This disease always reminds of my primary school years- children with their blue pump inhalers during PE. I always thought they were really cool puffing away.

However, though common, especially in childhood, asthma is not a mild childhood disease.

I took a history from an 67 year old woman of Caribbean origin- Mary- who was in hospital following a severe asthma exacerbation.

Here is the history I took from her:

PC: Severe shortness of breath/ exacerbation of asthma

HPC: 3 day history of worsening SOB

-during this episode she was very SOB, tight chested and weak

-cold-like symptoms- rhinorrhoea

-Her inhalers- Seretide (Salmeterol +  Fluticasone) + Ventolin (Salbutamol)- did not offer relief

-two asthma exacerbations in the past year

-asthma since childhood, disappeared when she was 16 and returned in her 40s

-usual symptoms of asthma: weak, tired, SOB, cough

-smoke and dust make asthma worse, no seasonal variation

PMHx: osteoarthritis, previous TIA, abdominal hernia, hiatus hernia, hypertension, hysterectomy, kidney stones



-Enalapril (ACE inhibitor- for hypertension)

-Amlodipine (Dihydropyridine calcium channel blocker- for hypertension)

-Clopidogrel (anti-platelet- stroke prevention because of previous TIA)

Seretide accuhaler (Salmeterol– long acting β2 agonist + Fluticasone– corticosteroid)

Ventolin (Salbutamol) accuhaler (short acting β2 agonist)

-Lansoprazole (proton pump inhibitor)

-Quinine Sulphate (anti-malarial that can also be used, as in Mary’s case, for leg cramps.)

-Tamsulosin HCl (α1 receptor antagonist- helps with passing kidney stones, by relaxing smooth muscle in the bladder neck)

-Bumetanide (loop diuretic)

-Fexofenadine (anti-histamine- Mary uses it to treat skin itching)

FHx: her children had asthma when young, mother died in 50s of a brain haemorrhage, hypertension and diabetes in the family

SHx: non-smoker, non-drinker, mobilises with a walking stick, lives with son and has a cleaner that helps with housework, used to be a social worker

On examination: transmitted upper airway sounds and diffuse expiratory wheeze

Management (from her notes):

-arrived on ambulance with a respiratory rate of 42 breaths/min, peak expiratory flow rate(PEFR) 240 L/min.

-immediate treatment on the ambulance:

  1. Salbutamol nebuliser + IM Hydrocortisone + Oxygen
  2. Ipratropium bromide nebuliser (anti-muscarinic)
  3. Salbutamol nebuliser

-Her PEFR improved to 280 L/min (normally 350-400) on the ambulance and further over her hospital stay

-Initially suspected infective exacerbation of asthma and clarithromycin and prednisolone were prescribed to take home for a few days

-However, bloods markers were non-suggestive of infection (CRP, WBC) and sputum cultures were negative so antibiotics were discontinued.

-Most likely a non-infective exacerbation of asthma


Definition: common chronic inflammatory condition of the lung airways characterised by reversible airflow limitation, airway hyper-responsiveness to a range of stimuli and inflammation of the bronchi. Airway limitation may be irreversible in chronic asthma as a result of airway remodelling and mucus impaction.

Aetiology/risk factors:

-Asthma can be classified as extrinsic (atopic) or intrinsic

-Atopic: reactions to common inhaled allergens such as dust mite, pollens, fungal spores (e.g. from Aspergillus fumigatus- rare cause, airborne spores)

-Intrinsic: often starts in middle age and no definite external cause can be identified

-Atopic individuals readily develop IgE antibodies against common environmental antigens

Risk factors for atopy: genetic predisposition (IL-4 gene cluster on Chr 5), childhood exposure to allergens, maternal smoking, intestinal bacteria, childhood infections, growing up in a relatively clean environment may predispose


-affects 5-8% of population

-increasing prevalence

-more common in developed countries (particularly UK, Australia, NZ)

⇒The primary abnormality in asthma is narrowing of the airway, due to smooth muscle contraction, thickening of the airway wall by cellular infiltration and inflammation, and the presence of secretions within the airway lumen.

⇒Key inflammatory cells and mediators: dendritic cells, Th2 lymphocytes, IL-3, IL-4, IL-5, IL-9, IL-13, B cells, IgE, mast cells, eosinophils, histamine, tryptase, prostaglandin D2, leukotriene C4, eosinophilic cationic protein.

⇒Chronically, re-modelling can occur. There is airway smooth muscle hypertrophy and hyperplasia. The airway wall is thickened further by collagen and matrix protein deposition below the basement membrane. The epithelia is damaged with loss of ciliated columnar cells and increased mucus-secreting goblet cells.


wheezing attacks, shortness of breath, chest tightness, cough (often nocturnal), sputum

-acid reflux (in 40-60%)

-tend to be intermittent, worse at night and in the early morning (quantification of nights per week of disturbed sleep can point towards severe asthma)

-provoked by triggers: house dust mite and its faeces (the major allergen), viral infections, cold air, exercise, irritant dusts, vapours and fumes (cigarette smoke, perfume), emotion and drugs (NSAIDs, aspirin, β-blockers)

-occupational asthma: triggered by materials encountered at the workplace, so typically improves on days away from work and holidays. Common occupations associated: animal handling, bakery (wheat, rye), pain sprayer, laundry work (biological enzymes)

-some patients have just 1-2 attacks per year, whereas others have chronic symptoms


-tachypnoea, audible wheeze

-hyper-inflated chest, hyper-resonant percussion note

-reduced air entry, reduced chest expansion

-prolonged expiratory time, bilateral expiratory poly-phonic wheeze

⇒Severe attack: inability to complete sentences, pulse >110bpm, resp rate >25/min, PEF 33-50% predicted

⇒Life threatening attack: silent chest, confusion, exhaustion, cyanosis, bradycardia, PEFR <33% predicted (PaO2 < 8kPa but PaCO2 4.6-6.0 kPa, SpO2 <92%) ⇒Near fatal attack: PaCO2 is raised, low pH (decreasing ventilatory effort due to exhaustion)


Diagnosis made on history and evidence of airflow obstruction (by spirometry of PEF) when symptomatic.

