Obstructive sleep apnoea syndrome

OSAS is predominantly a male disorder and the incidence among men is estimated to be as high as 1.25%. It is uncommon in premenopausal women, presumably due to the respiratory stimulant effect of progesterone. Major anatomical abnormalities are seldom seen; however, subtle structural narrowing of the upper airway is present in almost all patients with OSAS. A number of medical disorders are associated with and predispose to OSAS.

• Medical Disorders associated with OSAS

• Obesity

• Nasal pathology
  • Deflected nasal septum
  • Polyps
  • Turbinate hypertrophy
  • Tumour

• Adenotonsillar hypertrophy

• Excessive pharyngeal tissue
  • Large uvula
  • Redundant posterior wall tissue
  • Tumours
  • Macroglossia
• Excessive laryngeal tissue
  • Omega-shaped epiglottis
  • Large aryepiglottic folds
  • Tumours
• Other disorders
  • Hypothyroid goitre
  • Myotonic dystrophy
  • Shy-drager syndrome (multiple system atrophy with somnogenic abductor laryngeal paresis)
  • Micrognathia
  • Retrognathia

Alcohol can also predispose and/or induce sleep apnoea.

OSAS is due to the functional collapse of the upper airway during sleep. Structural abnormality of the upper airway predisposes to this collapse. The structural narrowing occurs mostly in the velopharyrnx and/or tongue base hypo- pharyngeal region. The site of obstruction to airflow has been localised to the supralaryngeal part of the airway, using fibre-optic pharyngoscopy, cine CT scanning, somnofluoroscopy and simultaneous recording of pressure in the oesophagus and supraglottic airway.

The occlusion begins in the oropharynx as the tongue comes into contact with the soft palate and posteriorpharyngeal wall, and this is followed by the progressive collapse of the lower pharygeal airway; the lateral oropharyngeal wall has been shown to collapse in a sphincteric manner. Narrowing of the airway necessitates the generation of a higher negative inspiratory pressure to maintain ventilation and, thus, leads to complete obstruction and apnoea. The consequent hypoxia and hypercarbia awakens the patient, and airway patency is restored during expiration coincident with the dissipation of negative intrathoracic pressure. Physiological aberration increases with the severity of apnoea.

The following changes are seen after the cessation of ventilation:

• increase in PaCO₂
• decrease in PaO₂
• decrease in pH
• sinus bradycardia (most common change)
• sinus pause
• atrioventricular block
• premature ventricular contractions

Sinus arrhythmias are due to oxygen desaturation and bradycardia responds to atropine. Hypoxia leads to catecholamine release, which, in turn, contributes to tachycardia on resumption of ventilation. Chronic and recurrent hypoxia puts a strain on the right side of the cardiopulmonary complex; this will aggravate or cause systemic and pulmonary hypertension, and eventually lead to cor pulmonale.

Clinical features of OSAS:

• Symptoms
  • Loud, intermittent snoring
  • Daytime sleepiness or hypersomnolence
  • Tiredness
  • Morning headaches
  • Nocturnal enuresis, loss of libido and impotence
  • Poor physical or intellectual performance
• Signs
  • Obesity
  • Structural narrowing of upper airway
  • Hypothyroidism
  • Clinical or radiological evidence of pulmonary hypertension, right ventricular hypertrophy and cardiac failure
  • Cardiac arrhythmias
• Laboratory findings
  • Polycythaemia
  • Alveolar hpoventilation (high PaCO2, low PaO2 and low pH)
  • Hypothyroidism (decreased T3, T4;increased TSH)

Most patients with OSAS are overweight and a significant proportion have short, thick necks. A history of noisy, intermittent snoring is present in almost all patients with OSAS and most are brought to the physician by their partner. Snoring is a sign of partial upper airway obstruction and is caused by vibration of the soft palate due to the airflow through the narrow airway. Snoring ceases when the obstruction becomes complete (i.e. apnoea).

Turbulent airflow causes noisy and heavy breathing which resembles inspiratory stridor.

Daytime sleepiness or hypersomnolence is a major incapacitating symptom, which may have serious social and economic consequences, including loss of job, frequent road accidents and divorce. It is caused by sleep fragmentation due to repeated nocturnal wakening. Even in the early part of this century childhood lethargy was often attributed to adenotonsillar hypertrophy.
Morning headaches, decreased libido and impotence are also common symptoms.

A detailed history is important and a thorough otolaryngological examination provides valuable information about the morphology of the airway. A general physical examination should also be carried out to detect any coexisting cardiopulmonary abnormalites.

