OSA.pptxhkryjkrykruksrtkjejyrjukfiylsuksryku

yjsrykjtudkulkldtilfy9;pfuo;

1. OBSTRUCTIVE SLEEP APNEA MODERATOR: DR. B.Y. PRAVEEN KUMAR PRESENTOR: DR. K. NAVYA KIRON

2. INDEX INTRODUCTION RESPIRATORY EVENT DEFINITIONS AND TYPES OBSTRUCTIVE SLEEP APNEA : HISTORIC PERSPECTIVE DEFINITION RISK FACTORS PATHOPHYSIOLOGY HEALTH CONSEQUENCES AND COMORBIDITIES APPROACH TO PATIENT

3. INTRODUCTION Sleep-related breathing disorders: Category Description 1. Obstructive Sleep Apnea (OSA) Recurrent upper airway obstruction during sleep causing apnea (cessation) or hypopnea (reduction) in airflow despite respiratory effort. 2. Central Sleep Apnea (CSA) Repetitive cessation of airflow due to lack of respiratory effort, often related to CNS disorders. 3. Complex/Mixed Sleep Apnea Features of both obstructive and central apneas. 4. Sleep-Related Hypoventilation Disorders Sustained hypoventilation during sleep; includes obesity hypoventilation syndrome and neuromuscular disorders. 5. Sleep-Related Hypoxemia Disorder Persistent low oxygen levels during sleep without clear apneas or hypopneas. Common in COPD and interstitial lung disease. 6. Isolated Symptoms & Normal Variants Includes snoring and upper airway resistance syndrome (UARS).

4. Respiratory Event Definitions and Types Apnea Cessation of airflow for at least 10 seconds. Hypopnea Reduction in airflow (≥30%) for at least 10 seconds with ≥4% oxyhemoglobin desaturation OR a reduction in airflow (≥50%) for at least 10 seconds with ≥3% desaturation or an EEG arousal. Respiratory Effort–Related Arousal (RERA) A sequence of breaths lasting at least 10 seconds with increasing respiratory effort or flattening of the nasal pressure waveform, leading to an arousal from sleep when the sequence does not meet criteria for apnea or hypopnea. Obstructive Continued thoracoabdominal effort in the setting of partial or complete airflow cessation. Central Lack of thoracoabdominal effort in the setting of partial or complete airflow cessation. Mixed A respiratory event with both obstructive and central features, generally beginning as central events and ending with thoracoabdominal effort without airflow.

5. OBSTRUCTIVE SLEEP APNEA

6. HISTORIC PERSPECTIVES The idea of obesity being associated with daytime somnolence : first written about by Charles Dickens in The Posthumous Papers of the Pickwick Club( 1837). Describes Joe, a boy so obese that he has difficulty breathing, sounds as if he is snoring even when awake, and frequently falls asleep while standing. 1956: Bickelmann and colleagues ; described the Pickwickian syndrome in a case report, titled “Extreme Obesity Associated with Alveolar Hypoventilation: A Pickwickian Syndrome.”

7. DEFINITION OSA is defined on the basis of Nocturnal and Daytime symptoms + Sleep study findings Diagnosis Based on: (1) Symptoms of Nocturnal breathing disturbances (snoring, snorting, gasping, or breathing pauses) during sleep, Or Daytime sleepiness or fatigue that occurs despite sufficient opportunity to sleep and is unexplained by other medical problems AND (2) ≥ 5 episodes of Obstructive apnea or hypopnea per hour of sleep ( The Apnea-Hypopnea Index [AHI= number of episodes divided by the number of hours of sleep]) in a sleep study

8. OSA also may be diagnosed in the absence of symptoms if : AHI is ≥15 episodes/hour Each episode of apnea or hypopnea  reduction in breathing for at least 10 s and ≥3% drop in oxygen saturation or a brain cortical arousal. OSA severity can be characterized by : Frequency of breathing disturbances (AHI)  Amount of oxyhemoglobin desaturation with respiratory events Duration of apneas and hypopneas, The degree of sleep fragmentation, The level of reported daytime sleepiness or functional impairment

9. RISK FACTORS Older age Obesity Male gender (2:1) Positive family history of OSA ( 2 fold higher risk) Mandibular retrognathia and micrognathia Genetic syndromes that reduce upper airway patency - Down syndrome, Treacher-Collins syndrome Adenotonsillar hypertrophy (especially in children), Endocrine syndromes (e.g., acromegaly, hypothyroidism).

