Pathology of bronchial asthma

2021-01-27 12:00 AM

Due to the action of inflammatory chemical mediators and the role of the autonomic nervous system including the cholinergic system, the adrenergic system and the non-adrenergic non-cholinergic system.


According to GINA 2002 (Global Initiative for Asthma), bronchial asthma is a chronic inflammatory disease of the bronchi in which the participation of many cells and many cellular components; chronic inflammation causes a coordinated increase in bronchial responsiveness that results in recurrent episodes of hissing, difficulty breathing, chest tightness, and cough, especially at night or in the early morning; These episodes are often associated with an extensive but variable bronchial obstruction that is often spontaneous or therapeutic in nature. The above basic views positively contribute to improving the quality of asthma diagnosis and treatment.


Asthma is a common disease, appearing at all ages, children make up the majority of adults, the rate of 2/1. Epidemiological studies in recent years show an average frequency of about 5%, children under 5 years of age 10%. Many recent studies show that this frequency has increased 3 - 4 times in the past decades.

The prevalence of bronchial asthma in France between the ages of 18 and 65 years is 3.9% (Charpin et al. 1987, Maladies respiratoires 1993, p. 335), 5% in Italy between the ages of 5 and 64 years (Paolette et al. 1989, Maladies respiratoires 1993, p 335). In Vietnam, in Hanoi, in 1991 it was 3.3%, in 1995 it increased to 4.3% (Vuong Thi Tam et al. In the report of the 1991-1995 review meeting of the National Institute of Tuberculosis and Disease Control. lung); In Ho Chi Minh City, the prevalence of bronchial asthma is 3.2 (1.39% (Pham Duy Linh et al. reported at the 5th Conference on Medicine and Pharmacy in Ho Chi Minh City from 25-27) / 11/1996), in the city of Hue, the prevalence of asthma in 2000 was 4.58 (1.12%).


Allergic asthma

Allergic asthma without bacterial infection:

Respiratory allergens: usually house dust, house bugs such as Dermatophagoides pt√©ronyssimus, blanket dust, animal claw feathers such as dogs, cats, mice, rabbits, etc ; pollen, plants, or occupation in textile workshops.

Allergies are aspirin, non-steroid anti-inflammatory, penicillin; eggs, certain dyes and food preservatives.

Asthma allergic bacterial infections:

Common bacteria are streptococcus pyogenes, streptococcus pneumonia, staphylococcus aureus ...

Virus: Commonly respiratory syncytial virus, parainfluenza, flu.

N warmer: N damage Cladosporium or Alternaria fungus, the fungus.

Asthma is not caused by allergies

Genetics:  family history, related antigens HLA harmony organization.

Stress: When exertion and especially when stopped exertion.

Weather: Cold air.

Endocrine disorders: During adulthood, pre-menstrual period, pregnancy, menopause.

Psychological factors: Anxiety, emotional conflict, emotional trauma.

Mechanism of pathogenesis

Asthma occurs through 3 processes


The basic process in the mechanism of bronchial asthma begins when the allergen passes and the body produces an allergic reaction through the role of the lgE antibody. Broncho-inducing cells include mast cells, polymorphonuclear leukocytes (eosinophils, eosinophils, neutrals), alveolar macrophages, mononucleosis, lymphocytes, and platelets that release mediators. inflammatory chemicals such as histamine, serotonin, bradykinins, thromboxane, prostaglandin, leukotriene, PAF and some interleukins.


Due to the action of inflammatory chemical mediators and the role of the autonomic nervous system including the cholinergic system, the adrenergic system and the non-adrenergic non-cholinergic system.

Increased bronchial response

Occurs after allergen enters the body, through the action of inflammatory cells. This is a non-specific pathological state for bronchial asthma.

Typical clinical symptoms of an asthma attack

Onset stage

Asthma attacks often appear suddenly at night, especially at midnight; The time to appear depends on many factors such as exposure to respiratory allergens, food, exertion, cold air, upper respiratory tract virus infection, etc. Symptoms such as the itchy nose, sneezing, water runny nose, tears, intermittent cough, restlessness etc ... but not always.

Exacerbation phase

Thereafter, dyspnoea occurs, slow breathing, rapid expiratory dyspnoea, during an asthma attack in the patient's chest, prominent accessory respiratory muscles, purple in the limbs may be followed. spread to face and body. Slow breathing, long hissing breath. Standing far away can hear the patient hissing or cockles. Hearing a lot of hissing and snoring. The difficulty of breathing long or short depends on the patient.

