1. Obstructive sleep apnoea(k.j.lee)
Sleep –disordered breathing; refers to a group of disorders caused by abnormal breathing patterns
that disrupt sleep.It includes upper airway resistance syndrome &OSA.The Hallmark symptom of
sleep-disordered breathing is snoring.
Apnoea:(means want of breathing)is defined as the cessation of respiration for 10 or more seconds.
Hyponoea :is a 50% or greater reduction in respiratory airflow for 10 or more seconds which results
in either arousal from sleep or a greater than 4% drop in oxyhemoglobin saturation.
Apnoea index is the number of apnoeas per hour of sleep.
Hyponoea index is the number hyponoeas per hour of sleep.
Apnoea /hyponoea index (AHI) or respiratory disturbance index which refers to the total number of
apnoea &hyponoea per hours of sleep.
There are three characteristic patterns of apnoea:
Central apnoea : is associated with the absence of airflow due to lack of ventilator effort.
Obstructive sleep apnoea: absence of airflow despite persistent ventilator effort as contraction of
the respiratory muscles such as diaphragm.
Mixed apnoea: includes both central & obstructive components
Upper airway resistance syndrome(UARS) refers to partial collapse of the upper airway reduction
with sleep fragmentation,arousals & day timesomnolence in the absence of measurable
apnea,hyponea, oxyhemoglobin desaturation.
Pathophysiology of OSA
The airway in the oropharynx &hypopharynx is depend on pharyngeal dilator muscle to maintain its
patency.(most prominent muscles are genioglossus &tensor palatine)
Patients with OSAS have narrow upper airway.Inspiring through a narrow passageway leads to
acceleration of airflow (venture effect) & negative pressure is generated at the edges of this
airstream.The faster the airflow ,the greater negative pressure (Bernoulli principal).
This negative pressure is countered during wakefulness by the activity of GH&TP in patients with
OSAS.During sleep ,this neuromuscular is lost.the loss of muscle tone is most pronounced during
rapid eye movement sleep.The combination of anatomic narrowing & loss of neuromuscular control
leads to airway collapse & cessation of airflow.
The switch to oral route for breathing changes the dynamic of upper airway predisposing to its
collapse.The stimulating effect of nasal airflow on breathing is lost.Nasal blockage increases the
negative inspiratory pressure augmenting the collapse of anatomically compromised airway.

2. Snoring is generated by vibrations of the pharyngeal soft tissue,the posterior edge of the soft
palate.uvula,tonsillar pillars are most common location.
Hypoxia & hypercapnia causes increase inspiratory effort to overcome the airway resistance.The
combination of hypoxia ,hypercapnia & increased ventilator effort causes sleep fragmentation &
arousals. With arousal, the pharyngeal muscle activity is restored & the airway opens.The patient
then hyperventilates to correct the blood gas , return to sleep& the cycle begins again.
Awake(narrow airway & compensatory pharyngeal dilators)
↓
Sleep
↓
Pharyngeal dilator muscle hypotonia
↓
Airway obstruction or collapse
↓
Obstructive apnoea
↓
Hypoxia & hypercapnia
↓
Increased ventilator effort
↓
Sleep arousal
↓
Regain pharyngeal muscle dilator tone
↓
Patent airway
↓
Correct hypoxia &hypercapnia
↓
Return to sleep & cycle begins again.

3. Clinical features of OSA
Daytime somnolence
Daytime fatique
Morning headache
Poor job performance
Depression
HTN
CVD
CVA
Risk factors for OSA
Obesity
Male
Age
Facial abnormalities; nasal obstruction,adenotonsillar
hypertrophy,macroglossia,micrognathia,retrognathia.
Family history
Sedative & alcohol
Endocrine abnormalities; hypothyroidism,acromegely.
Systemic disorders (down syndrome ,neuromuscular disordered,muscular
dystrophy,kyphoscliosis,amyloidosis.)
Clinical evaluation
1)History
2)Physical examination
may be divided into general & upper airway specific examinations.General examination
,obesity,HTH,endocrine &systemic disorders.
Upper airway examinationaims at determining the cause & site of airway narrowing .Anterior
rhinoscopy &fibreoptic nasal endoscopy.

