Specialist ENT OBSTRUCTIVE SLEEP APNEA

OBSTRUCTIVE SLEEP APNEA (OSA)

Definition: Obstructive sleep apnea is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. It is the most common type of sleep disordered breathing (SDB) and is characterized by recurrent episodes of upper airway (UA) collapse during sleep.

Definitions of respiratory events

Apnea is defined by the American Academy of Sleep Medicine (AASM) as the cessation of airflow for at least 10 seconds.

Hypopnea is defined as a recognizable transient reduction (but not complete cessation) of breathing for 10 seconds or longer. 

Obstructive events are characterized by continued thoracoabdominal effort in the setting of partial or complete airflow cessation. 

Central events lacks thoracoabdominal effort.

Mixed events have both obstructive and central features. They generally begin without             thoracoabdominal effort and end with several thoraco-abdominal efforts in breathing.

Pathophysiology

OSA is caused by soft tissue collapse in the pharynx. Transmural pressure is the difference between intraluminal pressure and the surrounding tissue pressure. If transmural pressure decreases, the cross-sectional area of the pharynx decreases.

Specialist ENT Screenshot 2020 11 29 book near final miscellaneous24

Anatomic factors leading to decreased transmural pressure

  • Enlarged tonsils.
  • Volume of the tongue.
  • Soft tissue.
  • Lateral pharyngeal walls.
  • Length of the soft palate.
  • Abnormal positioning of the maxilla and mandible.

Neuromuscular factors leading to decreased transmural pressure

  • Decreased Neuromuscular activity in the Upper airway, including reflex activity.
  • Reduced ventilatory motor output to upper airway muscles.
Neuromuscular factors leading to decreased transmural pressure
  • Vagal stimulation causes bradycardia. Bradycardia and hypoxia provoke serious cardiac rhythm disturbances i.e. premature beats asystole, ventricular tachycardia, cardiac arrest.

Etiology of OSA

A) Sex- Male to Female ratio 2:1.

B) Structural factors

  • Innate anatomic variations (facial elongation, posterior facial compression).
  • Retrognathia and micrognathia.
  • Mandibular hypoplasia.
  • Brachycephalic head form.
  • Inferior displacement of the hyoid.
  • Adenotonsillar hypertrophy, particularly in children and young adults.
Specialist ENT Screenshot 2020 11 29 book near final miscellaneous25
    • Syndromes- Pierre Robin syndrome, Down syndrome, Marfan syndrome, Prader-Willi syndrome.
    • High arched palate (particularly in women).
    • Nasal obstruction– Polyps, septal deviation, tumors, trauma, and stenosis.
    • Retropalatal obstruction– Elongated, posteriorly placed palate and uvula, tonsil and adenoid hypertrophy.
    • Retroglossal obstruction– Macroglossia and tumor.

C. Non-structural factors

    • Obesity.
    • Central fat distribution.
    • Old age.
    • Postmenopausal state.
    • Alcohol intake.
    • Sedative use.
    • Smoking.
    • Habitual snoring with daytime somnolence.
    • Supine sleep position.
    • Rapid eye movement (REM) sleep.

D. Other associated conditions

    • Hypothyroidism (macroglossia, increased soft tissue mass, myopathy).
    • Neurologic syndromes (post-polio syndrome, muscular dystrophies and autonomic failure syndromes such as Shy-Drager syndrome).
    • Stroke.
    • Acromegaly (macroglossia and increased soft tissue mass).
    • Environmental exposures (smoke, environmental irritants or allergens, alcohol and hypnotic sedative medications).
Epidemiology
  • Prevalence in US has been 2-4% for women and 4-9% for men. It remains undiagnosed in approximately 93% of affected women and 82% of affected men.
  • Seen in 2% of children, equal in boys and girls. Adenotonsillar hypertrophy is the major etiology.
  • Pregnancy IUGR is associated with pregnant women with untreated OSA.

Diagnosis

1.History

Nocturnal symptoms

    • Snoring, usually loud, habitual and bothersome to others.
    • Witnessed apneas, which often interrupt the snoring and end with a snort.
    • Gasping and choking sensations that arouse the patient from sleep.
    • Nocturia.
    • Insomnia.
    • Restless sleep, with patients often experiencing frequent arousals and tossing or turning during the night.

Daytime symptoms

    • Non-restorative sleep (waking up as tired as when they went to bed).
    • Morning headache, dry or sore throat.
    • Excessive daytime sleepiness (EDS) that usually begins during quiet activities (example, reading, watching television); as the severity worsens, patients begin to feel sleepy during activities that generally require alertness (example school, work, driving). Assessed using the Epworth Sleepiness Scale (ESS).
    • Daytime fatigue/tiredness.
    • Cognitive deficits- memory and intellectual impairment (short-term memory, concentration).
    • Decreased vigilance.
    • Morning confusion.
    • Personality and mood changes, including depression and anxiety.
    • Sexual dysfunction, impotence and decreased libido.
    • Gastroesophageal reflux.
    • Hypertension
    • Depression.

