1. Child with “OSA”
Anesthetic Considerations
BY
Eid Ali Gumaa
Assist. Professor of Anesthesia
Faculty of Medicine
Zagazig University
2013
2. Milestones
1837: Charles Dickens, in the
Posthumous Papers of the Pickwick Club,
described an obese boy named Joe with
excessive daytime somnolence.
Joe has become the prototype of the obesity-
hypoventilation syndrome, and probably
suffered from obstructive sleep apnea.
1918: Sir William Osler, was
subsequently coined the word „Pickwickian‟ to
describe such obese, hypersomnolent
patients.
1928: Berger, Human EEG alpha waves.
1937: Loomis, EEG Sleep stages described.
3. Milestones
1965: Gastaut et al. documented the
presence of repetitive obstructive apneas
during polysomnographic recording of an
obese Pickwickian patient.
The link between obesity, hypoventilation,
daytime somnolence, and upper airway
obstruction was now established.
1972: Guilleminault – coined the term
OSA.
1990: International Classification of Sleep
Disorders.
4. What is Sleep?
“a reversible behavioral state of
perceptual disengagement from and
unresponsiveness to the environment”
75% in Non-REM sleep
25% REM sleep –muscle atonia,
autonomic activation
5. NREM sleep:
Normal muscle tone
Regular respiration
Four stages of NREM sleep based on
EEG
Stage 1-small amplitude high
frequency waves resembling awake
state
Stage 4-large amplitude and lowest
frequency waves approaching REM
6. REM sleep:
Rapid eye movements.
Generalized hypotonia of muscles.
Irregular rate and depth of respiration.
Marked suppression of hypothalamic
regulation of homeostasis.
8. Definitions:
OSAS: describe a person with specific
symptoms and signs (daytime sleepiness,
cognitive dysfunction, snoring,
hypertension, and a narrow upper airway),
and a polysomnogram showing upper
airway obstruction.
associated symptoms have frequently been
described, including gastro-esophageal
reflux, nocturnal or unusually enuresis,
abnormal motor activity, and sweating
during sleep.
9. Definitions (Continue):
Apnea is cessation of airflow >10 sec,
ends in arousal
OSA- apnea with continued
respiratory efforts
Hypopnea –reduction in airflow of
50% with 4% desaturation, ends in
arousal
Apnea / Hypopnea Index (AHI)
10. Syndromes:
OSAS: AHI >5/ h. on polysomnography.
UARS: AHI <5/ h., excessive daytime
somnolence, elevated intra-thoracic
pressure
Primary Snoring: no polysomnogram
abnormalities
12. OSA severity scoring
Severe OSAModerate OSAMild OSA
Mouth breathing,
markedly increased
respiratory effort, loud
snoring and „snorting‟,
disrupted sleep
Mouth breathing with
moderate increase in
respiratory effort, +/-
snoring or „snorting‟,
restless sleep
Mouth breathing, slight
increased respiratory
effort, +/- snoring,
sleeps quietly at night
Clinical signs
Frequent prolonged
episodes of paradoxical
breathing, frequent
prolonged desaturation
Normal baseline SpO2,
repeated desaturation
to mid 80s
SpO2 in normal limits,
+/- minor dips
Sleep study
correlate
18. Upper airway resistance syndrome:
A group of children with:
Symptoms of (OSAS) excessive daytime somnolence but
Without polygraphic apnea and hypopneas.
Rather repeated central nervous system arousals, during
sleep
However, these children were found to have increased
respiratory efforts during sleep.
Using esophageal manometry as a measure of respiratory
effort, it was noted that such arousals were preceded
by increased respiratory effort.
19. The typical presentation of UARS
patients:
Daytime somnolence,
Not obese,
May or may not snore,
But typically has a narrowed upper
airway anatomy.
particularlyhypotension,Of interest,
postural hypotension, seems to be a
common finding in such patients, in
contrast to OSAS where hypertension is
the usual finding.
