SLEEP APNEU

R3
 INTRODUCTION
Obstructive sleep apnea (OSA) is a sleep-related breathing disorder
that involves periodic, partial or complete upper airway obstruction
despite an ongoing effort to breathe.
It is caused by the repetitive collapse or partial collapse of the
pharyngeal airway during sleep. This leads to apneas (complete
obstruction of the airway), hypopneas (partial obstruction leading to
desaturation) and respiratory effort-related arousals (RERAs partial
obstruction leading to arousal but no significant desaturation).
The prevalence of OSA is estimated to be 2% in women and 4% in men
 INTRODUCTION
The severity of the disease is determined by the number of these respiratory
events per hour, known as the RDI or respiratory disturbance index.
Central sleep apnea is a condition in which the brain's respiratory control center
is imbalanced during sleep. The brain does not respond to changing levels of
carbon dioxide.
During periods of apnea there is no effort to breathe, no chest wall movement
and no obstruction during pauses.
Central sleep apnea may be caused by conditions such as heart failure and
stroke.
OSA leads to disturbed sleep and possible daytime sleepiness. Consequently,
patients can be a danger to themselves and others, particularly if driving
More serious long-term consequences include:
a rise in sympathetic tone,
ischemic heart disease,
Hypertension (increased levels of catecholamines)
tachyarrhythmias,
deterioration in cognitive function,
pulmonary hypertension, cor pulmonale,
congestive heart failure,
cardiovascular accident/stroke and
sudden death.
These sequelae are the result of the physiologic consequences of the respiratory events
According to the National Commission on Sleep Disorders
Research, there are 38 000 cardiovascular deaths per year in the
United States secondary to OSA.

Untreated, the 15-year mortality for adults with severe OSA is

30%.

OSA in itself is associated with an increase in postoperative

complications and is an independent risk factor for increased
morbidity and mortality
Clinical features that suggest the presence of OSA include
increased neck circumference (> 17 inches in men > 16 inches
in women), body mass index 30 kg/m2, Mallampati score of 3 or
4, retrognathia, macroglossia, tonsillar hypertrophy, enlarged
uvula, high narrow hard palate, and/or nasal abnormalities

Continuous positive airway pressure (CPAP) is considered the

first line of treatment for patients with OSA; however, surgery
may be considered if this treatment is not tolerated
 DIAGNOSIS
OSA is diagnosed by clinical history and an overnight sleep study or
polysomnography (PSG). OSA is suspected by the occurrence of daytime
sleepiness, loud snoring, witnessed breathing interruptions or
awakenings due to gasping or choking.

Polysomnography includes monitoring of chest wall movement, airflow

dynamics, heart rate, blood pressure, arterial oxygen saturation,
electroencephalogram, electrooculogram, and chin electromyogram
during sleep
Obstructive events are recorded as apnea hypopnea index (AHI) or
respiratory disturbance index (RDI).
OSA is confirmed if the number of RDIs is >15 events per hour or greater
than five events per hour in a patient who also reports unintentional
sleep episodes during waking hours, daytime sleepiness, un-refreshing
sleep, fatigue, insomnia, waking up, breath-holding, gasping, choking, or
bed-partner description of snoring and breathing interruptions.
OSA is classified as mild, moderate or severe based on the respiratory
disturbance index.
Mild: RDI 514
Moderate: RDI 1529
Severe: RDI>30
 MEDICAL TREATMENT
Positive airway pressure (PAP) is considered the first line of treatment for
patients with OSA. PAP treatment attempts to maintain a competent
airway
through the application of continuous positive airway pressure (CPAP),
bi-level positive pressure (BiPAP) or auto-titrating positive pressure
(APAP).
It can be applied via the oral, nasal or oronasal route. PAP is the
treatment of choice for all severities of OSA. PAP has the potential to
reduce cardiac dysrhythmias, stabilize blood pressure, and improve
hemodynamics.
Behavioral treatment used in the treatment of OSA includes
weight loss, positional therapy, and avoidance of sedatives and
alcohol at bedtime
 SURGICAL TREATMENT

Patients turn to surgical correction in an attempt to find acure. Surgery

may be considered in patients who have obstructing anatomy that is
surgically correctable or when PAP or OA are inadequate or poorly
tolerated.
It may also be considered as an adjunct when obstructive anatomy
compromises other therapies
Indications for surgery depend on the severity of the sleep apnea,
symptoms, and comorbid conditions, and the anatomical location of the
obstruction.
Patients should be counseled on the surgical options, goals, risk,
benefits, and possible complications.
Surgical success has been defined as an AHI less than 20/h
and a reduction of the AHI by 50% or more after surgery.
Surgical cure is defined as AHI <5/h
 ANESTHETIC MANAGEMENT OF A PATIENT
UNDERGOING OSA

Preoperative management
Optimal care begins with a tailored preoperative assessment to aid
patient risk stratification and optimization
Preoperative history and physical exam
A thorough history and physical exam should be obtained evaluating all
of the patients' disease processes and co-morbidities. Patients with OSA
are more likely to have the comorbidities listed
 AIRWAY ASSESSMENT

Patients with OSA may be difficult to intubate or ventilate.

The upper airway abnormalities which lead to OSA can be the same
abnormalities which lead to a difficult airway. Snoring and OSA were
found to be independent risk factors for difficult mask ventilation.
Difficult intubation was found to occur eight times more often in
OSA patients than in control patients.

The patient should be educated regarding the possibility of an awake

intubation.
ASPIRATION PROPHYLAXIS AND PREOPERATIVE
SEDATION

Obese patients, due to their high intraabdominal pressure, larger gastric

fluid volume and lower gastric pH, may be at risk of aspiration.
Consideration should be given to aspiration prophylaxis with antacid,
proton pump inhibitor, and esophageal motility stimulant prior to
induction.
Unsupervised preoperative sedation should be avoided. OSA patients are
at higher risk of obstruction and apnea after the administration of
sedatives. If sedatives are to be given, it should only be done in a
monitored environment.
 CHOICE OF ANESTHETIC TECHNIQUE
General anesthesia with a secured, intubated airway is preferable
because of the risk of aspiration of blood from the surgical site and
the patient's likelihood of obstruction when sedated.
Anesthesia can be maintained using total IV anesthesia such as a
propofol infusion, due to its quick onset and offset. A short-acting
narcotic infusion such as remifentanil or alfentanil may also be used.
Insoluble anesthetic agents such as desflurane, which are more
quickly eliminated when discontinued, should be considered for
maintenance of anesthesia.
 Although controversial, systemic steroids may reduce airway
edema and can be given prior to surgery and several times
postoperatively.
Dexamethasone, 1015 mg, is given every 612 hours.
Antibiotics prevent infection-induced edema and may be
administered perioperatively
 POSTOPERATIVE MANAGEMENT

Analgesia
it is best to minimize opioids and sedatives, which may
suppress respiratory drive and lead to life-threatening hypoxia.
Mild pain can be treated with oral opioids, acetaminophen or
tramadol, best given in the liquid form.
 REFERENSI

Abdelmalak,Doyle. 2013. Anesthesia for Otolaryngologic Surgery

Cambridge Medicine.
THE END