2. Physical Examination

  • Obesity – Body mass index (BMI) greater than 30 kg/m2.
  • Large neck circumference – Greater than 17 inches in men and 15 inches in women.
  • Abnormal (increased) Mallampati score.
  • Narrowing of the lateral airway walls.
  • Enlarged tonsils.
  • Retrognathia or micrognathia.
  • High-arched hard palate.

3. Associated co-morbidities

  • Systemic arterial hypertension, present in approximately 50% of patients with OSA.
  • Congestive heart failure (CHF).
  • Pulmonary hypertension.
  • Stroke.
  • Metabolic syndrome.
  • Type 2 diabetes mellitus.

4. Diagnostic criteria for OSA 

Individuals must fulfill criterion A or B, plus criterion C to be diagnosed with OSAS:

A. Excessive daytime sleepiness that is not explained by other factors.

B. Two or more of the following that are not explained by other factors:

➣ Choking or gasping during sleep.

➣ Recurrent awakenings from sleep.

➣ Unrefreshing sleep.

➣ Daytime fatigue.

➣ Impaired concentration.

C. Overnight monitoring demonstrates 5 to 10 or more obstructed breathing events per hour during sleep or greater than 30 events per 6 hours of sleep. These events may include any combination of obstructive apnea, hypopnea, or respiratory effort–related arousals.

Investigations

  1. An overnight sleep study or polysomnography (PSG)– It is done in laboratory by measurement of sleep architecture and electroencephalographic (EEG) arousals, eye movements, chin movements, airflow, respiratory effort, oximetry, electrocardiographic (ECG) tracings, body position, snoring, and leg movements.
  2. Split-night PSG– Patients with a respiratory disturbance index (RDI) higher than 40 during the first 2 hours of diagnostic PSG should undergo a split-night PSG study. The final portion of the study is used for titrating the continuous positive airway pressure (CPAP) device.
  3. Multiple sleep latency test (MSLT)- Objective measurement of excessive daytime sleepiness (EDS). MSLT is generally used to confirm the diagnosis of narcolepsy in patients in whom narcolepsy is a consideration. Narcoleptic patients have rapid eye movement sleep on at least 2 of the 4-5 naps during the day.
  4. Drug-induced sleep endoscopy (DISE)- It is an evaluation technique that can be performed for patients with obstructive sleep apnea who are unable to tolerate positive airway pressure therapy (e.g., CPAP or BiPAP). The purpose of DISE is to improve the results of treatment with surgery and/or oral appliances.
  5. Dynamic MRI– It can accurately diagnose the cause and level of upper airway narrowing in patients with OSA. Surgery can be planned accurately after level of obstruction is confirmed.

Treatment

  1. Mild apnea has a wider variety of options.
  2. Moderate-to-severe apnea should be treated with nasal continuous positive airway pressure (CPAP).
  3. Conservative nonsurgical treatment includes
      • Weight loss- 10% reduction in weight leads to a 26% reduction in the respiratory disturbance index (RDI).
      • Avoidance of alcohol for 4-6 hours prior to bedtime.
      • Sleeping on one’s side rather than on the stomach or back.
  4. Nasal CPAP Therapy– The most effective treatment for OSA.
    • It increases the caliber of the airway in the retropalatal and retroglossal regions and maintains UA patency during sleep, preventing the soft tissues from collapsing.
    • Increases the lateral dimensions of the upper airway and thins the lateral pharyngeal walls.
  5. BiPAP Therapy.
  6. Oral Appliance Therapy.
  7. Surgical Correction of the Upper Airway
      • Nasal surgery (septoplasty, sinus surgery and others). 
      • Tonsillectomy ± adenoidectomy.
      • Uvulopalatopharyngoplasty (UPPP).
      • Laser assisted uvulopalatoplasty (LAUP).
      • Radiofrequency volumetric tissue reduction.
      • Lingual plasty.
      • Genioglossus and hyoid advancement.
      • Sliding genioplasty.
      • Maxillo-mandibular advancement osteotomy.
      • Tracheostomy.
  8. Pharmacologic therapy-
    • Modafinil is approved by the US Food and Drug Administration (FDA) for use in patients who have residual daytime sleepiness despite optimal use of CPAP. 
    • Selective serotonin reuptake inhibitor agents such as Paroxetine (Paxil) and Fluoxetine (Prozac) have been shown to increase genioglossal muscle activity and decrease REM sleep.

We Are Always Ready to Help You.
Book An Appointment

Specialist ENT section img
Specialist ENT contact img