Obstructive Sleep

Apnoea Syndrome
Definition

Sleep Apnoea syndrome is defined as

30 or more apnoeic episodes
during a 7 hour period of sleep
or
an apnoea index equal to or greater than 5.
3 types of Sleep apnoea syndrome

Mild 5 to 20/hr

Moderate 20 – 40/hr

Severe > 40/hr

 Introduction
•Burwell coined the term PICKWICKIAN syndrome
Obesity + Hypersomnolence + Pulmonary Hypoventilation + Cor Pulmonale.

•Ideal Night sleep is 7.5 to 8.5 hrs

•Sleep is a reversible behavioural state of perceptual disengagement from and

unresponsiveness to the environment.

•REM and Non REM sleep effects respiratory drive, stability and ventilator mechanisms
(decreased)
 IMPACT OF SLEEP ON RESPIRATION
REM – 20 % whereas NREM is 80 %

Arousal requires immediate cortical and reticular activation via increased respiratory drive, level
of ventilation, activation of cough reflex, activation of upper airway dilator and abductor
muscles.
•APNOEA >10 sec cessation of respiration during sleep leading to arousal.

•HYPOPNEIC EVENT Decrease in airflow in associated with Oxyhaemoglobin desaturation.

• APNOEA INDEX No of apneas occurring per hour of sleep.

•RDI = Respiratory Disturbance Index aka Apnoea/Hypopnoea index i.e. no of both apneas and
hypopnoeas occurring per Hr of sleep.

•RERA Absence of apnoea / hypopnoea with a 10 sec or more of progressive negative

esophageal pressure (Pes), culminating in arousal
 Sleep Disorders
•Respiratory and Non respiratory sleep disorders.

•Respiratory Sleep Disorders include 4 Syndromes

1. OSAH (Obstructive sleep apnoea/hypopnoea)
2. Central Sleep Apnoea/hypopnoea
3. Cheyne Stokes breathing
4. Sleep hypoventilation

•Obstructive Sleep Apnoea is constituent of Sleep Apnoea Syndrome (Obstructive, Central & Mixed)
OBSTRUCTIVE SLEEP APNOEA
•Defined as 5 or more respiratory events (apnoeas / hypopnoeas / RERAs) per hour of sleep lasting
≥10seconds in association with excessive day time somnolence, waking with gasping, choking, or breath
holding spells or witnessed spells of apnoeas, snoring or both,

•Usually accompanied by reduction in blood oxygen saturations of atleast 3% – 4% and is terminated by

brief, unconscious arousals from sleep.

• Can occur in association with other syndromes (pickwickian syndrome , central sleep apnoea, upper
airway resistance syndrome) or independently.
• Pickwickian syndrome with OSA
Arterial hypoxemia during wakefulness, Hypersomnolence, pulmonary HTN, with
chronic right heart failure and nocturnal hypoventilation.

•Diagnosis is confirmed by demonstration of increase in PaCO2 of greater than 10mmHg

during sleep.

•Snoring is usually the first manifestation of sleep disordered breathing.

EPIDEMIOLOGY AND RISK FACTORS
•Prevalence = 5%

• M:F = 2:1

•Obesity >120% of ideal body weight

•Fat in neck plays largest role 30% of snoring males with collar size >17 have sleep
apnoea
 Anatomical Abnormalities
Obstruction due to

•Nose – Deviated Nasal Septum, Polyps, Hypertrophied turbinated

•Oral cavity, Oropharynx – Elongated soft palate and uvula, tonsillitis, macroglossia, retrognathia

• Hypopharynx, Larynx – Laryngeal tumours, Omega epiglottis, Laryngotracheal stenosis

 Children
Congenital
Acquired
Others

CONGENITAL

• Nasal Obstruction – Choanal atresia, complete nasal agenesis, neonatal rhinitis, congenital cysts
of nasal cavity, dentigerous cysts etc
•Facial Skeletal anomalies – (Crouzon’s syndrome, Apert’s asso with narrow airway), glossoptosis,
micrognathia (Treacher Collin’s syndrome), Pierre robin syndrome (cleft palate).

