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Obstructive sleep apnea(OSA) syndrome

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... syndrome Sleep apnea Sleep apnea OSAS in children Obesity and obstructive sleep apnea in children Neuromotor factors Clinical features Complications ... – PowerPoint PPT presentation

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Title: Obstructive sleep apnea(OSA) syndrome


1
Obstructive sleep apnea(OSA) syndrome
  • V.S.???/CR???
  • Ri ???/???/???

2
Basic Data of the Patient
  • Name ?O?
  • Chart No. 5055863
  • Age 5 y/o
  • Gender Male
  • Body height 110 cm
  • Body Weight 22 kg

3
Chief Complaint
  • Restlessness during sleeping for several months

4
Brief Hx-1
  • This 5-year-old boy who was situs inversus with
    dextrocardia and valve insufficiency diagnosed at
    VGH had been suffering from snoring for several
    months.
  • There was no daytime somnolence and sleep awake.
  • He visited our podiatrist OPD and polysomnography
    was arranged. He was admitted for operation this
    time.

5
Brief Hx-2
  • The AHI was 6.9 per hour.
  • He was referred to our OPD for further
    evaluation. Local examination revealed bilateral
    hypertrophy tonsils and skull lateral view showed
    adenoid hypertrophy. Surgical intervention was
    suggested and his family accepted. He was
    admitted for operation this time.

6
Past History
  • 1. Situs inversus with dextrocardia and valve
    insufficiency, DM(-), HTN(-)
  • 2. Drug allergy NKDA
  • 3. Smoking denied
  • Drinking denied
  • Betel nut denied
  • 4. frequent UTI/URI

7
PE
  • Vital sign stable
  • Grade IIIII enlargement tonsils

8
Hemogram/BCS/PT/PTT
  • WBC 5.88 K/µL
  • RBC 4.06 M/µL
  • HB 11.8 g/dL
  • HCT 34.7
  • MCV 85.5 fL
  • MCH 29.1 pg
  • MCHC 34.0 g/dL
  • PLT 398.0 K/µL
  • RDW-CV 11.9
  • D-BIL 0.15 mg/dL
  • Alb 4.6 g/dL
  • T-BIL 0.67 mg/dL
  • AST 27 U/L
  • ALT 17 U/L
  • ALP 253 U/L
  • LDH 478 U/L
  • UN 10.0 mg/dL
  • CRE 0.5 mg/dL
  • Na 137 mmol/L
  • K 4.0 mmol/L
  • Cl 106 mmol/L
  • PT/PTT 11.0/34.1

9
Heart Echo 97/2/29
  • 2-D/Dopplar Findings1.Detro-position of the
    heart2.No chamber enlargement.3.LVEF 624.No
    intracardia anomaly.5.Mild TR, PG 16mmHg6.R't
    aortic arch. No CoA. No PDA.

10
Polysomnography (This April)
  • Lowest oxygen saturation 90
  • AHI 6.9 /hr.
  • Obstructive apnea 3.0 /hr.
  • Hypopnea 3.9 /hr.

11
Diagnosis
  • 1. Obstructive sleep apnea syndrome
  • 2. Adenoid vegetation
  • 3. Situs inversus with dextrocardia

12
Anesthesia (GA)
  • OP method UPPP
  • Pre-anesthesia evaluation ASA class II
  • Induction Atropine(0.2mg) Ketamine(455mg)
    Nimbex(3mg)
  • Maintenance Sevoflurane
  • IVF Lactic Ringer 200 c.c.
  • Recovery Atropine(0.4mg) Vagostin(1.9mg)

13
Post-OP (in recovery room)
  • Nausea/Vomiting Nil
  • Headache Nil
  • Sore throat Nil
  • Wound pain (Bain 1/3 amp)
  • Other complication Nil

14
Obstructive sleep apnea(OSAS) syndrome
15
Sleep apnea
  • Cessation or reduction in respiratory airflow ?
    abnormal gas exchange?hypoxemia and hypercapnia
  • Repetitive arousals caused by apneas and
    hypopneas ?sleep fragmentation and the loss of
    restorative sleep
  • Apnea cessation of air flow ? 10 seconds
  • Hypopnea airflow?of 25 or 50 and an oxygen
    saturation ?34
  • Apnea-hypopnea Index (AHI) Number of apneas and
    hypopneas per hour of total sleep time
  • Disease-defining therashold no consensus, AHI?5

16
Sleep apnea
  • Obstructive An event with absence of airflow
    but with continued respiratory effort
  • Central An event with absence of airflow and no
    respiratory effort
  • Mixed An event with characteristics of an
    obstructive and mixed event. These events
    typically start with a period that meets the
    criteria for a central event but will end with
    respiratory effort without airflow

17
OSAS in children
18
Obesity and obstructive sleep apnea in children
  • Redline et al obesity ( BMI? 28) was the
    strongest predictor of sleep-disordered
    breathing, 1/3 obese children abnormal PSG.
  • Deposition of adipose tissue (muscle and soft
    tissue)gt external compression
  • Increased chest wall and abdominal massgt reduced
    lung volumes

19
Neuromotor factors
  • Factors suggest neuromotor dactors
  • 1. obstruction while sleeping
  • 2. persisted OSAS after adenotonsillectomy
  • 3. recurrence during adolescence after
    adenotonsillectomy
  • 4. smaller pharynx, but stiffer, less
    collapsible
  • Reduced centrally mediated activation of their
    upper-airway musclesgt collapsibility ?

