Obstructive Sleep Apnoea Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Harris is a 56-year-old long-haul truck driver referred for assessment of excessive daytime sleepiness. His wife reports loud snoring for many years and, over the past two years, witnessed apnoeas several times per night. He dozes off at traffic lights and has had two near-miss motor vehicle incidents in the past six months. He is overweight with a body mass index of 36, has resistant hypertension uncontrolled on three agents including a diuretic, and recently diagnosed atrial fibrillation. [1]

On examination he is obese with a neck circumference of 46 cm, a blood pressure of 156 over 94, a crowded oropharynx with a Mallampati 4 view and grade 3 tonsillar hypertrophy, and a normal cardiovascular and respiratory examination otherwise. His Epworth Sleepiness Scale score is 17 out of 24, consistent with severe excessive daytime sleepiness. A home sleep apnoea test showed an apnoea-hypopnoea index of 42 events per hour with desaturation to 78 percent, consistent with severe obstructive sleep apnoea. [1]

His main problems are:

1. Severe obstructive sleep apnoea with excessive daytime sleepiness and a high motor vehicle accident risk — primary diagnosis
2. Resistant hypertension, likely driven in part by the OSA
3. Atrial fibrillation, with untreated OSA promoting recurrence
4. A commercial driving licence with medico-legal obligations for fitness to drive
5. Obesity, the dominant modifiable risk factor [1]

My plan addresses each in turn." [1]

Examiner probing questions and model answers

Q1: "How would you confirm the diagnosis, and is a home sleep apnoea test adequate in this patient?" [1]

"The diagnosis of OSA requires an apnoea-hypopnoea index of 5 or more on polysomnography or a validated home sleep apnoea test, accompanied by symptoms. His AHI of 42 is over 30 and therefore severe. A home sleep apnoea test is acceptable in a patient with a high pre-test probability of moderate-to-severe OSA and no significant comorbidity. However, given his atrial fibrillation and resistant hypertension, some units would obtain a full in-laboratory polysomnography to characterise the burden precisely, stage sleep architecture, and exclude central apnoeas. The home test under-detects hypopnoeas because it lacks electroencephalography to score arousals, so a negative or equivocal result in a convincing clinical picture must be followed by full polysomnography. In his case the result is unequivocally severe, so the diagnosis is secure, but I would discuss the polysomnography question with the sleep laboratory given his comorbidity." [1]

Q2: "What is the role of the Epworth Sleepiness Scale, and how do you interpret a score of 17?" [1]

"The Epworth Sleepiness Scale, developed by Murray Johns at the Epworth Hospital in Melbourne in 1991, is an eight-item, 0 to 24 self-report scale that quantifies the likelihood of dozing in eight common situations [1]. A score above 10 indicates excessive daytime sleepiness and warrants formal evaluation. A score of 17 is markedly abnormal, consistent with severe sleepiness, and explains his near-miss driving incidents. The ESS measures the consequence of OSA — sleepiness — rather than predicting the diagnosis, so it is used to quantify severity and monitor treatment response rather than to screen. I would recheck it after starting CPAP to document improvement."

Q3: "What is your immediate management?" [1]

"CPAP is first-line for severe symptomatic OSA. I would arrange CPAP titration — in-laboratory or auto-titrating — with attention to mask fit, heated humidification, and structured early follow-up, because adherence in the first month determines long-term success. I would set a shared adherence goal of at least 5 hours per night and arrange objective download of adherence data. Alongside CPAP, I would initiate lifestyle measures — weight loss, avoidance of alcohol and sedatives before sleep, lateral sleep positioning, and smoking cessation — and refer to a multidisciplinary weight-management service. Given his body mass index of 36, I would also discuss bariatric surgery as an effective option that can produce substantial weight loss and significantly reduce or resolve OSA." [1]

Q4: "He asks whether CPAP will prevent another heart attack. What do you tell him?" [1]

"I would counsel him honestly using the SAVE trial evidence. The SAVE trial, published in the New England Journal of Medicine in 2016, randomised over 2700 patients with moderate-to-severe OSA and established coronary or cerebrovascular disease to CPAP plus usual care versus usual care alone, and found no significant reduction in the primary composite of cardiovascular death, myocardial infarction, stroke, or related hospitalisation [4]. The key limitation was adherence — mean use was only 3.3 hours per night. CPAP did improve daytime sleepiness, mood, and quality of life.

In contrast, the observational study by Marin and colleagues in the Lancet in 2005 followed men for 10 years and found that untreated severe OSA had higher fatal and non-fatal cardiovascular events, while CPAP-treated patients approached the event rate of healthy controls [5]. The honest synthesis is that CPAP clearly improves his symptoms, sleepiness, blood pressure, and quality of life, and observational data suggest long-term cardiovascular and mortality benefit with good adherence, but the single large randomised trial in established disease was negative, partly limited by adherence. I would motivate him with symptom relief and sleepiness reduction, with cardiovascular benefit framed as likely but not proven."

