The document provides an overview of the diagnosis and management of obstructive sleep apnea (OSA), particularly emphasizing polysomnography as the gold standard for diagnosis. It discusses treatment options such as positive airway pressure therapy, behavioral therapies, oral devices, surgical interventions, and adjunctive therapies, highlighting CPAP as the mainstay treatment for OSA. Additionally, it covers various types of apneas, sleep study protocols, and the importance of follow-up assessments to evaluate treatment efficacy.

1. DIAGNOSIS AND
MANAGEMENT OF
OBSTRUCTIVE SLEEP
APNEA
Dr Kamal Bharathi S

2. Diagnosis Of Obstructive
Sleep Apnea
Polysomnography (PSG), the gold standard sleep study,
records many parameters while the patient sleeps:
 Electroencephalogram (EEG) to indicate sleep state,
 Electrooculogram (EOG) to monitor eye movements,
 Electromyogram (EMG) to measure muscle activity,
 Oronasal thermistor and nasal pressure sensors to
indicate respiratory airflow,
 Chest and waist bands to measure respiratory effort and
arterial oxygen saturation
These measurements are integrated to provide sleep
staging and to indicate apneas, hypopneas, and arousals.

4.  Obstructive apnea is the cessation of airflow for at
least 10 seconds with persistent respiratory effort.
 Central apnea is the cessation of airflow for at least 10
seconds with no respiratory effort.
 Mixed apnea is an apnea that begins as a central apnea
and ends as an obstructive apnea.
 The recommended definition of hypopnea is a 30% or
greater decrease in flow lasting at least 10 seconds and
associated with a 4% or greater oxyhemoglobin
desaturation

5. AHI (apnea-hypopnea index)
 The AHI (apnea-hypopnea index) is derived from the
total number of apneas and hypopneas divided by the
total sleep time.
 • A normal cutoff of 5–10 episodes per hour.

6. Obstructive sleep apnea
absence of flow despite paradoxical respiratory effort (blue arrows)

7. Central apnea
These are central apneas (2) with minimal oxygen desaturation. Note
there is no airflow and respiratory effort.

8. Mixed apnea,
a complete absence of nasal and air flow. A total absence of respiratory effort
at the beginning of the event (black thick arrow) is followed by gradual increase
in effort (blue thick arrow) which eventually breaks the apnea. An oxygen
desaturation is ≥3%

9. Hypopnea
This is an 18 sec hypopnea event. The airflow signal is reduced by 50%
during this event (small black arrow)

10. Various types of sleep studies

11. Level 1 study
 Level 1 study or in-hospital, in-laboratory, technician-attended,
overnight polysomnography (PSG) is the “Gold standard” for
evaluation of sleep disordered breathing.
 It remains the cornerstone for the diagnosis in patients of comorbid
sleep disorders, unstable medical conditions or complex sleep-
disordered breathing.
 Laboratory attended PSG (level 1) is not necessary in all patients
suspected to have OSA.
 Portable monitoring with devices (which should at least include
airflow, oxygen saturation and respiratory effort) is adequate for
diagnosis if
• Used in conjunction with comprehensive sleep evaluation
• In patients with high pre-test probability of moderate to severe OSA
• Without co-morbid sleep disorders or medical disorders like
pulmonary disease, neuromuscular disease, or congestive heart failure

12. Other indications for unattended
portable sleep study:
a. Severe clinical symptoms indicate OSA and initiation of
treatment is urgent and PSG is not readily available
b. Patients are unable to be studied in the sleep laboratory
(safety or immobility)
c. As a follow-up study when the diagnosis of OSA was
previously established by PSG and the intent of testing is to
evaluate the response to therapy (weight loss, surgery, oral
appliance)

13. Consequences Of Obstructive
Sleep Apnea

14. Management of OSA
 The decision to treat OSA should be based on its
severity, related symptoms, and medical comorbidities.
Options for the treatment of OSA include
 PAP Therapy,
 Behavioral Therapies,
 Mandibular Repositioning Devices,
 Surgical Treatments,
 Adjunctive Therapies.

15. Positive Airway Pressure
Therapies
 Colin Sullivan first described the use of nasal CPAP to
treat OSA in 1981.
 Today, CPAP remains the mainstay of therapy for most
patients with OSA.
 CPAP therapy increases airway caliber in the
retropalatal and retroglossal regions in particular, it
increases the lateral dimensions of the airway and thins
the lateral pharyngeal walls.

