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Obstructive sleep apnea (OSA). OR Obstructive sleep apnea/hypopnea syndrome (OSAHS). www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Definition. Recurrent episodes of partial or complete collapse of the upper airway during sleep.

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obstructive sleep apnea osa

Obstructive sleep apnea (OSA)


Obstructive sleep apnea/hypopnea syndrome



  • Recurrent episodes of partial or complete collapse of the upper airway during sleep.
  • May be associated with arousal from sleep &/or decrease in O2 saturation
  • Serious life threatening
  • 8yr mortality rate 40%
  • Underdiagnosed
type of disordered breathing event
Type of disordered breathing event
  • Central

An event with absence of airflow with no respiratory effort

  • Obstructive

An event with absence of airflow but with continued respiratory effort

  • Mixed

An event with characteristics of an obstructive & mixed event.

Start with a period that meets the criteria for a central event but will end with respiratory effort without airflow

type of obstructive breathing event
Type of obstructive breathing event
  • OSA

- Total cessation of airflow for 10sec or more despite continued ventilatory efforts

- with O2 desaturation of 4% or more.

  • Obstructive sleep hypopnea

-Decrease of 30-50% in airflow for 10 sec or longer with desaturation

  • Upper airway resistance

- Snoring during sleep without frank apnea or hypopnea,

does not result on desaturation



  • Loud disruptive snoring*
  • Breathing pauses (apneas)
  • Sudden arousals with choking*
  • Nocturnal sweating

Day time symptoms

  • Excessive daytime sleepiness* (falling asleep at work, when on telephone or whilst driving)
  • Unrefreshing sleep, morning headache (Co2, cerebral vasodilatation)
  • Fatigue, impaired concentration
  • Lethargy, Depression
  • Morning dry cough
  • Impotence, sexual dysfunction
  • Enuresis

Central sleep apnea

  • Uncommon
  • Physiological inhibition of breathing
  • Abnormal neurologic control of the diaphragm, resulting in the loss of respiratory drive

Obstructive sleep apnea

  • > 10% over 65 yr
  • Men > women
  • Episodic collapse & blockage of the upper airway during sleep despite continuous respiratory effort
  • Airflow obstruction can occur from soft palate to the hypopharynx posterior to the tongue
  • Upper airway patency- muscle tone, tissue mass, tissue consistency
  • Pharyngeal transmural pressure- difference between the pressure within the airway lumen & the pressure exerted by tissue surrounding the site of collapse
  • Decrease in pharyngeal transmural pressure
  • Pharyngeal dilator muscle tone prevents upper airway collapse. It is decreased during stage 4 & REM sleep which leads to narrowing of airway with turbulent airflow & snoring.
causes of osa
Causes of OSA
  • Obesity

-deposition of adipose tissue within the muscles & soft tissues surrounding the upper airway & ex compression from the neck

narrowing of the upper airway.

-↓lung volume, restrictive pulmonary defects, V/Q mismatch & hypoventilation

  • Pickwickian syndrome- severe form of OSA, morbid obese with Rt. Heart failure
  • Macroglossia, enlarged tonsils

further narrowing of the pharyngeal lumen, increases the likelihood of airway collapse during inspiration

  • Gravity – lateral position, by enlarging retropalatal & retroglossal aspect of the airway
contributing factors
Contributing factors
  • Abnormalities in the autonomic control of the pharyngeal muscles - acts by changing the balance between forces promoting the patency & those favouring its collapse
  • ↑ vagal tone, nocturnal paroxysmal asystole, episodic bradycardia, sinus node dysfunction
  • Autonomic chemoraceptors reacting to hypoxia, hypercapnia & acidosis trigger an inflammatory cascade HTN, insulin resistance, atherosclerosis & metabolic syndrome
  • Estrogen protection
  • Hormonal imbalance- acromegaly, cushing syndrome, hypothyroidism, DM
  • Airway moisture & surface tension in the fluid lining the upper airway, alter the function of pharyngeal sensory receptors
risk factors
Risk factors
  • Obesity –BMI >30kg/m2

