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									                          Interesting case

   ผู้ป่วยเด็กชายไทย อายุ 3 ปี ภูมิลาเนา อ.เมือง จ.เชียงใหม่
 Chief complaint : นอนกรนมา 1 ปี ก่อนมารพ.

 Present illness              : 1 ปีก่อนมารพ.มีประวัติรับประทาน

อาหารมากขึ้น แม่สังเกตว่าลูกอ้วนขึ้น มีหายใจเสียงดัง

เวลานอน นอนกรน มีหยุดหายใจเป็นช่วงๆประมาณ 4-5

วินาที จากนั้นมีหายใจแรง ไม่เขียว ถ้านอนตะแคงจะดีขึ้น

ไปรพ. แพทย์บอกต่อมทอนซิลโต แนะนาให้ผ่าตัด
Past History

         - เป็นบุตรคนเดียว คลอดปกติครบกาหนด
น้าหนักแรกคลอด3,420 กรัม หลังคลอดพัฒนาการปกติ
         - เป็น G6PD deficiency

Family History

       - มีทวดเป็นเบาหวาน
Physical Examination

Vital Signs : PR 108 , BP 100/55, T 37˚c,RR=32
BW =23.5,Height = 97 cm.

General appearance : A Thai boy look obesity
mild dyspnea ,no cyanosis,noisy breathing

HEENT : not pale conjunctiva,no icteric sclera
        no cyanosis,no neck vein engorged
        tonsil Rt. gr.3 , Lt. gr.4
        LN not palpable

Heart   : PMI at 5th intercostal space,MCL
          regular rhythm,normal s1,s2,no murmur
Lungs : inspiratory stridor
       rhonchi and wheezing both lungs

Abdomen : fatty contour,active bowel sound
          no hepatosplenomegaly,not tender

Extremities : no edema

Airway evaluation : Interincisor gap 3 cm
                      Thyromental distance 5 cm
                     Mallapati class III
                    no craniofacial anormally
                    no micronagthia
                    no retronagthia
                    no loose of teeth
Lab Investigation

1. CBC    Hb = 11.9 , Hct = 35.2 , WBC = 9,700
          Plt. = 460,000

2. U/A   pH 7, = 1.015,alb.-ve,sugar -ve
          WBC -ve, RBC -ve

3. BUN = 19, cr = 0.6, Na = 140, K = 4.0,
   Cl = 104, Total CO2 = 24 , BS = 75

4. PT = 9.8 ( 11.3) , PTT = 30.8 (33.8)
5. LFT    Total protein = 7.9 gm/dL
          Albumin = 4.7 gm/dL
          Globulin = 3.2 gm/dL
          Alkaline Phosphatase = 155 U/L
          Cholesterol = 196 mg/dL
          AST = 43 U/L
          ALT = 59 U/L

6. Lipid Profiles
            Triglyceride = 98 mg/dL
            Choresteral = 195 mg/dL
            HDL = 67 mg/dL
            LDL = 112 mg/dL
            VLDL = 20 mg/dL
            Chylomicron -ve
7. CXR

8. Film lateral neck

9. EKG

         Operation : Adrenotonsillectomy
   Obstructive sleep apnea syndrome

  # Sleep apnea = cessation of air flow at the
    mouth and nose for at least 10 s during

  # Central sleep apnea = no airflow at the
    nose and mouth occurs and there is no
    respiratory movement

  # Obstructive sleep apnea = absence of
    airflow at the mouth and nose despite
    respiratory movement
# Hypopnea = partial upper airway obstruction
  during sleep causing at least a 50%
  reduction in airflow with respiratory

# Mixed sleep apnea = a period of central apnea
  followed by an obstructive apnea episode

Epidemiology of SAS

- Sleep apnea syndrome is a common disorder,
  the estimate prevalence in middle-aged adult
  population = 1-4%

- In children = 0.7-2% ,Thailand = 0.69%
- Most common in children age 2-5 years old.

