Asthma (from Greek "asthma" meaning "panting" is reversible chronic inflammation of the airways, causing airflow obstruction and bronchospasm.

Patient information

Whoa.... bit confused here  In short, what is asthma?
It's inflammation of the airways. You could call it airway-itis. Specifically, it's of the bronchioles.

What are bronchioles?
The lower portions of the airways, right down at the lungs. It also happens to be the narrowest portions!

Wait... that'd make it reversible bronchio-litis. That's a real thing! So what's the difference between bronchiolitis and asthma?
Bronchiolitis is inflammation usually caused by some virus, usually the RSV virus. Asthma on the other hand is an allergy-type reaction !

You say it's reversible. How?
If you remove the trigger. Or take medications.

• Wheezing (expiratory) → and Prolonged expiratory phase, because whereas inhalation if an active process, exhalation is a passive process, meaning effects of bronchoconstriction are even greater [during exhalation]
• SOB
• Dry cough → mucus is so far down in the lungs, it is near impossible to bring up
• Chest tightness

[Severe] asthma attack (aka status asthmaticus, asthma emergency):

• Use of accessory muscles of respiration
• Paradoxical pulse (pulse weaker during inhalation, and stronger during exhalation)
• Over inflation of the chest
• Cyanotic blue skin (lack of oxygen)

• Acute asthma exacerbation (aka asthma attack), is classified according to the frequency of Sx, FEV1 (forced expiratory volume in 1 second), and peak expiratory flow rate:
  • Moderate, w/ worsening Sx, peak flow <80% best/predicted, no features of acute severe asthma
  • Acute severe asthma (aka status asthmaticus), w/ any 1 of peak flow <50%, RR>=25bpm, HR>=110bpm, unable to complete sentences in 1 breath. It doesn't respond to inhalers and oral steroids
  • Life threatening, w/ any 1 of altered LOC, exhaustion, arrhythmia, hypotension, cyanosis, silent chest, poor respiratory effort, peak flow <33%, ox sats <92%, PaO2<8 kPa, "normal" PaCO2
  • Near fatal, high PaCO2 and/or requiring mechanical ventilation
• Cause, including:
  • Atopic (extrinsic), which is a predisposition toward development of type 1 hypersensitivity reactions
  • Non-atopic (intrinsic)

• In atopic asthma, IgE is produced systemically by type 1 hypersensitivity (allergy/immediate, mediated by IgE) triggered by environmental factors. In non-atopic asthma, IgE is produced locally
• IgE causes inflammation (swelling, exudation, eventually mucus plugging) in the airways, causing:
  • Bronchoconstriction (i.e. obstruction of the small airways) due to constriction of the surrounding smooth muscle. This causes difficulty for air to escape → wheeze, SOB
  • Goblet cell hyperplasia, causing excessive mucus production → cough
  • Airway remodelling, including scarring and thickening → air trapping (can't be exhaled by lungs), chest tightness

• Family Hx (genetic- immune related)
• Environmental factors:
  • Hygiene hypothesis (i.e. due to reduced childhood exposure to non-pathogenic bacteria/viruses, because of cleanliness and decreased family size - asthma is lower on farms and households w/ pets)
  • Use of antibiotics in early life
  • Delivery by C-section (due to lack of healthy bacterial colonization acquired through birth canal)
  • Obesity (decreased respiratory function due to buildup of fat, and adipose tissue is pro-inflammatory)
• Triggers:
  • Night time, early morning
  • Exercise
  • Cold air
  • Allergens
  • Irritants (smoking, pollution, chemicals, dust mites, cockroaches, animal dander, mold, perfumes, stress)
  • Bacterial, or Viral respiratory infections (RSV, rhinovirus)

• Components of the atopy triad, including:
  • Eczema/Atopic dermatitis
  • Allergic rhinitis (hay fever)
  • Asthma
• GERD (gastro-esophageal reflux disease)
• OSA (Obstructive sleep apnea)
• Anxiety disorders, mood disorders

• Symptoms
• Postbronchodilator test, where spirometry (>6yo) is <80%, but improves by more than 12% following administrator of Tx, a bronchodilator (e.g. salbutamol)
• Bronchial challenge test, where the Pt breathes in methacholine or histamine, which both provoke bronchoconstriction. Pt's with pre-existing airway hyperactivity, e.g. asthmatics, will react more powerfully to the drugs

Patient information

In kids, you commonly see the ocassional dry cough, and once in a while, perhaps a wheeze or shortness of breath. They do enjoy a run around ! Is there a more legit way of figuring out if there's really an issue?
There is indeed! The Postbronchodilator test and the Bronchial challenge test.