1. Fat deposition around the upper airway can decrease upper airway size.

2. Neck circumference greater than 16 inches in female or greater than 17 inches in males

  • Male, middle age, Race,
  • Family history, Alcohol consumption ( phargl msc tone)
  • Craniofacial abnormalities
  • Habitual snoring & gasping noted by bed partner
  • Daytime sleepiness
  • Hypertension
  • High mallampati score
  • Unexplained polycythemia, room air hypoxemia or signs of right sided heart failure.
other causes of daytime sleepiness
Other causes of daytime sleepiness
  • Sleep deprivation
  • Shift work
  • Depression
  • Narcolepsy
  • Hypothyroidism
  • Sedatives
  • Excessive alcohol
  • Idiopathic hypersomnolence
  • Neurological conditions: previous head injury, previous encephalitis, parkinsonism, dystrophica myotonica
indices on disordered breathing severity
Indices on disordered breathing severity
  • Apnea-hypopnea index (AHI) (severity of OSA)

no. of apnea & hypopneas per hr of total sleep time

  • Apnea index

no. of apnea per hr of total sleep time

  • Hypopnea index

no. of hypopneas per hr of total sleep time

  • Central apnea index

no. of central apnea per hr of total sleep time

  • Arousal index - no. of arousal per hr of sleep
  • Body position, NREM & REM sleep
indices on disordered breathing severity1
Indices on disordered breathing severity
  • Mild: AHI – 5 - 14 events per hr
  • Moderate: AHI 15 – 30 events per hr
  • Severe : AHI> 30 per hr
the stages of snoring
The stages of snoring

Non REM sleep

  • High alertness to deep sleep. Stage 1 to 4
  • Changing pattern of electrical activity in the brain
  • Skeletal muscle start to relax

REM sleep

  • Brain activity looks similar to wakefulness
  • Absence of skeletal muscle tone so effectively paralysed

Conventional snoring

  • Stage 3-4, later in 1 & 2

Sleep apnea

  • REM sleep
  • A sleep study or a polysomnogram

-Standard test for OSA

- Identifying abnormal or disordered breathing pattern during sleep

  • Simultaneous recording of multiple physiological signals

rt. & lt. electro-oculograms

submental electromyogram


  • Distinguish wakefulness from sleep & determine the distribution of different sleep stages over the course of the night
  • Impedance plethysmography to assess breathing patterns with measurements of respiratory efforts
  • Airflow – oronasal thermistor (temp change) or a nasal cannula (pressure changes)
  • Oxygen saturation
  • Body position
  • electrocardiogram – arrhythmias
  • Epworth sleepiness scale (ESS) max – 24

best available tool to guide the clinician as to the pt’s perception of his sleepiness

normal < 11

mild subjective daytime sleepiness 11-14

mod subjective daytime sleepiness 15-18

severe subjective daytime sleepiness >18

  • Hypertension
  • Obesity
  • Diabetes mellitus
  • Coronary artery disease
  • Cerebral vascular disease & stroke
  • Congestive heart failure
  • Cardiac dysrhythmias
  • Gastroesophageal reflux disease
pathophysiological consequences

↑sympathetic tone

systemic HTN

pulmonary HTN


art. hypoxemia

art. hypercarbia

rt. heart failure

lt. heart failure



myocardial ischemia



personality changes

cognitive deficits

accident prone

Pathophysiological consequences
  • AHI >15,
  • More than ten 4% desaturation/hr

1.Behavioural interventions



behavioural interventions
Behavioural interventions
  • To lose wt.
  • life modifications
  • Stop smoking
  • No alcohol esp in the evening
  • No sedatives
  • Discourage from sleeping on their back by using Triangular pillow – space for the pt’s arm under the head to encourage sleeping on the side
nonsurgical management
Nonsurgical management

The American Academy of Sleep Medicine guidelines recommend

  • Continuous positive airway pressure CPAP

AI > 20, symptomatic pt with AHI > 10

  • Function as a mechanical stent to maintain upper airway patency th. out all phases of sleep breathing
  • Nasal CPAP- proper use eliminates excessive day time sleepiness, reduce HTN, improve neurocognitive function
  • Increased augmentation of lung volume
  • Increase in the tone of the upper airway
  • Improved LVF
  • Reduce morbidity in pt with CHF
  • Reduction in the sympathetic tone
nonsurgical management1
Nonsurgical management
  • Nasal CPAP highly effective & acceptable in 72-91%
  • Bulky, noisy, difficult to bring on trips & require electricity
  • Pts who sleeps in lt position knock the mask off.
  • Intolerance by the pt’s partner
  • Claustrophobia, nasal congestion, chest discomfort & inconvenience

