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Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
Obstructive sleep apnoea(OSA)
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Obstructive sleep apnoea(OSA)

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OSA is an entity that is increasingly being managed by otolaryngologists...Hope this presentation helps to clear any doubts regarding its diagnosis and management!

OSA is an entity that is increasingly being managed by otolaryngologists...Hope this presentation helps to clear any doubts regarding its diagnosis and management!

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  • 1. Dr Dhaiirya JoshiResident ,IGGMC
  • 2.  Physiology of sleep Definitions Pathophysiology of OSA Clinical features Investigations Medical Management Surgical Management
  • 3.  Obstructive sleep apnoea syndrome described as Pickwikian syndrome in Charles Dicken‟s work-‟The Pickwick papers” Guilleminult,Eldridge and Dement described first sleep apnoea in 1973,and established first sleep clinic.
  • 4.  Behavioral and neurobiological state which is characterized by a change in the state of consciousness and bodily as well as neurological behavior. Involuntary cyclic process which is dependent on environmental and internal circumstances of an individual
  • 5. Divided intoREM (Rapid Eye Movement) sleepNREM (Non-Rapid Eye Movement) based on Environmental Responsiveness General Physiology EEG waveforms (of muscle and eye movement) Muscle tones Mental activity
  • 6. Principal characteristics of REM and NREM sleep REM SLEEP SLOW-WAVE/NREM SLEEP EEG De-synchrony EEG Synchrony (slow (irregular, low voltage waves) high freq) Lack of Muscle Tones Moderate Muscle Tones Rapid Eye Movement Slow or Absent Eye Movement Genital Activity Lack of Genital Activity Dreams Dreams - Increased autonomic activity
  • 7. NREM sleep divided into 4 stages Stages 1 and 2- EEG voltage low and freq mixed. Stages 3 and 4- EEG voltage high and freq slow. So also referred as Slow wave sleep(SWS) Stage 2 – Predominant sleep stage 50% of sleep time
  • 8. REM sleep Occurs 1st time 90 min after onset of sleep Recurs 4-6 times throughout night Accounts for 25% of total sleep Increasing age, alcohol and sedatives decrease REM sleep. Helps in brain development, promote learning and strengthening memories.
  • 9.  Reticular activating system-promotes wakefulness when active. Controls the intrinsic sleep drive, which increases with time spent awake. Adaptive sleep drive-influenced by behavioral responses to environment and reflex responses to sensory stimulation.
  • 10.  Suprachiasmatic nucleus- - Controls the circadian rhythm. - Keeps the sleep/wake cycle in sequence with the environment,but does not initiate sleep. Melatonin - Released by pineal gland in response to darkness. - Promotes sleep. - Acts on suprachiasmatic nucleus to change circadian rhythm and reduce body temp.
  • 11.  Reduced chemical and mechanical drives to breathe. Respiratory output via phrenic nerve and other motor nuclei to spinal cord. NREM sleep- Diaphragmatic activity - N Intercostal ms activity – -Expansion of ribcage and diaphragmatic activity. REM sleep – Diaphragmatic activity – - Intercostal ms activity -
  • 12.  REM sleep - Reduction of lung compliance. - Decrease in lung volume. - Increases V/P mismatch. - Increase in abdominal contribution to breathing. So overall-reduction in ventilation
  • 13.  Hypoventilation with mild hypoxemia and hypercapnia. Metabolic rate reduced by 10-25 %. Arterial PCO2 increases- 0.5 kPa Arterial PO2 decreases – 0.5-2 kPa Hypocapnic apnoeic threshold more sensitive. Upper airway dilating capacity decreases partially due to hypercapnoea due to hypoventilation.
