Obstructive Sleep Apnea & UPPP Overview

Obstructive Sleep Apnea (OSA)

• OSA is recurrent upper airway obstruction during sleep, causing hypoxia and hypercarbia.
• OSA increases risk of cardiovascular, neuropsychological, and endocrine problems, and reduced quality of life.
• Significant underdiagnosis; up to 93% of women and 82% of men with moderate-severe OSA remain undiagnosed. Prevalence in the US is estimated at 2% for women and 4% for men. Surveys suggest a much higher potential risk, with 21% of women and 31% of men potentially at risk.
• OSA increases perioperative risk due to difficult intubation, coexisting conditions, and life-threatening apnea. OSA patients are at increased risk of postoperative respiratory complications, including severe oxygen desaturation.
• OSA is associated with significant morbidity, due to chronic, frequent upper airway obstruction during sleep leading to hypoxia and hypercarbia.
• OSA is a syndrome with periodic, partial or complete upper airway obstruction during sleep, resulting in episodes of apnea-hypopnea, frequent arousals, oxygen desaturation, and daytime hypersomnolence.
• Apnea is cessation of airflow for >10 seconds with effort to breathe. Hypopnea is abnormal respiration with at least 30% reduction in airflow or thoracoabdominal movement for ≥10 seconds and 4% oxygen desaturation.
• Polysomnography diagnoses OSA, with severity based on the Apnea-Hypopnea Index (AHI). Higher arousal index, lower SaO2, and reduced slow-wave sleep are common in OSA patients.
• Typical OSA patient profile: loud snorer, BMI ≥35 kg/m², age ~50, neck circumference ~17 inches, and male.
• Pathophysiology is multifactorial, involving upper airway anatomy, motor control, ventilatory control, and arousal threshold.
• Upper airway segments (nasopharynx, oropharynx, hypopharynx) vulnerable to collapse due to lack of bony support.
• Pharyngeal dilator muscles (tensor palatini, genioglossus, hyoid) maintain airway patency during wakefulness. Muscle tone loss during sleep (NREM and REM) contributes to airway collapse.
• Obesity contributes to OSA by increasing fat deposition (uvula, tonsils, tongue, etc.) obstructing the airway.
• Poor upper airway motor control during sleep, muscle damage, further worsen obstruction.
• Ventilation instability (increases/decreases in respiratory output) impacts pharyngeal dilator muscles and, alongside fat deposition, contributes to obstruction.
• Apnea, hypoxemia, and hypercarbia trigger increased respiratory effort, neural stimulation, arousals, vocalization, extremity twitching, turning, gasping, or snorting.
• Hyperventilation after obstruction can lower CO2, reducing respiratory drive and contributing to subsequent apnea.
• Repeated obstruction-hypoxemia-hypercarbia cycles cause sleep fragmentation, sympathetic hyperactivity, inflammation (higher CRP and interleukin-6), endothelial dysfunction, and metabolic dysregulation, increasing cardiovascular, neuropsychological, and endocrine risks.
• OSA affects cardiovascular (hypertension, left ventricular failure, arrhythmias, nocturnal angina, MI), cerebrovascular (CVD, stroke), pulmonary (pulmonary hypertension, right-sided heart failure), neuropsychological (daytime somnolence, impaired cognition, accidents, depression, anxiety), and endocrine (obesity, glucose intolerance, diabetes, decreased testosterone, growth hormone) systems.

Uvulopalatopharyngoplasty (UPPP)

• Perioperative risk is determined by OSA severity, surgery invasiveness, and postoperative opioid needs.
• Anesthetic management for UPPP involves identifying and managing potentially difficult airways.
• Close monitoring is essential for airway obstruction and bleeding.
• Careful titration of postoperative opioids is crucial.
• Preoperative Period
  • Preoperative evaluation is crucial, including history, physical exam (airway focus), STOP-BANG, review of systems for coexisting conditions, difficult intubation factors, prior anesthetic issues.
  • Preoperative testing (ECG, stress test, chest X-ray, electrolytes, CBC, coagulation panel), sleep study review (or moderate OSA assumption if no study). CPAP settings and instructions. Inpatient/outpatient suitability, monitoring based on OSA severity, comorbidities, anesthetic type, opioid needs, age.
• Perioperative Risk Prediction (using ASA Practice Guidelines for OSA)
  • Severity of OSA (none = 0, mild = 1, moderate = 2, severe = 3; subtract 1 if CPAP pre/postop; add 11 if PaCO2 >50 mmHg)
  • Invasiveness of surgery (superficial = 0, moderate sedation/general = 1, peripheral spinal/epidural =1, airway/major general = 2, 3)
  • Postoperative opioid needs (none = 0, low dose oral = 1, high dose = 3)
  • A + B + C = Overall risk score (0-6). Score of 4 = potentially increased risk; 5 or 6 = significantly increased risk.
  • Examples (as provided).

Postoperative Complications of UPPP

• Respiratory (1.1% to 11%): laryngospasm, postobstructive pulmonary edema, airway obstruction and oxygen desaturation, emergent tracheotomy, reintubation, pneumonia.
• Hemorrhage (0.3% to 14%): immediate or several days later.
• Hypertension (2% to 70%).
• Cardiovascular (0.3%): arrhythmias, cardiac arrest, angina, MI, cerebrovascular accident, pulmonary embolism.

Postoperative Management of Severe OSA after UPPP

• Anesthetic considerations: decreasing postoperative pain, ensuring adequate oxygenation, observing for airway obstruction, positioning patient laterally or semi-recumbent, CPAP resumption.
• Severe OSA Patients: High risk for opioid-induced airway obstruction, requiring close monitoring in a recovery room, and ideally in an intensive care unit for at least 24 hours.
• Pain Management: Nonsteroidal antiinflammatory drugs (opioid-sparing effect) should be considered.
• Oxygenation: Supplemental oxygen and continuous pulse oximetry. Maintain baseline or 90% O2 saturation.
• Positioning: Lateral or semi-recumbent.
• CPAP: Restart CPAP postoperatively

Awake Fiber-Optic Intubation Procedure

• Discuss need for awake fiber-optic intubation with patient and surgical team.
• Obtain IV access and administer 0.2 mg glycopyrrolate IV.
• Prepare difficult airway cart with fiber-optic bronchoscope, atomizer, nebulizer, nasal trumpets, viscous lidocaine/lubricant, Ovassapian and Williams airways, oxygen/suction, applicators, bag-valve mask, and additional intubation equipment.
• Verify bronchoscope function, practice scope rotations.
• Topicalize airway: 4% lidocaine atomizer/nebulizer, 5% lidocaine ointment, Neo-Synephrine spray/lidocaine for nasal intubation, and local anesthetic nerve blocks (glossopharyngeal and superior laryngeal).
• Oral intubation with Williams/Ovassapian airway to keep scope midline, or pass ETT past the scope for nasal intubation.
• Inject additional lidocaine onto vocal cords via scope side port or perform transtracheal injection to block recurrent laryngeal nerve.
• Suction and oxygen as needed with scope.
• Observe vocal cords (pull scope back if pink tissue seen). Jaw thrust or cricoid pressure for better visualization.
• Pass scope through cords, advance avoiding carina. Slide ETT over scope; if resistance, rotate ETT 90° counterclockwise.
• Confirm placement, induce general anesthesia.