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OBSTRUCTIVE SLEEP APNEA AND ITS ANAESTHETIC MANAGEMENT

www.anaesthesia.co.in. Dr. Pabitra Biswas MD, PGT drpb2010@gmail.com. OBSTRUCTIVE SLEEP APNEA AND ITS ANAESTHETIC MANAGEMENT. Dept. of Anaesthesiology Calcutta National Medical College and Hospital Kolkata. Definitions.

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OBSTRUCTIVE SLEEP APNEA AND ITS ANAESTHETIC MANAGEMENT

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  1. www.anaesthesia.co.in Dr. Pabitra Biswas MD, PGT drpb2010@gmail.com OBSTRUCTIVE SLEEP APNEA AND ITS ANAESTHETIC MANAGEMENT Dept. of Anaesthesiology Calcutta National Medical College and Hospital Kolkata

  2. Definitions • Apnea is defined as a complete cessation of air flow for more than 10 sec. • Hypopnea is defined as air flow reduction more than 50% for more than 10 sec • Obstructive sleep apnea hypopnea syndrome (OSAHS) may be defined as the coexistence of unexplained day time sleepiness with at least 5 obstructive breathing events (apnea or hypopnea) / hr of sleep .

  3. Obstructive sleep apnoea-complete cessation of airflow during breathing lasting 10 seconds or longer despite maintenance of neuromuscular ventilatory effort and occuring 5 or more time per hour of sleep accompanied by a decrease of at least 4% of SaO2.

  4. Epidemiology • In middle age the prevalence of overt OSA is approximately 4% in men and 2% in women. • It is estimated that 80% of pts. are undiagnosed. • OSA is strongly correlated with obesity, in particular morbid obesity (BMI > 40kg/m2 or a BMI > 35kg/m2 with significant comorbidities). • OSA is found in 40% of obese females and 50% of obese males

  5. Obese • BMI – 32.4-35 (women) 31.2-35 (men) • Severe obesity: • BMI 35-40 • Morbid obesity • BMI – 40-50 • Super obesity - > 50 • BMI – weight in kg / height in meter2

  6. Predisposing Condition • OBESITY • Age more than 50 years • Male gender • Neck circumference more than 40 cm • Nasal/pharyngeal/laryngeal obstruction • Craniofacial abnormalities (such as Down syndrome, micrognathia and achondroplasia) • Neuromuscular disorders • Use of alcohol, sedatives and cigarettes

  7. Pathophysiology • Apnea occurs when pharyngeal airways collapse • Pharyngeal airways collapse when there is decrease tone of the pharyngeal dilator muscles (genioglossus and geniohyoideus) • This occurs during REM sleep • In obese patients increased adipose tissue in the neck and pharyngeal tissues narrows the airway further, predisposing to airway closure during sleep • In non-obese patients tonsilor hypertrophy or craniofacial skeletal abnormalities may lead to airway narrowing and sleep apnea

  8. Pathophysiology • In OSA patients neural control mechanism generating pharyngeal dilator muscle tone are active in the awake state to overcome the relatively smaller upper airway. • Sleep & anesthesia substantially attenuate pharyngeal dilator muscle activity. • It is this combination of anatomical structure and neural compensatory mechanism that is responsible for development of OSA. • With airway obstruction inspiratory efforts increase as arterial oxygen desaturation progresses, leading to partial arousal from sleep & a sudden opening of airway • A short period of hyperventilation follows until sleep deep ens and airway obstruction recurs, repeating the cycle

  9. Physiological Changes • Arterial hypoxemia • Arterial hypercarbia • Polycythemia • Systemic hypertension • Cardiac rhythm disturbance • Right ventricular failure • There is an increased incidence of heart disease, cerebrovascular events and sudden death

  10. Signs and Symptoms • Excessive sleepiness during the day • Poor concentration • Fatigue • Increased risk of accident • Snoring

  11. Differential Diagnosis • Insufficient sleep • Shift work • Psychological causes • Drugs • Narcolepsy • Idiopathic hypersomnolence

  12. Diagnosis • Sleep history • Epworth sleepiness score > 11 • Polysomnographic examination • Physical assessment of obesity, jaw structure, upper airway and blood pressure

  13. Diagnosis

  14. Polysomnography - It is a sleep study during which the patients electro encephalogram, electromyogram, electroocculogram,, electrocardiogram, capnogram, nasal or oral pulse oximetry and room noise are typically monitored or recorded • The results are recorded as Apnea Hypopnea Index • It is derived from the total no of episodes of apnea or hypopnea divided by the total sleep time • Mild OSAHS – 5-15 per hr • Moderate OSAHS 15-30 per hr • Severe OSAHS more than 30 per hr • Arousal index (AI) – no of arousals per hr • Respiratory disturbance index (RDI) = AHI + AI

  15. Whom to treat • There is evidence obtained from randomized controlled trial (RCT) that treatment improves symptoms, sleepiness, driving, cognition, mood, quality of life and blood pressure in patients who have an Epworth score of more than 11, trouble some sleepiness while driving or working and > 15 apneas and hypopneas per hr of sleep

