Obstructive Sleep Apnoea — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr David Harris, 56 years old. [1]

Presenting complaint: Two-year history of progressively worsening loud snoring, witnessed apnoeas reported by his wife, and excessive daytime sleepiness. He has had two near-miss motor vehicle incidents in the past six months while driving his truck. [1]

Past history:

• Hypertension for 12 years, now resistant — blood pressure 156 over 94 on amlodipine 10 mg, perindopril 10 mg, and indapamide 2.5 mg
• Atrial fibrillation, diagnosed 8 months ago, currently rate-controlled with metoprolol; on apixaban for stroke prevention (CHA2DS2-VASc 3)
• Dyslipidaemia on atorvastatin 40 mg
• Gastro-oesophageal reflux disease
• No prior cardiac or cerebrovascular event [1]

Social and occupational history:

• Long-haul truck driver for 30 years — holds a commercial (heavy vehicle) licence
• Smoked 30 pack-years, quit 5 years ago
• Drinks 30 standard drinks per week (above recommended limits)
• Sedentary lifestyle; diet high in fast food
• Married; wife provides the corroborative history of snoring and apnoeas [1]

Current medications:

• Amlodipine 10 mg daily, perindopril 10 mg daily, indapamide 2.5 mg daily
• Metoprolol 50 mg twice daily
• Apixaban 5 mg twice daily
• Atorvastatin 40 mg nocte
• Pantoprazole 40 mg daily [1]

Examination findings (trainee elicits):

• Obese, comfortable at rest, no cyanosis or clubbing
• Body mass index 36, weight 112 kg, neck circumference 46 cm, waist circumference 118 cm
• Blood pressure 156 over 94 (right arm, seated), heart rate 72 irregularly irregular
• Oropharynx: Mallampati class 4 view, grade 3 tonsillar hypertrophy, large dependent uvula and soft palate, retrognathia with overjet
• Cardiovascular: irregularly irregular pulse, normal heart sounds, no murmurs, no elevated jugular venous pressure, no peripheral oedema
• Respiratory: clear lung fields, normal breath sounds, no signs of right heart failure
• No acromegalic or hypothyroid features [1]

Investigations:

• Epworth Sleepiness Scale score: 17 out of 24
• Home sleep apnoea test: apnoea-hypopnoea index 42 events per hour (severe, over 30), nadir oxygen saturation 78 percent, desaturation index 38 per hour
• Electrocardiogram: atrial fibrillation, left ventricular hypertrophy by voltage criteria
• Echocardiogram: mildly impaired left ventricular function (ejection fraction 50 percent), left atrial dilatation (44 mm), pulmonary artery systolic pressure 32 mmHg (normal)
• Bloods: HbA1c 44 mmol per mol (prediabetes range), total cholesterol 5.8, LDL 3.9, normal renal and hepatic function, TSH normal [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Harris is a 56-year-old long-haul truck driver referred for assessment of excessive daytime sleepiness. His wife reports loud snoring for 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 obese with a body mass index of 36, has resistant hypertension uncontrolled on three agents including a diuretic, recently diagnosed atrial fibrillation, and prediabetes. [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 an irregularly irregular pulse consistent with his atrial fibrillation. His Epworth Sleepiness Scale score is 17 out of 24. 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 and hazardous alcohol intake, the dominant modifiable risk factors
6. Prediabetes and dyslipidaemia as part of his metabolic syndrome [1]

My plan addresses each in turn." [1]

Management plan: [1]

1. Confirm and grade severity (immediate): The diagnosis of severe OSA is secure on the home sleep apnoea test (AHI 42, over 30, with significant desaturation). Given his atrial fibrillation and cardiovascular disease, I would discuss with the sleep laboratory whether a full in-laboratory polysomnography is warranted to characterise the burden precisely and exclude central events, but treatment should not be delayed. [1]

2. Initiate CPAP (immediate): With severe symptomatic OSA, CPAP is first-line. I would arrange CPAP titration with attention to mask fit, heated humidification, and structured early follow-up, setting a shared adherence goal of at least 5 hours per night with objective adherence monitoring. [1]

