Bronchial asthma in children

and adolescents
 GINA: history and purpose of creation
• in 1993 the National Institute of the Heart, Lungs and Blood(National
Heart, Lung, and Blood Institute) The United States, together with
the World Health Organization (WHO), created a working group that
developed

• The global strategy for the treatment

and prevention of asthma is GINA.
• Goals GINA:
– reduced asthma disability
– reduction in the frequency of premature deaths from asthma
– ensuring a fruitful and active life of patients,
 Asthma rule
All that is accompanied by
wheezing is asthma until proven
otherwise.
 Definition
• AD is a chronic allergic disease of the respiratory tract
involving many cells and cellular elements.
• Chronic inflammation causes the development of bronchial
hyperreactivity, leading to recurring episodes of wheezing,
shortness of breath, chest tightness and coughing, especially at
night or in the early morning.
• These episodes are usually associated with widespread, but
varying in severity, airway obstruction, which is often
reversible either spontaneously or under the influence of
treatment.
• Bronchial asthma is a heterogeneous disease
characterized by chronic inflammation of the
airways.
• AD is determined by the presence of a history of
variable respiratory symptoms such as
wheezing, chest tightness, cough, the severity of
which varies with time, as well as a variable
limitation of the speed of the air flow on the
exhale
• The prevalence of AD in different countries
varies from 10 to 30%.
• Prevalence among adults in the Republic of
Kazakhstan - 1.7% - 3.5%
• The frequency of asthma in Western Europe and
North America is decreasing; in Asia, Africa and
Latin America, on the contrary, it is increasing
• Mortality rates are weakly correlated with the
prevalence of the disease.
• In 50% of children, BA symptoms develop by 2
years, in 80% - by school age.
• At an early and preschool age, boys are sick
more often than girls, with the onset of puberty
(after 10 years), the frequency of a girl’s disease
is often the same
• In girls with obesity and especially early onset of
puberty, bronchial asthma is more common.
• BA urban residents get sick more often
than rural
• The risk of BA in children from families
with high social status is higher than from
poor families
• BA is most severe in children from families
with low social status, with the onset of
puberty
 Etiology of bronchial asthma
Factors affecting the development and
manifestations of AD are divided into 2 groups:
Determining factors, i.e. causing the development
of the disease
Symptom triggers

GINA 2014. www.ginasthma.org

 Classification of bronchial asthma
BA form - atopic, non-atopic

Severity: - intermittent
- light persistent
- moderate persistent
- heavy persistent
Current - exacerbation (onset)
- remission
BA controlled, partially controlled, uncontrolled
 Internal factors:
• Genetic predisposition:
• 3 gene groups:
• 1 - susceptible to atopy, responsible for sensitization,
total IgE
• 2 - predisposing to bronchial hyperreactivity
• 3 - for the development of eosinophilic inflammation
• Obesity
• Floor
• Source: Global Strategy for Asthma Management and
Prevention. Revised 2014
 External factors causing asthma
exacerbation - triggers
• Allergens
• Viral respiratory infections,
mycoplasma, chlamydia
• Hyperventilation during
physical and emotional stress
• Weather change (cold air)
• External irritants (tobacco
smoke, xenobiotics, pungent
odors, smoke during frying)
• Vaccines, medicines, food
• Compact family
 BA triggers in children