Bilevel positive airway pressure (bilevel PAP)

  • Improved pt comfort, tolerance
  • Provide ventilatory assistance for pts who require high CPAP(COPD)
nonsurgical management2
Nonsurgical management

Adjustable oral appliances

To enlarge the airway by keeping the tongue in an ant position or displacing the mandible forward (jaw thrust technique)

1.Mandibular repositioning devices (MRD)

  • snoring or mild to mod OSA, unable to tolerate CPAP
  • High compliance (50-75%)
  • Xerostomia, dental pain,temporomandibular joint pain, excessive salivation & changes on occlusion

2. Drugs

  • Protriptyline, acetazolamide, progesterone, theophylline
  • Modafanil
  • Fluoxetine

3. Nocturnal O2 therapy

  • Severe arterial desaturation
surgical management
Surgical management

Aim :

  • relieving site-specific problems in the upper airway
  • increasing pharyngeal caliber & reducing pharyngeal resistance during sleep

Complete evaluation:

  • recent polysomnogram,
  • head & neck exam (flexible nasopharyngeal fiberoptic exam),
  • assessment of disproportionate anatomy (elongated soft palate, thickened uvula, large base of tongue, DNS,enlarged tonsils, hypertrophic nasal turbinates & hypoplastic or retrognatic mandible),
  • imaging studies (cephalometrics or CT scan)
surgical management1
Surgical management

1.Uvulopharyngopalatoplasty (UPPP)

2. Tonsillectomy

3. Nasal sx

4. Tracheostomy

5. Jaw advancement techniques

6. Minimally invasive techniques

  • Genioglossus advancement
  • Multilevel radiofrequency tissue ablation
  • Tongue-base suspension
  • Future research - Muscle strengthening with transcutaneous neuromuscular stimulation
preoperative assessment
Preoperative assessment

Identifying pts – questions for exploring

  • Do people tell you that you snore?
  • Do you wake up at night with a feeling of shortness of breath or choking?
  • Do people tell you that you that gasp, choke or snore while sleeping?
  • Do you awake feeling almost as or more tired than when you went to bed?
  • Do you often awake with a headache?
  • Do you often have difficulty breathing through your nose?
  • Do you fight sleepiness during day time?
  • Do you fall asleep when relaxing after meals?
  • Do other comment on your sleepiness during the day?
pre anesthetic visit
Pre anesthetic visit
  • Weight & height
  • Neck circumference
  • Abnormally small size mandible
  • Nasal patency
  • Upper airway for obvious obstruction (IL)
  • Tongue (macroglossia), dentition
  • Pharynx (tonsillar size, uvula, lumen size)
  • BP
  • RS, CVS, CNS ex
  • FEV1, FVC
  • Hypothyroidism, acromegaly, Marfan’s syndrome
next step
Next step

Nonurgent procedure

  • Evaluation by a sleep specialist
  • Primary treatment.
  • Milder – conservative
  • Mod to severe - initiation of CPAP therapy


  • improvement in some cardiovascular squeal within several wks of initiation of therapy
  • 4-6wks - ↓tongue volume & ↑ pharyngeal tone
  • reduce the risks of difficult airway management
  • perioperative respiratory embarrassment
  • improve cardiovascular function
approach to guide anesthetic management
Approach to guide anesthetic management
  • Management of the airway should be conservative, with measures taken to minimize hypoxia secondary to airway obstruction or apnea
  • Cautious, titrated administration of sedatives, monitoring & observation of pt.
  • Adequate preoxygenation if plan is to ablate spontaneous ventilation
  • LMA & emergency airway devices s/b immediately avilable.
  • Regional anesthesia with careful sedation
approach to guide anesthetic management1
Approach to guide anesthetic management
  • Maintenance of general anesthesia s/b with the use of newer, shorter acting drugs to minimize the duration of postoperative ventilatory depression.
  • Extubation – in difficult airway, in conservative fashion, pt. strength & level of consciousness
  • Adequate postoperative analgesia
  • NSAIDS, local anesthetics for incision infiltration, epidural analgesia, peripheral nerve blocks
  • Minimize administration of large dose of narcotics
anesthesia technique
Anesthesia technique
  • Regional anesthesia

