Bronchial Asthma
Alena Vlachová
Definition
Chronic inflammatory disease with inflammation due to complex interaction between inflammatory cells,mediastors and airways cells
The chronic inflammationis associated with hyperresponsivenes that leasd to reccurent episodes of wheezing,breathlessness,chest tightess and coughing,particulary at night or in the early morning
These epizodes are usually associated with widespread but variable airflow obstruction withing the lung, that is often reversible either spontaneously or with treatment.
Airway structure
Mucosa is composed of epithelial cells that are capable of specialized mucous production and a transport
Basement membrane Smooth-muscle matrix extending to the
alveolar entrances Predominantly fibrocartilaginous or
fibroelastic -supporting connective tissue
Cellular elements
Mast cells are involved in the complex control of releasing histamine ad other mediators
Basophils, eosinophils and macrophages are responsible for extensive mediastors release in the early and late stage bronchial asthma
Stretch and irritans receptors
Cholinergic motors nerves which innervate the smooth muscle and glandular units
Patophysiology
is complex involves following components: airway inflammation intermitent airflow
obstruction bronchial
hyperresponsiveness
Airway inflammation
Eosinophilic 50% of all patients may have atopic
history IgE mediated reaction -Th2cell produce
cytokines (IL -5,IL-6,IL-4,IL-9,IL-13) eosinophils, epithelial cells,
macrophages
Airway inflammation
Neutrophilic -usually severe asthma -IL-8, matrix-metaloproteinasis -often non immunologic ( smoking,
infection) -often irreversible obstruction - poor response to inhal. steroids
Paucigranulocytic marker of inflammation does not exist no response to steroids
Airflow obstruction
Variable : Acute -bronchoconstriction -airway edema -mucus production Airway remodeling during chronic
inflammation
Bronchial hyperresponsivenes
Airflow obstruction ..hyperinflation.. increased intra-alveolar pressure with alteration in circulation ...ventilation-perfusion mismatch ..compensatory vasocontriction
in early stage of airflow obstruction : hypoxemia without hypercapnia - respiratory alkalosis
later increased work of breathing, increased oxygen consumption: hypoxemia with hypercapnia - respiratory acidosis
Etiology Enviromental allergens – house dust mites,
animal allergens, fungi... Viral respiratory tract infection Exercise,hyperventilation Gastroesophageal reflux disease Chronic sinusitis or rhinitis Aspirin or nonsteroidal anti-inflammatory
drugs, sulfit sensitivity Obesity Enviromentall pollutans, tobacco smoke
Etiology Occupational exposure Irritans -eggs, household sprays, paint
fumes Various high and low-molecular weight
compounds -eggs, nsects,plants, latex, rubber, diisocyanates,anhydrides, wood dust,..
Emotional factors or stress Perinatal factors-prematurity and increased
maternal age, maternal smoking, genetics
Epidemiology 5-10% of the population 40% asthmatics are smokers! common in industriazed countries prevalence raises in developing countries In US asthma prevalence is higher in black In childhood predominantly in boys
(m:f..2:1) 2/3 of asthma cases are diagnosed under
the age of 18 After puberty predominantly in females In older than 40 predominantly females
Dg and assessment of asthma
History – family, occupation, drugs, hobbies, diseases
Physical examination Pulmonary function tests Sputum analysis
Dg and assesment of asthma
Laboratory: blood tests, IgE, ECP, ABG FeNO CXR, CT Examination of upper airways Allergic screening Examination of expired air or sputum:
leukotriens ( B4,D4,C4...)
Levels of Asthma Control (GINA 2006)Characteristic Controlled
(All of the following)
Partly Controlled(Any measurepresent in any week)
Uncontrolled
Daytime symptoms
None (twice or less/week)
More than twice/week
Three or morefeatures of partly controlledasthma present İn any week
Limitations of activities
None Any
Nocturnal symptoms/ awakening
None Any
Need for reliever/rescue treatment
None (twice or less/week)
More than twice/week
Lung function (PEF or FEV1)
Normal < 80% predicted or personal best(if known)
Exacerbations None One or more/year*
One in any week
Clinical features May be normal Dry cough Shortness of breath Wheezes, classically expiratory Chest tightness Chest deformity / hyperinflation – long-
lasting or poorly controlled asthma Severe -life threatening asthma may have no
wheezing and a silent chest , tachypnoea, tachycardia or bradycardia, cyanosis, use of accessory respiratory muscles, anxiety, general distress, pulsus paradoxus , exhaustion, confusion or coma.