• Allergens
• Respiratory infection - virus-induced
asthma, chlamydia, mycoplasma
• Exercise stress
 Comorbid conditions in AD in
children
• Allergic rhinitis
• Chronic rhinosinusitis
• Atopic dermatitis
• Obesity
• GERD
• Food allergy
• Obstructive Sleep Apnea Syndrome
 Pathogenesis
Allergic reactions go through 3 stages.
1. Immune stage: upon repeated contact with an allergen in
a sensitized organism, it binds to IgE antibodies
(antigen-antibody reaction). The first contact is
sensitizing. The second is allowing
2. The pathochemical stage is accompanied by the release
of biologically active substances, inflammatory
mediators, activation of the complement system,
proteolytic enzymes, blood coagulation factors.
Degranulation of basophils, eosinophils, histamine
release, ACC, lysosomal enzymes
3. Pathophysiological - changes in CVS, RO, blood, central
nervous system (edema, mucus hypersecretion,
bronchospasm, decreased blood pressure, itching,
burning, pain)
 Allergic response phases
• Early phase - acute inflammation (bronchospasm)
• - Occurs 5 to 15 minutes after exposure to a
causative allergen (antigen-antibody)
• Activation of basophils, mast cells in the interaction
of specific IgE with a causative allergen induces the
release of inflammatory mediators (histamine,
serotonin, tryptase, histamine releasing factor,
kallikrein, kinins, FAT, leukotrienes)
• Morphological manifestations - bronchiolospasm,
extravasation, hypersecretion, edema.
• The early phase is easily eliminated and completely
reversible with timely adequate treatment
Late phase - chronic allergic inflammation
The development of chronic inflammation is
realized with the participation of eosinophils,
basophils, Th-2 lymphocytes (interleukins: IL-
4, IL-5, IL-9, IL 13, which regulate the
process of eosinophilic inflammation and the
production of IgE B-lymphocytes),
monocytes, neutrophils, platelets fibroblasts.
The leading role belongs to eosinophils,
which damage the bronchial epithelium and
T-lymphocytes located in peripheral DP and
actively involved in inflammatory reactions.
Source: Global Strategy for Asthma
Management and Prevention. Revised 2007
 BA pathogenesis
• Chronic allergic inflammation
• Bronchial hyperreactivity
• Bronchial Remodeling
 Structural changes in BA
Remodeling of AW - chronic, possibly irreversible changes that develop
in BA, which can persist for more than 6 years even in the absence
of clinical symptoms and after discontinuation of treatment:
• Angiogenesis and hypervascularization leading to thickening of the
bronchial wall
• Chronic cell infiltration with inflammatory cells (T-lymphocytes and
eosinophils)
• Deposition of collagen and thickening of the basement membrane
• The decrease in the elasticity of the walls of the DP
• Hypertrophy and hyperplasia of smooth muscles and mucous
glands
• Obstruction of the bronchi with mucous secretion
• The development of chronic allergic inflammation, increased
bronchial obstruction, decreased treatment effectiveness
 Clinic of bronchial asthma
• Spasmodic cough, dry, frequent
• Dyspnea
• Wheezing in the distance
• Labored breathing
• Chest tightness
• Difficulty breathing out
• Swollen chest
• Feeling of fear
• Sweating
• Forced situation
• Dry wheezing on both sides in the lungs
• Low PSV (below 80%)
 BA phenotypes
• Infants - 0 to 2 years old (virus-induced)
• Preschoolers - 3 - 5 years (AD - virus-induced, AD associated with
physical activity, allergen-induced AD)
• The presence of atopy is a factor in the persistence of AD,
regardless of whether the role of allergens as triggers of the disease
is proven.
• If it is not possible to establish allergens, then this phenotype type
should be characterized with great care as non-allergic
(unspecified) BA.
• However, this can only mean that the causative allergen has not yet
been identified.
• Source: Geppe N.A. "Recommendations for AD in children
PRACTALL"
 BA phenotypes
Schoolchildren - 6 - 12 years old
More often allergen-induced, including seasonal
A common virus-induced form of BA remains
The severity of the disease is a serious problem in the treatment of
allergen-induced asthma.
Teens
Atopic BA may first appear in adolescence
Possible development of non-atopic asthma (NSAIDs intolerance,
neuroendocrine dysfunction, chemical pollutants, occupational
hazards)
The emergence of additional problems when choosing tactics of
management and treatment.
Source: Geppe N.A. "Recommendations for BA in children PRACTALL"
Phenotypes of bronchial asthma
(GINA 2014)
• Allergic BA
• Manifested in childhood
• Association with AZ (blood pressure, food,
drug allergy, AR, in personal and / or
family history).
• In sputum cytology - eosinophilia.
• Good effect from IGKS
Phenotypes of bronchial asthma
(GINA 2014)
• Non-allergic BA -
• Not related to allergies.
• More common in adults
• Sputum cytology - neutrophilic
inflammation, less often eosinophils
• The response to treatment for IGC is
worse than for ABA
Phenotypes of bronchial asthma
(GINA 2014)
• Late onset BA
• Start in adulthood
• More common in women
• No allergy
• To achieve the effect, higher doses of IHC
are required.
• Possible refractory to the treatment of IHC
Phenotypes of bronchial asthma
(GINA 2014)
• BA with fixed airflow rate limitation
• Development in patients with a prolonged
course of asthma due to remodeling of the
bronchial wall
• The development of fixed irreversible
airway obstruction
Phenotypes of bronchial asthma
(GINA 2014)
• BA in obesity
• Severe respiratory symptoms
• Minor eosinophilic inflammation of the AW
 Diagnostic criteria for asthma
• The presence of more than one respiratory symptom (wheezing,
wheezing, chest tightness, coughing)
• Symptoms worsen at night or immediately after waking up, early in
the morning
• Symptoms are variable in time and in intensity
• Symptoms are triggered by physical exercise, allergens, laughter,
weather changes, cold air, irritating substances (smoke, exhaust
fumes, pungent odors)
• Symptoms appear or worsen with ARVI
• A key criterion for BA - bronchial obstruction is completely reversible
on its own or under the influence of drugs
 Questions to Suspect AD
1. Are there episodes of "whistling", wheezing in the
chest?
2. Does cough bother me at night?
3. Are there paroxysmal coughs or wheezing after
exercise?
4. Do wheezing, wheezing, or coughing occur after
contact with allergens or irritants of the airways?
5. Is there a prolonged (> 10 days) cough after a cold?
6. Do anti-asthma drugs bring relief?
 Characteristic signs of AD in children GINA 2014

