Bronchial extrinsic asthma J45.0

Variable, intermittently occurring, fully or partially reversible airway obstruction caused by allergenic environmental substances or substances from the working environment as a result of inflammation and hyperreactivity of the airways. Clinically, extrinsic (as well as intrinsic) bronchial asthma is characterized by a sudden shortness of breath due to bronchoconstriction. Status asthmaticus (severe asthma attack) is a severe asthma attack that lasts for at least 24 hours and is refractory to therapy.

Preferably in children and adolescents, but all age groups can be affected.

Prevalence in adults about 5%; in children up to 10%.

m:w=2:1

About 15% of the population suffer from unspecific bronchial hypersensitivity.

Allergic disposition, genetic factors: if both parents suffer from allergic bronchial asthma, children have a 60-80% risk of developing the disease.

About 25% of patients with allergic rhinitis also develop bronchial asthma during their lifetime (so called floor change).

People with polymorphisms in the ORMDL3 gene have a 70% increased risk of developing bronchial asthma.

IgE-mediated hypersensitivity reaction of the immune system of the immediate type against inhalation allergens. These are proteins to which most people do not have an allergic (pathological) reaction. The pathogenesis of allergic asthma begins with sensitization. The allergen is phagocytized by an antigen-presenting cell of the bronchial system (APC = alveolar macrophage - dendritic cell) and the antigen in question is presented on its surface as part of the MHC-II complex. After migration into a regional lymph node, contact is made with a naive T-helper cell, which differentiates into a Th2 cell and is thus capable of producing the Th2-specific cytokines(Il-4, interleukin-5, interleukin-9, interleukin-13) with which plasma cells are stimulated to produce allergen-specific IgE antibodies. Other lymphocyte populations such as gamma-delta T cells, Th17 cells, Th9 cells and ILC2 are also involved.

Consecutive IgE-mediated eosinophilic inflammation of the bronchial mucosa with release of inflammatory mediators from mast cells, basophilic leukocytes and macrophages induces epithelial damage of the bronchial mucosa, hyperplasia of goblet cells, contraction of bronchial muscles, mucosal edema and secretion of tough mucus. The following mast cell mediators play a pathogenetic role in IgE-mediated inflammation: histamine, leukotrienes, bradykinins, prostaglandins, enzymes such as tryptase and chymase, proteoglycans and chemokines (including Il-4, interleukin-5, TNFalpha, RANTES = CCL5, eotaxin).

Autonomic innervation of the bronchial tubes plays a further role in the pathogenesis of the allergic asthma reaction. Dysfunctions of the bronchodilatorily active acetylcholine receptors can be detected. Furthermore, pro-inflammatory neuropeptides such as substance P are released from autonomous C-fibres.

Late consequences of eosinophilic inflammation of the bronchial mucosa are chronic remodelling processes (remodelling) with fibrosis and hypertrophy of the smooth muscles.

The cause of the unspecific hypersensitivity of the airways, which is also present in the forms of extrinsic (as well as intrinsic) asthma, is ultimately unknown.

• Triggering (or co-triggering) factors that are suitable for inducing asthmatic reactions:
• physical exertion (exercise induced asthma - see also Wheat-dependent exertion-induced anaphylaxis).
• Infections: Viral, bacterial and mycotic infections can induce an asthma attack in both extrinsic and intrinsic asthma.
• Other factors: Temperature influences such as cold, psychological stress.

Allergic (extrinsic) asthma begins in childhood.

The diagnosis "asthma" is a clinical diagnosis. It is based on characteristic complaints and symptoms and evidence of airway obstruction and/or bronchial hyperreactivity. It is characterised by the repeated occurrence of attacks of breathlessness and/or chest tightness and/or coughing with or without sputum, often at night.

The bronchial obstruction may occur immediately, within minutes, or only after an interval of 4-8 hours after allergen exposure.

If general complaints such as muscle pain, arthralgias or fever with BSG elevations and leucocytosis occur 6-8 hours after exposure to the allergen, exogenous allergic alveolitis must be considered.

The symptoms can be intermittent, e.g. situational (e.g. workplace-related: flour dust, isocyanates) or site-related (e.g. animal contact), seasonal, e.g. pollen count (seasonal allergic asthma) or continuous.

Auscultatory: Dry background noises (wheezing, whistling, humming) during auscultation, possibly to be provoked by forced expiration; prolonged expiration.

In case of severe obstruction with pulmonary hyperinflation or pronounced emphysema often very quiet breathing sounds (silent lung).

During the seizure, the patient sits upright and breathes with the aid of the respiratory muscles

In case of severe respiratory distress (especially in children): thoracic retractions (especially jugulum, intercostal, epigastric);

If the patient becomes exhausted, possibly respiratory alternans (alternation between thoracic and abdominal breathing)

Proof of the signs of airway obstruction may be missing in the symptom-free interval.

Chronic cough without asthma (as asthma equivalent) may be an indication of bronchial asthma.

Tachycardia: possible pulsus paradoxus (inspiratory blood pressure drop >10mmHg)

Stage classification of the airway obstruction (see also classification according to degrees of asthma control).

