear to improve over time;
- are worse during the night and early morning hours;
- they occur in response to some specific event such as physical activity or exposure to allergenic substances such as dust or pollen.
Diagnosis of bronchial asthma
Diagnosis is based on anamnesis, physical examination and the performance of various tests and examinations.
Anamnesis
Typically, patients presenting with an asthmatic attack complain of chest tightness, difficulty breathing, wheezing and/or coughing.
The onset of these symptoms may be rapid or gradual.
When symptoms appear rapidly, they may also disappear quickly following appropriate treatment.
Although some idea of the severity of the asthmatic attack can be derived from the history, the degree of dyspnoea is not in itself a reliable predictor of severity.
Although the presence of dyspnoea and wheezing may be suggestive of bronchial asthma, other conditions, such as congestive heart failure, bronchitis, pulmonary embolism and upper airway obstruction, may also show similar symptomatology.
In many cases, it is the patient’s age, pathological history, physical examination and the results of laboratory tests and chest X-ray that will confirm the diagnostic suspicion.
Objective examination
The clinical examination provides important objective information useful in confirming the diagnosis and assessing the severity of the obstruction.
Inadequate assessment of the patient’s clinical status can be a fatal error, as it can lead to inadequate treatment and clinical control.
Clinical findings associated with bronchial asthma include:
- tachypnoea;
- use of accessory muscles of respiration;
- prolongation of the expiratory phase;
- increased antero-posterior diameter of the chest;
- presence of expiratory hisses;
- presence of intercostal indentations.
The severity of the asthmatic attack is suggested by the obvious use of the accessory muscles of respiration, the presence of a paradoxical pulse, the extent of tachypnoea and the presence of inspiratory and expiratory hisses.
The use of the accessory muscles of respiration is secondary to pulmonary hyperinflation which, by causing a flattening of the diaphragm, makes ventilation less efficient.
The prolongation of the expiratory phase occurs because, as the intrapulmonary airways are obstructed, the movement of air out of the lung is slowed.
Increased antero-posterior diameter of the chest occurs in the presence of air entrapment and pulmonary hyperinflation.
The hissing is related to the rapid airflow in the narrowed airways, which causes them to vibrate.
Respiratory retractions are related to the intermittent depression of the skin surrounding the rib cage during each inspiratory effort.
They occur when a significant drop in intrapleural pressure causes the skin overlying the chest wall to sink inwards.
The significant intrapleural pressure drop is also responsible for the reduction in pressure during inspiration (paradoxical pulse).
It is not uncommon to observe that the patient, during an asthmatic attack, leans forward while fixing his hands or elbows on a nearby table, as this position provides a significant mechanical advantage for the accessory muscles of respiration.
Other examinations
In addition to routine peripheral blood tests, other examinations and tests may be useful, in particular X-rays, spirometry, bronchial provocation tests, haemogasanalysis and tests to detect allergies.
The chest X-ray is very useful in identifying the presence of complications such as pneumonia, atelectasis, or pneumothorax.
In the absence of complications, the chest X-ray typically shows hyperinflation of the lung fields affected by the asthmatic process.
During an asthmatic attack, it is typically not possible to perform full pulmonary function tests, but it is, however, indicated to perform a simple spirometry test at the patient’s bedside.
This examination may, in fact, be useful in assessing the extent of the obstructive process and responsiveness to therapy.
Measurement of peak airflow and forced expiratory volume in 1 second (FEV1) is commonly used for this purpose and is, moreover, easy to assess unless the patient is severely dyspnoic.
A peak airflow of less than 100 l/minute or an FEV1 of less than 1.0 litre suggests the presence of severe obstruction.
Bronchial provocation tests are useful in identifying the degree of airway reactivity in patients with symptoms typical for bronchial asthma, but who present with normal findings on pulmonary function tests.
Methacholine is the compound most frequently used in bronchial provocation tests, as it increases parasympathetic tone in airway smooth muscle, causing bronchospasm.
Bronchial asthma patients show a greater than 20 % reduction in FEV1 in response to methacholine, while healthy subjects show little or no response. Read more:
Bronchial provocation test with methacholine: execution, preparation, risks
Bronchial hyperreactivity: meaning, symptoms, diagnosis and treatment
- ABGs are extremely useful for assessing the severity of the asthmatic attack, if the bronchospasm is so severe that the patient cannot perform the forced expiration manoeuvre. The degree of hypoxia and
- of hypercapnia present are a reliable guide in assessing the severity of airway obstruction. Typically, paC02 decreases with the onset of the asthmatic attack, whereas a normal or increased paC02 value indicates the presence of a more severe degree of obstruction or that the patient is beginning to experience respiratory fatigue. Additional signs of fatigue include tachypnoea, diaphoresis, paradoxical abdominal breathing, sensory disturbances and reduced peak airflow. Paradoxical abdominal breathing is observed as an inward movement of the abdominal wall during inspiration and is associated with the appearance of diaphragm fatigue. Read more: Arterial haemogas analysis: procedure, interpretation, is it painful?
The importance of a rapid diagnosis
An important objective in the assessment of an acute asthmatic attack is related to the efficiency of the clinical examination.
This is always valid in the medical field and even more so in the case of asthma: many asthma patients require immediate treatment, so an experienced physician will be the one who is able to perform an efficient and rapid assessment, without further delaying the start of therapy.
