This document provides an overview of obstructive sleep apnea syndrome (OSA) in both adults and pediatrics. It defines OSA and discusses symptoms, risk factors, pathophysiology, diagnosis using polysomnography, and various treatment options including weight loss, CPAP, oral appliances, surgery, and drugs. For children, it notes key differences in presentation compared to adults and conditions commonly associated with pediatric OSA such as adenotonsillar hypertrophy. The gold standard treatment is adenotonsillectomy for children and weight loss and CPAP for adults.

1. O.S.A SYNDROME IN ADULTS AND
PAEDIATRICS DIAGNOSIS &
MANAGEMENT
Presenter- Dr Abhineet Jain
Moderator– Dr R.R. Barle

2. Definition
 Sleep related breathing disorder originating from
partial airway collapse and increased upper
airway resistance to episodes of hypopnea or
complete airway collapse with sleep apnea.

3. Frequently used terminology
 Apnea-cessation of airflow for at least 10 sec.
 Hypopnea- reduction in airflow(>30%) at least 10
sec. with >3% oxyhemoglobin desaturation.
 Obstructive- continued tracheobronchial effort in
setting of airflow cessation.
 Central-lack of tracheobronchial effort in setting
of airflow cessation.
 Mixed- event with both obst. & central causes.

4.  Apnea index- no. of apneas /hr of total sleep
time.
 AHI- No of apneas and hypoapneas/hr of total
sleep time.
 REARs index- no of REARs /hr of total sleep
time.
 RDI –no. of apneas,hypoapneas,REARs /hr of
total sleep time.

5. Types
Snoring U.A.R.S.
 Sound generated by
pharyngeal soft tissue
vibration.
 May occur in isolation
with absence of asso.
Insmonia/daytime
sleepiness/frequent
arousals/-ve PSG
study.
 Pt. with snoring who
experience daytime
somnolence and
somatic complaints
with effort related
frequent arousals but
DON’T match criteria
for OSA syndrome.

6. OSA syndrome-
 Pt with snoring having 5 or more respiratory
events with associated daytime
somnolence,waking and gasping.each episode
lasting for >10 sec with oxydesaturation by > 3-
4%

7. Symptoms
 Loud snoring
 Restless sleep
 Observed apnea,choking
 Excessive daytime somnolence
 Morning fatigue/headache
 Memory loss/ depression/mood changes.
 Nocturnal enuresis/sweating
 Women -more to have
insomnia,palpitations,ankle oedema.

8. Pathophysiology
 Etiology and mechanism of collapse of airway is
multifactorial but is largely due to interaction of
easily collapsible upper airway with relaxation of
pharyngeal dilator muscle, which happens during
sleep.
 It is not only structural compromise but also because
of abnormalities of complex reflex pathways that
control action of pharyngeal dilator muscles, may fail
to maintain patency.
 Genioglossus is the most important muscle in
maintaining patency in OSA pt.

9. Risk Factors
 Obesity
 Soft tissue
hypertrophy.
 Retrognathia
 Increased Vertical
facial length
 Increased vertical
length of post. Airway
 Increased cervical
angulation.
 Adenotonsillar
hypertrophy.
 Increased distance of
hyoid from mandible
plane.
 Decreased
mandibular/maxillary
projection.

10. Consequences of OSA--
 Hypertension/ arrythmias /CAD.
 Pulmonary htn./stroke/ sudden death.
 Metabolic syndrome
 GERD
 Neurocognitive disorder.

11. Diagnosis-
 Epworth sleepiness scale- to asses daytime
sleepiness. Score of > 10 in OSA pt.
 General para.- BM,neck circumference,blood
pressure.
 Physical examinations of nose ,oral cavity &
oropharynx,neck.
 Fibreoptic nasopharyngoscopy with Muller’s
maneuver in awake pt.

12. Cont..
 Drug induced sleep videoendoscopy- greater
promise of identifying site of obstruction during sleep
and useful for directing surgical intervention.
 MRI– a good soft tissue imaging but
cant,differentiate between OSA and non- OSA.
 GOLD STANDARD- nocturnal polysomnography

13. Few imporatnt physical findings
Nasal obstruction
Oropharyngeal
obstruction
 Septal deviation.
 Turbinate
hypertrophy.
 Nasal valve collapse.
 Adenoid hypertrophy
 Polyps and tumors.
 Large soft palate.
 Tonsillar hypertrophy
 post. Pharyngeal wall
banding.
 Macroglossia.
 Large mandibular tori.

14. Hypopharyngeal
obstruction Laryngeal obstruction
 Lateral wall collapse.
 Omega shape
epiglottis.
 Lingual tonsil
hypertrophy.
 Retro and
micrognathia.
 True cord paralysis.
 Laryngeal tumors.