10. PATHOPHYSIOLOGY During inspiration: * During wakefulness: Dilator muscle Activity↑ = Airway patent

11. Upper Airway Anatomy related factors: Contains a collapsible portion  from the Hard palate to the L arynx Ability of the upper airway to change shape and momentarily close, is essential for speech and swallowing during wakefulness, this feature also provides the opportunity for collapse during sleep. Obesity, soft tissue hypertrophy and craniofacial characteristics such as retrognathia  impaired upper airway anatomy by ↑ the extraluminal pressures surrounding the upper airway. The airway may collapse at different sites, such as

12. Obesity : Major risk factor ↑ Fat deposition around the neck and parapharyngeal spaces → narrow and compress the upper airway - offset the effects of dilator muscles Impairment of metabolism, ventilation, and lung volume → mismatch between alveolar ventilation and pulmonary perfusion. ↓ lung volume  ↓ functional residual capacity ↓ lung volume  ↓ pharyngeal upper airway size due to tracheal and thoracic traction aka- Tracheal tug  ↑ airway collapse

13. Nasal obstruction: High degree of nasal resistance (nasal septal deviation or polyps)  airway collapse by ↓ intraluminal pressure downstream in the pharynx. Contributes to open-mouth breathing during sleep  increases upper airway collapsibility, decrease the efficacy of dilator muscles and breaks the seal between tongue and palate  tongue falls posteriorly  occludes airway Snoring can be caused by nasal obstruction. Adenotonsillar hypertrophy major cause of OSA in children.

14. Craniofacial variations : ↑ Distance of the hyoid bone from the mandibular plane ↓ Mandibular and maxillary projection Downward and posterior rotation of mandibular and maxillary growth ↑ Vertical facial length ↑ Vertical length of the posterior airway ↑ Cervical angulation

15. Fujita classified the patterns of obstruction by Anatomic Location: Type I : Collapse in the Retropalatal region only Type II: Collapse in both Retropalatal and Retrolingual regions Type III: Collapse in the Retrolingual region only.

16. Passive Critical Closing Pressure ( Pcrit ) ; Used to measure the functional collapsibility of the upper airway Luminal pressure at which the upper airway collapses when airway support (positive pressure) is suddenly withdrawn without activating the pharyngeal dilator muscles Measured by: Mask connected to a device that can apply both positive and negative pressure After maintaining a prolonged positive airway pressure, the pressure is suddenly reduced. Pcrit is recorded at the point where the airway collapses passively Normal individuals : Pcrit is below −5 cm H₂O → their airway is more stable and less collapsible OSA patients: Pcrit is above atmospheric pressure → their airway collapses more easily.

17. Upper Airway Dilator Muscle Activity and Reflex Responsiveness Neuromuscular tone contributes to the patency of the upper airway During sleep this tone decreases  airway collapse Genioglossus muscle - important muscle in maintaining airway patency in OSA Awake OSA patients show higher genioglossus and tensor palatini activity than normal individuals. This compensates for their structurally narrower or more collapsible airway. If the muscles fail to increase activity in response to collapsing pressures (e.g. during sleep), it leads to airway obstruction → OSA.

18. Ventilatory Control Stability Loop gain refers to the sensitivity of the respiratory control system to changes in carbon dioxide (CO₂) levels. It reflects how strongly the body responds to disturbances in ventilation. Low Loop Gain : stable respiratory system High Loop Gain: Indicates an unstable control system . Even small ↑ in CO₂ = excessive ventilatory responses (overcompensation). These large responses lead to: Rapid drops in CO₂  suppressing respiratory drive  hypoventilation , and again a rise in CO₂ : vicious cycle of instability In OSA , this instability causes: Large negative intraluminal pressures during inspiration. Greater tendency for the upper airway to collapse .

19. Arousal from Sleep Low Arousal Threshold Easily awakened in response to small changes in intrathoracic pressure (like from airway narrowing) Disrupts sleep continuity , preventing progression to deeper sleep stages . Consequences: Less time in stages with higher genioglossus muscle activity . Reduced pharyngeal dilator tone , which increases airway collapsibility . Too sensitive → Too frequent awakenings → Poor airway muscle compensation. High Arousal Threshold Less easily awakened , even when CO₂ builds up or during apnea. Allows more time for CO₂-mediated muscle compensation to restore airway patency. If too high : Apneas - persist longer . ↑ oxygen desaturation Delayed arousal may worsen the physiological impact of apneas.