Relapse phase

After a few minutes or a few hours, the asthma attack gradually subsides. At this time, hear the lungs detected a lot of moisture, a little snoring. Sputum much signalling the asthma attack is gone.

Period between attacks

Between attacks, the above symptoms disappear. Clinical examination is normal at this time. However, if doing some tests such as exercise, using acetylcholine, then still detect bronchial hyperresponsiveness.

Subclinical symptoms

Explore respiratory function

Ventilation disorders:

Measurement of FEV1 (maximum expiratory volume in the first second) and FEV1 / FVC (Tiffanie ratio): During an episode of less than 80% reduction compared to theory.

PEF (peak expiratory flow) measurement: During an episode less than 80% less than theoretical.

Blood gas:

Measure PaO2, PaCO2, SaO2, and blood pH, this is an additional test to assess the degree of respiratory failure.

Allergy tests:

Skin test: Using the prick method, red skin is positive.

Test for antibodies: Like agglutination antibodies, the precipitating antibody is usually lgG, lgM.

Quantification of total lgE and specific lgE.

Chest film:

During an asthma attack, the chest swells, the rib spaces widen, the diaphragm is lowered, the lungs light up, the hilum is darkened.


Implementing the quadrants

Personal history of allergy:

Such as eczema, urticaria, previous exposure to allergens, a family history of asthma, allergies or other factors such as exertion, cold, etc.

Spasmodic stenosis syndrome:

K they breathe slow, mainly expiratory lung hiss heard many rans, ran snoring, the film shows images of lung emphysema.

Nature of dyspnoea:

The dyspnoea is regressive in nature, responding well to bronchodilators, bronchodilator therapy with positive beta 2 agonists ie, after using beta 2 agonists, FEV1> 200ml and FEV1 / FVC> 15%.

Differential diagnosis

A patient who has a history of heart valve disease such as mitral stenosis, open aortic valve, high blood pressure, difficulty breathing fast, the 2 periods, lungs heard many flashes of fluid retention, few ran snoring, CXR shows image retention, ECG to further verify the cause.

Exacerbation of chronic obstructive pulmonary disease:

C √≥ history of the chronic obstructive pulmonary disease usually caused by smoking, syndrome infection, difficulty breathing fast, without a history of personal and family allergy or asthma, pulmonary rales moisture to bead together with snakes and snoring, bronchial rehabilitation with negative beta 2 agonists.

Severity level


Symptoms occurred <1 time / week.

Short outbreaks.

Night symptoms <2 times / month.

FEV1 or PEF ≥ 80% compared with theory

Variable PEF or FEV1 <20%


Symptoms occurred> 1 time / week but <1 time / day.

Outbreaks can interfere with activity and sleep.

Night symptoms> 2 times / month.

FEV1 or PEF ≥ 80% compared with theory.

The PEF or FEV1 variation is 20 30%.


Symptoms occur every day.

Outbreaks affect activity and sleep.

Night symptoms> 1 time / week.

Daily use of an agonist nebulizer (2 short effects

FEV1 or PEF 60-80% compared with the theory

Variable PEF or FEV1> 30%


Symptoms occur every day.

There are frequent outbreaks.

Symptoms usually occur at night.

Limit physical activity.

FEV1 or PEF ≤ 60% compared with the theory.

Variable PEF or FEV1> 30%


Acute complications

Severe acute asthma: C may originate from severe acute asthma threatening syndrome, which may correspond to an acute episode of asthma that does not respond to conventional treatment and worsens; or happens very acute sometimes within minutes. It is a critical condition with a short life-and-death prognosis.

Diagnosis should be made early and urgent.

Respiratory signs:

The severe respiratory condition with cyanosis, sweating, shallow tachypnoea, frequency above 30 beats/min with muscle markers pulling the respiratory muscles.

Perceptual Disorders: anxiety with wrestling or vice versa, drowsiness can gradually enter a coma.

Slow breathing may indicate respiratory muscle weakness and warn of respiratory arrest.

Lung hearing: Silence both sides of the lungs.

Peak expiratory flow rate of fewer than 150 litres/min.

PaO2 < 60 mmHg, PaCO2 > 45 mmHg.

Blood pH <7.38.

Cardiovascular signs:

Rapid pulse is usually over 120 times/minute, the slow pulse is a very serious sign signalling stop circulation.

