CHILDHOOD ASTHMA Flashcards

1
Q

Definition

A

Asthma is a chronic inflammatory, obstructive airway disease resulting from spasm of airway muscle, increased mucus secretion, and inflammation.

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2
Q

Epidemiology

A

•The actual prevalence of asthma in Nigerian children is not known
•Asthma is one of the leading childhood chronic respiratory disorder.
•Prevalence of asthma is on the increase worldwide.
•Asthma is the most common chronic disease among children

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3
Q

Ateiology

A

The exact cause is unknown
•Interplay between genetics and environmental factors
•Positive family history
•Environmental factors – Maternal smoking, childhood exposure to tobacco smoke, lack of exclusive breastfeeding etc

•Risk factors
Family history of atopy
Urbanization
Low birth weight/ prematurity
Exposure to tobacco smoke/air pollution early in life
Viral respiratory infections
Exposure to some environmental allergens
Overweight/obesity

•Triggers
Viral infections( Rhinovirus C)
Damp mouldy bedroom
Household pets
Cigarette smoke
Mosquito coil
cockroaches
House dust mite allergy, Feathers, dog hair, cat fur, grass pollen, flower pollen, cow milk allergy
Ascaris infection
Volatile organic compounds
Drugs – beta blockers, NSAIDS, Cocaine, Heroin, contrast agents
Cold air, exercise etc

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4
Q

Pathogenesis

A

The airways of asthmatics are hyper-responsive to a variety of stimuli including cold air, atmospheric irritants, various drugs, and hyperventilation.
•This hyper-responsiveness is genetically determined
•The inflammatory process in asthmatics is with a deviation in the maturation of helper T lymphocytes to a sub-type Th2
•Th2 secretes soluble cytokines eg interleukin-3, GM-CSF, etc which lead to recruitment of Ig E, mast cells, basophils and eosinophils

•Also, toxic substances such as leukotrienes major proteins, Eosinophils cationic protein etc are released when there is exposure to antigens
•The toxic substances lead to denudation of bronchial epithelium
•Persistent airway structure leads to airway remodelling
•Substances (protein kinase C and neuropeptide) cause bronchoconstriction and increased mucus secretion
• Airflow limitation – inflammation of the airways, bronchospasm,

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5
Q

Clinical presentations/Diagnosis

A

History-Cough-Wheeze-Dyspnea-Chest tightness-Mucus production(+ or -)-Family history of atopy/ asthma-Triggers

•Examination-
-general physical exam -in respiratory distress,
-detailed respiratory exam-tachypnea; tactile fermitus may be reduced, hyper resonance on percussion, rhonchi
-CVS exam; tachycardic

evidence of allergic disease- rhinitis, eczema

•Investigations
-No recognized gold standard method of diagnosis is available in children 5 years and younger
-Therapeutic trial-(short acting beta 2 agonist and low dose inhaled corticosteroid) for 2-3 months - Marked clinical improvement during treatment and deterioration when treatment is stopped support diagnosis
-•Other tests- tests for atopy, chest radiograph
•Exhaled Nitric oxide- elevated fractional concentration of exhaled nitric oxide recorded > 4weeks from any URTI in pre-school children
-fbc; increased eosinophils
-serum IgE estimation
-skin prick test ; to determine hypersensitivity to allergens >2mm in +I’ve

•Lung function tests
-Spirometry
To demonstrate reversibility-
- Measure PEF or FEVI
-inhalation of two puffs of a short acting bronchodilator
- Measure the PEF or FEV1 after about 15-30 minutes after inhalation.
- An increase in FEV1 of > 12% is indicative of asthma
•Exercise challenge- A fall in FEV1 of >12% of predicted or PEF > 15% after 6 minutes intensive exercise

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6
Q

Management

A

•Depends on the degree of severity
-Acute exacerbation
-Chronic state
➢Intermittent
➢Mild persistent (chronic)
➢Moderate persistent (chronic)
➢Severe persistent (chronic)

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7
Q

Classification of chronic stable asthma

A

According to daily symptoms, night symptoms and lung function test

And findings;
Confused
Oxygen saturation
Talks in
Heart rate
Central cyanosis
Wheeze intensity
FEV1, PEFR

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8
Q

Management

A

Quick history/examination
•Classify severity
•Resuscitate
•General principle- Short acting beta2 agonist, Oxygen and Steroid

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9
Q

Treatment for mild

A

Mild- salbutamol by MDI/Spacer(6 puffs<6, 10 puffs for>6 years)
•Review every 20 min(pre and post) and repeat if need be.

Mild – If good response- discharge on beta 2 agonist as needed(hourly for next 4 hours, then 4hrly for the next 2 days)
•If poor response treat as moderate asthma

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10
Q

Treatment for moderate

A

start oral prednisolone within 1 hour of admission then daily for next 2 days
Give iv hydrocortisone if you can’t give prednisolone to avoid aspiration.
Provide written asthma action plan
Discharge home on low dose ICS only or LTRA

Oxygen as indicated if SPO2< 94%
•Add nebulized `Ipratropium bromide
•If child becomes stable discharge home with instructions as in mild

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11
Q

Treatment of severe

A

Severe-
SOS; salbutamol by nebulizer, oxygen, steroids (prednisolone)

Nebulizing salbutamol dosage;
<5yrs give 2.5mg every 20mins
>5yrs give 5mg
If no improvement
Nebulized ipratrobium bromide

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12
Q

Treatment of Life threatening

A

•Life threatening - Admit to ICU
-Magnesium sulphate
-Aminophylline
Do chest x-ray
•Counseling
•Follow -up

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13
Q

Differential diagnosis

A

•Foreign body aspiration
•Gastroesophageal reflux disease
•Tuberculosis
•Tracheomalacia

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14
Q

Prevention

A

•Primary
-Exclusive breastfeeding
-Health education
•Secondary prevention
-Avoidance of triggers
-Appropriate management of chronic state
Tertiary
Prevention of complications of care
Give minimum effective dose ;steroids complications m

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