3. Lifestyle measures: Weight loss (a 10 percent reduction can reduce the AHI by approximately 50 percent), reduction in alcohol intake to recommended limits, avoidance of alcohol and sedatives before sleep, and a structured exercise program. Given his body mass index, I would refer to a multidisciplinary weight-management service and discuss bariatric surgery. [1]

4. Manage the cardiometabolic comorbidities: Optimise antihypertensives with general medicine, acknowledging CPAP may improve control over months. Manage his atrial fibrillation with cardiology. Address prediabetes and dyslipidaemia. [1]

5. Driving and medico-legal: As a commercial driver, he must cease driving until his OSA is treated and he meets fitness-to-drive criteria. I would counsel him, notify the licensing authority, involve his employer and occupational health, and plan for return to driving once his Epworth is under 10 and objective CPAP adherence is satisfactory. [1]

Examiner discussion questions

Q: "The home sleep apnoea test was used here rather than polysomnography. When is a home test acceptable, and when must you do a full polysomnogram?" [1]

"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 — no moderate or severe cardiopulmonary disease, no neuromuscular disease, and no suspicion of a non-respiratory sleep disorder such as narcolepsy. The home test records fewer channels — typically nasal airflow, oximetry, and respiratory effort — so it under-detects hypopnoeas because it lacks electroencephalography to score arousals, and it may underestimate severity. A negative or equivocal home test in a convincing clinical picture must be followed by full polysomnography. In this patient, with his atrial fibrillation and resistant hypertension, some units would obtain a full polysomnogram to characterise the burden precisely and exclude central events, but his result is unequivocally severe and treatment should not be delayed." [1]

Q: "His Epworth score is 17. Tell me about this scale." [1]

"The Epworth Sleepiness Scale, developed by Murray Johns at the Epworth Hospital in Melbourne in 1991, is an eight-item self-report scale that asks the patient to rate, on a 0 to 3 scale, the likelihood of dozing in eight common situations, for a total of 0 to 24 [1]. A score above 10 indicates excessive daytime sleepiness. A score of 17 is markedly abnormal and consistent with severe sleepiness, explaining his near-miss driving incidents. The ESS measures the consequence of OSA rather than predicting the diagnosis, so it quantifies severity and monitors treatment response. I would recheck it after starting CPAP to document improvement."

Q: "Walk me through the cardiovascular evidence for CPAP. Will it prevent him having a stroke or heart attack?" [1]

"This is best discussed using two studies. 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 [2]. 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 [3]. And 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 [4].

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." [1]

Q: "How will you address CPAP adherence? He is a truck driver who lives a long way from the clinic." [1]

"Adherence is the central determinant of his real-world benefit, so I would invest heavily in the strategy. First, correct mask selection and fitting — I would trial nasal, oronasal, and nasal-pillows masks against his anatomy and comfort. Second, heated humidification to reduce nasal dryness and mucosal irritation. Third, education about the disease and the consequences of untreated OSA, including the driving risk, to build motivation. Fourth, proactive management of side-effects — mask leak, nasal congestion, claustrophobia, and aerophagia. Fifth, structured follow-up in the first weeks, with objective download of adherence data at each contact, and telehealth or phone support given his distance. Adherence in the first month predicts long-term use, so intensive early support is the priority. I would set a shared goal of at least 5 hours per night." [1]

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

"This is a public-safety issue and a medico-legal duty. 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 and falls towards normal with effective CPAP. 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. 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. If he continued to drive against advice, my duty to report would become mandatory." [1]

Q: "He says he cannot tolerate the mask. What are his options?" [1]

"I would revisit the adherence strategy first — most apparent CPAP intolerance can be overcome with intensive support, different mask types, humidification, and treatment of side-effects. If he genuinely cannot tolerate CPAP, the main alternative is a mandibular advancement splint, which is less effective than CPAP on average but often better tolerated. However, given his severe disease and obesity, a splint alone may be inadequate. [1]