20. Clinical assessment:
Diagnosis may be wrong in 50 % cases
Loud snoring + witnessed apneas
identified OSAHS with sensitivity 78%
and specificity 67%
Neck circumference <37cm , >48 cm
are associated with low and high risk
of OSA
Obesity (BMI>30) independent risk
factor but ~ 50% cases are not obese
23. Obstructive apnea: Complete cessation of
airflow despite efforts to breathe
Desaturation
Obstructive apnea
Respiratory paradox
Snore
24. Hypopnea:Reduction in airflow compared
to baseline, associated with desaturation:
Desaturation
Hypopnea
Progressively increasing
respiratory effort
25. Pediatric OSAS:
2% of children
Boys = Girls
Peak at age 2:5 years
Peak OSA =Peak ATH
26. Pediatric OSAS:
Snoring- severity not predictive
Many are mouth breathers (Adenoid
facies 15% have OSA)
Excessive daytime sleepiness
Obesity Vs. Fatty
Increased respiratory effort
27. Pediatric OSAS:
Impaired growth
* Possible impairment of release or end-
organ response to GH
* Increased caloric effort with respiration
* Difficulty with eating
Cor pulmonal
Associated with GERD
28. Clinical features of OSA in children and adults
ObesityAdenotonsillar hypertrophy
Craniofacial disorders
Chromosomal abnormalities
Hypotonia
Causes
ObeseFailure to thriveWeight
CommonUncommonDaytime sleepiness
Cognitive impairment
Poor vigilance
Hyperactive
Poor school performance
Secondary enuresis
Neurobehavioural
Adults and Children
Type II OSA
Children
Type I OSA
Clinical features
Middle age2-6 yearsPeak age
Male>>femaleMale=femaleGender
29. Anesthesia Considerations:
High rate of comorbidity (COPD, CAD,
etc)
Pre-op. CPAP/BiPAP
Short, obese neck / retrognathia –
setup for disaster unless prepared
Post-op. HTN
Post-obstructive pulmonary edema
30. Anesthesia Considerations:
Identification of children at high risk for
complications after adenotonsillectomy
Age < 3 years or Weight < 15 Kg.
Severe OSA
Failure to thrive
Cardiac complications
Obesity
Prematurity
Recent URTI
Craniofacial abnormalities
31. Anesthesia Considerations:
Children with OSA with a cold should be
postponed for 4 weeks.
Children with signs and symptoms
suggestive of severe OSA with cardiac
involvement need to be assessed by a
cardiologist prior to surgery
The improvement is not immediate, but
children are dramatically improved in
the weeks after surgery.
33. Induction:
May be gaseous or intravenous, depending
on the child and the preference of the
anesthetist.
Immediately after induction” with the loss
of pharyngeal tone “ airway almost
obstruct & may be relieved by jaw thrust
and the application of CPAP.
As soon as the child is deep enough an oral
airway should be inserted and effectively
relieves the obstruction.
34. Induction (Continue):
Children with severe micrognathia (expected will
not be easy to intubate) a cautious gas
induction is sensible in this situation.
Intubation and electively ventilation of children
with severe OSA, usually using a short acting
non-depolarising NMBDs.
Intubation under deep anesthesia without muscle
relaxant is unwise in this situation.
Suxamethonium should be used if non depolarising
agents are not available.
35. Maintenance& Recovery:
Children with severe OSA have been
estimated to require 50% less opioid than
normal children due to increased opioid
sensitivity.
Analgesia should be carefully titrated to effect,
Simple analgesics should be used.
Awake Extubation at the end of surgery.
Opioid analgesia should be kept to a minimum
in the postoperative period.
Insertion of a nasopharyngeal prong airway
(NP airway) for these children at the end of
surgery
36. Postoperative:
Airway obstruction is not relieved immediately after
surgery in children undergoing adenotonsillectomy for
severe OSA. This is mainly due to edema and swelling
at the operation site, which improves in the first 24-
48 hours after surgery.
The child is nursed on the high dependency area (HAD)
with the NP airway in position for the first night at
least – it is very important to regularly do suction the
airway with soft suction catheter.
Careful overnight observation, using saturation
monitoring as part of routine monitoring on the ward /
HAD , but do not administer oxygen to those with
severe OSA unless required.