An essential part of asthma attack assessment is also to avoid the use of unnecessary diagnostic tools, especially when the patient is acutely suffering: this allows treatment to be started earlier, avoiding costs for both the patient and the NHS and avoiding invasive and risky examinations, such as a bronchoscopy.
Treatment
Initial treatment should be directed at achieving adequate oxygenation, ensuring bronchodilation and reducing airway inflammation.
Most patients suffering an acute asthmatic attack develop hypoxaemia secondary to a V/Q imbalance.
In some cases, the hypoxaemia will be severe enough to be life-threatening, but can almost always be corrected by adequate oxygen therapy.
Numerous drugs can be used to achieve bronchodilation and reduce airway inflammation, such as beta2-stimulants, xanthines, parasympatholytics and steroids.
In most mild cases, bronchospasm can be reversed by the use of beta2-adrenergic stimulants administered aerosolally.
Inhaled beta-agonist bronchodilator compounds offer the following advantages over orally administered bronchodilators: faster onset of clinical effect, lower dosage requirements, lower incidence of systemic side effects and better airway protection from irritant compounds.
The most common mode of administration of bronchodilator compounds is using pre-dosed inhalers (MDI), which are popular precisely because they are easy to use.
Aerosol bronchodilator treatment with small-volume nebulisers (SVN), on the other hand, is useful in those patients who are unable to use the MDI.
SVN treatment is most often prescribed every 4-6 hours, but during a severe bronchospastic crisis it may be given more frequently, albeit with close monitoring.
Finally, continuous bronchodilator nebulisation therapy may prove useful if the asthma patient does not respond to conventional therapy and is close to respiratory failure.
Therapy with oral or intravenous theophylline is indicated in patients who do not respond to treatment with aerosol beta-agonists, or when the asthmatic attack is severe.
During a severe acute asthmatic attack, if the patient does not respond adequately to beta-agonists and intravenous theophylline, intravenous corticosteroids may be combined.
The anti-inflammatory effect of the latter may, however, take several hours to fully manifest itself, so this treatment should be started as soon as possible if required.
In addition, if conventional bronchodilators do not have the desired effect, therapy with ipratropium bromide may be initiated.
The physician should also avoid giving patients certain drugs with an acute asthmatic attack.
Sedatives can, in fact, trigger ventilatory failure and should only be used if the patient is intubated and mechanically ventilated. Inhaled corticosteroids, acetylcysteine, sodium cromoglycate and aerosols with high-density substances may worsen bronchospasm as they tend to irritate the airways.
Other treatment goals include treatment of airway infections, mucolysis and adequate hydration.
Hydration improves the patient’s respiratory condition by encouraging the release of secretions.
Favourable prognostic signs include improvement in vital signs, pa02, lung auscultation, sensorium and respiratory mechanics.
Since each of these parameters considered alone can be confusing, it is always best to assess several parameters at once in order to obtain a more accurate picture of the patient’s response to current therapy.
If the patient becomes fatigued despite treatment, mechanical ventilation is then required.
The decision to intubate and ventilate the patient can be a difficult one, especially when the blood gas data are inconclusive.
In this case, the combined use of the clinical findings, haemogasanalytical data and peak flow values described above and in the clinical case below will provide the most reliable data for assessing the need for mechanical ventilation.
The ultimate goal of asthma treatment is to prevent or, at least, decrease the number of future attacks by reducing the level of airway reactivity.
Consequently, once the acute episode has passed and the patient has recovered, it is necessary to assess the severity of the underlying asthmatic pathology.
This can be done through careful anamnestic collection, respiratory function tests and, in selected cases, provocative tests.
The latter are especially useful in assessing patients with suspected occupational bronchial asthma
Particularly useful in enabling the patient to assume an active, independent lifestyle is education, which consists of avoiding irritants, using appropriate medication and avoiding their side effects.
In this regard, current international guidelines on the treatment of asthma identify inhaled corticosteroids as the cornerstone of the therapeutic approach to asthma.
These guidelines show the tendency to reserve the use of ‘short-acting’ beta2-stimulants for administration on an as-needed basis, avoiding their continuous use; in fact, while this approach may be sufficient to control the asthmatic disease in its mild-intermittent forms, in mild-persistent, moderate-severe forms it is necessary to combine the regular administration of corticosteroids as maintenance therapy.
The careful application of this treatment protocol in maintenance not only reduces the severity of asthmatic symptoms, but also allows the patient to improve his or her quality of life; one of the most important objectives in the treatment of reversible bronchitis is thus achieved.
Long-acting inhaled beta2-stimulants such as salmeterol, which exert a bronchodilator effect of at least 12 hours, are particularly well suited to accompanying steroids in the maintenance therapy; this effect is much more prolonged than that of short-acting inhaled beta2-stimulants such as salbutamol, which are characterised by a duration of action of only 4-6 hours.
Long-acting beta2-stimulants are an elective indication in the prolonged symptomatic treatment of bronchospastic states, where they provide effective control of daytime and night-time symptoms and superior protection against exercise-induced symptoms.
Their regular use also makes it less necessary to resort to ‘short-acting’ beta2-stimulants, which nevertheless retain their therapeutic role in treating the acute episode.
Finally, the use of sodium cromoglycate helps to stabilise mast cells so as to prevent them from releasing substances with pharmacological action, such as histamine, which can in fact cause bronchospasm.
Training the patient in the use of peak flow assessment devices (autonomous monitoring of the degree of airway obstruction) can be helpful in knowing when to increase medication intake and seek medical advice.
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