•Macroglossia – (Down syndrome, Beckwith Weidman syndrome), haemangioma of floor of mouth.

•Pharyngeal Swelling – Lingual thyroid, thornwald cyst, brachial cleft cyst, thyroglossal duct cyst,
haemangioma
ACQUIRED CONDITIONS

•Traumatic – Septal haematoma

•Inflammatory – Tonsillitis, adenoiditis

•Neoplastic – Juvenile angiofibroma

•Iatrogenic – Stenosis of nasopharyngeal isthmus

OTHER CONDITIONS

•Pharyngeal Muscle dysfunction

•Genetic predisposition
•Endocrine disorders (hypothyroidism, acromegaly)
•Alcohols, Sedatives
• Neuromuscular diseases – Cerebral palsy, Duchene Muscular Dystrophy
• Mucopolysaccharidosis
PATHOGENESIS
•Posterior movement of tongue and palate into apposition with the posterior pharyngeal wall
resulting in occlusion of nasopharynx and oropharynx.

•The resulting airway obstruction initiates a primary sequence of events that may repeat itself
hundreds of times each night.

• Posterior movement of tongue and palate

Airway obstruction with continued respiratory efforts
Apnoea Asphyxia Brief Arousal Restoration of upper airway patency
Sleeps & cycle continues
 CLINICAL FEATURES
Night Time Symptoms

Loud, habitual snoring

Witnessed apneas
Nocturnal awakenings
Gasping and choking episodes during sleep
Nocturia
Abnormal body movements
Day time symptoms

Unrefreshing sleep
Daytime headaches
Excessive daytime sleepiness
Lack of concentration, poor memory, irritability, personality changes
May lead to automobile or work related accidents
Decreased libido
• Nocturia may be related to negative pleural pressure increased dilatation of left atrium release of ANP (Atrial
Natriuretic peptide)

•Excessive daytime sleepiness can be subjective or objective.

• Subjective EDS scoring system Epworth Sleepiness Scale (ESS) >10 is significant

•Objective EDS measurements include Multiple Sleep Latency Test.

• Nocturnal palpitations, skipped heart beats, Cardiac Arrhythmias are common in these patients.
SEQUELAE
EXAMINATION

•Detailed history including genetic

•Associated medical conditions like hypothyroidism.

•HTN, DM, Hypertriglyceridaemia should always be looked for (Metabolic syndrome)

•Height, Weight, BMI Neck circumference Blood pressure Craniofacial Morphology.

•Oral cavity, oropharynx and larynx to be looked for any anatomical or pathological abnormality.

• Malampatti score.
 INVESTIGATIONS

•To assess patients general condition

•Differentiate simple snoring and sleep apnoea and determine severity of any apnoeas /
hypopnoeas.
•To assess site of obstruction

TO ASSESS GENERAL CONDITION

• CBC, TFT, Chest Xray (Cardiamegaly, pulmonary disorders), ABG analysis (arterial blood
gas), Lung function tests.
 TO DIFFERENTIATE SIMPLE SNORING
FROM OSA
Pulse Oximetry (during apnoea oxygen saturation falls and returns to normal once apnoea relieved,
Pulse rate is also measured)

ODI (Oxygen desaturation Index) i.e. no of times, oxygen saturation falls by 4% averaged out per hour.
ODI of >15 may suggest OSA.

 ‘Mini Sleep’ Study system Pulse oximetry + Video footage + Sound recording (best known is visilab)

Home multichannel testing (HMT) home overnight respiratory monitoring. Includes nasal/oral flow,
chest and abdominal movements, pulse oximetry are most popular. However, home monitoring without
EEG will not determine when the patient is asleep during the night.
 Overnight Polysomnography
GOLD STANDARD

Measures – Sleep state (EEG, EOG, EMG), Respiratory variables (Abdominal & chest wall
movements, oral or nasal airflow, End tidal CO2, Arterial oxygen saturation with pulse oximetry.
Non respiratory variables include ECG, EMG, Sleeping position, Audio video recording.