Postbronchodilator. Bronchial challenge. Big words, what do they mean!
You can essentially do 1 of 2 things. Both require the use of a spirometer, which you blow into and it measures the amount of air that is blown out. The test can either involve giving a medication to see if more air can be blown out, as the medication is supposed to improve things! Or alternatively, give something that will make it worse, and because asthma involves extra reactive airways, should make it drastically worse.

What is considered bad on a postbronchodilator?
FEV1<80%, which improves by >12% after you give a drug to dilate the bronchioles.

I think I'll opt for the medication The anti-medication sounds sort of evil!
Sure thing

• SOB + cough:
  • Bronchiolitis - wheeze
  • COPD - wheeze
• SOB:
  • Tracheal stenosis - SOB (esp exertional), stridor
  • Congestive heart failure - SOB (esp exertional, lying down, at night while sleeping), tiredness, leg swelling
• Cough:
  • Foreign body aspiration - choking, chronic cough [if in the bronchi]
  • ACEi cough
• Allergic rhinitis - runny nose, itching, sneeze

• Prevent initial sensitization:
  • Limit maternal smoking
  • Breastfeeding
  • Increased environmental exposure to daycare, large families, pets (unless if there is allergies to said pet)
• If already sensitized, avoid allergens and triggers (refer above)

Relievers, for use in the short term:

• Treatment of acute symptoms with:
  • Inhaled SABA's (e.g. salbutamol)
  • +Ipratropium bromide (anticholinergic)
  • For exacerbations, +Inhaled corticosteroids
• In severe cases:
  • ABC's, including mechanical ventilation
  • IV corticosteroids
  • +IV magnesium sulfate → provides bronchodilating effect in severe acute asthma

Source: Dokter Online

Preventers, for use in the long term:

• In exercise induced asthma → inhaled SABA's before exercise
• Mild persistent asthma (>2 attacks/week):
  • Low dose inhaled corticosteroids (Beclometasone, Fluticasone, Budesonide)
    • ​Alternatives include Leukotriene antagonists (Montelukast), Mast cell stabilizer (Cromoglicic acid, Nedocromil)
  • +LABA's (aka symptom controller, e.g. Formoterol, Salmeterol)
  • Note that combination medications combine corticosteroid+LABA, e.g. Seretide (fluticasone+salmeterol) or Symbicort (budesonide+eformoterol)
• Moderate (daily) asthma:
  • +Oral corticosteroids

Source: Hospira

Patient information

Can you cure asthma?
No . Like any allergy, you can't make it go away. But you can take steps to prevent an allergy from occuring in the first place, or if it occurs, medication to help it.

There's a lot of medications there!! Do you take them all?
No. It's a bit of trial and error. SABA's come first.

What are SABA's?
Short acting beta agonists. LABA is the long acting version of it. They have a positive effect on beta adrenergic receptors, which amongst other things, opens up the airways.

So you can breath? Yayyy !!!
Indeed.

Nebulizer or inhaler, which one should I go with?
Research shows it really doesn't matter. But no special breathing technique is required to use a nebulizer. Many people also think the nebulizer is better because it's more expensive and fancy looking, they often see nebulizers used in the hospital, and because it takes longer to administer believe it to be more effective. Even in hospitals, research shows that inhalers are just as effective, and with less side effects.

If that fails, corticosteroids are next. Aren't steroids what body builders to get big muscles, and of course the little infamous side effect... . What do they do?
Like the pun. And yes indeed! Remember everything in the body is linked. Not only do steroids make your body go bazoink. It also makes your immune system go bazoink too!

Why do you go from inhaled to other ways to give corticosteroids?
If mucus has fully plugged up a person's lungs... the medication cannot cross from the lungs into the blood stream ! So we eventually give it through an injection into a vein - that's called "IV".

What if that IV corticosteroids fails?
Magnesium sulfate, which we also give by IV.

For long term, how do inhaled corticoseroids compare against LABA's?
Inhaled corticosteroids are the most effective for long term control. We try them before LABA's, because they have been linked to severe asthma attacks.

• Education, and drawing up an asthma action plan (source):
  • Assess severity of Sx, including when well controlled, getting worse (e.g. cold Sx, cough), severe, life-threatening (SOB)
  • Treatment required [depending on severity], including preventer, reliever, symptom controller

• Atopic asthma is more common than non-atopic
• The occurrence of asthma has increased significantly since the 1970s
• Annually, 235-300m people globally were Dx with asthma, resulting in 250k deaths

• Bronchiolitis
• Reactive airway disease (the Dx in kids <2yo)
• COPD (irreversible inflammation)
• Inhaler (how to use)
• Nebulizer (how to use)