4. Retropalatal region is a common site for airway collapse.Poor visualization of the uvula or posteror
edge of the soft palate using tongue depressor ,suggest an oropharyngeal/retropalatal site of airway
obstruction.Mallampati &Friedman classification.
Gr-1,tonsils are contained within the tonsillar pillars.
Size-2,tonsils extend to the posterior pillars,
Size-3,extend beyond the pillars but not to midline,
Size-4,extend to the midline.
Dynamic assessment of the airway involves the Muller manoeuvre.A fibreroptic laryngoscope is
passed through the nostril &positioned directly on above the segment to be evaluated.Patients are
asked to inhale forcefully at end expiration aganist occluded oral &nasal passages.The site & degree
of airway collapse is determined.This is performed with the patient in a sitting &lying position.A
greater than 40% narrowing of the airway at the level of the tongue base /hypopharynx suggests
poor outcome with uvulopalatopharyngoplasty.(the degree of constriction at the level of the tongue
base can be estimated based on occlusion of the vallecula & extend that epiglottis is pushed
posteriorly towards the posterior pharyngeal wall.)
3) Imaging
both CT &MRI are not routinely used inthe clinical evaluation of the patient with sleep apnoea.
4)Polysomnography
:(sleep study) can be obtained at home or laboratory.A standard polysomnography cosists of EEG
that determines stage of sleep &arousal;
EOG that differentiates REM & Non-REM phases of sleep based on eye movement.
EMG :submental EMG for additional scoring of sleep stage & wakefulness.
EMG of anterior tibialis muscle to monitor periodic limb movement.
ECG : to monitor cardiac arrhythmia.
Pulse oximetry: to record oxygen saturation.
Measurement of nasal & oral airflow.
Measurement of chest & abdominal wall motion to evaluate respiratory efforts.
Snoring sound with a microphone.
In the laboratory polysomnography may be full night & split night study.Full night allow for a more
complete diagnostic evaluation.In the split night study ,the first half of the study is diagnostic&
second half titration &initation of the therapy.

5. Treatment of OSA
Once the diagnosis is confirmed by polysomnography,if the RDI(Respiratory disturbance index) is
more than 20 events per hour of sleep &lowest oxygen saturation is less than 86%.
The nature &aggressiveness of the treatment are guided by patients signs& symptoms ,daytime
somnolence ,sign of cardiovascular dysfunction,result of the polysomnography including RDI,extend
of arterial oxygen desaturation,sleep disruption,arrhythmia.The treatment include
behavioural,medical &surgical interventions.
Behavioural interventions
Weight loss should be encouraged.Alcohol ,smoking & sedative should be avoided.
The patients are advised to improve sleep hygiene with regular sleep schedule &sufficient amount of
sleep. Sleep apnoea is worse in the supine position.so avoid this position.
Medical intervention
Medical treatment has a limited role in the treatment of OSA.Nasal decongestant,intranasal
steroid,&antihistamines are helpful.
Protrityline or fluoxetine may reduce the number of apnoea in some patients.
Supplemental oxygen is beneficial with severe oxyhemoglobin desaturation. It reduces apoea related
arrhythmia,oxygen therapy does not prevent the nocturnal respiratory events &sleep fragmentation.
Oral &Dental appliance may be effective in the treatment of habitual snoring.
Continuous positive airway pressure is the mainstay of treatment for OSA.CPAP serves as pneumatic
stent for the upper airway with prevention of collapse.The pressure requirement is determined
during polysomnography when the pressure is titrated until the majority of the respiratory events
are abolished.
Surgical intervention
Nasal surgery: septoplasty ,inferior turbinectomy,polypectomy, nasal valve procedures,alone or
combination.
Palatopharyngoplasty:The presence of more than 30 to 40 % narrowing in the hypopharynx /tongue
base region on Muller manoeuvre predicts poor outcome with palatopharyngoplasty.
1) Laser –assisted uvulopalatoplasty:It involves amputation of the uvula & making two lateral
incision in the soft palate which induce retraction of the soft palate &stiffen the
palate.current indication snoring & mild OSA.
2) Radiofrequence volume reduction of soft palate (somnoplasty): to produce submucosal
coagulation necrosis & later scar formation,which results in volumne contraction &soft
tissue stiffening.
3) Tonsillectomy:adenotonsillar hypertrophy is a common cause of OSA.

6. 4) Uvulopalatopharyngoplasty: excision of excessive soft tissue at the free margin of the soft
palate (sparing the underlying muscle),uvula,posterior lateral pharyngeal wall. Tonsil are
excised,excessive tissue along posterior pillars are removed,anterior &posterior pillars are
sutured together.
Hypopharyngeal/Tongue base surgery:
1)Lingual tonsillectomy.
2) Midline glossectomy
3)hyoid Myotomy &suspension with glenoid tubercle advancement.
4)Radiofrequency volumetric tongue base reduction.
5) Mandibular advancement.

7. 4) Uvulopalatopharyngoplasty: excision of excessive soft tissue at the free margin of the soft
palate (sparing the underlying muscle),uvula,posterior lateral pharyngeal wall. Tonsil are
excised,excessive tissue along posterior pillars are removed,anterior &posterior pillars are
sutured together.
Hypopharyngeal/Tongue base surgery:
1)Lingual tonsillectomy.
2) Midline glossectomy
3)hyoid Myotomy &suspension with glenoid tubercle advancement.
4)Radiofrequency volumetric tongue base reduction.
5) Mandibular advancement.