20
Clinical features
  • Snoring, labored breathing, paradoxical
    respiratory effort, observed apnea, restlessness,
    sweating, unusual sleep positions and enuresis
  • Normal height and weight or obesity, failure to
    thrive and developmental delay
  • Tonsillar hypertrophy (adenoids correlate with
    the severity of OSAS on PSG)

21
Complications
  • Chronic nocturnal hypoxemia and sleep
    fregmentation
  • Growth impairment, decreased growth hormone
    (growth spurt after adenotonsillectomy)
  • Cardiovascular pulmonary hypertension, cor
    pulmonale, and heart failure
  • Neurocognitive deficits, learning problems,
    behavioral problems, attention deficit
    hyperactivity

22
Evaluation
  • Gold standard polysomnography(PSG)
  • PSG differentiate between primary snoring and
    OSAS has lower functional residual capacity and
    higher respiratory rate?desaturate with
    relatively short apnea ?apneas lt 10-second may be
    significant
  • Degree of PSG abnormalities that produce sequelae
    is yet unclear

23
Surgical treatment
  • Adenotonsillectomy is the mainstay of treatment
    for OSAS .
  • Down syndrome or obesity tend to improve after
    adenotonsillectomy, although additional treatment
    may sometimes be needed.
  • Uvulopalatopharyngoplasty, a tongue reduction,or
    a craniofacial reconstruction has also been used
    in selected cases.
  • Tracheostomy

24
Medical treatment
  • When Surgery is contraindication or failure.
  • CPAP
  • BiPAP
  • Supplemental oxygen has been shown to improve
    oxygenation in patients with OSAS, it does not
    alter the increased work of breathing
  • Few individuals develop a marked rise in their
    Pco2 in response to supplemental oxygen

25
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26
Preanesthesia evaluation
  • History
  • CXR ,EKG , Cardiac echo if needed
  • VBG
  • In most cases, OSAS is considered a chronic
    health condition and warrants a classification of
    ASA II.
  • Children who experience respiratory failure that
    requires mechanical ventilatory support and those
    who have severe anatomical malformationsof the
    airway or morbid neurologic disease may be
    classified as ASA III
  • or IV.

27
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28
Intraoperative anesthetic plan
  • Those children will present with exacerbation of
    obstructed breathing and apnea when under the
    affects of anesthesia.
  • Children with OSAS show an exaggeration of the
    blunted respiratory drive in response to opioid
    and BZD administration
  • and are at risk for airway obstruction
  • Presedation with opioids or benzodiazepines or
    both before surgery should be used with
    appropriate preoperative monitoring

29
Intraoperative anesthetic plan
  • A neuromuscular blockade for children with OSAS
    is often used to facilitate endotracheal
    intubation with an oral RAE endotracheal tube.
  • Skilled clinicians and the equipment for managing
    a difficult airway, such as a fiber-optic
    laryngoscope as well as a laryngeal mask airway,
    also should be readily available.

30
Intraoperative anesthetic plan
  • the two person ventilation method and laryngeal
    mask airway are reported to be helpful in adult
    with OSAS .
  • The jaw thrust to treat airway obstruction in
    these patients is the most useful and is superior
    to the chin lift.
  • Antireflux medications and antisialagogue drugs
    are important adjuncts to consider for the
    prevention of aspiration and laryngospasm in the
  • OSAS population

31
Intraoperative monitoring
  • Continuous EKG , end-tidal gas, and carbon
    dioxide concentrations, pulse oximetry and
    temperature.
  • A-line is rarely needed.

32
extubation
  • Deep extubation is not suitable because the
    child with OSAS will be less likely to breath
    spontaneously and maintain airway patency
  • while under the residual effects of
    anesthesia.
  • Children with OSAS are extubated when they are
    fully awake and demonstrating markers of airway
    muscle control such as age-appropriate
    respiratory rate without assisted ventilation in
    OR or ICU.

33
Postoperative care
  • Children with severe OSAS or cardiovascular
    disease or those who are recovering from
  • airway or craniofacial surgery should be
    monitored after surgery in the pediatric
  • intensive care unit.
  • Patients who do not experience respiratory
    compromise during the initial recovery phase
    still may require continued monitoring because
    obstructive apnea may recur along with the return
    of REM sleep on postanesthesia day 2 or 3.

34
Respiratory support
  • The use of supplemental oxygen during recovery
    from anesthesia in the child with OSAS is
    controversial.
  • Hyperoxygenation can mask hypoventilation, making
    it difficult to determine the severity of
    postoperative apnea.
  • Children who experience postanesthetic hypoxemia
    should be evaluated first for pulmonary edema,
    atelectasis, and pneumonia.

35
Pain management
  • Opioid analgesics will further depress
    respiratory drive and relax the pharyngeal
    dilator muscles, must be used judiciously during
    the postoperative period.
  • Acetaminophen seems to be the safest choice as
    either a narcotic-sparing or a primary analgesic,
    with limited risk of bleeding or airway compromise

36
Conclusion
  • Preanesthesia evaluation is important.
  • Opioid is relative contraindication.
  • Jaw thurst position with RAE endo tube is better
    choice.
  • Postanesthesia monitoring with adequate
    respiratory support helps patients a lot.

37
References
  • Obstructive Sleep Apnea Syndrome in Children,
    Preetam Bandla, MD, Anesthesiology Clin N Am 23
    (2005) 535 549
  • Demographics and Diagnosis of Obstructive Sleep
    Apnea, Tracey Stierer, MDa,, Naresh M. Punjabi,
    MD, PhD, Anesthesiology Clin N Am 23 (2005) 405
    420
  • Anaesthesia and sleep apnoea, J.A. Loadsman nad
    D.R.Hillman, British Journal of Anaesthesia
    86(2) 254-66(2001)
  • Millers anesthesia, 6th ed.
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