Asthma and Severe Asthma — Written Clinical Reasoning

SAQ 1 — Integrated Management of Severe Asthma (20 marks, 30 minutes)

Prompt: Outline your integrated management plan for this patient, including confirmation of the severe asthma diagnosis, phenotype assessment, pharmacological escalation including biologic selection, and comorbidity management. Justify each decision with reference to evidence. ^[1]

Model Answer

Step 1 — Confirm this is severe asthma and exclude mimics (4 marks): ^[1]

This patient meets the ERS/ATS definition of severe asthma: she remains uncontrolled (frequent exacerbations, nocturnal waking, ongoing symptoms) despite high-dose ICS-LABA plus a LAMA plus maintenance oral corticosteroid. Before any escalation, three checks are mandatory: ^[1]

1. Confirm the diagnosis — she has variable airflow limitation (16% and 280 mL reversibility), so asthma is confirmed. Exclude asthma-COPD overlap (she is a never-smoker with fully reversible obstruction — overlap is unlikely), allergic bronchopulmonary aspergillosis (send Aspergillus-specific IgE and precipitins; total IgE is raised but not to the ABPA range of above 1000 IU/mL), and vocal cord dysfunction (the high FeNO and reversibility argue against a pure VCD picture, but laryngoscopy may be warranted given refractory symptoms).
2. Confirm adherence and technique — the stem states pharmacy refill records confirm full adherence and technique is good on observation. The high FeNO (58 ppb) on high-dose ICS is therefore NOT a non-adherence signal here — it reflects active T2 inflammation despite therapy, supporting true severe T2-high disease. (A directly-observed ICS trial is the standard confirmatory step when adherence is uncertain, but here it is already established.)
3. Phenotype — eosinophils 460/microL (at least 300) and FeNO 58 ppb (at least 50) on maximal inhaled therapy confirms a T2-high eosinophilic phenotype. She is a biologic candidate. ^[1]

Step 2 — Problem list (2 marks):

1. Severe T2-high eosinophilic asthma, uncontrolled on high-dose ICS-LABA + LAMA + low-dose OCS
2. Maintenance oral corticosteroid exposure → osteopenia (bone protection needed)
3. Allergic rhinitis and chronic rhinosinusitis with nasal polyps (T2 comorbidity)
4. Obesity (BMI 33) — contributes to symptoms and steroid resistance
5. Occupational exposure (bakery worker — flour/aeroallergen sensitisation) ^[1]

Step 3 — Biologic selection (6 marks): ^[1]

She is T2-high with eosinophils and FeNO elevated, has nasal polyps (a Type 2 comorbidity), and is oral-steroid-dependent. The best single choice is dupilumab (anti-IL-4 receptor alpha, 300 mg SC every 2 weeks after a loading dose): ^[1]

• Exacerbation reduction and FEV1 improvement in moderate-to-severe uncontrolled T2-high asthma (QUEST, Castro 2018 — PMID 29782217). ^[1]
• Oral-corticosteroid-sparing benefit, directly addressing her maintenance prednisolone and osteopenia (VENTURE, Rabe 2018 — PMID 29782224). ^[2]
• Treatment of chronic rhinosinusitis with nasal polyps, addressing her upper-airway comorbidity — a decisive advantage over a pure anti-IL-5 in this patient. ^[1]

A reasonable alternative is an anti-IL-5 pathway agent (mepolizumab 100 mg SC every 4 weeks — exacerbation reduction shown in MENSA, Ortega 2014 — PMID 25199059 ^[3] — or benralizumab 30 mg SC at weeks 0, 4 then every 8 weeks). However, neither treats nasal polyps as a primary indication. Omalizumab is less compelling given her polysensitisation and the superior dual benefit of dupilumab. ^[1]

Plan: start dupilumab, trial for 3-4 months, and taper oral prednisolone once exacerbation rate and FeNO fall. Define a meaningful response as at least a 50% reduction in exacerbations and/or a successful prednisolone taper. ^[1]

Step 4 — Oral corticosteroid management and bone protection (3 marks):

• Taper prednisolone once the biologic is established; aim to discontinue if possible. Do not stop abruptly (adrenal suppression risk — she has been on 7.5 mg daily long-term, so a slow taper over months with a stress-dose plan is required).
• Bone protection: calcium and vitamin D supplementation; arrange a DEXA scan (osteopenia already documented — repeat to monitor); consider a bisphosphonate if T-score worsens or if she remains on prednisolone. Screen for steroid-induced diabetes (HbA1c) and hypertension. ^[1]

Step 5 — Comorbidity and lifestyle management (3 marks):

• Allergic rhinitis / nasal polyps: intranasal corticosteroid (e.g. mometasone) and saline irrigation; dupilumab will address the polyps; consider ENT input if obstructive.
• Obesity: weight-management referral; obesity worsens inflammation and steroid response; bariatric consideration only if BMI continues to rise.
• Occupational assessment: as a bakery worker she is at high risk of flour-dust sensitisation (occupational asthma). Arrange specific IgE to flour/wheat/alpha-amylase and consider serial peak flow monitoring at and away from work; an occupational physician referral and workplace exposure reduction (RPE, ventilation) may be the single most effective intervention if sensitisation is confirmed. ^[1]

Step 6 — Communication, action plan and follow-up (2 marks):

• Provide a written asthma action plan with traffic-light zones and an oral corticosteroid starter pack.
• Enrol in a severe asthma service for biologic administration and monitoring (ACQ-5, AQLQ, exacerbation log, FeNO and eosinophil trend).
• Shared decision-making: explain the biologic rationale, the 3-4 month assessment window, and the goal of steroid freedom; discuss funding/PBS or local criteria for ongoing therapy. ^[1]