- min affecting resp drive

- maintain arousal response during apneic episode

  • Sedation must be carefully administered & monitored, it will worsen hypoventilation
  • General anesthesia with regional anestheisa allow rapid restoration of consciousness
  • Outcome depends on type of sx.
  • Neuraxial opioid have been ass with unexpected degree of ventilatory depression
anesthetic management
Anesthetic management
  • Anesthetic drugs profoundly influence control of the respiratory system, which is already dysfunctional
  • Exaggerated responses
  • Thiopentone, propofol, opioids, benzodiazepines & nitrous oxide- reduce the tone of the pharyngeal musculature that acts to maintain airway patency.
  • Response to Co2 in children with OSA & tonsillar hypertrophy is diminished
  • Depressed ventilation – 50% apnea after 0.5µg/kg of fentanyl
  • Shorter acting drugs
rapid sequence induction
Rapid sequence induction

To reduce the risk of pulmonary aspiration

  • Pharmacological agent with or without gastric suctioning
  • Reduce gastric volume & acidity
  • Rapid acting hypnotic agent & MR to limit apneic time & providing non hypoxemic apneic period
  • Absence of mask ventilation after a preoxygenation – FRC is reduced → faster desaturation → safe apneic pr. is reduced from >5min to < 2-3min.
  • Absence of mask ventilation → atelectasis. Constant CPAP during preoxygenation & gentle ventilation with PEEP during induction significantly reduce atelectasis
rapid sequence induction1
Rapid sequence induction

Cricoid pressure – correct application

  • Initiate with a forceof 20N as the induction started & to increase the force to 30N as loss of consciousness occurs
  • Adversely affect mask ventilation (directly posterior with gradual release)
  • Adversely affect laryngoscopy view (backward & upward laryngeal displacement)
  • More difficult LMA insertion
  • Less successful intubating LMA
  • Trendelenburg position, suction available & graded release of cricoid pressure
rapid sequence induction2
Rapid sequence induction

Difficult airway

  • Sp. Alteration in airway anatomy & physiology – difficult mask ventilation & intubation
  • Diabetes mellitus (limited jt mobility syndrome)
  • paramount concern - Ability to assure oxygenation & ventilation
  • Secondary concern – difficult airway & inadequate anesthetic depth during difficult airway management
muscle relaxant
Muscle relaxant


  • 0.6mg/kg
  • Fasciculation – rise in gastric pressure (40mmHg)
  • Rapid onset & short duration of action
  • Rapid return of spontaneous ventilation


  • Faster onset
  • Longer duration – not for pts with difficult airway
  • Less side effects
intraoperative monitoring
Intraoperative monitoring
  • According to type of sx, comorbidities
  • TEE – ventricular filling & function
  • Intra-arterial catheter to monitor blood pressure
  • Metabolic alkalosis can result in mild hypoventilation. Maintenance of baseline bicarbonate
  • Challenging
  • Deep extubation – occasionally practiced
  • Fully conscious
  • Intact upper airway reflexes
  • Adequate muscle strength
  • In the OT or in ICU with facility for reintubation
  • Difficult intubation cart
  • Noninvasive mechanical ventilation immediately after extubation
postoperative consideration
Postoperative consideration

Immediate: PACU

  • Most complications – first 2hr
  • continuous monitoring, depending on I/O complications
  • frequent assessment of s/s of airway problems
  • 1 in 500 pt will require reintubation
  • Difficult intubation
  • Continuous O2 thr. Face mask or nasal CPAP (if nasogastric tube in place then seal of nasal CPAP is not adequate)
  • Posture & positioning – HOB 300 (↑ stability of the upper airway)
  • Adequate blood pressure control –