  • 14.  OBSTRUCTIVE SLEEP APNOEA(OSA) Condition characterized by repetitive upper airway obstruction leading to apnoea and hypopnoea causing sleep fragmentation, cardiovascular stimulation and oxygen desaturation during sleep.More than 5 apnoeas per hour of sleep. UPPER AIR WAY RESISTANCE SYNDROME(UARS) Increased respiratory efforts(as identified by esophageal pressure measurements) with frequent arousals as measured from EEG during diagnostic overnight polysomnography,but without apnoeas and hypopnoea
  • 15.  OBESITY HYPOVENTILATION SYNDROME(OHS) Daytime respiratory failure in presence of obesity(BMI > 30kg/m2 ) in absence of airway obstruction from respiratory spirometry. Respiratory failure is defined as PaCo2 > 45mmHg and PaO2 < 70mmHg CENTRAL SLEEP APNOEA ◦ Cessation of ventilation during sleep due to loss of ventilatory drive ◦ ≥ 10 second pauses with no associated respiratory effort
  • 16.  Upper airway more prone to collapse if -Upper airway narrowing -Decreased intraluminal pressure -Extraluminal pressure increased When –ve pressure by inspiratory muscles exceeds the force generated by dilator muscles Collapse Critical pressure(Pcrit) – pressure reqd to collapse upper airway.
  • 17.  OSAH +ve Pcrit with airway collapsing at atmospheric pressure. So +ve pressure to relieve obstruction. Normally –ve pressure required to collapse airway.
  • 18.  Upper airway dilating muscles influencing -Hyoid position- eg Geniohyoid -Tongue position- eg Genioglossus -Palate position- eg Tensor palitini Geniohyoid and genioglossus – Phasic inspiratory activity maintained during NREM sleep. Tensor palatini – Tonic actvity which decreases during sleep.
  • 19.  Upper airway dilating muscles activated by –ve airway pressure stimulating nasal and laryngeal receptor. Activity by hypoxia. Progesterone dilating activity. Serotonin dilating activity and reduced in patients with OSA.
  • 20.  Supine position- -Posterior displacement of tongue and mandible. -Loss of tone and gravity. -More marked in REM sleep. Obesity- fat deposition around upper airway. Shape of airway - More oval upper airway. Chronic vascular over perfusion-upper airway edema.
  • 21.  Upper airway edema secondary to mechanical trauma during snoring and recurrent airway obstruction. Further reduction in airway – perpetuates obstruction Overuse myopathy of dilating muscles due to increase workload. Chronic sleep deprivation impairs dilating activity.
  • 22.  Obesity Strongest risk factor for OSA ◦ Present in > 60% of patients referred for a diagnostic sleep evaluation Alters upper airway mechanics during sleep 1. Increased parapharyngeal fat deposition: neck circumference: > 17” males > 16” females With subsequent smaller upper airway  increase the collapsibility of the pharyngeal airway
  • 23. 2. Changes in neural compensatory mechanisms that maintain airway patency:  diminished protective reflexes which otherwise would increase upper airway dilator muscle activity to maintain airway patency3. Waist circumference Fat deposition around the abdomen produces  reduced lung volumes (functional residual capacity) which can lead to loss of caudal traction on the upper airway  low lung volumes are associated with diminished oxygen stores
  • 24. MALE GENDER Increased neck and waist circumference Pharyngeal airway length ? Women not reporting the classic symptoms ? Differential response of bed partner to symptoms of obstructive breathing during sleep ? Healthcare providers have lower index of suspicion for considering OSA in men than women
  • 25.  CRANIOFACIAL ABNORMALITIES• Mandibular body length• Retrognathia• Tonsilar hypertrophy• Enlarged tongue or soft palate• Inferiorly positioned hyoid bone• Maxillary and mandibular retro position• Decreased posterior airway space
  • 26.  OTHER• Smoking• Alcohol consumption• Sedatives (benzodiazepines)  reduce nerve output to compensatory dilator muscles  increase OSA severity in patients with preexisting syndrome.