Q5: "How do you approach his resistant hypertension and atrial fibrillation?" [1]

"OSA is the single commonest identifiable cause of resistant hypertension, present in up to 80 percent of resistant hypertensives, and the mechanism is sympathetic overdrive from intermittent hypoxia plus endothelial dysfunction. A non-dipping nocturnal blood pressure pattern is characteristic. Effective CPAP produces a modest but real fall in blood pressure of approximately 2 to 3 mmHg systolic on meta-analysis, often greater in resistant hypertension. I would liaise with general medicine or nephrology to optimise his antihypertensives, acknowledging that CPAP may improve control over months. [1]

For his atrial fibrillation, OSA is strongly associated — the negative intrathoracic pressure swings stretch the atrial walls, the intermittent hypoxia and afterload surges remodel atrial myocardium, and untreated OSA predicts both new-onset AF and recurrence after cardioversion or ablation. I would manage his AF on its merits with cardiology — rate or rhythm control and anticoagulation by CHA2DS2-VASc — with the expectation that treating the OSA may reduce recurrence after a rhythm-control strategy. I would screen him for diabetes and dyslipidaemia as part of comprehensive cardiovascular risk reduction." [1]

Q6: "What are your obligations regarding his commercial driving licence?" [1]

"This is a public-safety issue and a medico-legal duty. The approach is threefold. First, I would counsel him immediately that he must cease driving until his OSA is treated and he meets fitness-to-drive criteria. The risk of a crash is approximately 2 to 7 fold higher in untreated OSA. I would document this advice and his response. [1]

Second, for a commercial (heavy vehicle) driver, the reporting obligation is more stringent than for private drivers. Under the Austroads fitness-to-drive standards, a confirmed diagnosis of OSA requires effective treatment and demonstration of satisfactory control — objective CPAP adherence data and resolution of sleepiness, with an Epworth under 10 — before a commercial licence is granted or renewed. I would notify the licensing authority and involve his employer and occupational health. [1]

Third, I would plan for return to driving once his Epworth is under 10, his CPAP adherence is at least 4 to 5 hours per night documented objectively, and he reports no residual sleepiness at the wheel, with periodic review thereafter. I would communicate this compassionately but firmly, framing treatment as the enabler — effective CPAP restores driving fitness, usually within weeks — and document the entire conversation and the notification." [1]

Q7: "What if he cannot tolerate CPAP?" [1]

"The main alternative for a CPAP-intolerant patient is a mandibular advancement splint, which is less effective than CPAP at reducing the AHI on average but often better tolerated. However, given his severe disease and obesity, a splint alone may be inadequate. I would revisit the adherence strategy first — different mask types, heated humidification, behavioural support, and treatment of side-effects — because most apparent CPAP intolerance can be overcome with intensive support. [1]

If he genuinely cannot tolerate CPAP, I would consider hypoglossal nerve stimulation, supported by the STAR trial, which showed a 68 percent median AHI reduction in CPAP-intolerant moderate-to-severe OSA [6]. However, the body mass index threshold is under 32 to 35 and he is at 36, so he would need weight reduction first, which again points to bariatric surgery as a key part of his management. Surgery such as uvulopalatopharyngoplasty has limited and inconsistent evidence and is not a reliable stand-alone cure for severe OSA."

Q8: "What is his long-term prognosis?" [1]

"With effective treatment and good adherence, the prognosis is good — his sleepiness, blood pressure, and quality of life improve, and his driving fitness is restored. Observational data, including the Marin study, suggest that effective CPAP normalises the cardiovascular risk of severe OSA towards that of healthy controls. Without treatment, he faces a continued high risk of motor vehicle accident, progressive hypertension, atrial fibrillation recurrence, and an increased risk of stroke and cardiovascular events. The Yaggi study in the New England Journal of Medicine in 2005 established OSA as an independent risk factor for stroke and death after adjustment for vascular risk factors [3]. The dominant determinant of his prognosis is adherence to effective therapy, which is why the adherence strategy and the driving framework are so central to his care."

Short Case Discussion

Scenario: "Examine this patient with obstructive sleep apnoea. Concentrate on the features relevant to the diagnosis."

Candidate presentation (model): [1]

"I examined Mr Harris. He is an obese man with a short, thick neck. His body mass index is elevated and his neck circumference is 46 cm. His blood pressure is 156 over 94. [1]

On oropharyngeal inspection he has a Mallampati class 4 view with grade 3 tonsillar hypertrophy and a large dependent uvula, consistent with a crowded upper airway. Cardiovascular examination reveals a regular pulse but an elevated blood pressure; heart sounds are normal with no evidence of right heart failure. [1]

In summary, these findings are consistent with the obstructive sleep apnoea phenotype — central obesity with a crowded oropharynx — and the elevated blood pressure is consistent with the cardiometabolic association of his condition." [1]

Examiner: "What features would suggest advanced disease with pulmonary hypertension?" [1]

"Advanced OSA may progress to pulmonary hypertension and cor pulmonale. I would look for a loud pulmonary component of the second heart sound, a right ventricular heave, an elevated jugular venous pressure, a tricuspid regurgitation murmur, and peripheral oedema. However, when a patient with OSA presents with marked daytime hypercapnia, severe pulmonary hypertension, or cor pulmonale, I would suspect the overlap syndrome of OSA combined with COPD or obesity hypoventilation syndrome, which carries a substantially worse prognosis and requires bilevel positive airway pressure rather than CPAP alone. I would check arterial blood gases and an echocardiogram to assess for these complications." [1]

Examiner: "How would you investigate him?" [1]

"The gold-standard investigation is polysomnography to determine the apnoea-hypopnoea index and grade severity. A home sleep apnoea test is acceptable in high pre-test probability without complex comorbidity. I would quantify his sleepiness with the Epworth Sleepiness Scale, screen for diabetes and dyslipidaemia, obtain an electrocardiogram and — given his atrial fibrillation — an echocardiogram to assess for pulmonary hypertension and structural heart disease. If there were any suggestion of daytime hypercapnia or obesity hypoventilation syndrome, I would check arterial blood gases." [1]