Sleep disorders

Question 1

Screening questionnaires/evaluation tools for undiagnosed OSA

Answer 1

STOP BANG: with score 3/8: Sens 93%, Poor specificity (32%)

Berlin Questionnaire (Sens 82%, Spec 39%)

OSA 50 - Developed in Australian GP setting - Score ≥ 5 94% sens and 31% spec for moderate-severe OSA

Question 2

OSA 50 elements

Answer 2

Question 2

STOP BANG

Answer 2

Snoring,
Tiredness,
Observed apnoeas,
Pressure (Blood)
BMI,
Age,
Neck circumference,
Gender

Intermediate to high risk of OSA if score ≥3/8
* Sens 93% for AHI >15,
* NPV 90% for AHI > 15
* Poor specificity (32%)

Question 3

ESS elements

Answer 3

• Standardised measurement of subjective sleepiness
• Not sensitive or specific for the diagnosis of OSA
• Moderate correlations with objective measurements of sleepiness such as Mean Sleep Latency Test and Maintenance of Wakefulness Test performed in sleep laboratories
• Weak correlations with all measurements of OSA severity e.g. AHI

Question 4

OSA treatment

Answer 4

Risk factor modification
* Weight reduction, reduce alcohol intake
* Medication – avoid opioids, (benzodiazepines)
* Positional therapy – highly efficacious if used in those with only positional OSA (up to 25%)

Devices to Splint Upper Airway during sleep
* CPAP (Continuous Positive Airway Pressure) Therapy
* Oral Appliances (mouthguards) – moderate effectiveness, expensive

Surgical Options– Tonsillectomy, Bariatric surgery

Radical Maxillofacial/ENT surgery - rare, usually a “last resort” for those who are intolerant of CPAP, variable efficacy, long term data needed

Question 5

2 types of PAP for OSA

Answer 5

Continuous airway pressure (most common – requires determination of individual optimal pressure)

Auto-adjusting pressure (APAP device).

Question 6

Proven benefits of CPAP

Answer 6

• Improves daytime sleepiness, depression, cognitive function, QOL, systolic>diastolic BP
• Reduces risk of MVAs (Untreated OSA associated with 4-7 fold increased risk of MVA)
• No RCT evidence that CPAP decreases CV mortality (despite lots of observational evidence) SAVE study, RICCADSA study

Question 7

Obesity hypoventilation syndrome triad

Answer 7

1. Awake hypercapnia (PaCO2 > 45 mmHg)
2. BMI >30 kg/m2
3. SDB when other causes of hypoventilation excluded (e.g. lung disease, neuromuscular disease)

Question 8

Prevalence of OHS

Answer 8

approx. 0.3% of population,

up to 50% if BMI > 50 kg/m2

Up to 1/3 present with acute on chronic respiratory failure and/or right heart failure

Question 9

Pathophysiology of OHS

Answer 9

Increased leptin resistance (and mechanical load in general) lead to blunting of ventilatory response

OSA exacerbates

Question 10

CV disease associated with OHS

Answer 10

HTN (up to 80%), Pulmonary Hypertension, RHF

Question 11

Treatment for OHS

Answer 11

• Weight loss is an effective treatment option (usually >25-30% of body weight required)
• Positive airway pressure (PAP) almost certainly improves survival (RCT unethical); reduces hypercapnia, right heart failure, pulmonary hypertension; improves symptoms

Question 12

Which PAP to use in OHS (CPAP or NIV)

Answer 12

CPAP usually first choice if significant co-existing OSA → monitor carefully over next 2-3 mo (symptoms, ABG…)

If minimal /mild OSA but significant hypoventilation/respiratory failure→ NIV may be needed from outset

If presents acutely with acute on chronic hypercapnic respiratory failure-> NIV usually commenced and may be changed to CPAP when acidaemia resolves

Question 13

Sleep disordered breathing in heart failure

Answer 13

May be either OSA or Cheyne Stokes Respiration – Central Sleep Apnea (CSR - CSA) or a mix

Question 14

Treatment for Cheyne-stoke breathing in heart failure

Answer 14

optimise heart failure therapy

If OSA present, CPAP may improve EF, BP, exercise capacity and QOL (No evidence that PAP reduces mortality in heart failure)

If CSR present, can consider trialling CPAP, oxygen, Bilevel PAP (NIV)

Adaptive Servo Ventilation (ASV) – now CONTRAindicated in CSR with EF <45%

Question 15

Narcolepsy Type 1 diagnosis

Answer 15

Excessive daytime sleepiness for at least 3 months
One of :
* Definite cataplexy and a positive MSLT
* Or low CSF hypocretin

Exclusion of other causes

Question 16

Narcolepsy Type 2 diagnosis

Answer 16

• EDS for at least 3 months
• Cataplexy is absent
• Positive MSLT
• Or Normal CSH Hypocretin

Exclusion of other causes

Question 17

Pathophys narcolepsy

Answer 17

autoimmune destruction of hypothalamic neurones that produce Hypocretin (Orexin) which regulates arousal and transition between wake and sleep

Question 18

Treatment of narcolepsy

Answer 18

stimulant therapy such as Dexamphetamine or wake promoting agent such as Armodafinil,

usually SSRI/SNRI used for cataplexy

Question 19

MSLT procedure

Answer 19

series of 4 or 5 - 20 minute naps set 2 hours apart with measurement of sleep latency

Mean Sleep latency of < 8 minutes associated with 2 sleep onset REM periods strongly suggests a diagnosis of Narcolepsy

2 week sleep diary and/or Actigraphy should be performed prior to test (exclude sleep restriction)
Urinary drug screen often performed