HTN due to pain, hypercarbia, anxiety. VASOTRAC device for BP monitoring

postoperative consideration1
Postoperative consideration

Disposition from PACU

  • Preop AHI, CPAP dependence
  • RVF, LVF, Lung disease, Degree of obesity, Nature of sx
  • Mild OSA & min comorbidities for minor sx

discharge on the day of sx

  • Mod OSA & intermediate comorbidities for interm.risk sx

admission to a standard M or Sx unit

  • Severe OSA with CPAP at home & multiple comorbidities

closer observation on ICU or intermediate care unit depending on the nature of the sx

perioperative issues for osa sx
Perioperative issues for OSA sx
  • Max with in 2hrs of sx
  • Airway obstruction, laryngospasm, desaturation & postop pul oedema
  • Postop. Hemorrhage
  • HTN
postoperative pain managment
Postoperative pain managment
  • Narcotics use is dangerous
  • After GA- Propensity of REM sleep during the first several days
  • After iv opioid, epidural opioid, PCA → resp depression culminating to resp arrest
  • Prevention – HOB, CPAP, limit narcotics
  • NSAIDS – 20-35% decrease in opioid use
  • Resp depression – supplemental O2, iv naloxone
  • nasal or oral airway
  • CPAP
  • endotracheal intubation (difficult)
  • emergency cricothyroidotomy (difficult)
postop additional consideration
Postop. additional consideration
  • Early ambulation
  • Proper position in bed
  • Sleeping position
  • Physical therapy
  • Skin breakdown (lack of adequate oxygen delivery, poor vascularity of adipose tissue)
  • Pressure sore (proper padding)
osa in children
OSA in children
  • Preschoolers, equal in boys & girls


  • Airway anatomy – upper airway narrowing (Adenotonsillar hyperthrophy, craniofacial anomalies, obese BMI >28)
  • Obesity
  • Neuromotor factors – reduced, centrally mediated activation of their upper airway muscles
osa in children1
OSA in children

Clinical features

  • Snoring, labored breathing, paradoxical resp effort, observed apnea, restlessness, sweating, unusual sleep position, enuresis
  • Day time – mouth breathing, poor school performance, excessive day time somnolence, morning headache, fatigue, hyperactivity, aggression & social withdrawal
  • Failure to thrive, developmental delay
  • Physical - mouth breathing, nasal voice quality, retrognathia or micrognathia, pul HTN
osa in children2
OSA in children



2.CPAP - if adenotonsillectomy is C/I or sypmtomatic after sx

3.Tracheostomy –

craniofacial anomalies

neuromuscular syndromes

can not tolerate CPAP or BiPAP

risk factors for resp distress after sx
Risk factors for resp distress after sx
  • Age < 3yr
  • Bleeding
  • Concurrent resp infection
  • CHD, craniofacial disease
  • Failure to thrive
  • H/O cor pulmonale, premature birth
  • Neuromuscular disease
  • Obesity
  • Other cong abnormalities or syndrome
  • Severe OSA
  • Throat pack not removed
osa in children3
OSA in children


  • Due to ch. Nocturnal hypoxemia & sleep fragmentation
  • Pul HTN, cor pulmonale, heart failure
  • Hypertrophy of ventricles
  • Dysregulation of the mean blood pressure – end-organ damage & ↑ risk for CV disease
  • Neurocognitive deficits, learning problems, behavioral problems & attention deficit hyperactivity disorder.


  • Polysomnography: age appropriate interpretation

differentiate primary snoring & OSAS

pac in children
PAC in children
  • History – detailed birth & medical history
  • Growth assessment, recent RTI, behavioral & school performance
  • Polysomnography review
  • CXR, ECG, echo
  • ABG – comp metabolic alkalosis in response to chr hypercarbia to identifying prolong OSAS
  • Severe anatomical malformation of the airway or morbid neurological disease – ASAIII & IV
  • Alternative airway devices including emrg trcheostomy
  • Anticipation of need of postop ventilation
  • Prevention of gastroesophageal reflux
  • Management of neurological disease - seizure
intraoperative anesthetic plan
Intraoperative anesthetic plan
  • Collapse of upper-airway structures & diminished arousal response to elevation of CO2 under anesthesia
  • Inhalational induction – dose dependent relaxation of genioglossus muscle
  • Exaggeration of the blunted resp drive in response to opioid & benzodiazepine adm & at risk for resp obstruction
  • Jaw thrust to tr obstruction is the most useful & superior to chin lift. Lateral position