16. CPAP therapy
Advantage:
 being noninvasive,
 smaller, portable, and quieter,
 provide data on patient adherence patterns, mask leaks,
and the effectiveness of the delivered CPAP pressure
 improvements in daytime sleepiness among those with the
highest AHIs,
 Improve euro-cognitive performance,
 cardiovascular outcomes including overall mortality
 modest reduction in BP among patients with hypertension
and OSA.

17.  CPAP therapy is indicated in all patients with moderate
or severe sleep apnea (i.e., an AHI ≥15 events/h) and in
those patients with mild OSA who have associated
symptoms, as noted previously.
 The optimal pressure can be determined during a
titration polysomnogram or using out-of- laboratory
treatment algorithms in conjunction with portable
monitoring for OSA diagnosis.

18.  CPAP can be delivered using a variety of interfaces.
 Nasal masks,
 Nasal inserts, or
 Full-face masks.
 Ensure that the patient has a well-fitting interface.
 Mouth leaks, which often result from mouth breathing
while using a nasal mask, can render CPAP ineffective.

19. Nasal Mask
Pillow Mask
Full face Mask

20. Complications Associated
with CPAP
 Nocturnal arousals
 Rhinitis, nasal irritation, and dryness
 Aerophagia
 Mask and mouth leaks (dry mouth in morning)
 Facial rash or irritation
 Difficulty with exhalation
 Claustrophobia

21. Bilevel PAP (BiPAP)
 BIPAP: Bilevel systems (EPAP & IPAP) deliver higher
pressures during inspiration and lower pressures during
expiration.
EPAP
• To stabilize the upper airway at end expiration so that
the airway is sufficiently patent to permit the patient to
trigger delivery of IPAP by generating low‐level inspiratory
volume or flow.
IPAP
• To prevent upper‐airway closure and partial obstruction
(hypopnea) during the inspiratory phase of breathing.

22. BPAP type
BPAP‐S (spontaneous mode )
 Patients may breathe with their own frequency, with
the BPAP supporting both phases of respiration (IPAP and
EPAP)
BPAP‐ST(spontaneous‐timed mode with backup rate)
 It guarantees a certain number of breaths per minute ,
if the patient does not initiate a breath within a
specified period.
 Inspiratory time must be set, which tells the machine
the maximum time allowed for inspiration.

23. Indications for BiPAP
OSA
 BPAP and CPAP showed no differences in the
improvement of AHI, ESS, or sleep quality.
 No differences in adherence or comfort level among
BPAP and CPAP users of OSA pt without coexisting
respiratory disorders.
 prefer BPAP over CPAP
– Comorbid obesity
– Daytime hypercapnia

24. Indications for BiPAP
Central Sleep Apnea
 Primary CSA
 CSA caused by
• Cheyne‐Stokes breathing pattern
• High‐altitude periodic breathing
• Drugs or substances such as opioids.
 Complex CSA
 BPAP with ST mode is useful to treat patients with CSA
syndromes

25. Autotitrating PAP
 Autotitrating CPAP, or auto-CPAP, adjusts CPAP during
use by detecting airway flow, snoring, apneas, and
inspiratory flow limitation.
 Each auto-CPAP unit uses a different algorithm for
abolishing apneas.
 The use of auto-CPAP for OSA titration is associated with
substantially lower costs compared to in-laboratory
CPAP titration.

26. Intraoral Devices
 Oral devices aim to alter the position of the upper
airway structures, thereby enlarging airway caliber or
reducing airway collapsibility during sleep.

27.  The tongue retaining device (TRD)- maintain the tongue
in a forward position during sleep.
 Palatal lifting devices and
 Mandibular advancing devices- produce downward
rotation and advancement of the lower jaw during
sleep.
 In choosing an oral device, attention to its adjustability
(modifiability over time) and
 titratability (ability to alter jaw position by adjusting
the appliance) are important.

28. Indication:
 patients with primary snoring, or
 mild-to-moderate OSA who prefer them to CPAP or do not respond
to, are not appropriate candidates for, or who fail treatment
attempts with CPAP.
 Patients treated with an intraoral device are recommended to have
follow-up PSG to verify efficacy.
Adverse effect:
 Excessive salivation
 Temporary discomfort after awakening
 Mucosal dryness
 Transient discomfort in teeth, gum and TMJ Headache
 Distal migration of upper dentition

29. a novel treatment modality was introduced involving application
of intraoral negative pressure via an oral interface connected to a
vacuum pump in an attempt to stabilize upper airway tissue in
patients with OSA

30. Position Therapy
 Sleep in the supine position- more conducive to airway
obstruction by virtue of gravity’s effect on the tongue.
 The lateral position is associated with increased
maximum cross sectional upper airway area and lower
closing pressure of the passive pharyngeal airway
compared to the supine position.