Hypoglossal nerve stimulation, supported by the STAR trial, showed a 68 percent median AHI reduction in CPAP-intolerant moderate-to-severe OSA [5], but the body mass index threshold is under 32 to 35 and he is at 36, so he would need weight reduction first. This again points to bariatric surgery as a key part of his management — substantial weight loss can markedly reduce or resolve OSA and may bring him into the threshold for hypoglossal stimulation if he still needs it. Surgery such as uvulopalatopharyngoplasty has limited and inconsistent evidence and is not a reliable stand-alone cure for severe OSA."

Q: "He drinks 30 standard drinks a week. What is the relevance?" [1]

"Alcohol depresses upper airway dilator muscle tone and worsens OSA, particularly in the hours before sleep. His hazardous intake is likely contributing to his disease severity and his hypertension. Reducing alcohol intake to recommended limits is an important part of his lifestyle management, alongside weight loss, and may improve his AHI and blood pressure independently of CPAP. I would counsel him on safe drinking limits, refer him to a drug and alcohol service if there is any suggestion of dependence, and recheck his sleep study and blood pressure after lifestyle changes." [1]

DCE Short Case — Examination in OSA

Instruction

"Examine this patient with obstructive sleep apnoea. Concentrate on the features relevant to the diagnosis. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates

• Inspection — central obesity, a short thick neck, a plethoric facies
• Oropharyngeal inspection — a crowded airway with a high Mallampati grade (class 3 or 4), enlarged tonsils, a large or oedematous uvula and dependent soft palate, macroglossia, and retrognathia or overjet
• Cardiovascular — elevated blood pressure (often resistant); in advanced disease a loud pulmonary component of the second heart sound or a right ventricular heave [1]

Presentation template

"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 an irregularly irregular pulse consistent with atrial fibrillation and 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]

Discussion template

1. Summarise findings — "central obesity, crowded oropharynx, and elevated blood pressure, consistent with severe OSA with cardiometabolic comorbidity."
2. Differential of crowded oropharynx — tonsillar hypertrophy, macroglossia (consider acromegaly, hypothyroidism, Down syndrome), retrognathia.
3. Investigations — polysomnography or home sleep apnoea test for the AHI; Epworth Sleepiness Scale; screen for diabetes, dyslipidaemia; electrocardiogram and echocardiogram for cardiovascular consequences. [1]

Examiner: "What craniofacial and soft-tissue features predispose to OSA?" [1]

"The predisposing features fall into two groups. The craniofacial features are retrognathia (a receded mandible), micrognathia, maxillary hypoplasia, and an overjet, which shorten the mandibular compartment and crowd the tongue into a smaller pharyngeal space — these explain OSA in non-obese patients. The soft-tissue features are macroglossia, tonsillar and adenoidal hypertrophy (the commonest cause in children), uvulopalatal hypertrophy, and nasal obstruction from a deviated septum or polyps. Obesity compounds all of these by depositing fat in the lateral pharyngeal walls and around the tongue, narrowing the lumen and increasing extraluminal tissue pressure. Approximately 80 percent of OSA patients are overweight or obese." [1]

Examiner: "What is the mechanism by which OSA causes hypertension?" [1]

"The repetitive intermittent hypoxia during apnoeas activates the chemoreflex, producing surges in sympathetic nerve activity and systemic blood pressure with each event. Over time, this sympathetic overdrive, combined with oxidative stress and endothelial dysfunction from the cyclical hypoxia-reoxygenation, produces sustained hypertension. The characteristic finding is a non-dipping nocturnal blood pressure pattern on 24-hour ambulatory monitoring, because the blood pressure surges continue through the night. OSA is the single commonest identifiable cause of resistant hypertension, present in up to 80 percent of resistant hypertensives. Effective CPAP produces a modest but real fall in blood pressure of approximately 2 to 3 mmHg systolic, often greater in resistant hypertension." [1]