  • 27. NOCTURNAL SYMPTOMS Snoring – reflects the critical narrowing - population survey: habitual snorers 25% of men, 15% of women - prevalence increases with age - the most frequent symptom of OSA - absence makes OSA unlikely (only 6% of patients with OSA did not report)
  • 28.  Witnessed apneas Nocturnal choking or gasping - report of waking at night with a choking sensation; passes within a few seconds Insomnia - sleep maintenance insomnia - few have difficulty initiating sleep
  • 29. DAYTIME SYMPTOMS Excessive daytime sleepiness(EDS) - severity can be assessed  subjectively = questionnaires (Epworth Sleepiness Scale)  objectively MSLT = Multiple Sleep Latency Test MWT = Maintenance of wakefulness Test Osler Test
  • 30.  Fatigue Memory impairment Personality changes Morning headaches or nausea Depression
  • 31. American Academy of Sleep Medicine Criterias A. Excessive daytime sleepiness that is not better explained by other factors B. Two or more of the following that are not better explained by other factors: -choking during sleep -recurrent awakenings -unrefreshing sleep; -daytime fatigue -impaired concentration C. AHI (five or more obstructed breathing events per hour during sleep)
  • 32. QUESTIONNAIRE Does pt snore? Is the pt or the partner troubled by snoring? How severe is the snoring?Audible if in the same room in an adjacent room? downstairs/anywhere in the house? next-door noeghbour? Is the snoring positional or does it occur in all sleep positions?
  • 33.  For how long pt has been snoring? Are there clinical features suggestive of OSA? regular multiple apnoeic episodes most nights? cerebrovascular complications like stroke, HTN,MI. endocrine co-morbidity like DM or hypothyroidism.
  • 34. Are the any aggravating factors? alcohol,how many per week? smoking how many per day? passive smoking? current wt and whetehr this is increasing? previous tonsil or adenoid surg? other upper aerodigetive tract abnormalities?
  • 35.  Have any conservative treatment tried such as wt loss,mandibular advancement splints or nasal valve dilators? Does this pt represent an anesthetic risk? is airway anatomically difficult? does the pt have cardiovascular,repiratory or cerebral disease that would significantly increase risk of anaesthesia?
  • 36. Examination of oropharynx,hypopharynx andlarynx to establish whether Nasal airway is patent Postnasal space is small There is long redundant soft palate with swollen uvula Palatine and/or lingual tonsils enlarged Tongue base is prominent There is large floppy epiglottis Vocal cord palsy Retrodisplaced Mandible Retro-displaced hyoid complex Dental malocclusion or large tongue
  • 37. FRIEDMAN PALATE POSITION
  • 38. TONSIL SIZE
  • 39. PALATE VARIATIONS
  • 40. ESS > 15 significant
  • 41. OVERNIGHT OXIMETRY Measures O2 saturation and provides pulse data. Assumes that when individual has apnoea or hyponoea O2 saturation falls. Once apnoea or hyponoea relived- O2 saturation rises. Falls and rises – Oxygen dips Dip of 4 or more % regarded as meaningful.
  • 42.  Oxygen desaturation index(ODI)- No of times O2 saturation falls by 4% per hr. ODI > 15 /Hr siggestive of OSA. Good specificty and +ve predictive value but poor sensitivity and _ve predictive value. In UK some sleep centres use it as a sceening test
  • 43. HOME MULTI CHANNEL TESTING Kit consists of -Nasal/oral flow by pressure cannulae -Chest and abdominal movts by Velcro belts -Pulse oximetry Disdvantage- Sensor failure and loss of signal Chest and abdominal belts allow to determine if apnoeas are related to respiratory effort -Central apnoea – no chest or abdominal movts -OSA – movts +
  • 44. HOME MULTI CHANNEL KIT
  • 45.  Apnoea- compete cessation of airflow for atleast 10secs irrespective of oxygen desaturation or arousals. Hypopnoeas – Reduction in airflow(amplitude of signal) between 50 -90%(with or without a 3% O2 desaturation and/or EEG arousal) OR - Reduction in airflow of <50% + 3% or more O2 desaturation and/or EEG arousal
  • 46. POLYSOMNOGRAPHY Measurements ◦ EEG, EOG, submental EMG – used to identify stages of sleep ◦ Airflow – measured by nasal prongs with pressure transducer, give a quantitative measure of inspiratory airflow ◦ Respiratory Effort ◦ O2 saturation ◦ ECG ◦ Body position ◦ Anterior tibialis EMG – to detect limb movements
  • 47.  Derived Information ◦ Total Sleep Time ◦ Sleep Efficiency ◦ Sleep stage latency ◦ Sleep stage distribution ◦ Arousals ◦ Apneas ◦ Hypopneas ◦ Indices ◦ Snoring ◦ Body position ◦ Oxygen desaturations ◦ Limb Movements
  • 48. Apnea-Hypopnea Index (AHI) – total number of apneas and hypopneas per hour of sleep. Mild- 5 to 20 per hour. Moderate- 21 to 30 per hour. Severe- >30 apnoea per hour.