PO2 low to 8kPa, pCO2 up to 5-6 kPa!!!
Differential diagnosis of asthma
COPD Tumours Upper airway obstruction Thromboembolic disease Vocal cord dysfunction Foreign body aspiration Infection Left heart failure Gastroesophageal reflux disease
Vasculitis PAH ILD Hyperventilation sy Cystic fibrosis
Differential diagnosis of asthma
Classification according to severity
Intermittent Mild persistent Moderate persistent Severe persistent Patient with asthma of any level of
severity can have mild, moderate or severe exacerbation
Pharmacologic management
Control agent :inhaled or systematic steroids leucotriens modifiers inhaled cromones long acting bronchodilatators theophylline-long acting anti IgE specific immunoterapy Relief agent: short acting bronchodilatators systemic steroids short acting theophylline
Stepwise management of chronic asthma
1.step:mild intermitent:avoid alergen, RABA on demand
2.step: regular preventive terapy: RABA+ add: ICS or leucotriens modifiers
3.step: RABa +ICS +add LABA or long acting theophylline or leucotrien modifiers
RABA + increase ICS 4.step: step 3 + increase ICS + leucotrien
modifiers + long acting theophyline 5.step: step 4 + systemic CS + anti IgE
Non pharmacologic management
Allergen avoidance No smoking ! Dietary factors Weight reduction Physiotherapy - breathing techniques Patient education Bronchial thermoplasty
Hospital treatment of acute asthma
B2agonists -nebulised 5-10 mg/h Anticholinergic drug- nebulised Steroid IV or oral MgSO4 Theophylline -IV aminophyllin 5mg/kg Antibiotics –in case of infection Rehydratation Oxygen
Acute severe asthma Severe bronchospasm refractory to
usual treatment Identification of high risk asthmatics :
History: Previous life threatening attacs (CO2,
intubation) Frequent ER visits Hospitalization in last year Recent steroid use Deterioration on steroids
Acute severe asthma Clinical features :
HR more than 130, RR more than 25 PEF 33-50% of predicted or best Paradoxical thoracoabdominal motion Silent chest Confusion, lethargy, fatigue Patient can´t speak Bradycardia Respirarory insuficiency
Treatment of acute severe asthma Oxygen
Beta (2) agonists - in almost all situations inhaled b2 terapy schould be given prior to parenteral (!side effects).
But in little airflow parenteral : epinephrine: SC: 0,3-0,5mg q20-30 min IV: 4-8 ucg/min Via ETT: 5 ml of 1:10000 salbutamol : nebulizace 5-10 mgq 15
min 0,1-0,2 ucg/kg/min
Treatment of acute severe asthma
Anticholinergic agens -in severely obstructed patient drug deposit in the more proximal airways where cholinergic receptors are located
ipratropium MDI 4-9puffs q 15min or cont.
atropine IV 20mg /kg -! side effects ! glycopyrrolate IV 10 mg/kg ! Side effects! Corticosteroids - take 4-12 hours to show
an effect hydrocortison 10-15mg/kg/day- 500 mg
=metylprednisolone 40-120 mg 4-6 h
Treatment of severe acute asthma
Theophyllines : loading dose 3-6 mg/kg, IV 0,2-0,9 mg/kg/hr !side effects !
Magnesium sulfate: 10-12 mmol/20 min
Intubation decision Progressive exhaustion Respiratory arrest Decreased level of consciousness Persistent respiratory acidosis (pH
<7,2) Hypoxemia (SaO2 < 90%) Hypercapnia is not indication for
intubation ?-studies show improvement after aggresive use of bronchodilatators
Alternative treatments of severe acute asthma
Volatile anestetics Heliox ECMO Pulmonary lavage