The paradoxical circuit causes the pulse to decrease amplitude during the inlet, which can be determined by measuring the systolic pressure between the expiration and the expiration period usually above 20 mmHg.

Heart failure acute with signs of right heart failure.

Blood pressure may increase in association with an increase in Paco2, and hypotension in extreme cases.


Due to the broken air bubble.

Bronchitis - lung infections:

Normal cause by Streptococcus pneumonia, Haemophilus influenza, Staphylococcus aureus, mycoplasma pneumonia, legionella pneumophila.

Chronic complications

When punctured multi-lobular perforation:

Often there is difficulty breathing during exertion, during heavy work, purple lips and limbs, chest deformity in the shape of chicken breast or barrel shape, percussion, and a decrease in sound.

Sediment volume and functional residue capacity increase, there is a disorder of coordinated ventilation, the PaO2 decreases only in the later stages and the PaCO2 increases only in the later stages.

Chronic respiratory failure:

Purple and dyspnoea: Fast shallow breathing, exhalation of lips closed, sign of HOOVER.

Chronic obstructive pulmonary failure with a marked decrease in sediment volumes, mean and peak flow rates, increased pulmonary dilation, limited chronic respiratory failure with decreased lung volume, decreased lung relaxation, depending on degree of impairment with a PaO2 below 65-70 mmHg and a PaCO2 above 43 mmHg.

Difficulty breathing gradually increases from difficulty breathing with exertion, to difficulty breathing when climbing a slope or climbing stairs, to difficulty breathing when walking fast on a flat road, to difficulty breathing slowly on a flat road, finally difficulty breathing when doing light work such as cleaning, undressing, and later having difficulty breathing while resting. Purple lips, limbs, face if heavy purple body.

Right heart failure symptoms: Clinical and subclinical.

PaO2 decreases to 70 mmHg, PaO2 increases by 50-80mmHg, SaO2 <75%, blood pH can decrease <7.2.


Management of bronchial asthma in steps

Step 1 (Interstitial asthma):

In intermittent bronchial asthma, the severity of an exacerbation varies from patient to patient and over time. Severe exacerbations are very rare.

The drug used in most patients with mild-distance bronchial asthma is a fast-acting nebulizer 2 agonist, in addition to either chromone or a leukotriene antagonist. Anticholinergics, oral β2 agonists, or short-acting theophylline can be interfered with nebulized β2 agonists, although these drugs have a slow onset of action and are often at risk of multiple effects. side effect more. Often more severe or prolonged exacerbations may require the use of a short course of oral glucocorticoid therapy.

Level 2 (Mild persistent asthma):

Patients with mild persistent bronchial asthma should receive daily medication to complete and maintain asthma control. The first treatment is an anti-inflammatory drug that is taken every day. Selective treatment of an aerosolized glucocorticoid (200 - 500μg Beclomethasone dipropionate, or Budesonide, 1000 - 250μg fluticasone divided 2 times/day). Alternatives are slow-release theophylline, chromones, and anti-leukotriene, but these are less effective than aerosolized glucocorticoids or are only effective in some patients. Long-term treatment of slow-discharge theophylline requires monitoring the concentration of theophylline in serum with a therapeutic concentration of 5-15μg / ml.

In addition to the above routine treatment, patients with second-line bronchial asthma can use a fast-acting nebulizer β2 agonist, but not more than 3-4 times/day.

Other bronchodilators may be used as anticholinergics, fast-acting β2 agonists, or short-acting theophylline, although these have a slow onset of action and are often at risk. has more side effects.

If long-term therapy is initiated with slow-release theophylline, chromone or leukotriene resistance, and symptoms persist after 4 weeks of treatment, then aerosolized glucocorticoid should be used. Nebulized glucocorticoid can be used initially instead of other drugs, or used together.

Tier 3 (Moderate persistent asthma):

Patients with moderately persistent bronchial asthma require daily medication to achieve and maintain control of bronchial asthma. The treatment of choice is the combination of an aerosolized glucocorticoid (200 - 1000 μg beclomethasone dipropionate, 400 - 1000 μg budesonide, 250 - 500 μg fluticasone divided 2-3 times/day) with a 2 to 2 long-acting aerosol β2 agonist. /day.

A combination of aerosolized glucocorticoid with a long-acting aerosol 2 agonist is a good and favourable combination.