Pathogenesis & Pathophysiology

- During normal respiration-->genioglossus &
  geniohyoid muscles act as the main muscle
  groups in maintainina pharyngeal airway

- During inspiration-->tone in these muscles
  counteracting intraluminal pharyngeal pressure
  generate by the respiratory pump muscles.
- During sleep--> Force of dilatory muscles

                 negative intraluminal pressure

                 inspiratory collapse
                 of the upper airway

- Obstructive sleep apnea results from
  a narrowing of the airway and occurs as a
  consequence of an anatomical reduction in the
  upper airway or incoordination of upper airway
  dilatory muscle activity.
- When OSA occurs,the site of the obstruction
  can be anywhere from the nasopharynx to the

  1. Anterioposterior displacement of the tongue
     against the posterior pharynx

  2. Posterior displacement of the soft palate by
     the tongue against the posterior pharynx

  3. Opposition of the lateral pharyngeal wall

  4. Circular closure of the pharynx
              Anesthesia                                          Sleep Onset

 Muscle                Decreased Upper                          Decreased CO2
Weakness             Airway Muscle Activity                      Increased O2

  Small                    Upper Airway                      Relief of Obstruction
 Airway                     Narrowing                        Restoration of Airflow

Tonsils and              Obstructive                            Increase Upper
 Adenoids          Hypoventilation And Apnea                 Airway Muscle Activity

                                                               Arousal from Sleep

                                          Increased Ventilatory Effort
Predisposing factors to OSA

Anatomic factors that narrow the upper airway
 # Adenotonsillar hypertrophy
 # Trisomy 21
 # Other genetic or crainofacial syndromes
   associated with
       - Midface hypoplasia
       - Small nasopharynx
       - Micrognathia or retrognathia
       - Choanal atresia or stenosis
       - Macroglossia
       - Cleft palate
 # Obesity
 # Nasal obstruction
   # Laryngomalacia
  # Sickle cell disease
  # Velopharyngeal flap repair

Neurologic factors that decrease pharyngeal
muscle dilator activity

 # Medications--> sedatives or general anesth.
 # Brain stem disorder--> Chiari malformation,
                          birth asphyxia
 # Neuromuscular disease
PRIMARY EVENTS                                        CLINICAL FEATURES

                        Vagal bradycardia
  Sleep onset                                      “Unexplained” nocturnal death
                      Ectopic cardiac beats
                                                      Pulmonary hypertension
    Apnoea         Pulmonary vasoconstriction
                                                         Right heart failure
                    Systemic vasoconstriction          Systemic hypertension
   O2, CO2
      pH           Stimulation of erythropoiesis           Polycythaemia

  Arousal from                                           Excessive daytime
                      Cerebral dysfunction                   Sleepiness
                                                      Intellectual deterioration
                        Loss of deep sleep              Personality changes
 Resumption of         Sleep fragmentation              Behavioral disorders
                     Excessive motor activity              Restless sleep
 Return to sleep
Obstructive sleep apnea                           Increased circulation blood volume
Obesity hypoventilation
                                                       Increased stroke volume

Hypoxia / hypercapnia                                  Increased cardiac output

                                                           LV enlargement

  Pulmonary arterial      RV enlargement
    hypertension          And hypertrophy              Increased LV wall Stress

                                                            Eccentric LV
                             RV failure                                                     Hypertension

                                            LV diastolic                          LV systolic
                                            Dysfunction                           Dysfunction

  Pulmonary venous                                                                          Ischaemic heart
                                                              LV failure
    hypertension                                                                                disease
Clinical features of sleep apnea syndromes
 # Nocturnal events
     - Snoring
     - Restless sleep with frequent movements
     - Sudden arousals with choking or shortness
       of breath
     - Nocturnal awakenings and insomnia
     - Nocturnal enuresis or frequent nocturia
     - Nocturnal sweating
 # Diurnal history
     - Excessive daytime sleepiness
     - personality changes
     - Morning headaches
     - Morning dry throat - Sexual dysfunction

  - Reduced sleep latency by EEG
  - Obesity
  - Hypertension
  - Cardiac dysrhythmias
  - Upper airway abnormalities
  - Pulmonary hypertension
  - RV hypertrophy
  - Cardiomegaly
  - Peripheral edema
  - Polycythemia