  • 49.  Respiratory effort-related arousal(RERA) – events like hypopneas, with less than 4% drop in saturation Respiratory disturbance index(RDI) Apneas + hypopneas+ RERA‟s/hour -RDI > 5 is considered OSA -RDI 5 –20, mild -RDI 20 –40, moderate -RDI > 40, severe
  • 50. DYNAMIC NASOPHARYNGOLARYNGOSCOPY Flexible fiberoptic scope to examine the upper airway. Determine whether there are any fixed blockages in the upper airway such as a deviated septum or nasal polyps. Demonstrate the dynamic behaviour of the airway under conditions that promote collapse or which help to prevent collapse.
  • 51. Flexible Fiberoptic ScopeView of the nasopharynxStructures to note are theadenoids and the depthand height of thenasopharynx.
  • 52.  View of the velopharynx The velopharynx is bounded by the soft palate (top), the back of the throat, and a muscle complex on each side. View of the oropharynx and hypopharynx This is the part of the upper airway that contains the tonsils and the tongue.
  • 53.  View of the glottis
  • 54. 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%.
  • 55. MULLER‟S MANOEUVREResting airway Severe airway collapse during Mullers manoeuvre
  • 56. JAW THRUST OR 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).
  • 57. JAW THRUSTResting airway Airway with jaw thrust
  • 58. SLEEP NASOENDOSCOPY[Drug induced sleep endoscopy (DISE)] 1st described by Croft and Pringle in 1991 Pt sedated with propofol to a level sufficient to induce snoring. Operator examines upper aerodigestive tract in supine position to determine levels of obstruction. Anaesthetist must be present with full cardiac monitoring and resuscitation facilities. Respiratory stimulants can be used to encourage snoring.
  • 59. Sleep nasoendoscopy gradingsGrade Obstruction 1 Simple palatal level snoring/palatal flutter 2 Single level palatal obstruction 3 Palatal level obstruction with intermittent oropharyngeal involvement 4 Sustained multi segmental obstruction 5 Tongue base level obstruction 6 Isolated epiglottic involvement
  • 60. ESOPHAGEAL MANOMETRY Used in conjunction with screening sleep studies to diagnose apnoeas and hypoapnoeas. Evaluate relationship between reflux and OSA.
  • 61. 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 pts with OSA-very close correlation with videoendoscopy found. Not widely used due to high cost and time taken. Sleep in an MRI machine may not be representative of normal sleep patterns.
  • 62. 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
  • 63. CEPHALOMERTRYFor 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 Gngnathion
  • 64. NASAL SPRAY TESTUsing topical nasal decongestant on alternatenights and comparing severity of snoring andapnoea.
  • 65. STANFORD METHODCraniofacial Measurements Palatal Height (distance D - F): mm =P Maxillary Intermolar Distance: mm = Mx Mandibular Intermolar Distance: mm = Mn Overjet: mm = OJ Angle AC is 20 degrees
  • 66. The Stanford Score = {P + (Mx - Mn) + 3 x OJ} + {[Max(BMI - 25, 0)] x (NC/BMI)} = {Craniofacial Score} + {Obesity Score} If > 70 patient has OSA; and if < 70, there is a 10% chance of OSA If the jaw is too small, there will not be enough room for the tongue. This is reflected in the Craniofacial Score. If the person is obese and/or has a very thick neck it can lead to collapse of the throat during sleep. This is reflected in the Obesity Score.
  • 67.  Weight Loss/Exercise Nasal Obstruction/Allergy Treatment Sedative Avoidance Smoking cessation Sleep hygiene ◦ Consistent sleep/wake times ◦ Avoid alcohol, heavy meals before bedtime ◦ Position on side ◦ Avoid caffeine, TV, reading in bed
  • 68. SLEEP POSITION TRAINING Use of a tennis ball sewn into the back of a night shirt as a means of training the patient to avoid the supine position and sleep in the lateral position.
