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