Symptoms Characteristic symptoms of asthma

cough Recurrent / persistent unproductive cough that intensifies at

night or occurs with physical exertion, laughter, crying,
exposure to tobacco smoke in the absence of concomitant
SARS
wheezing Recurrent sighting during sleep, under the influence of triggers
(physical activity, laughter, crying, exposure to tobacco smoke,
pollutants)
Shortness of breath or Physical activity, laughter
shortness of breath

Decreased activity Does not run, does not play like other children, quickly gets
tired on walks

Allergic history or The presence of other diseases (AR or AD). Relatives in the
allergy in relatives first generation of relatives

Trial treatment with Clinical improvement within 2-3 months of basic treatment and
low doses of ICS or worsening after withdrawal
CDBA
 Indications for an alternative
diagnosis in children under 5 years
old
• Lack of body weight gain
• The onset of symptoms in the first months of life or at a
very young age, especially in combination with the lack
of an increase in MT
• Respiratory Symptom Vomiting
• Constant wheezing
• Lack of response to drugs for BA control
• Lack of association of symptoms with standard triggering
factors (ARVI)
• Focal pulmonary or SS symptoms, "drumsticks"
• Hypoxemia unrelated to ARI
 Evaluation of AD in adults, adolescents, and
children 6–11 years old (GINA 2014)
Assessment of AD control - symptom control and future risk
of adverse outcomes Clinical control criteria for the last 4
weeks:
• absence (or no more than 2 times a week) of
symptoms in the daytime; • lack of restrictions on daily
activities, including exercise; • lack of symptoms at night
or awakenings caused by asthma; • absence (or no more
than 2 times a week) of the need for taking symptomatic
drugs; • normal or near normal lung function; • lack of
complications
 Complications of BA
• Lung atelectasis
• Mediastinal and subcutaneous
emphysema
• Spontaneous pneumothorax
• Emphysema
• Pulmonary heart
 Clinic of asthmatic status
• Cough
• Suffocation
• Wheezing in the distance
• Difficult wheezing
• Anxiety, fear, sweating
• Swollen neck veins
• Tachycardia
• High blood pressure
• "Dumb Light"
 First aid for asthma attack
• Sublime head end
• Reassure baby
• Oxygen therapy until saturation> 90%
• Ventolin inhalation through a spacer or nebulizer (mild
attack of 0.1 mg / 0.02 ml / kg, moderate - 0.15 mg / 0.03
ml / kg, severe attack - 0.15 mg / 0.03 ml / kg every 20
minutes)
• Evaluation of effectiveness after 20 minutes:
• shortness of breath
• improved breathing
• 15% increase in PSV
 First aid for asthma attack
• Long-term therapy (24-48 hours or more) -
ventolin 0.15 mg / 0.03 ml / kg every 4-6 hours
or inhalation of berodual (0.5 ml / 10 drops up to
6 years, 6-14 years 0.5 -1.0 ml / 10-20 drops)
• In a severe attack of asthma (total obstruction of
the bronchi, obstruction with a viscous secretion)
eufillin 2.4% solution in / drip 4-10 mg / kg / day
(0.15 ml / kg), GC parenteral
• Infusion of glucose-salt solutions (1: 1) 30.0-50.0
ml / kg, at a rate of 10-15 drops / min
 Contraindicated in asthma attack
• 1st generation antihistamines
• Sedatives
• Herbal preparations, mustard plasters, banks, rubbing
• Calcium preparations
• Mucolytics
• Antibiotics (only in the presence of pneumonia or other
bacterial infection)
• Prolonged bronchodilators (theophylline)
• Beta 2 Dagonists DD (Salmoterol, Fenoterol)
• The use of Eufillin v / m, in candles, inhalation