In addition other variables can be measured including penile tumescence, and multilevel
oesophageal manometry.
 TO ASSESS SITE OF OBSTRUCTION
1. Nasopharyngoscopy

2. ACOUSTIC REFLECTION Non invasive technique based on analyzing reflected sound waves
from the respiratory system which provides calculation of upper airway area as a function of
distance from the incisors. In OSA there is reduction in upper airway area compared with
normal controls.
3. CEPHALOMETRY relation between various soft tissue and bony landmarks based on carefully
taken lateral X rays.

4. FLUOROSCOPY to measure upper airway closure during sleep in patients with sleep apnoea

5. CT SCAN

6.MRI

7. Esophageal manometry
 MULLER’S MANOEUVRE
The patient is asked to breathe in while the mouth is closed
and the nose is pinched shut.

This generates a –ve pressure in the upper airway.

 Just snorers, slight inward movement of the soft palate and the back of the throat but the
glottis remains visible.

 OSA show varying degrees of collapse in the side walls of the velopharynx, at the base of the
tongue, and at the back of the throat which narrows the airway by more than 25%.
 JAW THRUST/MANADIBULAR
ADVANCEMENT
Enlarges the airway by several mechanisms mostly the base of the tongue is
pulled forward. Also lifts the pharyngeal muscles off the spine and places them
under tension.

Enlarges and stabilizes the airway at several levels.

Patients who show a good response to this manoeuvre can use a dental
appliance for treatment of their snoring or OSA (provided that their teeth are in
good shape)
 SLEEP NASOENDOSCOPY[Drug induced
sleep endoscopy (DISE)
1st described by Croft and Pringle in 1991

Patient sedated with propofol to a level sufficient to induce snoring.

Operator examines upper aerodigestive tract in supine position to determine levels of

obstruction.

Anesthetist must be present with full cardiac monitoring and resuscitation facilities.
Respiratory stimulants can be used to encourage snoring.
 DYNAMIC ULTRAFAST MRI
Can be used in awake and asleep pts to assess the site of obstruction.

 Midline saggital and cross sections at various levels most useful.

In awake patients with OSA-very close correlation with videoendoscopy found.

Not widely used due to high cost and time taken and sleep in an MRI machine may not be
representative of normal sleep patterns.
3-DIMENSIONAL CT
 Retropalatal space is most relevant area.

Gives an idea about modifications in palatal surgeries required to increase lateral dimensions of
this space
CEPHALOMETRY:
For size of airway,bulkiness of surroundingtissues & anatomical abnormalities

S sella
N nasion
ANS anterior nasal spine
A subnasale
B supramentale
PAS posterior airway space
Go gonion
Gn gnathion
STANFORD METHOD
Craniofacial Measurements
Stanford Score
 NASAL SPRAY TEST
This test involves using a topical nasal decongestant on alternate nights and comparing the

severity of snoring and apnoea. If the decongestant results in improved symptoms it may be

worth treating nasal abnormalities to help in snoring

TREATMENT
General Measures: Avoid sedatives, hypnotics and alcohol Weight loss

MEDICAL THERAPY
Pharmacological Agents –
a) Protriptyline (decreases REM sleep)
b) Others include Azetazolamide, Theophylline, nicotine, methoxyprogesterone
c) Oxygen therapy – Limited use, arterial oxygenation tried
d) Nasal Dilators tried
 Specific Medical therapies
A. Positional therapy – (LATERAL POSITION)

A. Positive Airway pressure

• CPAP – mainstay of treatment, acts as pneumatic splint(prevents collapse of airway and avoids OSA)
• Bi-level systems
• Auto CPAP
Oral Appliances

• Tongue retaining devices

• Mandibular advancing devices
• Snore guard
• Palatal Lifting devices
• NAPA (Nocturnal Airway Patency Device
 CPAP
MECHANISM OF ACTION
Acts as pneumatic splint, whereby blowing air via a tube and mask through the nasal and/or oral
passageway, will support the pharyngeal and palatal walls, preventing collapse of the airway.

