DEFINITION
• Asthma: Chronic inflammatory condition of the lung airways resulting in episodic airflow obstruction.
• Chronic inflammation results in airways hyperresponsiveness (AHR) to provocative exposures
• Management aims: 1. Reduce proinflammatory environmental exposures and 2. DAILY anti-inflammatory medications (ie. corticosteroids) and 3. Control any comorbidities that may worsen asthma
AETIOLOGY
• Cause not fully determined
• Combination of environmental exposures and inherent biological and genetic vulnerabilities
• **Causal environments: Inhaled allergens, viral RTIs, chemical/biological air pollutants/irritants eg. tobacco smoke.
o Exposure to these in predisposed host result in prolonged pathogenic inflammation and aberrant repair -->
Lung dysfunction develops.
o This abnormal growth and development in early life leads to abnormal airways at mature age
GENETICS
• More than 100 gene loci linked to asthma.
• Loci contain
• Other genes:
ENVIRONMENT
• Injurious/severe LRTI of the airways that manifest as *pneumonia and *bronchiolitis are risk factors for persistent asthma.
• Other infections/Microbes
• Allergens – Inhalant allergens > food allergens
• Irritants/Pollutants e.g. Tobacco smoke
• Stress
RISK FACTORS (Must Know)
See box -> (M > F) ->
Lecture: “ASTHMA PREDICTIVE INDEX (API)”
- Tucson cohort 1980-present
- >/= 4 eps of wheeze + 1 major OR 2 minor predicts asthma
APPLIES TO CHILDREN <=
- *MAJOR: 1. Parental asthma, 2. Atopic dermatitis (eczema), 3. Inhalant allergen sensitization
- MINOR: 1. Eosinophilia > 4%, 2. Wheezing outside of colds, 3. Food allergen sensitization, 4. Allergic
rhinitis
POINTS
Approximately 80% of all asthmatic patients report disease onset prior to age 6!!
- BUT only a minority of children who experience
recurrent wheezing go on to persistent asthma
- Maternal asthma is the single most important risk factor for asthma development
2 main types of childhood asthma: 1. Recurrent wheezing 2. Chronic asthma
PATHOGENESIS
Airway obstruction in asthma results from numerous pathologic processes:
• In small airways, airflow is regulated by smooth muscle encircling the airways lumens – bronchoconstriction
of these bronchiolar muscle bands restricts and blocks airflow (Parasympathetic system stimulates bronchoconstriction)
• ALSO, a cellular inflammatory infiltrate AND exudates containing mainly eosinophils, can fill and obstruct airways AND induce epithelial damage and desquamation into the airways lumen.
• ALSO, helper T lymphocytes (CD4) and other immune cells produce proallergenic, proinflammatory cytokines (IL-4, 5 and 13) that mediate the inflammatory process.
ALL CONTRIBUTE TO AIRFLOW OBSTRUCTION (LOOK AT EACH AND JUST OBVIOUSLY SEE HOW)
CLINICAL MANIFESTATIONS AND DIAGNOSIS
***NOTE FROM LECTURE: The most likely diagnosis in children with recurrent wheezing is asthma, regardless of the age of onset, evidence of atopic disease, precipitating causes, or frequency of wheezing
MOST COMMON CHRONIC SYMPTOMS:
• Intermittent DRY COUGHING
• EXPIRATORY WHEEZE
Other symptoms in older children/adults:
• Shortness of breath
• Chest tightness
**NB**: The respiratory symptoms are WORSE AT NIGHT!!
Others are subtle/nonspecific: Limited physical activity, general fatigue (may be due to sleep disturbance)
• ***MUST ASK ABOUT PREVIOUS BRONCHODILATOR USE IN HISTORY!!:
o Symptomatic improvement with treatment supports asthma diagnosis!