20. HEALTH CONSEQUENCES OF OSA System Affected Key Effects of OSA Mechanisms 🧠 Sleep & Arousal Daytime sleepiness, poor concentration, increased accident risk Sleep fragmentation, intermittent hypoxia ❤️ Cardiovascular System ↑ Risk of: Coronary artery disease, heart failure (with or without reduced EF), arrhythmias Sympathetic overactivity, RAAS activation, intrathoracic pressure swings 🧠 Cerebrovascular System ↑ Stroke risk Hypoxia, endothelial dysfunction 💊 Blood Pressure Regulation Prehypertension, nondipping pattern, resistant hypertension ↑ Sympathetic activity, RAAS changes, altered fluid balance 🧬 Metabolic System ↑ Risk of: Insulin resistance, type 2 diabetes, dyslipidemia Inflammation, oxidative stress, hormonal imbalance 🚗 Functional Impact ↑ Risk of motor vehicle and occupational accidents Excessive daytime sleepiness

21. APPROACH TO PATIENT

22. SYMPTOMS AND HISTORY

23. The Epworth Sleepiness Scale (ESS) is a widely used tool that assesses daytime sleepiness OSA may be suspected in patients with an ESS score >10 STOP-BANG questionnaire

24. PHYSICAL EXAMINATION FINDINGS * Neck circumference- at the level of cricothyroid membrane is measured Collar size should not exceed 42 cm in males and 37.5 cm in females *

25. INVESTIGATIONS 1. Polysomnogram (PSG) Gold standard for diagnosis Records various parameters which include:

26. 2. Fiber-optic Nasopharyngoscopy and Laryngoscopy: A flexible endoscope is passed through the nose and Müller’s maneuver is performed in an awake patient, who generates negative pressure by inhaling against a closed glottis with the nose and mouth closed- to trigger airway collapse. Level of pharyngeal obstruction can be found Helps guide surgical decision making when the area of collapse is purely retropalatal Drawback: less useful in patients who have multilevel obstruction

27. 3. Drug-induced sleep endoscopy (DISE) : Involves the use of fiberoptic nasopharyngoscopy to evaluate the site of airway collapse during pharmacologically induced sleep To better identify the site or sites of obstruction in patients with OSA and to guide more effective surgical intervention. Dynamic obstruction observed during sedated endoscopy may more accurately reflect airway obstruction during natural sleep than during an awake examination A proposed method of standardizing DISE findings called the velum , oropharynx , tongue base , epiglottis ( VOTE)

28. 4. Radiologic techniques: Ce phalometric radiograph : two-dimensional representation of the airway, a standardized evaluation system with broad availability and relatively low cost. Awake Computed tomography (CT) and Dynamic CT during sleep Magnetic resonance imaging (MRI) and cineMRI (which captures images at short time intervals to allow assessment of dynamic movement of soft tissues) Fluoroscopy and Somnofluoroscopy Primary advantage : high anatomic resolution of dynamic airway movement during sleep without the presence of an endoscope that might potentially alter airflow Poor sensitivity for diagnosing OSA Can be used to illustrate postoperative anatomic changes that correlate with improved PSG parameters

29. TREATMENT MEDICAL / CONSERVATIVE MANAGEMENT : Weight reduction - for all overweight patients. Bariatric surgeon consultation for morbid obesity Optimize sleep duration (7–9 h) Positional therapy: Side sleeping Treat nasal allergies/ obstruction- Decongestants Avoidance of Alcohol and sedatives Oral appliances – for mild to moderate OSA , who cannot tolerate CPAP Continuous positive airway pressure (CPAP) - Standard medical therapy with the highest level of evidence for efficacy.