Diagnosis of OSAS

• General investigations
  • History
  • Otolaryngologic examination
  • Haemoglobin
  • Arterial blood gas analysis
  • Thyroid function test
  • ECG
• Specific investigations
  • Fibre-optic laryngoscopy (sitting and supine)
  • Polysomnography
  • Transcutaneous oxygen monitoring or ear-lobe oximetry
  • Somnofluoroscopy (lateral fluoroscopic examination of upper airway during sleep with synchronous polysomnography)
  • CT scanning and cine CT scanning (during sleep)

Laboratory investigations may demonstrate polycythaemia, which is due to hypoxic stimulation of bone marrow. A chest radiograph and ECG are helpful to evaluate cardiopulmonary status and to identify any coexisting abnormality. Spirometry is also useful; a sawtoothed pattern is indicative of possible airway obstruction during sleep. A sleep study should be undertaken which should include continuous arterial oxygen and ECG monitoring, and polysomnography to measure airflow through the nose and mouth, as well as thoracic cage movements. Earlobe oximetry and transcutaneous oxygen monitoring are occasionally used to confirm desaturation during apnoea.

One of the methods used to localise the site of obstruction is fibre-optic pharyngoscopy with or without Mueller’s manoeuvre which is carried out in both the sitting and supine position. Mueller’s manoeuvre involves vigorous inspiration with the nose and mouth closed. The movements of the pharyngeal wall during this manoeuvre reportedly replicate obstructive events occurring during sleep. Fibre- optic pharyngoscopy would yield better information if it could be performed during sleep, but this is impractical.

All these investigations are commonly performed and enable the necessary distinction to be made between type, frequency and severity of apnoeaic episodes, and their incidence during rapid eye movement (REM) sleep and non- REM sleep.

Management of OSAS is summarised below.

Medical

• Weight loss
• Avoidance of CNS depressants, including alcohol
• Respiratory stimulants (e.g. progesterone, acetazolamide and theophyline)
• Protriptyline
• Continuous positive airway pressure
• Tongue retaining devices
• Position alarm
• Nasopharyngeal intubation
• Treat associated medical disorders

Surgical

• Adenotonsillectomy
• Nasal surgery (submucus resection, septoplasty, polypectomy, turbinectomy)
• Uvulopalatopharyngoplasty
• Tracheostomy
• Mandibular advancement or reconstruction
• Expansion hyoidplasty
• Weight reduction surgery

Management may be medical or surgical, depending on the predominant type of apnoea, and the severity of functional and physiological aberration. All patients, irrespective of type of apnoea, should be advised to avoid CNS depressants, including alcohol. Weight reduction should be strongly encouraged as it can decrease the severity of apnoea in obese patients. In morbid obese patients, weight reduction surgery could be considered.

Medical: progesterone, which is a recognised repiratory stimulant, has been found to be beneficial in OSAS. However, decreased libido, impotence and alopecia are major side-effects in male patents and limit its frequent and long- term use.

• Acetazolamide, which is a carbonic anhydrase inhibitor, stimulates respiration by increasing the concentration of hydrogen ions in arterial blood and has been useful in some cases.
• Protriptyline, which is a non-sedating tricyclic antidepressant suppresses REM sleep and is indicated in those patients with little or no apnoea associated with non- REM sleep.
• Theophyiline, which increases hypoxic ventilatory drive, has been used successfully in premature infants.

The use of tongue retaining devices (TRD) and nasal continuous positive airway pressure (CPAP) is effective, but patient compliance is poor; nasal CPAP splints the airway open with positive pressure and TRD prevents retrolapse of the tongue during sleep. A position alarm is appropriate for patients who have moderate to severe apnoea in the supine position, but little or no apnoea in the lateral position.

Surgical: adenotonsillar hypertrophy is a common cause of pediatric sleep apnoea and adenotonsillectomy is curative. Micrognathia and retrognathia are amenable to mandibula corrective surgery (reconstruction or advancement).

Tracheostomy is the only totally effective treatment but because of the special care required and the possible complications, it is not a preferred primary treatment. It is only indicated in patients with severe apnoea, which is not amenable to other forms of surgical treatment and oxygen desaturation below 50% or a bradycardia of 40-45 beats/ minute with significant arrhythmias. Uvulo-palato-pharyngoplasty (UPPP) was introduced as a new surgical procedure for the treatment of OSAS in 1981 and has since been modified.The procedure involves tonsillectomy, amputation of the uvula and appropriate (4-6 mm) resection of the soft palate and redundant pillars of fauces.

The success rate has been reported to be 25-75%. It is most effective when the obstruction is in the velopharyngeal sphincter area. In lower pharyngeal (i.e. hypopharynx, tongue base, epiglottis and/or ayepiglottic fold) obstruction, other surgical procedures, such as tracheostomy or Mandibular-hyoid reconstruction are required.