Obstructive Sleep Apnea (OSA)
Anesthesia Implications
Anesthesia Implications
Reduced FRC and oxygen reserve – the patient will tend to desaturate much quicker than those without OSA.
Compromised airway patency – anticipate airway obstruction during induction, emergence, and postoperatively. Airway obstruction also creates a high risk for negative pressure pulmonary edema for patients breathing spontaneously.
Without diagnosis – A large percentile of patients with OSA will not be formally diagnosed. Patients exhibiting risks of the condition should be evaluated using the STOP-BANG questionnaire.
High pulmonary hypertension risk – it is estimated that 50% of patients with OHS have pulmonary hypertension
Surgery qualification – in 2012, the Society for Ambulatory Anesthesia (SAMBA) produced a consensus statement that indicates the patient with KNOWN OSA patient could be considered for ambulatory surgery if they were medically optimized and could use CPAP postoperatively. Patients PRESUMED to have OSA could have ambulatory surgery as long as management was performed using a non-opioid approach.
Pathophysiology
Apnea is defined as the cessation of breathing for periods longer than 10 seconds. Collapse of pharyngeal tissues causes apnea. Pharyngeal muscle tone maintains the airway patent during sleep, but as that tone is lost, the patient will begin to snore, which may progress to OSA.
More than 5 incidents of apnea in one hour is indicative of sleep apnea syndrome
Primary risk factors include: Male gender, obesity (BMI > 30), and middle aged. CNS depressants such as alcohol or sleep aids can worsen the problem.
Treatment typically includes using oral appliances, positive pressure to keep the airway patent (CPAP), and oxygen.
Reduced FRC is the result of obesity, the most common cause of OSA.
Cognitive function can be reduced by OSA due to “sleep fragmentation”, or frequent arousal during sleep.
Systemic inflammation is common in these patients. This is triggered by adiopocytokines which are released by adipose tissue.
OSA may progress to Obesity Hypoventilation syndrome (OHS). This syndrome is caused by the body’s tolerance to hypercarbia. Characteristically, these patients fail to make respiratory effort during airway obstruction (known as central sleep apnea).
OHS may further progress to pickwickian syndrome. This syndrome essentially culminates all of the symptoms typically associated with obstructive sleep apnea because it represents the most extreme version of the problem. These include obesity, daytime hypersomnolence, hypoxemia, hypercarbia, polycythemia, respiratory acidosis, pulmonary hypertension, and right ventricular failure.
OSA can be caused by obesity (the primary cause), postpolio syndrome, and midface hypoplasia
OSA can be the causative factor for secondary hypertension and cor pulmonale
OSA is a common disorder in patients with achondroplastic dwarfism and down syndrome
Additional Notes:
Assessments for OSA:
Berlin Questionnaire: An end score of ≥ 2 is a high risk patient for OSA
STOP Questionnaire: Answering yes to 2 or more questions is considered high risk
STOP-BANG Questionnaire: Answering yes to 3 or more questions is considered high risk
Resources:
STOP-BANG questionnaire (The answer of ‘yes’ to 3 or more of the questions below indicates a high risk for OSA) :
Snoring – Can your snoring be heard behind closed doors?
Tired – Do you have daytime sleepiness or fatigue?
Observed Apnea – Has anyone observed you stop breathing?
Blood Pressure – Do you have high blood pressure?
BMI – BMI more than 35?
Age – Older than 50 years?
Neck Circumference – Neck Circumference greater than 40cm?
Gender – male gender?
Hines. Stoelting’s anesthesia and co-existing disease. 7th edition. 2018. p.36, 47, 185, 193, 298, 329, 391, 655