  • 69. CONTINUOUS POSITIVE AIRWAY PRESSURE(CPAP)
  • 70. CPAP Mainstay of treatment Acts as a „pneumatic splint‟. Blowing air via a mask and tube supports pharyngeal and palatal walls to prevent collapse. Two types -Fixed pressure type -AutoCPAP
  • 71. CPAP
  • 72. MASKS Can be nasal or full face. Chin straps can be used keep mouth closed. Kept in place with Velcro straps. Have expiratory port to prevent reinhalation of expired air.
  • 73. SETTING UP ON CPAP Patient education Group video workshops Pressure(cm H2O)=(0.16 x BMI) + (0.13 x NC) + (0.04 x AHI) – 5.12 NC=Neck circumference Split night- Diagnostic PSG and halfway through night CPAP started. Set fixed pressure is 95th percentile-pressure reqd to elilimnate 95% of apnoeas and hypopnoeas.
  • 74.  Has been shown to objectively ◦ Decrease blood pressure ◦ Decrease day time sleepiness Problems By 3 years of treatment 12-25% have discontinued treatment due to ◦ Mask discomfort ◦ Claustrophobia ◦ Aerophagia ◦ Nasal stuffiness ◦ Skin abrasions ◦ Ulcerations over nasal bridge ◦ Leaks ◦ Rarely pulmonary barotrauma
  • 75.  BiPAP ◦ Useful when > 6 cm H2O difference in inspiratory and expiratory pressures ◦ No objective evidence demonstrates improved compliance over CPAP
  • 76. ORAL APPLIANCES Mandibular advancement device Tongue retaining device ◦ Protrude the mandible forward and hold tongue more anteriorly, away from the posterior pharyngeal wall ◦ More effective in patients with mild – moderate OSA, AHI 5-15
  • 77. INDICATIONS FOR SURGERY Apnea-Hypoapnea index>15 O2 desaturation<90% AHI>5 or<14 with day time sleepiness. Upper airways resistance syndrome. Cardiac arrhythmias with obstruction.
  • 78.  Nasal Surgery ◦ Limited efficacy when used alone ◦ Verse et al 2002 showed 15.8% success rate when used alone in patients with OSA and day-time nasal congestion with snoring (RDI<20 and 50% reduction) Adenoidectomy (children)
  • 79. Uvulopalatopharyngoplasty(UPPP) 1st described by Ikematsu in 1950‟s. Popularized by Fugita in 1985. Resection of strip of soft palate and uvula + tonsillectomy. Tonsillar pillars then sutured. Used in pts of severe snoring with OSA.
  • 80. COMPLICATIONS OF UPPP Severe post op pain. Haemorrage. Respiratory obstruction due to laryngospasm. Post –op pulmonary edema. Velopharyngeal insuffiency. Nasopharyngeal stenosis. Dry throat due to loss of lubricating function of uvula. Voice changes. Taste disturbances.
  • 81. Cahali, 2003 proposedthe new LateralPharyngoplasty techniquefor patients withsignificant lateralnarrowing
  • 82.  Laser Assisted Uvulopalatoplasty(LUAP)
  • 83.  Introduced by Kamami in France,1993. Can be done as OPD procedure. Lignocaine+adrenaline injected at the base of uvula and 1cm lateral to midline on soft palate. Partial vapourization of the uvula with a CO2 laser. Stiffens soft palate and minimizes palateal flutter. May require repeated sessions.
  • 84. LAUP
  • 85. RADIOFREQUENCY ABLATION
  • 86.  Similar to diathermy but -lower power (2-10 W) -lower tissue temperatures(60-90o C ) -freq of 460 Hz Applied to specific submucosal sites causing -fibrosis of muscular layer -volumetric tissue reduction 3 types of radiofrequency devices -Somnus unit -Celon device -Coblator unit
  • 87. Pillar Palatal Implant System Three Implants Per Patient Implants are• made of Dacron®• 18 mm in length and 1.8 mm in diameter• meant to be permanent• can be removed FDA Approved for SNORING FDA Approved for mild to moderate SLEEP APNEA - AHI UNDER 30
  • 88.  Antibiotic 1 hour pre-op Mouth Rinse (chlorhexidine gluconate or equivalent) Hurricane or Equivalent Topical Spray Ponticane or Equivalent Topical Jelly Anesthetic, optional. Local Anesthetic Infiltration: 2 to 3 cc. Beginning at the junction of the Hard and Soft Palate inject entire “Target Zone”. (lidocaine with epinephrine or equivalent) Have available: Flexible Scope, Angled Tonsil Forceps
  • 89. 2 m.m. apart Minimum Palate Length 25 mm
  • 90.  Needle through the mucosa layer into the muscle. The insertion site should be as close to the junction of the hard and soft palate as possible. Needle advancement continued in an arcing motion until the “Full insertion depth marker” is no longer visible.