o BUT lack of improvement with bronchodilator/corticosteroid therapy is inconsistent with asthma and should prompt consideration of “ASTHMA-MASQUERADING CONDITIONS”
• ***MUST ASK ALL Triggers***: Physical exertion, hyperventilation (laughing), cold or dry air, airway irritants/allergens (incl smoking at home, pets etc), respiratory infection (induce airway inflammation – eg. RSV, rhinovirus, adenovirus, influenza, parainfluenza, mycoplasma pneumoniae, chlamydia pneumoniae). ENVIRONMENTAL HISTORY IS VITAL
• **Ask about risk factors: SEE RISK FACTORS ABOVE AND OTHER DIFFERENTIALS OF WHEEZE
From lecture: HISTORY FOR A WHEEZING PATIENT:
o Age of onset
o Course of onset (Acute vs. chronic)
o Cough
o Shortness of breath
o Cyanosis
o Chest pain
o **Exercise-induced symptoms
o Postnasal drip
o Snoring
o Spitting up
o Greasy stool (cystic fibrosis)?
o **Eczema
o Choking
o Triggers
o Cold air
o Allergic rhinitis
o Weight loss
o Recurrent infections
o Birth history
o Environmental history
o Smokers at home
o Number of siblings
o Occupation of inhabitants at home
o Pets
o TB exposure
o Worms
o ***Family history of Atopy/Asthma
o ***Past use and response to bronchodilators
o Food allergies
o Co-morbid conditions
History suggestive of asthma
o Intermittent episodes of wheezing
o Seasonal variation
o Family history of asthma and/or atopy
o Good response to asthma medications
o Positive asthma predictive index
**History suggestive of a diagnosis other than asthma
o Poor response to asthma medications/bronchodilators
o History of neonatal or perinatal respiratory problems
o Wheezing since birth - congenital abnormality
o Associated with feeding or vomiting
o History of choking associated with cough & SOB
o Poor weight gain
o Recurrent ear or sinus infections
o Wheezing with little cough - Mechanical cause of obstruction- small airways, airway malacia
o Symptoms vary with position (TM)
o Progressive dyspnea, tachypnea, exercise intolerance & failure to thrive suggest interstitial lung disease
Examination (See Notes on wheezing for general wheezing examination)
• ***Chest findings are often normal!! – Ask for deeper breaths -> May elicit wheezing
In extremis -> Airflow may be so limited that wheezing cannot be heard
DIFFERENTIAL DIAGNOSIS
[**CLASSIFY: Upper vs. Middle vs. Lower respiratory tract conditions**]
[ALSO: Extraluminal compression vs. Intraluminal obstruction vs. Intrinsic change in airway dimension]
Also depends on the age group (see lecture)
Other common causes of intermittent chronic coughing --> GER, rhinosinusitis SEE TABLE BELOW - * = More common ones
DIFFERENTIAL DIAGNOSIS OF CHILDHOOD ASTHMA
UPPER RT CONDITIONS MIDDLE RT CONDITIONS LOWER RT CONDITIONS
- Allergic rhinitis *
- Chronic rhinitis *
- Sinusitis *
- Adenoidal or tonsillar hypertrophy
- Nasal foreign body - Laryngotracheobronchomalacia *
- Laryngotracheobronchitis (e.g., pertussis) *
- Chronic bronchitis from environmental tobacco smoke exposure *
- Vocal cord dysfunction *
- Foreign body aspiration *
- Laryngeal web, cyst, or stenosis
- Vocal cord paralysis
- Tracheoesophageal fistula
- Vascular ring, sling, or external mass compressing on the airway (e.g., tumor)
- Toxic inhalations Viral bronchiolitis * Gastroesophageal reflux *
Bronchopulmonary dysplasia (chronic lung disease of preterm infants)
Pneumonia
Pulmonary oedema (e.g., congestive heart failure)
Causes of bronchiectasis: Cystic fibrosis
Immune deficiency
Allergic bronchopulmonary mycoses (e.g., aspergillosis)
Chronic aspiration
Immotile cilia syndrome, primary ciliary dyskinesia Bronchiolitis obliterans
Interstitial lung diseases Hypersensitivity pneumonitis
Pulmonary eosinophilia, Churg-Strauss vasculitis Pulmonary hemosiderosis
Tuberculosis
Medications associated with chronic cough:
Acetylcholinesterase inhibitors
β -Adrenergic antagonists
Angiotensin-converting enzyme inhibitors
LABORATORY FINDINGS
1. PULMONARY FUNCTION TESTS (Spirometry and Peak flow)
POINT: ‘Forced expiratory airflow measurement’ helpful in diagnosis and monitoring efficacy of therapy
A. Spirometry is helpful as an objective measure of airflow limitation
o **Valid spirometry measurements depend on a patient’s ability to perform a full, forceful, prolonged expiration, usually feasible in children > 6 yrs. old. Reproducible spirometric efforts are an indicator of test validity; if the FEV 1 (forced expiratory volume in 1 sec) is within 5% on 3 attempts, then the highest FEV 1 effort of the 3 is used
Normative values for FEV 1 have been determined for children on the basis of height, gender, and ethnicity
o Because asthmatic patients typically have hyperinflated lungs, FEV 1 can be simply adjusted for full expiratory lung volume — the forced vital capacity (FVC) — with an FEV 1/FVC ratio.