• Stage I (mild): Low dyspnoea, diffuse wheezing
• Stage II (moderate): dyspnea at rest, use of accessory respiratory muscles, loud gushing, normal or restricted gausal exchange
• Stage III (severe): severe dyspnoea, cyanosis, use of accessory respiratory muscles, gulling or absence of breathing sounds (silent lung), pulsus paradoxus (with the over-inflation of the lungs, at a capacity of <1.25 l per second, a drop in systolic blood pressure during inspiration runs parallel; RR expiratory 10 mm Hg higher than inspiratory). Gaussian exchange significantly restricted.
• Stage IV (acutely life-threatening): severe dyspnoea, cyanosis, lethargy, confusion, pulsus paradoxus (drop in systolic blood pressure during inspiration >30-50mm Hg).

Classification by degrees of asthma control. The degree of asthma control depends on the symptoms prevailing during the day and night, restrictions in daily activities, lung function, the need for emergency medication and the frequency of exacerbations

• Grade 1 Controlled bronchial asthma
• Grade 2 Partially controlled bronchial asthma
• Grade 3 Uncontrolled bronchial asthma

Detailed anamnesis

Proof of variable and/or stress-induced airway obstruction by means of a pulmonary function test (see spirometry below)

Allergological step-by-step diagnosis (prick test, specific IgE in serum, eosinophilic granulocytes and ECP elevated in blood and sputum)

ECG: Signs of right heart strain

Lab. CBC, chem panel, SGS (CRP). Sputum test

COPD

Reflux diseases: in patients with gastroesophageal reflux there may be minute amounts of nocturnal aspiration of gastric secretion. A hyperreactive bronchial system can react to this with chronic coughing and bronchitic symptoms.

Atypical pneumonia (protracted course)

Pulmonary artery embolism

Heart failure/cardiovascular diseases

Aspiration, e.g. foreign bodies

Neuromuscular diseases (respiratory pump disorders)

Postinfectious disorders (e.g. pertussis, bronchiolitis obliterans)

Bronchiectasis

Psychosomatic respiratory disorders (psychogenic hyperventilation,

vocal cord dysfunction (e.g. vocal cord dysfunction - VCD)

Chronic persistent cough of other etiology

Spontaneous pneumothorax

Chronic obstructive bronchitis with/without emphysema (COPD)

Trachobronchomalacia

Diffuse parenchymatous lung diseases (including exogenous allergic alveolitis, sarcoidosis) Tuberculosis

Cystic fibrosis (cystic fibrosis)

The goal of all asthma therapy is to achieve or maintain the status of controlled asthma. By assessing the degree of control, the therapy goal is also defined at the same time.

Note: Each patient should receive a written therapy plan (with emergency plan and the necessary emergency medication) and asthma training.

The following therapy goals should be aimed for depending on the patient's age and concomitant diseases:

• Normalization or achievement of the best possible lung function and reduction of bronchial hyperreactivity;
• Improvement of the health and asthma-related quality of life;
• reduction of asthma-related mortality.

Pharmacotherapy: If the trigger mechanism of the asthma attack can be blocked by medication, drug therapy is indicated. The most important anti-asthmatic drugs are available for inhalation application.

Note: In the case of several dosage forms of one active substance, inhalation application should be preferred.

The drugs are divided into:

• Therapeutic agents for rapid symptomatic therapy
• and
• Long-term Therapeutics

Need therapeutics for rapid symptomatic therapy

• SABA=Short acting beta-2-agonist: Rapid acting beta-2 sympathomimetic. These include: fenoterol, salbutamol, terbutaline and the protracted formoterol.
• Inhaled short-acting beta-2 sympathomimetic (SABA) plus anticholinergic as a fixed combination: Fenoterol plus ipratropium
• Theophylline (drops or solution = preparations with rapid release of active ingredient)

Long-term Therapeutics

• Inhaled corticosteroids (ICS= Inhaled Corticosteroid): Beclomethasone, Budesonide, Fluticasone and others
• LABA = long acting beta-2 agonist: inhaled long acting beta-2 sympathomimetics. These include: formoterol, salmeterol
• Leukotriene receptor antagonist (LTRA): montelukast
• Combination preparations ICS/LABA: formoterol/beclometasone, formoterol/budsonide, salmeterol/fluticasone

Other medicines (to be used only in justified cases):

• Systemic glucocorticosteroids
• Theophylline (preparations with delayed release of active ingredient)
• Omalizumab: Anti-IgE treatment with the monoclonal antibody: Omalizumab is an option for adults and children 6 years and older with severe persistent (IgE-mediated) allergic asthma.

SCIT/SLIT: Specific immunotherapy for allergic asthma: The use of specific subcutaneous (SCIT) or sublingual immunotherapy (SLIT) for allergic asthma requires an individual indication, as their efficacy in asthma is not assured according to current studies. It is recommended in cases of sensitization to a few allergens and short duration of illness. Contraindicated is the specific immunotherapy for uncontrolled or severe asthma at FEV1 ≤ 70% of the target value (for adults).

Note: In principle, specific immunotherapy is not a substitute for effective anti-asthmatic pharmacotherapy.

Step-by-step scheme of long-term asthma therapy see below Bronchial asthma (overview)

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