Although a combination of nebulized glucocorticoid with a long-acting nebulizer β2 agonist is most effective, patients with persistent bronchial asthma can alternate medications such as the slow-release theophylline and agonists. β2 long-acting, anti-leukotriene drugs.

In addition to regular daily therapy, a fast-acting nebulizer β2 agonist can be used for reliever therapy, but not more than 3-4 times a day. Nebulized anticholinergics, rapid-acting β2 agonists, or short-acting theophylline can be substitutes for short-acting 2 agonists, although they have a slow onset of action and or are at risk for more side effects.

Level 4 (Severe persistent asthma):

In severe persistent bronchial asthma, the treatment goal is to achieve the best results - minimal symptoms, need for minimum rapid-acting nebulizer β2 agonists, best PEF, minimal exacerbations show about 1 time/day, and minimal side effects. Therapy is primarily a higher dose aerosolized glucocorticoid (> 1000 μg beclomethasone dipropionate / day in combination with a 2-daily-acting aerosol 2 agonist.

Long-acting nebulizer β2 agonists are the drug of choice, but alternative drugs such as slow-release theophylline, long-acting 2 agonists, and anti-leukotriene can be used. These drugs may be in addition to combination therapy of high-dose nebulized glucocorticoid with long-acting aerosol β2 agonists. Rapid-acting aerosol β2 agonists are also used when needed. If necessary, oral glucocorticoid can be taken in the lowest dose, preferably for a single tent in the morning to minimize systemic side effects.

High-dose aerosolized glucocorticoid may be used, but this use has not been shown to cause less systemic side effects than with an equivalent oral glucocorticoid dose. But this treatment is very expensive and can cause local side effects like a sore mouth. There is no evidence from studies recommending the use of aerosolized glucocorticoid in stable bronchial asthma in adults.

Supportive treatment

Oxygen therapy: when needed, oxygen is about 2l / min.

Antibiotics: Only used when bronchopulmonary superinfection.

Treatment of severe acute asthma attacks

Oxygen therapy: Must be performed immediately without waiting for blood gas results, high volume 6l / min if there is no chronic respiratory failure, if there is severe respiratory failure, low output 2l / min.


Beta 2 stimulants: Terbutaline (Bricanyl) 1 ampoule of 0.5 mg is the first aid measure at the patient's home.

When hospitalized, use Salbutamol nebulizer, 1 ml containing 5 mg mixed with 4 ml of physiological solution through an aerosol machine for inhalation for 10-15 minutes, can be repeated depending on clinical progress, every 30 minutes. Salbutamol can be administered intravenously continuously with an automatic syringe, the initial dose is usually 0.1 - 0.2 μg / kg/min, increasing the dose by 1 mg/hour according to the clinical course.


Indication of only beta-2 stimulants has failed; Initial dosage is usually 0.5 - 1 mg/hour intravenously by auto syringe.


Can be combined, used intravenously with 5% Glucose solution continuously at a dose of 0.5 - 0.6 mg / kg / hour.

Antibiotics: Used when there is an accompanying bronchopulmonary infection, cephalosporines, macrolides or respiratory fluoroquinolones can be used.


Methylprednisolone (Solumedrol) 60-80mg every 6 hours.

Breathing machine:

Is indicated in the asphyxiant form or in the body where drug therapy has failed to cause respiratory muscle depression.

Follow up the patient

The goal of treating acute asthma attacks is to get the symptoms to decrease rapidly and improve lung function as quickly as possible while minimizing the side effects of medications.

If initial treatment has no results, if the PaCO2 is still low, treatment can be continued in the hospital room; but if the PaCO2 increases and the pH becomes acidic, the patient should be referred to the recovery room for assisted ventilation.

For severe acute bronchial asthma is a medical emergency, urgent hospitalization is required in the respiratory resuscitation department. If a diagnosis of threatening severe asthma syndrome or severe acute asthma or severe asthma is at home, the patient should be referred immediately to the emergency department by an equipped ambulance.

Preventing asthma attacks from recurring

Currently, according to GINA, it is recommended that Seretide be used in the maintenance treatment of asthma attack and it has been found that patients with bronchial asthma treated with Seretide have a very little occurrence of severe asthma attacks.

Avoid adverse environmental factors

Avoid unnecessary physical activity.

Avoid contact with dust, smoke, especially cigarette smoke and other irritants.

Avoid contact with people with respiratory infections.

Keep the environment fresh.