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Perioperative Management of the Sleep Apnea Patient Grand Rounds Richard Browning, M.D.

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Presentation on theme: "Perioperative Management of the Sleep Apnea Patient Grand Rounds Richard Browning, M.D."— Presentation transcript:

1 Perioperative Management of the Sleep Apnea Patient Grand Rounds Richard Browning, M.D.

2 Goals Review Incidence Define OSA & OSH Learn how to diagnose Understand the pathophysiology Develop a plan for pre-, intra- and post- op management

3 Incidence Among middle-aged adults – 4% of men & 2% of women Estimated that 80-95% are undiagnosed Testing increasing 124% every 3 years Therefore, diagnosis of OSA will increase 5 to 10-fold over next decade.

4 Causes / Risk Factors Obesity, Obesity, Obesity Increasing age Male gender Structural abnormalties Tonsillar hypertrophy, nasal pathology Alcohol, smoking and family history

5 Causes / Risk Factors Up to 90% of adult patients with OSA are obese OSA parallels the obesity epidemic

6 Table 1. Distribution by Age of Categorical Levels of AHI* (AHI=Apneas + Hypopneas/Hour of Sleep) Habitual Snoring AHI > 5 AHI > 10 AHI > 15 Age (Yrs) (%) (%) (%) (%) <25 14 10 2 0 26-50 41 26 15 0 >50 46 61 50 36 AHI = Apnea Hypopnea Index

7 Definition of OSA OSA is defined as a cessation of airflow for more than 10 seconds despite continuing ventilatory effort, 5 or more times per hour of sleep and a decrease of more than 4% in S a O 2.

8 Definition of OSH OSH is defined as a decrease in airflow of >50% for >10 seconds, 15 or more times/hour of sleep, and often with  in S a O 2.

9 Oropharynx With Tonsillar Hypertrophy Normal Oropharynx Anatomy of the Obstructed Airway Exam: Tonsillar Hypertrophy

10 Pediatric Sleep Apnea Sleep with Sleep ApneaChild’s Enlarged Palatine & Adenoidal Tonsils

11 Exam: Oropharynx Patient With the Crowded Oropharynx

12 Physical Exam Guilleminault C et al. Sleep Apnea Syndromes. New York: Alan R. Liss, 1978. Structural Abnormalities

13 Airway Anatomy 3 collapsible pharyngeal segments Nasopharynx, posterior pharynx to soft pallate Retroglossal pharynx, uvula to epiglottis Retroepiglottal pharynx

14 Pathophysiology of Apnea

15 Patency Depends on pharyngeal dilator muscles which stiffen and distend the airway during inspiration.

16 Patency 3 segments are controlled by: A. Tensor palatini B. Genioglossus* C. Hyoid bone muscles *Most important

17 Genioglossus Muscle Activity is phasic with inspiration Activity decreases with sleep Almost ceases with REM sleep Abolished in OSA at onset of APNEA Increases with arousal

18 What Happens with Normal Sleep?

19 Normal Sleep 4 to 6 cycles of N-REM sleep followed by REM sleep 4 stages of N-REM with progressive slowing of EEG

20 Normal Sleep Stage 3 and 4 N-REM and REM are very deep levels of sleep Progressive generalized loss of muscle tone Restorative periods of sleep

21 Normal Sleep Progressive decrease in muscle activity and resultant increase in upper airway resistance.

22 Pathophysiology of Apnea

23 Airway Collapse Occurs with loss of muscle activity Increased subatmospheric pharyngeal pressure MRI reveal anterior and lateral wall collapse

24 Obesity Effects Airway Anatomy Adversely Inverse relationship between obesity and pharyngeal area Fat deposits in the uvula, tongue, tonsillor pillars, aryepiglottic folds and lateral pharyngeal walls.

25 Obesity Effects Airway Anatomy Adversely Increase fat deposits change shape of pharynx Decreases efficiency of normal muscle function Increase extra-mural pressure All conspire to increase propensity for collapse

26 Obesity Effects Airway Anatomy Adversely Therefore, neck obesity is more important than generalized obesity in determining risk of OSA.

27 Physiologic Consequences of OSA

28 Pathophysiology of Sleep Apnea Awake: Small airway + neuromuscular compensation Loss of neuromuscular compensation + Decreased pharyngeal muscle activity Sleep Onset Hyperventilate: correct hypoxia & hypercapnia Airway opens Airway collapses Pharyngeal muscle activity restored Apnea Arousal from sleep Hypoxia & Hypercapnia Increased ventilatory effort

29 Clinical Consequences Cardiovascular Complications Morbidity Mortality Sleep Fragmentation Hypoxia/ Hypercapnia Excessive Daytime Sleepiness Sleep Apnea

30 Diagnosis of OSA Clinical A. Obesity BMI >30 Kg/M 2 B. Snoring / Apnea / Arousal C. Daytime Sleepiness D. Increased Neck Circumference >42 cm

31 Diagnosis of OSA Gold Standard is a sleep study EEG, EOG, Airflow sensors, E T CO 2 esophageal pressure, chest and abdomen movement, submental EMG, oximetry, BP, EKG

32 AHI APNEA – Hypopnea Index 6-20, 21-50, >50 per hour Mild, Moderate, Severe O 2 SAT usually reported

33 Anesthesia Effect Propofol, Thiopental, Opioids, Benzodiazepines, NMBs, Inhalational Anesthestics cause pharyngeal collapse First 3 days are greatest risk for apnea from drug-induced sleep

34 Surgical Effects Sleep architecture is disturbed first 3 days Days 4-6, patients experience REM sleep rebound Apnea risk increased for 1 week post-op

35 Surgical Effects REM sleep disturbance is surgical stress related and proportional to magnitude of surgery REM rebound may contribute to poor hemodynamic outcomes from profound sympathetic activation

36 OSA Risk Conclusions Perioperative complications increase with severity Anethestic drugs and surgical stress exacerbate baseline problem May play significant role in unexplained MIs, stroke or death

37 Perioperative Management Make diagnosis and grade severity Thorough airway assessment and plan for intubation to extubation Plan for pain management Plan for post-op monitoring

38 OSA Severity Inpatient vs. Outpatient Regional vs. General Pre-op Nasal CPAP

39 Airway Assessment OSA independent factor for difficult intubation may be as high as 5% Limited jaw protrusion, abnormal neck anatomy, obesity, moderate to severe OSA consider awake intubation Good topicalization, limit sedatives Be prepared

40 Pain Management Regional or local anesthetic technique NSAID Clonidine / Dex IV narcotic, no basal infusion

41 Extubation High risk, 5% post-extubation obstruction Fully reversed, fully awake Semi-upright position Oral or nasal airway Be prepared

42 Monitoring O 2 SAT and close observation post-op in PACU, resume N-CPAP Inpatients continuous pulse oximetry monitoring until stable Outpatients may be discharged if they meet discharge criteria and the surgical acuity dictates

43 Conclusions Increased # and severity Diagnostic challenge Airway management risk Post-op challenge for pain, monitoring and resource management


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