THE EQUIPMENT
Continuous positive airway pressure machines provide either a constant blowing pressure (fixed
pressure) or vary pressure depending on the presence of apneas.
The masks may essentially be nasal or full face.
 SETTING UP ON CONTINUOUS POSITIVE
AIRWAY PRESSURE

Patients differ as to what level of pressure is necessary to eliminate the vast majority of apnoeas
and hypopnoeas.

METHOD OF TITRATION is to admit a patient for overnight diagnostic Polysomnography, and

halfway through the night, when the severity and the diagnosis of OSA have been confirmed, to
commence CPAP for the second half of the night.

This is referred to as a SPLIT NIGHT.

CPAP titration technique – The starting pressure is usually approximately 4 cm H20 and the pressure is
increased quickly until all apnoeas and hypopnoeas are eliminated.

Another technique increasingly used is to send the subject home with an autoCPAP machine. Most
autoCPAP machines will collect data on compliance, leaks and pressure profile.

 Advantage of autoCPAP over fixed pressure CPAP is an improvement in long-term compliance because
pressure can be altered as appropriate to the apnoea severity during the night, and also the average
pressure can be reduced throughout the night
 SIDE EFFECTS
1. Claustrophobia
2. Nasal Stuffiness
3. Skin abrasions and leaks
4. Ulceration of bridge of nose
5. Air swallowing or pulmonary barotraums
6. Treatment failure due to poor complaince
 SURGICAL TECHNIQUES
INDICATIONS
 SURGERIES INCLUDE :
1. RFTVR (Radiofrequeny tissue volume reduction)

2. Palatal Advancement with Z plasty

3. UPPP (Uvulopalatopharyngoplasty)

4. Modified UPPP

5. LAUP

6. Lingualplasty
7. Laser Midline Glossectomy

8. Genioglossus Advancement

9. Sliding genioplasty

10. Maxillomandibular advancement osteotomy

11. Bimandibular advancement

12. Hyoid Expansion

13. Tracheostomy
 RFTVR
Submucosal application of the radiofrequency energy to the midline soft palate. Initial
treatment directed at a point approximately midway between the hard and soft palate junction
and the base of the muscular uvulae.

 Subsequent treatment if necessary is directed more distally towards base of uvula. Usual target
temperature = 85 degree and average energy delivered is 500 to 600 J.

Complications – Submucosal ulceration.

 UPPP
Where obstruction is at upper pharyngeal or velopharyngeal level

 85 percent success rate in snoring. Remove tonsils, trimming faucial pillars, removal of uvula
and variable amount of soft palate mucosa, then suturing anterior and posterior faucial pillars
and anterior and posterior soft palate mucosa.

Modified UPPP-------- Tonsil not excised.

Complications of UPPP
Palatal Advancement with Z plasty

LMG i.e. Laser Midline Glossectomy : approximately 2.5 x 5cm midline tongue tissue is excised.
Might also require lingual tonsillectomy, reduction of aryepiglottic folds and partial
epiglottectomy. Usually combined with tracheostomy for airway protection.
LAUP
RFA
Pillar Palatal Implant System
Preferred Patients
Tongue based Procedures
Radiofrequency ablation – tongue based
FRIEDMAN ALGORITHM
Lingualoplasty: Same as LMG plus destruction of extra lingual tissue posteriorly and laterally

Maxillomandibular Advancement osteotomy: Le fort 1 maxillary osteotomy and advancing

maxilla forwards.

Bimandibular Advancement: Bony cuts posterior to last molar.

Hyoid Expansion: Hyoid cut in 3 pieces one anterior and 2 lateral. These pieces reanchored to an
arch bar like device which holds the pieces in an expanded manner and thus enlarging airway
COMPLICATIONS : pain and hemorrhage.
Thank you