30. Continuous Positive Airway Pressure (CPAP) Delivered through a nasal or nasal-oral mask CPAP works as a mechanical splint to hold the airway open, thus maintaining airway patency during sleep. Rates of adherence to CPAP treatment are highly variable (average, 50–80%)

31. The CPAP machine was invented in 1980 by Colin Sullivan , an Australian physician and professor.

32. TREATMENT SURGICAL TREATMENT : Indications: AHI >5 and <14 with symptoms or comorbidities AHI >15 Oxyhemoglobin desaturation <90% Upper airway resistance syndrome, preferably with objective improvement of neurocognitive dysfunction and medical therapy Significant cardiac arrhythmias associated with obstructions Unsuccessful or refused medical therapy and desire for surgery Medically stable enough to undergo recommended procedures

33. Preoperative examination and planning : Discussion between the anesthesia team and the surgeon regarding plans for airway management. Stepwise algorithm includes : using an oropharyngeal airway to prevent airway obstruction by the tongue refraining from using paralyzing agents until the patient can be easily ventilated with a mask preparing alternative methods of ventilation in case intubation is unsuccessful. The surgeon should also have a frank discussion with the patient about the possibility of Tracheotomy . Site of obstruction must be determined in each patient to determine the type and extent of surgical intervention – DISE

34. Surgical Treatment OROPHARYNGEAL PROCEDURES

35. Nasal surgery: Nasal septoplasty, Inferior turbinate reduction, Adenoidectomy, Nasal tumor or polyp resection and Nasal valve reconstruction - based on pathology Treats nasal obstruction associated with OSA Unlikely to significantly improve OSA when used alone Improving nasal patency may help restore physiologic breathing and may allow for the use of nasal CPAP in patients previously unable to tolerate it Consideration should be made to address nasal obstruction as an initial step in OSA management so as to facilitate better CPAP adherence

36. Palatal surgery: UVULOPALATOPHARYNGEOPLASTY: Fujita and colleagues: described the UPPP, the first palatal procedure for OSA treatment Most commonly performed surgical procedure for OSA UPPP with tonsillectomy was developed to eliminate palatal obstruction by resection of redundant palatal and pharyngeal tissue. Often misused as the first-line surgical therapy for OSA regardless of coexistent patient factors such as obesity, retrognathia, and the existence of other sites of obstruction thus-it is often unsuccessful in treating OSA The site of pharyngeal collapse has a marked effect on the probability of the success of UPPP.

37. Laser-Assisted Uvulopalatoplasty (LAUP): Office-based surgical procedure that was introduced in 1990 Progressively shortens and tightens the uvula and palate through a series of carbon dioxide laser incisions and vaporizations Most of the uvula is amputated, and the soft palate is incised by vertical trenches up to the muscular sling 1–2 cm lateral to the uvula. Surrounding mucosal or tonsillar pillar tissue may also be vaporized.

38. Elevoplasty Technique involves: 3 fully resorbable (Polydioxanone), barbed suture implants insertion into the soft palate under topical and local infiltration anesthesia The bidirectional, self‐anchoring suture configuration incorporates tiny barbs spaced evenly in a helical array on either side of a nonbarbed midsegment. Net result: Stiffening and shortening of the soft palate without the need for surgical knots or swaged needles. Each implant provided preloaded into a specialized suturing needle delivery device

39. Gently traction on the silk sutures causes mild tissue apposition (“accordion‐ ing ”) and results in elevaton , shorten, and stiffen the soft palate. The proximal barbs engage with tissue to maintain the tension The Elevo suture implant is provided preloaded into a specialized suturing needle delivery device

40. TRANSPAL ATAL ADVANCEMENT PHARYNGOPLASTY : Introduced by Woodson and colleagues Aims to decrease retropalatal obstruction by altering the bony hard palate and the soft tissue attachments of the posterior maxilla a 1-cm portion of the hard palate is removed, and the soft palate is then advanced and secured medially and laterally in the tensor aponeurosis, which enlarges the retropalatal region. Used for persistent retropalatal obstruction after UPPP

41. Z-PALATOPLASTY : Introduced by Friedman and associates Primary or revision palatal procedure in selected patients RADIOFREQUENCY ABLATION of Soft palate: Safe and well tolerated with minimal adverse outcomes More useful in improvement of snoring > OSA

42. PILLAR IMPLANTS: Placement of three woven polyester implants, which stiffen the palate Porosity of the implants  formation of a fibrotic capsule  connects the three implants and further stiffens the palate Advantages : Single office visit Minimal morbidity Reduce snoring Commonly used to treat snoring and mild OSA.