-Demonstration of variable (at least 15%) airflow limitation by measurement of PEFR (Peak Expiratory Flow Rate) or FEV1 (Forced Expiratory Volume in 1 second)

-Measure PEFR morning, day and night- most asthmatics will show diurnal variation with a ‘morning dip’ (>20% variation on >3d for 2 wks)

-Increase after inhalation of a bronchodilator (>15% improvement in FEV1)

-Decrease after 6 minutes of exercise

-Spirometry: obstructive defect- decreased FEV1/FVC, increased Residual Volume

Histamine or methacholine challenge in difficult cases- inhale gradually increasing doses to demonstrate bronchial hyper-sensitivity as a fall in FEV1. (Contra-indicated in poor lung function)

Skin prick tests in all cases to identify any allergic causes. Measure of allergen- specific IgE in the serum is also sometimes used.

-CXR shows hyperinflation or may identify pulmonary shadows associated with allergic bronchopulmonary aspergillosis (Aspergillus fumigatus spores as a rare cause of asthma. There is also peripheral blood eosinophilia in ABPA, may do Aspergillus serology).

⇒Acute attack: PEF, sputum culture, FBC, U & E, CRP, blood cultures  (looking for signs of infection)

-ABG: usually shows normal or slightly decreased PaO2 but decreased PaCO2 as they are hyperventilating. If PaCO2 is normal or raised, transfer to HDU/ITU for ventilation as this means failing respiratory effort (i.e. they are tiring of breathing so much).

-CXR to exclude infection or pneumothorax


-smoking cessation and avoidance of precipitating factors and exposures, including occupational exposure. β-blockers are absolutely contra-indicated and individuals intolerant of aspirin should avoid all NSAIDs.

-Drugs: most delivered directly into lung as aerosols or dry powder inhalers. Asthma is managed with a stepwise approach which depends partly on repeated PEFR measurement by patient. Patients should be educated on proper inhaler technique and use of peak flow meter to monitor PEFR 2x day. They should be educated to enable them to alter their medications according to symptoms and PEFR and given specific advice on what to do in emergency.

-start at step most appropriate to severity, moving up if needed or down if control is good >3 months

rescue courses of prednisolone may be used at any time

Step 1: occasional short-acting inhaled β2-agonist (e.g. salbutamol) as required for symptom relief. If used >1/day, or night-time symptoms, go to step 2.

Step 2: add standard dose inhaled steroid (e.g. beclometasone, 200-800μg/day), or start at dose appropriate for disease severity and titrate as required.

Step 3: add long-acting inhaled β2-agonist (LABA e.g. salmeterol 5oμg/12h). Usually added to low dose steroid as combination inhaler e.g. Seretide = salmeterol + fluticasone)

if LABA is beneficial, but inadequate, continue LABA and – increase dose of beclometasone to 800μg/day.

0r continue LABA and- may try oral leukotriene receptor antagonist (e.g. montelukast/ zafirlukast) or oral theophylline (methylated xanthine derivative- PDE inhibitor) or long acting muscarinic antagonist (e.g. tiotropium bromide)

if LABA is ineffective, discontinue and consider increasing the dose of beclometasone/ corticosteroid

Step 4: consider, in conjunction with previous therapy, trials of:

beclometasone up to 2000μg/day

-modified release oral theophylline

-modified release oral β2-agonist

-oral leukotriene receptor antagonist

long acting muscarinic antagonist

Step 5: add regular oral prednisolone (1 dose/day at lowest possible dose)

continue with high dose inhaled steroids

refer to asthma clinic

Management of acute asthma attack:

Salbutamol 5mg nebulised with oxygen and give oral prednisolone (40-50mg) or IV hydrocortisone (100mg) or both if very ill.

-Start oxygen if saturations <92% (aim for 94-98%).

-If life threatening features present-carry on with salbutamol nebulisers (every 15 min or 10mg continuous/hour), add in ipratropium bromide to nebulisers (0.5 mg), and a single dose of magnesium sulphate (1.2-2g IV over 20 min).

-If improving within 15-30 mins- nebulised salbutamol every 4 hours and oral prednisolone continued for 5-7 days (40-50mg). Supplemental O2 if needed.

-If not improving refer to ICU for consideration of  ventilatory support and intensifying medical therapy e.g. aminophylline, IV salbutamol.

Complications: growth retardation, chest wall deformity (e.g. pigeon chest), recurrent infections (give flu jab), pneumothorax, respiratory failure, death-

Prognosis: ~1000 asthma deaths in the UK in 2009, 50% were >65 years old

Most childhood asthmatics either grow out of asthma in adolescence or suffer much less as adults. A significant number of people develop chronic asthma later in life.

References: Kumar & Clark’s, cheese and onion, British Thoracic Society 2016 asthma guidelines, rapid medicine

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