  • 91. INSPECTION Inspect the needle insertion site. If a portion of the implant is exposed, it must be removed with a hemostat. Inspect the nasal side of the soft palate using a Flexible Naso Scope. If the implant is exposed, it must be removed. An angled tonsil forceps is recommended.
  • 92. PREFERRED PATIENT BMI less than 32 AHI Less than 30 No Obvious Nasal Obstruction Small to Medium Sized Tonsils Mallampati Class І or Class ΙΙ Friedman Tongue Position I and II Minimum 25mm Palate to treat
  • 93. TONGUE BASED PROCEDURES These are rarely done alone Part of multilevel surgery Knowledge of anatomy and important structures is critical Address the tongue base by three mechanisms -Tissue reduction -Improved tension -Increased airway space
  • 94. TONGUE BASE ANATOMY Hypoglossal nerve, lingual artery neurovascular bundle Foramen cecum and sulcus terminalis Retromolar trigone Lingual tonsil Epiglottis Hyoid
  • 95. Radiofrequency base of tongue ablation Advantages -Relatively safe (3.5% overall complication rate) -Can be performed on outpatient basis -Can be performed in as little as one sitting DisadvantagesCan only ablate a small amount of tissue
  • 96. Submucosal minimally invasive lingual excision(SMILE) Lingual arteries found and marked using doppler Midline of tongue one centimeter anterior to the circumvallatepapillae an incision is made using 15 blade Coblator wand to ablate tissue to vallecula Stay within 1 cm of midline, and medial to the markings for artery Leave open for drainage
  • 97. SMILE
  • 98. LASER MIDLINE GLOSSECTOMY AND LINGUALPLASTY
  • 99. GENIOGLOSSUS ADVANCEMENT
  • 100. REPOSE(SUTURE SUSPENSION OF TONGUE) Intraoral incision is made in the frenulum and a titanium screw is placed in the lingual cortex of the geniotubercle Permanent suture is passed through the paramediantongue musculature to the tongue base and then back through. 1 cm lateral to midline, and 1 cm below foramen cecum Pulls the tongue base anteriorly Increase tension, and posterior airway space
  • 101. LINGUAL SUSPENSION
  • 102. HYOID MYOTOMY AND SUSPENSION◦ Advances hyoid bone anteriorly and inferiorly◦ Advances epiglottis and base of tongue◦ Performed in conjunction with other procedures◦ Dysphagia may result
  • 103. Maxillary-Mandibular Advancement ◦ Severe disease ◦ Failure with more conservative measures ◦ Midface, palate, and mandible advanced anteriorly ◦ Limited by ability to stabilize the segments and aesthetic facial changes ◦ Performed in conjunction with oral surgeons ◦ Temporary or permanent paresthesia
  • 104. TRACHEOSTOMY Ultimate treatment modality Temporary treatment while other surgery is done Morbid obesity Severe OSA when more conservative treatment failed,refused or not tolerated Life threatening cardiopulmonary complications Significant anesthetic/surgical risks Once placed, uncommon to decannulate
  • 105. ALGORITHMS Stanford Protocol• Riley et al 1992 Studied 2 phase approach for multilevel site of obstruction• Phase 1: Genioglossal advancement, hyoid myotomy and advancement, UP3• Phase 2: Maxillary-Mandibular advancement in 6 months if phase 1 failed• Reported >90% success rate in patients who completed both phases• Testing is done at 6 months
  • 106. FRIEDMAN ALGORITHM Chance of success with surgical management decreases with increasing Friedman stage Stage I and II patients have good success with UPPP and tongue base procedures Stage III and IV patients have much lower rates of success following UPPP/tongue base

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