child with osa anesthetic considerations

Child with “OSA”Anesthetic Considerations

BY

Eid Ali GumaaAssist. Professor of Anesthesia

Faculty of Medicine

Zagazig University

2013

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.

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.

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

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

REM sleep:

Rapid eye movements.

Generalized hypotonia of muscles.

Irregular rate and depth of respiration.

Marked suppression of hypothalamic regulation of homeostasis.

Sleep Disordered Breathing:

Sleep-Disordered Breathing (SDB):

Obstructive Sleep Apnea Syndrome (OSAS)

–Obstructive Sleep Hypopnea Syndrome (OSHS)

–Upper Airway Resistance Syndrome (UARS)

Heavy Snorers Disease (HSD):

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.

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)

Syndromes:

OSAS: AHI >5/ h. on polysomnography.

UARS: AHI <5/ h., excessive daytime somnolence, elevated intra-thoracic pressure

Primary Snoring: no polysomnogram abnormalities

OSAS:

AHI SaO2 (%)

Mild 5–20 >85

Moderate 21–40 65–84

Severe >40 <65

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 dipsSleep study correlate

Control of Airway Patency:

Pathophysiology

Anatomy-Obesity

–Nasal Obstruction

–Pharyngeal Obstruction

Jaw

Tongue

Palate

Physiology–Failure of dilator muscles

–Excessive intra-thoracic pressure

Consequences of OSAS:

Hypertension

Ischemic heart disease

Myocardial dysfunction & arrhythmias

Cerebro-vascular disease

Mood, neurocognitive, behavioral

–Increased industrial/traffic accidents

Increased mortality.

Consequences of OSAS:

Consequences of OSAS:

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.

The typical presentation of UARS patients:

Daytime somnolence,

Not obese,

May or may not snore,

But typically has a narrowed upper airway anatomy.

particularly hypotension,Of interest, postural hypotension, seems to be a common finding in such patients, in contrast to OSAS where hypertension is the usual finding.

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

Polysomnography:

EEG

EOG

EMG

ECG

Oronasal airflow

Pulse oximetry

Respiratory efforts

Snoring

Position

Leg movements

Normal Sleep Study:

Obstructive apnea: Complete cessation of airflow despite efforts to breathe

Desaturation

Obstructive apnea

Respiratory paradox

Snore

Hypopnea:Reduction in airflow compared to baseline, associated with desaturation:

Desaturation

Hypopnea

Progressively increasing respiratory effort

Pediatric OSAS:

2% of children

Boys = Girls

Peak at age 2:5 years

Peak OSA =Peak ATH

Pediatric OSAS:

Snoring- severity not predictive

Many are mouth breathers (Adenoid facies 15% have OSA)

Excessive daytime sleepiness

Obesity Vs. Fatty

Increased respiratory effort

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

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

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

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

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.

Premedication:

Sedative premedication should be avoided for children with OSA.

Parents to accompany the child to the anaesthetic room to reduce the child‟s

anxiety.

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.

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.

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

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.

Thank you………….