1. CBC ---> polycythemia

2. ABG ---> respiratory acidosis + met.alkalosis

3. EKG,CXR --> RV hypertrophy

4. Film lateral neck --> narrowing upper airway

5. Polysomnography ( PSG )

    Apnea Index = จานวนครั้งที่มีการหยุดหายใจต่อ

1. Avoid alcohol,sedatives,sleep deprivation and
   supine sleep posture--> induce or worsen
2. Weight reduction

3. Treat underlying --> surgical correction

4. Application of CPAP

5. Intra-oral appliance
         --> Tongue-retaining device

6. Tracheostomy
Plan of anesthesia

1. Preanesthetic period
     - evaluation
     - preparation
     - premedication

2. Intraoperative management
      - induction
      - intubation
      - maintenance of anesthesia
      - recovery

3. Post anesthetic care
Preanesthetic evaluation
1.Patients history & physical examination
  --> to detemine the ease of mask ventilation
       and tracheal intubation
2.Lab investigation
  --> CBC & Coagulation parameter
  --> CXR
  --> EKG
  --> antibiotic,diuretic
  --> premedication
          - sedative drug
          - antisialagogue
          - preemptive drug
          - prophylactic antiemetic

  - pulse oximeter
  - precordial chest piece
  - capnograph
  - EKG
  - Peek airway pressure
 1. Inhalation induction
      - smooth transition from spontaneous to
        assist ventilation-->ease to management
        of a difficult airway
      - effects of anesthesia reversible if difficult
        in maintaining airway
      - The use of inhalational agents in patient
         with pulmonary hypertension has been
        reported to lower pulmonary arterial
      - un pleasant for the child and result in
        coughing & laryngospasm,especially if
        anticholinergic premedication has not been
- Most inhalation agents have a myocardial
  depressant effect in the high concentrations
  required for induction

- Sevoflurane has smoother and more rapid
  inhalational induction and faster emergence
  compare with halothane

- Nitrous oxide has been reported to produce a
  rise in pulmonary artery pressure
Intravenous induction

 - rapid,does not produce an excitation phase and
   reduces the likelihood of vomiting and
- may be complete loss of upper airway with an
  inability to ventilate the lungs
- if the upper airway becomes obstruct during
  induction can relieve by jaw manipulation,
  the use of an oral or nasal pharygeal airway
  or the use of CPAP
- All anesthetic drug should be titrated to just
  the desire effect,prefer using short acting

 - Tracheal intubation is the prefer option for
adenotonsillectomy and in children with
associate craniofacial abnormalities this can
proove difficult

 - Intubation can be facilitated by using high
concentrations of inhalation agents in the
spontaneously breathing child.

 - Alternatively,a muscle relaxant can be used to
facilitate intubation
     @ suxamethonium => short acting
                       => cardiac arrhythmias
     @ nondepo. => longer onset,duration
               =>prolong ventilate=>regur.
               => if complete airway obstruct.
                   Difficult to reverse

- Awake intubation may be difficult in
  uncooperative child.

- Blind nasal intubation is an alternative
  technique in skill hands.
- The laryngeal mask airway has been used
  successfully in many cases of failed intubation
  and its elective use in ENT surgery is becoming

      LMA ---> no aspiration of blood
          --> one study found recovery to be
               significant better,with less
               airway obstruction when
               compare with tracheal tube
          --> extra vigilance because of the
               danger if it dislodge
Maintenance anesthesia

- Spontaneous or controlled ventilation should
  be used for adenotonsillectomy is controversial
- In the USA advocate control ventilation.
- In the UK advocate spontaneous ventilation

- Nondepolarising Muscle relaxant should be
  used intermediate acting than longer acting

- The use of opioids during anethesia may result
  in respiratory depression,especially in the
  postoperative period.
        ---> should be limited and short-acting
              opioids use
- The use of nitrous oxide and volatile agents
may be beneficial to decrease the amount of
opioids required to maintain anesthesia.

- When pulmonary hypertension is present,
nitrous oxide may cause a marked increase in
pulmonary vascular resistance and pulmonary
arterial pressure

- Perform only in the fully awake alert patient.
- Respiratory monitoring is imperative after
  extubation,and all equipment and personnel
  necessary for airway management must be
  immediately available.
- Extubation in the lateral position,with slight
  head down tilt,will ensure safe drainage of blood
  if rebleeding should occur

Postoperative management
-Positioning--> sitting posture in OSAS+obesity
            --> tonsil position in tonsillectomy
-Oxygen therapy
   prevent early episode desat.-->add 28% O2
   concern that O2 may increase apnea duration
   ---> CO2 retention
   -systemic opioids use with extreme caution
   -NSAIDs ---> caution
CPAP therapy
- Nasal CPAP may also be used to maintain
  pharyngeal patency in patients demonstrating
 recurrent apnea after extubation.


Postoperative nausea and vomiting

Acute postoperative pulmonary edema

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