15.  Obesity
 Achondroplasia.
 Chest wall deformity.
 Marfan’s syndrome.
 Redundant cervical adipose tissue.

16. PSG parameters-
 EEG
 EOG
 ECG
 Pulse Oximetry
 Nasal and oral airflow
monitors- pressure
trasducers.
 EMG- Ant.
Tibial/submental.
 Chest/ abdom. Effort
monitors.
 Tracheal microphone.
 Body position
monitors.
 Optional
ET-Co2 monitor.
Esophageal pressure
monitor

17. Medical treatment
 Weight loss measures
 CPAP- gold standard.it acts as a pneumatic splint
to prevent upper airway collapse both during
inspiration & expiration. It has shown
improvement in quality of life,reduction in AHI.,
Reduced cardiovascular risk.
 BiPAP- delivers a separate adjustable lower
expiratory/ high inspiratory positive airwau
pressure . It improve adherence in selected group
of pt. especiallybthose with Neuromuscular
/ventilatorty disorder

18.  APAP--It is AUTOMATED.the pressure changes
in response to variation in airflow
magnitude,limitation, snoring, or airway
impedance.
 Oral Appliances- in mild to moderate OSA by
increasing post. Oropharyngeal airway.
Adherence rate is high.
 Tooth /jaw muscle pain / excessive salivation are
common problems.

20.  Drugs- fluticasone, monteleukast proved to be
effective in those with rhinitis/ adenotonsillar
hypertrophy. Duration of Rx-6 weeks.
 Modafinil- to reduce residual sleepiness of OSA
pt. on CPAP use. NOT TO BE USED in absence
of DEFINITIVE treatment of OSA. It acts as a
central stimulant of postsynaptic – alpha
adrenergic receptors.
 Topical nasal decongestants in pt.with nasal
obstruction with OSA with mini.releif.
 Nasal strip dilators makedly releif of
snoring,sleepiness in non OSA pt.

21. Surgical treatment
 Indications
I. AHI>5 and <14 with excessive day time
sleepiness.
II. AHI >15
III. SIGNIFICANT arrhythmias with airway
obstructions.
IV. Unsuccessful or refused medical therapy.
V. Medically stable enough to under go surgery.
VI. UARS preferably with objective improvement of
neurocognitive dysfunction on medical Rx.

22. Surgical procedures-
 Majority of pt. has combination of retropalatal
and retro glossal obst. Isolated areas of
obstruction are less common.
 pt,. with laryngeal obstruction should be treated
appropiately and be considerd for tracheostomy
if improvement is not achieved surgically or with
CPAP.

23. Treatment options-
Nasal surgery Palatal surgery
 Septoplasty
 Inferior turbinate
reduction.
 Adenoidectomy.
 Polyp resection.
 Nasal valve reduction.
 Palatal radifrequency
 Pillar implants
 Tonsillectomy
 UPPP
 Transpalatal
advancement
pharyngoplasty

24. UPPP

25. Hypopharyngeal surgery
 Lingual tonsillectomy.
 Partial midline glossectomy.
 Tongue base radiofrequency.
 Mandibular osteotomy & genioglossal advn.
 Hyoid myotomy & suspension.
 Tongue suspension suture.
 Maxillomandibular osteotomy & advancement.

26. GENIOGLOSSUS
ADVANCEMENT

27. Post operative period
Complications Airway care
 Pain
 airway obstruction
 Hemorrhage
 Wound dehiscence.
 Palatal incompetence
 Death
 Nasopharyngeal
stenosis.
 Nasal CPAP should
be used in 1st
postoperative night to
keep oxygen satu.
>90%.
 In pt. with severe
OSA use CPAP for 2
weeks

28. OSA Syndrome In Paediatrics
 It has been defined as episodes of upper airway
obstruction during sleep that are usually
associated with a reduction in oxy hemoglobin
saturation, hypercarbia or both.
 A unique feature is obstructive hypoventilation
where continuous partial airway obstruction
leads to paradox. Efforts,hypercarbia ,often
hypoxemia. Its diagnosis needs Et-CO2
monitoring.

29. Childhood Vs Adult
presentation adult children
Excess daytime sleep ++ +/_
obesity major minor
Under wt. --- ++
Daytime mouth
--- ++
breathing
Arousal/sleep diruption ++ --/+
management Medical mainly Surgical is definitive in
many

30. Symptoms Consequences
 Snoring/ paradox.
Breathing movements
 Night time
restlessness
 Enuresis
 Mouth breathing
 Nasal obstruction.
 Change of voice
 Failure to thrive.
 Inattention/hyperactivi
ty/learning debt
 Cor pulmonale which
is generally reversible
with Rx.

31. Conditions with OSAS
 Adenotonsillar Hypertrophy/chonal stenosis/cleft
palae with repair./cystic hygroma/oropharyngeal
papillomatosis.
 Obesity.
 Hypothyrodism.
 Cerebral palsy.
 Down syndrome/pierre robin syn./treacher collin
syn./MPS/klippel-feill syndrome/achondroplasia.

32. Acute /rapid progressive OSAS
 In Children Suggest rapid enlargement of
lymphoid tissue in the pharynx or other lesion
rapidly growing near airway, as seen in infectious
mononucleosis/ malignat and benign head and
neck tumor respectively.

33. Management
medical surgical
 Fluticasone nasal
spray
 BiPAP/CPAP- in those
who fail to tespond or
unfit for surgery.
Hypoventilation with
central apnea as
risk.
 Supplemen. O2 only
in under monitoring.
 Adenotonsillectomy.
 UPPP is not widely
used as alone. It is
used in conjuction
with adenotonsil in
neuromuscular
disorder pt.
 Craniofacial surgery.
 Tracheotomy- severe
OSAS in NM disorder
pt.

34. Thank you