Obstructive Sleep Apnea Annette Hulse, DO Sep 17 2016 www.SantaCruzOsteopathy.com/Slides

Sleep Disordered Breathing Snoring Upper Airway Resistance Syndrome Sleep apnea Obstructive Central Mixed

Snoring Loud/harsh during sleep, due to tissue vibration from the flow of air through membranous structures (the soft palate, uvula, and the pharyngeal walls) that do not have cartilaginous support What determines the "stiffness" of the pharyngeal wall is not fully understood; the tissues are both distensable and collapsable

Snoring Any stage of sleep (most common in Stages 2,3,4) Inhalation > exhalation Worse with alcohol or other depressants Worse with asthma, colds, congestion, allergies, smoking More common with obesity or weight gain ~ 50% of all people snore at some point Men (40%) > women (24%) Men less likely to snore after age 70

Obstructive Sleep Apnea

Upper Airway Patency Structural Neuromuscular Craniofacial structure Surrounding soft tissue (including adipose, tongue size, lateral pharyngeal walls) Vascular structures (fluid displacement to lateral pharyngeal walls) Neuromuscular Including thoracic-upper airway link (caudal traction)

Sleep Stages NREM (non-REM) sleep - consists of Stage 1 (transitional sleep), Stage 2 (light sleep), and Stage 3 and 4 (slow wave). Most information about upper airway patency is primarily from NREM sleep due to difficulty of achieving REM sleep with invasive testing REM sleep - also called Rapid Eye Movement sleep, is when the most vivid dreaming occurs. Paralysis of skeletal muscles Most people have higher AHI numbers in REM than non- REM (skeletal muscle paralysis during REM)

Prevalence of OSA Age 30 – 49 Age 50-70 Men 10% 17% Women 3% 9% How many apneic events do you need to be diagnosed with OSA?

AHI: Apnea-Hypopnea Index Apnea: stop breathing for 10 seconds or more Hypopnea: at least a 30% decrease in airflow for 10 seconds or more (usually measured as 3% decrease in O2 Sat). AHI = (apneas + hypopneas)/hours of sleep Alternatively Respiratory Disturbance Index (RDI) may be reported; it includes not only apneas and hypopneas, but may also include other, more subtle, breathing irregularities

Gradations of OSA None/Minimal: AHI < 5 per hour AHI 5-15 per hour – Mild OSA AHI 15-30 per hour – Moderate OSA AHI ≥ 30 per hour – Severe OSA

Pathophysiology of OSA Thought to be Excessive arousals increase sympathetic drive Hypoxias Disruption of sleep architecture (REM vs. non-REM sleep) / sleep fragmentation Risks (causation) Daytime sleepiness (driving, operating machinery, attention to detail) Increased cardiovascular risk – documented increase in HTN with severe OSA Other risks uncertain (may include impaired glucose tolerance, stroke, pulmonary HTN)

Symptoms of OSA Morning headaches Difficulty concentrating Daytime sleepiness Memory loss Nocturia Snoring

Symptoms of OSA in Children Snoring Daytime sleepiness Neurocognitive effects ADHD, behavioral disorders, memory & learning, poor school performance, developmental delay, aggressive behavior Enuresis Tonsil & adenoid hypertrophy

OSA in Children More often during REM sleep Smaller lung capacities  become more hypoxic and more hypercapnic Typically do not awaken Often mouth breathers, frequent URIs Sleep in unusual positions, night sweats, morning headache

How Do We Diagnose Sleep Apnea? “Sleep study” aka polysomnography

Polysomnography (PSG) A sleep study measures sleep cycles and stages by recording: Air flow in and out of lungs The level of oxygen in your blood Body position Brain waves (EEG) Breathing effort and rate Electrical activity of muscles (EMG) Eye movement (EOG) Heart rate & EKG

Arousals Any sudden change on Electroencephalographm EEG from a deeper sleep stage to a lighter sleep stage. It may be related to an apnea, a hypopnea, a leg movement, or it may be "spontaneous” Greater than 10 arousals per hour is abnormal

How is Sleep Apnea Treated?

Traditional Treatment CPAP – nasal or oral Treats SYMPTOMS

Oral Repositioning Devices Oral devices reposition the mandible forward (anteriorly) to increase airway space behind the tongue; also may include tongue retaining device.

Surgery Surgery may stiffen, remove or reposition tissues in and around your throat, including Soft palate & uvula Tonsils & adenoids Tongue Upper & lower jaw (MMA) MMA ~ #35% “curative”

Ablation

Upper Airway Stimulation

Traditional Treatments --Children

Traditional Treatments for Children Tonsillectomy & Adenoidectomy (rarely curative) Rapid palatal expansion

Preferred Treatment Myofunctional therapy ~ 50% improvement in AHI + Osteopathic Treatment Functional dental appliance CPAP if needed for symptom control

Osteopathic Considerations Upper airway fluid retention decreases with better cranial/facial bone excursion with PRM Hypopneas can be influenced by rib compliance and lung mechanics Airway patency influenced by vascular fluid retention in pharyngeal areas (e.g., thoracic inlet, cervical lymphatics) Diaphragm excursion a significant player in lung mechanics (C3- C5, phrenic nerve) Address sympathetic tone Note that CPAP will impede diaphragm excursion, rib compliance, and lung mechanics

Example of ALF in Sleep Uses alternative to PSG that you can use with your patients from Sleepimage.com N-REM sleep – more white area is better REM sleep – more to the left is better

Baseline

Baseline

Baseline

With CPAP

With CPAP

With CPAP + ALF

REM-With CPAP

REM-With CPAP + ALF