 Asthmatic status
• AS - a protracted, severe asthma attack
due to severe obstruction of the PD “dumb
lung”, due to obstruction of the bronchi of
different calibers with mucous and
mucopurulent secretions, edema of CO
and bronchospasm.
 Asthmatic status
• Stage 1 - stage of relative compensation.
The clinical picture of a protracted asthma
attack:
• Anxiety, arousal of the child
• In the lungs, a significant amount of dry
wheezing, buzzing wheezing on the
background of weakened breathing.
Ineffective cough.
• Blood pressure increased
 Asthmatic status
• Stage 2 - progressive DN (decompensation)
• A child conscious, agitated or apathy
• Difficulty breathing
• The skin is pale cyanotic, moist, clammy
• Signs of NK: puffy face, neck vein swelling
• In the lungs, breathing is sharply weakened,
wheezing is less, areas of the "silent lung"
• Tachycardia, blood pressure lowered
• Bronchodilators are ineffective
 Asthmatic status
• Stage 3 - hypoxic hypercapnic coma
(increasing extracardial tamponade of the
heart and NK, brain hypoxia)
• Consciousness is oppressed, coma, cramps
• Diffuse cyanosis, shallow breathing
• Auscultatory - “dumb lung”, the tops of the
lungs are heard
• Deaf tones, bradycardia
• Low blood pressure
 AS treatment
• Respiratory support initially non-invasive methods against sedation,
oxygenation 40% through the mask
• Oxygen therapy (saturation to a level not lower than 92%)
• In the early stages of AS - timely hydration of sputum and techniques that
facilitate its evacuation
• Basic therapy - in / in the introduction of aminophylline 4-5 mg / kg (0.15-2.0
ml / kg) jet for at least 10 minutes, then drip for 6-8 hours in
• dose of 0.6-0.8 mg / kg / hour.
• For stopping AS - aminophylline - 10-15 mg / kg
• To all patients with AS GC iv intravenously: 1-2 mg / kg / day (stage 1 AS),
3 mg / kg / day (stage 2 AS), 7 mg / kg / day (stage 3 AS)
• Ht Crystalloid Infusion

• Inhalation of beta2-agonists and anticholinergic drugs begin only after

breathing is restored in “silent zones”
 Primary prevention
• Avoid exposure to environmental tobacco smoke
during pregnancy and the first year of a baby’s
life
• Birth promotion through natural ways
• Promoting natural feeding in relation to its
overall health benefits
• If possible, avoid the use of paracetamol,
including by mother, and broad-spectrum
antibiotics
 Primary prevention
• Nutrition - Breastfeeding
• The risk of developing BA in children born by Caesarean
section is higher than in children born naturally.
• Maternal intake of Vit D and E during pregnancy - low
risk of developing obstructive diseases in children
• Maternal smoking during pregnancy is an effect on the
health of the infant at an early age, and smoking after
childbirth is only on the development of AD in older
children.
• The impact of microflora - BA prevention (hygienic
hypothesis, microflora hypothesis, biological diversity
hypothesis)
Role of Vit D in the prevention of diseases in
children
• The risk of exacerbation of AD (5-18 years) is 500-2000
IU / day for 1-12 months
• Reducing the risk of acute respiratory viral infections in
young children (age 1 month) 800 IU / day course 6
months
• Prevention of FA infection (7-14 years) 800 IU / L course
6 months
• Prevention of influenza and exacerbation of bronchial
asthma (7-14 years) 1200 IU / day course 6 months
• Prevention of atopic dermatitis in the winter (4-14 years)
1000 IU / day course 1 month