o
BUT these measures alone are NOT diagnostic of asthma as numerous other conditions can cause airflow reduction
Bronchodilator response to an inhaled β -agonist (e.g., albuterol) is > in asthmatics than nonasthmatics; an improvement in FEV 1 ≥ 12% or > 200 mL is consistent with asthma.
IMPORTANT TABLE (NELSON’S)
B. Peak expiratory flow (PEF) monitoring devices provide simple and inexpensive home-use tools to measure airflow and can be helpful in a number of circumstances. Patients must practice over 2-3 weeks to determine a “personal best”, preferably at times when they a not symptomatic
• Peak flow rate monitoring can be accurately performed by most patients > 5 years
• ** PEFR < 80% predicted for height/patient’s personal best should trigger the administration of an inhaled short-acting beta2 -agonist
• A PEFR < 50% of the patient’s personal best should trigger both administration of an inhaled short-acting beta2 -agonist AND immediate medical attention
SEE MY FULL NOTES ON PEFR
NOTE WELL: PEFR and FEV1 are different. Forced expiratory volume over 1 second (FEV1) is a dynamic measure of flow used in formal spirometry. It represents a truer indication of airway obstruction than does peak flow rate. Although peak flow rate usually correlates well with FEV1, this correlation decreases in patients with asthma as airflow diminishes.
2. Radiology
The findings of chest radiographs (PA and lateral views) in children with asthma often appear to be normal, aside from subtle and nonspecific findings of hyperinflation (flattening of the diaphragms) and peribronchial thickening
CXR:
• Hyperinflation (Flattened ribs and diaphgram, Increased number of ribs over hemidiaphragm, Right diaphragm same level as left)
• Flattened hemi-diaphragms
• Peribronchial cuffing
• Atelectasis
Chest radiographs can be helpful in identifying abnormalities that are hallmarks of asthma masqueraders (aspiration pneumonitis, hyperlucent lung fields in bronchiolitis obliterans), and complications during asthma exacerbations (atelectasis, pneumomediastinum, pneumothorax).
TREATMENT **MUST SEE ENTIRE UHWI OFFICIAL EMED DOCUMENT**
• SEE GINA GUIDELINES
• SEE SUMMARY OF THE STEP UP AND DOWN APPROACH FROM A CONCISE SOURCE!!
• MUST SEE UHWI OFFICIAL EMED DOCUMENT AND GINA FOR MANAGEMENT OF EXACERBATION
***ASTHMA IS A CHRONIC CONDITION THAT IS OFTEN BEST MANAGED WITH DAILY ICS
CONTROLLER MEDICATION as monotherapy or with adjunctive therapy***
***NOTE WELL: Remember patient education AND control of environmental factors AND comorbidities (eg.
GER, rhinitis, sinusitis etc.)***
NELSON’S: During initial patient visits, a basic understanding of the pathogenesis of asthma (chronic inflammation and AHR underlying a clinically intermittent presentation) can help children with asthma and their parents understand the importance of recommendations aimed at reducing airways inflammation. It is helpful to specify the expectations of good asthma control resulting from optimal asthma management. Explaining the importance of steps to reduce airways inflammation in order to achieve good asthma control and addressing concerns about potential adverse effects of asthma pharmacotherapeutic agents, especially their risks relative to their benefits, are essential in achieving long-term adherence with asthma pharmacotherapy and environmental control measures.
GINA (GLOBAL INITIATIVE FOR ASTHMA) GUIDELINE
Based on GINA guidelines, must use this table to determine level of control, which will determine when to “Step-up” management, using the table on the next page
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