32. Nasal Expiratory Positive
Airway Pressure
 Delivered via a novel device with a one-way mechanical
valve that provides high expiratory resistance in the
setting of very low inspiratory resistance.
 Positive pressure resulting from the high expiratory
resistance during exhalation stents open the upper
airway, rendering it less likely to collapse on subsequent
inhalation and increases end expiratory lung volumes.
 Nasal EPAP appears to reduce AHI and improve
subjective sleepiness in patients with mild-to-moderate
OSA.
 Nasal EPAP can be considered as an alternative therapy
in individuals with mild-to-moderate SDB who are
unable to tolerate CPAP therapy.

34. Pharyngeal Muscle
Stimulation
 The genioglossus muscle is the largest
airway dilator muscle.
 Electrical stimulation causes tongue protusion
and stiffening of the anterior pharyngeal wall.
 Attempts at muscle stimulation have enlarged upper
airway diameter and reduced apneas and hypopneas
during sleep
 The branches of the hypoglossal nerve that innervate
the genioglossus (motor).

35.  Studies have demonstrated efficacy, including improved
airflow, reduced AHI, and improved symptoms, as well
as safety and compliance with the use of newer
implantable hypoglossal nerve stimulators.

36. Surgical Treatment Of OSA
 The leading objective for presurgical evaluation is to
identify the primary site(s) of obstruction.
 Fiberoptic laryngoscopy, drug-induced sleep endoscopy,
or imaging can be used to classify the obstruction of the
airway at the nasal, oropharyngeal, and/or
hypopharyngeal level.
Lingual tonsil
image from
nasopharyngeal
endoscopy
Lateral
cephalogram
demonstrating
decreased
airway space &
low-positioned
hyoid

37. Beginning with the nasal exam, assessment for the following clinical
findings:
 • External and internal nasal valve collapse
 • Septal deviation
 • Turbinate and/or mucosal hypertrophy
Oropharyngeal, maxillary, and mandibular skeletal exam signs consistent
with an increased risk of having OSA are:
 Constricted maxilla
 • High-arched palate
 • Elongated soft palate/uvula
 • Narrowing of tonsillar pillars
 • Adenotonsillar hypertrophy (grade 3 or 4)
 • Micro- and retrognathia
 • Microgenia

38. Surgery for Obstructive Sleep
Apnea
 Nasal surgery (septoplasty, sinus surgery, and others)
 Tonsillectomy ± adenoidectomy
 Uvulopalatopharyngoplasty (UPPP)
 Laser-assisted uvulopalatoplasty (LAUP)
 Radiofrequency volumetric tissue reduction
 Lingular tonsillectomy
 Genioglossus and hyoid advancement (GAHM)
 Sliding genioplasty
 Maxillomandibular advancement osteotomy
 Tracheostomy

39.  Phase 1 surgeries- Surgeries aimed at reducing
obstruction at the nasal, palatal, and lingual levels.
 Phase 2 surgery- maxillomandibular advancement
(MMA)

40.  Septoplasty and turbinate reduction- common nasal
surgical procedure.
 Tonsillectomy and adenoidectomy is the primary therapy
for children with OSA.
 Tracheostomy is virtually 100% effective in eliminating
obstructive apneas. Associated with negative impact on
patients’ quality of life. Reserved for patients with severe
OSA who have failed medical or surgical therapy.
 Maxillomandibular advancement osteotomy- procedure
with substantial reduction in AHI.
 Uvulopalatopharyngoplasty (UPPP) with or without
tonsillectomy as a sole surgical procedure does not have a
consistent effect on the AHI

41. 1. Pre-operative three-dimensional airway volume analysis.
Six-month postoperative three-dimensional airway volume
analysis, showing significant
objective improvement in airway volume.
Maxillomandibular Advancement

42.  Laser-assisted uvulopalatoplasty- involving removal
of the uvula and a part of the soft palate with a
carbon dioxide laser.
 Radiofrequency volumetric tissue reduction (i.e.,
radiofrequency ablation [RFA]), a minimally invasive
technique, has been employed to treat turbinate
hypertrophy and reduce the size of the base of the
tongue.
 Genioglossus advancement with hyoid myotomy
involves movement of the tongue forward without
moving the mandible, with the leading aim of
achieving a larger-caliber airway.

43. MEDICATIONS
 Stimulants, such as modafinil, can also be utilized as
adjunctive therapy for residual sleepiness in patients
who remain symptomatic despite adequate treatment
for SDB.
 Dosage- 200 to 400 mg daily

44. Thank
You…!!!