Obstructive sleep apnoea

Of OSA, Question 8 from the first paper of 2001 asked the candidates specifically: "What are  the potential long-term complications of this syndrome?" Less specifically, the college frequently throws obese hypercapneic patients at the candidates (Question 1a from the second paper of 2000, Question 14 from the second paper of 2011).

The best resources for this, aimed at intensivists:

• The OSA page from LITFL

• This 2014 overview article from the Annals of Internal Medicine
• This article from the Lancet (Jordan et al, 2014)
• Park et al (2011) from the Mayo Clinic Proceeding
• The Australasian Sleep Association's OSA fact sheet

Definition of OSA

Table 2 from the Park article (2011) lists some of the defining features of OSA.  In order to meet the criteria, one must undergo a formal polysomnographic sleep study, and demonstrate the following features:

• Apnoeic episodes of greater than 10 seconds in duration (or recordable pulse oximetry desaturation by more than 4%)
• At least 5 of these episodes per hour, with associated symptoms:
  • Daytime somnolence
  • Impaired cognition
  • Mood disorders
  • Insomnia
  • Hypertension
  • Ischaemic heart disease
  • History of stroke
• OR: over 15 of these episodes, irrespective of what symptoms you think you have.

This definition comes from a 1999 position statement by the American Academy of Sleep Medicine, which has also been endorsed by the Australasian Sleep Association.

STOP-BANG is a tool devised for pre-admission clinic staff, to screen OSA patients preoperatively and thereby predict those who will have clinically relevant perioperative complications.

The items in this screening tool are as follows

• Snoring ("loud enough to be heard through closed doors")
• Tiredness (daytime somnolence)
• Observed apnoea
• Pressure - high blood pressure
• Body mass index in excess of 35
• Age is over 50
• Neck circumference over 40cm
• Gender is male

Each item scores a 1 or 0. A total score in excess of 3 has an 84% sensitivity of predicting OSA; a score in excess of 5 predicts moderate-to-severe OSA. Other similar tools exist, of which the best known is probably the Berlin Questionnaire.

Pathophysiology of OSA

Question 8 from the first paper of 2001 also asked the candidates to discuss the pathophysiology of obstructive sleep apnoea.  An excellent review article from Thorax (Fogel et al, 2004) is available to answer this. One may summarise by saying that there is a combination of anatomical predisposition and exacerbating factors.

The delicate eyes of visual learners may be offended by this big confusing diagram:

Instead, in a thousand words:

• The oropharynx is a muscular tube which depends on muscle tone for patency.  
• Three muscle groups are involved:
  • muscles influencing hyoid bone position (geniohyoid, sternohyoid)
  • the muscle of the tongue (genioglossus)
  • the muscles of the palate (tensor palatini, levator palatini)
• During sleep there is a loss of background muscle tone.
  • This occurs mostly during REM sleep
  • Neuromuscular coordination is lost: the normal increase in upper airway tone with inspiration does not occur.
• This is exacerbated by drugs, alcohol, bulbar stroke, myopathy, etc.
• Several anatomical defects may coexist, which narrow the upper airway:
  • Acromegaly
  • Retrognathia
  • Macroglossia, eg. in Down syndrome
  • Fat infiltration of oropharyngeal tissues
  • Oedema (as a part of generalised oedema)
  • Upper airway infection, eg. tonsillitis
• The combination of narrowed airway, reduced airway muscle tone and lost inspiratory coordination results in complete upper airway obstruction with inspiration.
• The resulting apnoeic episodes have several pathological features:
  • Hypoxia
  • Hypercapnea
  • Extremely negative intrathoracic pressure
• This has pathological consequences (listed in the Park article)
  • Due to chronic REM sleep deprivation:
    • Daytime somnolence
    • Mood disturbances
    • Cognitive impairment
  • Due to chronic hypoxia:
    • Pulmonary hypertension (due to chronic hypoxic vasoconstriction)
    • Right ventricular hypertrophy and right heart failure`
    • Polycythaemia
  • Due to chronic hypercapnea:
    • Reset respiratory drive centre
  • Due to the influence of the above on cardiovascular function:
    • Hypertension
    • Increased risk of myocardial infarction
    • Atrial fibrillation (3-4 fold higher odds)
    • Increased risk of stroke (likely due to polycythaemia and hyperviscosity)
  • Associated with OSA, but not necessarily caused by it:
    • Decreased seizure threshold (independently associated with epilepsy)
    • Diabetes (somehow, it is an independent risk factor)
    • Increased risk of post-operative reintubation
    • Impotence

Risk factors for OSA

Young et al (JAMA, 2004) offer a good overview of the risk factors:

• Established risk factors:
  • Obesity
  • Central body fat distribution
  • Large neck girth
  • Craniofacuial and upper airway abnormalities (eg. acromegaly, retrognathia, macroglossia, enlarged tonsils, and so forth)
• Suspected risk factors:
  • Smoking
  • Menopause
  • Use of alcohol before sleep
  • Nocturnal nasal congestion

If one really wanted to, one could come up with a shitload more. Lets face it: how many causes of narrowed upper airway or poor upper airway tone are there? Lets say, drug use is a risk factor. would the rapidly scribbling exam candidate then go on to offer greater granularity, separating the drugs into benzodiazepines, barbiturates, opiates, volatile anaesthetics, etc? Would one mention stroke, adding bulbar palsies? Musclular dystrophy? What about myasthenia gravis? Airway tumours? It could be lost time in return for few marks.