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).
• Oral-corticosteroid-sparing benefit, directly addressing her maintenance prednisolone and osteopenia (VENTURE, Rabe 2018 — PMID 29782224).
• 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 (mepolizumab 100 mg SC every 4 weeks, or benralizumab 30 mg SC at weeks 0, 4 then every 8 weeks), both of which reduce exacerbations in severe eosinophilic asthma (MENSA, Ortega 2014 — PMID 25208643; benralizumab also steroid-sparing in ZONDA). 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]

SAQ 2 — Acute Severe Asthma: Emergency Management (20 marks, 30 minutes)

Prompt: A 29-year-old man with known asthma presents to the emergency department with worsening wheeze and breathlessness over 6 hours after a viral illness. On arrival: respiratory rate 30, heart rate 128, SpO2 91% on room air, unable to complete sentences, using accessory muscles, widespread wheeze with reduced air entry. PEF is 35% of his best (best 560 L/min). Discuss the immediate severity assessment, the sequential emergency management with doses and timing, and the criteria for intensive care escalation. [1]

Model Answer

Severity assessment (3 marks): [1]

He meets criteria for an acute severe attack (any one of PEF 33-50% of best, RR at least 25, HR at least 110, inability to complete sentences). He also has SpO2 below 92%, which is a life-threatening feature. He must be managed in a high-acuity area with continuous monitoring (ECG, SpO2, repeated PEF). An arterial blood gas is indicated given the life-threatening feature and severity, to assess PaCO2 and acid-base status. [1]

Key teaching point: A "normal" PaCO2 (4.6-6.0 kPa) in a patient breathing at RR 30 is ABNORMAL and life-threatening — he should be hyperventilating to a low CO2. A normal or rising CO2 signals ventilatory failure and impending arrest. [1]

Immediate management — first 15-30 minutes (6 marks): [1]

1. High-flow oxygen via mask to target SpO2 93-95%. In asthma there is no risk of oxygen-induced CO2 retention; give adequate oxygen. (In contrast to COPD, where oxygen is titrated cautiously.)
2. Nebulised salbutamol 5 mg (driven by oxygen at 6-8 L/min) — repeat every 15-20 minutes for the first hour (up to 3 doses). Driving the nebuliser with oxygen prevents worsening hypoxia.
3. Nebulised ipratropium bromide 500 mcg added to each of the first three salbutamol nebulisers — the combination is more effective than salbutamol alone in severe attacks.
4. Systemic corticosteroid — prednisolone 40-50 mg orally if he can swallow, OR hydrocortisone 100 mg IV (200 mg IV is acceptable in very severe attacks). Give EARLY — steroids take 4-6 hours to work; do not wait. Oral and IV are equally effective. [1]

Second-line therapy if not responding (4 marks): [1]

5. IV magnesium sulfate 2 g (1.2-2 g) over 20 minutes — for acute severe asthma not responding to initial nebulised bronchodilators and steroids. Cochrane (Kew 2014 — PMID 24865567) showed a 25% reduction in hospital admissions (NNT 7). Monitor for flushing, hypotension and areflexia. [1]

Escalation (5 marks): [1]

If he deteriorates or fails to improve:

• Continuous nebulised salbutamol (5-10 mg/hour) with repeated ipratropium.
• Consider IV salbutamol (250 mcg bolus then infusion 3-20 mcg/min with cardiac monitoring) — carries tachyarrhythmia, lactic acidosis and hypokalaemia risk; second-line.
• IV aminophylline (5 mg/kg loading over 20 min then infusion) — narrow therapeutic window; rarely used, reserve for refractory cases. [1]

Intubation criteria — any one of:

• Deteriorating consciousness, exhaustion, or apnoea
• Rising PaCO2 despite maximal medical therapy
• Silent chest with failing respiratory effort
• Cardiac arrest or peri-arrest (bradycardia, severe hypoxia) [1]

NIV is controversial in acute asthma and not routinely recommended; if used, only in ICU by experienced staff, and never as a substitute for intubation in a patient meeting life-threatening criteria. [1]

Intubation of a severe asthmatic is high-risk: ketamine is the preferred induction agent (bronchodilator, maintains BP); ventilate slowly with a long expiratory time to avoid breath-stacking and dynamic hyperinflation (permissive hypercapnia). Involve ICU/anaesthetics EARLY, before arrest. [1]

Discharge planning (2 marks): [1]

Discharge only when clinically stable on inhaled therapy and PEF at least 75% of best sustained for at least 4 hours. The discharge bundle:

1. Continue oral prednisolone 40-50 mg for 5 days (no taper for a short course).
2. Optimise the inhaled controller — step up; an asthma admission is a sentinel event.
3. Written asthma action plan with traffic-light zones and an oral corticosteroid starter pack.
4. Check inhaler technique (observe the patient); use a spacer with an MDI.
5. Follow-up within 48 hours (primary care/rapid-access) and in a respiratory clinic within 4 weeks to reassess control and consider step-down. [1]

An asthma admission markedly raises the risk of further severe attacks and asthma death in the following year — the single most evidence-based readmission-prevention intervention is ensuring the patient leaves on ICS-containing therapy with a written action plan. [1]