  • Standard
  • Invasive – heart failure, pul HTN, severe bronchospasm, ABG
  • Challenging
  • Deep extubation – occasionally practiced
  • Laryngospasm – Mg, midazolam premedication
  • Adequate muscle strength, age app resp rate without assisted ventilation
  • In the OT or in ICU with facility for reintubation
  • Noninvasive mechanical ventilation immediately after extubation

Post op care

  • Resp failure, ↑ apea episodes, ac airway obs, atelectasis, pul edema
  • Circulatory failure – pul HTN, COR pulmonale
  • Ped. ICU – severe OSA, cvs disease, airway sx, craniofacial sx
  • 2-3 days post sx bec OSA may recur along with the return of REM sleep
respiratory support
Respiratory support
  • Supplemental O2 – may prolong apnea time & prevent the frequency of hypoxemic episodes
  • Postop hypoxemia –


pul oedema,



  • CPAP or BiPAP
  • Mechanical ventilation
  • ABG – can guide extubation decisions
respiratory support1
Respiratory support

Postop pul oedema –

  • ↑ pul blood flow & pul microvascular pressures which occur as pt generates an exceeding high negative inspiratory force while inhaling against a collapsed pharynx or closed glottis
  • Diffuse punctate hemorrhages
  • S/S – hypoxemia, cough,

serous, frothy or bloody sputum

crepts in the lung field

diffuse haziness on CXR

  • Reintubation, invasive or non invasive positive pressure ventilation, O2, diuretic
surgical management2
Surgical management

1.Uvulopharyngopalatoplasty (UPPP):

  • removal of a rim of the soft palate & the uvula (1964)
  • combined with tonsillectomy
  • Result: enlarge oropharyngeal airway
  • Success rate 40-50% (drop in the RDI >50% or an absolute RDI <20)
  • Drop in success rate if retrolingual narrowing in present from an enlarged tongue or crowding in the region of the hypopharynx
  • Side effect: Decrease ability to use nasal CPAP
surgical management3
Surgical management

2. Tonsillectomy

  • Airway blockage – palatine tonsils
  • ↓ AHI < 50%
  • Children with adenoidectomy
  • Temperature controlled radiofrequency tissue ablation in office setting under LA
  • Electrocautery

3. Nasal sx-

  • Improve compliance of CPAP
  • After max medical therapy
  • Septoplasty & turbinate reduction
  • ↑ nasal resistance or obstruction may ↑the negative pressure of the airway during inspiration → collapse of the velopharyngeal area & the hypopharyngeal regions
surgical management4
Surgical management

4. Tracheostomy

  • Last measure
  • Life threatening severe OSA
  • Inability to tolerate CPAP
  • Pickwickian syndrome – nighttime ventilatory support

5. Jaw advancement techniques

  • Enlarging the posterior airway
  • Le fort I & bilateral mandibular osteotomies to move tongue & entire midface forward, typically app. 10mm
  • Success rate 97%
  • Alter facial appearance
  • With other sx
surgical management5
Surgical management

6. Minimally invasive techniques

a. Genioglossus advancement

  • retropalatal & retrolingual obstruction
  • Guided trephine system
  • With UPPP
  • 67% success rate
  • >50% reduction in the resp disturbances

b. Multilevel radiofrequency tissue ablation

  • Multilevel obstruction: tongue base & soft palate
  • Office based, LA
  • Significantly improve the AHI & AI
surgical management6
Surgical management

c. Tongue-base suspension

  • ↓ post obstruction of the tongue base during sleep
  • With UPPP
  • Titanium screw is inserted into the post aspect of the mandible at the floor of the mouth
  • Loop of permanent suture extending thr the tongue base is att to the mandible screw

d. Future research

  • Muscle strengthening with transcutaneous neuromuscular stimulation to counteract muscle dysfunction that may be contributing to the collapse of the upper airway