43. Oropharyngeal Surgery: ISOLATED TONSILLECTOMY Patients with large tonsils and mild-to moderate OSA. HYPOGLOSSAL NERVE STIMULATION: Electrical stimulation of the hypoglossal nerve has been proposed as a method to improve the neuromuscular tone of the pharynx during sleep, particularly the genioglossus. Implantable hypoglossal nerve-stimulating device was developed  detects the onset of the inspiratory phase of respiration through chest wall pressure sensors, allowing the electrical stimulation of the hypoglossal nerve to be timed with inspiration.

44. LATERAL PHARYNGOPLASTY : First described by Cahali . The technique involves:

45. EXPANSION SPHINCTER PHARYNGOPLASTY: Preoperative view of the oropharynx Exposure of the palatopharyngeus (vertical fibers) Elevation of the palatopharyngeus. Rotation and tunneling of the palatopharyngeus toward the hamulus. Suture suspension and approximation.

46. TONGUE-BASE PROCEDURES: For Retrolingual collapse Partial midline glossectomy (PMG), Lingualplasty RFA of the tongue base In selected patients: lingual tonsillectomy, reduction of the aryepiglottic folds, and partial epiglottectomy are also performed. Lingual tonsillectomy in combination with palatal surgery

47. Hypopharyngeal Surgery: GENIOGLOSSAL ADVANCEMENT (GA) : Genial tubercle of the mandible, (anterior attachment of the genioglossus muscle) is mobilized by means of limited osteotomy The segment is then advanced and fixed into place at the inferior aspect of the osteotomy

48. HYOID MYOTOMY/MANDIBULAR SUSPENSION: Aims to enlarge the retrolingual airway by fixing the major dilators of the pharynx forward without changing dental occlusion. Hyoid is mobilized via inferior myotomy and fixed anteriorly and inferiorly by attachment to the thyroid cartilage

49. Maxillomandibular Advancement: ↑the retropalatal and retrolingual airway The maxilla and mandible are advanced by means of Le Fort I maxillary and sagittal-split mandibular osteotomies. Usually performed after other surgical intervention has been unsuccessful, Complications : malocclusion, relapse, nerve paresthesia , nonunion or malunion, temporomandibular joint problems, infection, bleeding, and the need for subsequent dental work.

50. Tracheotomy: Traditional gold standard of surgical management of OSA. Relieves OSA by completely bypassing the portion of the airway that most commonly collapses during sleep. However, the associated psychosocial problems, perceived inconvenience, and morbidity  rarely makes tracheotomy a desirable surgical option.

51. Indications: Failed all other OSA treatments Life-threatening OSA and are unable to tolerate CPAP, Patients who are neurodevelopmentally impaired/ morbidly obese Temporary measure for patients undergoing base of tongue surgery.

52. POSTOPERATIVE MANAGEMENT Increased chance of postoperative airway obstruction due to multisite surgical treatment of OSA  because of resultant edema in multiple sites in the upper airway Post-anesthesia sedation along with altered respiration secondary to narcotic pain medications can be additive in patients with an already compromised airway Hospitalization is recommended Admission to ICU  in multilevel surgery Patients with severe OSA use CPAP for the first 2 weeks after surgery Postoperative PSG be carried out in 3 to 4 months to evaluate the response to surgery.

53. REFERENCES Flint PW, Haughey BH, Lund VJ, Niparko JK, Richardson MA, Robbins KT, Thomas JR, Lesperance MM, editors. Cummings Otolaryngology: Head and Neck Surgery. 7th ed. Philadelphia: Elsevier; 2021. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 21st ed. New York: McGraw-Hill Education; 2022. Kryger MH, Malhotra RK. Atlas of Clinical Sleep Medicine. 3rd ed. Philadelphia: Elsevier; 2022 Won CHJ, Li KK, Guilleminault C. Surgical treatment of obstructive sleep apnea : upper airway and maxillomandibular surgery. Proc Am Thorac Soc . 2008;5(2):193–9. doi:10.1513/pats.200708-135MG. Friedman M, Gillespie MB, Shabdiz FA, Hiltzik DH, Meyer TA, Ahn J, Catalano PJ, Joseph NJ. A new office-based procedure for treatment of snoring: The S.I.Le.N.C.E . study. Laryngoscope . 2021;131(3):624–9. doi:10.1002/lary.28803.

54. Thank YOU