  16. Treatment • Continuous positive airway pressure (CPAP). CPAP therapy works by blowing the airway open during sleep usually with pressures of 5-20 cmHg. CPAP has been shown in randomized placebo controlled trials to improve breathing during sleep as well as sleep quality. Positive airway pressure is delivered through a nasal mask and is the initial treatment of choice of clinically significant obstructive sleep apnea • Mandibular repositioning splint - MRS work by holding the lower jaw and tongue forward thereby widening the pharyngeal air way

  17. Treatment • The use of drugs to treat obstructive sleep apnea has not shown to be reliably affective. • Surgical treatment of OSA include tracheostomy, laser assisted palatal surgery and maxillofacial surgical procedures (Genioglossal advancement).

  18. OBESITY AND CHANGES IN C.V.S.

  19. OBESITY AND CHANGES IN RESPIRATORY SYSTEM

  20. Obesity associated system wise comorbid conditions • RESPIRATORY SYSTEM- • Dyspnoea • Obstructive sleep apnoea. • Obesity hypoventilation syndrome. • CARDIOVASCULAR SYSTEM- • Hypertension of pregnancy. • Congestive heart failure. • Thromboembolic manifestations. • Pulmonary embolism. • MUSCULOSKELETAL SYSTEM- • Low back pain. • Immobility. • Osteoarthritis of knees and hips. • GASTROINTESTINAL SYSTEM- • Reflux disease, fatty liver, cholelithiasis, hernias, cancer • ENDOCRINE- Type 2 diabetes, dyslipidemia, P.C.O.D.

  21. Airway Assessment • Routine parameters • Mallampati classification • Temperomandibular joint assessment with inter incisor distance • Mentohyaoid distance • Dentition • Parameters specific for OSAHS and obesity • Pretracheal adipose tissue thickness • Circumference • Hypertrophic tonsils and adenoids

  22. Anticipated Difficult Intubation • Pretracheal adipose tissue > 1 inch (2.5 cm) at the level of the vocal cords as determined by USG • Neck circumference • > 40 cm - 5% chance of difficult intubation • > 60 cm – 35% chance of difficult intubation • Obligate mouth breathers – Adenotonsillar hypertrophy

  23. Preoperative Investigation • Hemoglobin • TC, DC, Platelet count • FBS • PPBS • Urea, Creatinine • CXR (PA View) • ECG • Consultation with cardiologist and pulmonologists (echo, spirometry and liver function test may be needed • Polysomnography in heavy snorers

  24. Assessment of potential vascular access sites.

  25. Cuff size for blood pressure. • Unless the length of the cuff exceeds the circumference of the arm by 20% the SBP and DBP may over estimate the true blood pressure. • Direct arterial blood pressure measurement may be useful. • Intra arterial catheter can perform repeated blood gas sampling .

  26. Operating table and position. • It is difficult to lift the patient from the trolley to the OT table. • Selection of appropriate sized OT table is very important. • Ramp position is widely accepted for intubating obese patients. • This position aligns the oral, pharyngeal and tracheal axis and frees the mandible to accommodate the tongue. • Nowadays electronic TABLE RAMP is used in many operating tables.

  27. Proper padding is to be applied on the pressure points as because prolonged surgery might lead to tissue necrosis and sepsis.

  28. MONITORING • 1.Pulse rate • 2.Oxygen saturation • 3.NIBP • 4.Arterial blood pressure in selected cases. • 5.ECG • 6.Capnograph. • 7.Neuromuscular monitor. • 8.CVP and PCWP monitoring used very infrequently due to technical difficulties in placing these lines.

  29. REGIONAL ANESTHESIA • Epidural or spinal anaesthesia is safe and feasible in patients with large body habitus. • Technically more difficult. • Tendency of the catheter to migrate out of the epidural space. • Longer needle and ultra sound probe may be needed. • Smaller epidural space in obese, so there will be increased cephalad spread of the drug. So dose should be adjusted accordingly.

  30. Preoxygenation • Studies have shown that the rate of development of hypoxemia in patients during apnea, was faster in obese patients than in patients with normal BMI. • THIS CAN BE DELAYED BY: • Pre oxygenation with 30 degree head up position. • Use of 10cm.water CPAP during pre oxygenation in the supine position. • Mask application of PEEP/mechanical ventilation after induction.

  31. Difficult Bag Mask Ventilation • B earded individuals. • O besity(BMI>26). • N o teeth. • E lderly(age>55). • S norers.

  32. PRE ANESTHETIC MEDICATION • Benzodiazepines and opioids to be avoided as much as possible. • Glycopyrrolate 5 microgm. per kg as anti secretory agent. • Dexmedetomidine 1 microgm. per kg for 10 mins. Then 0.2-0.7 microgm.per kg per hour as sedative, anxiolytic, analgesic. It can also blunt stress response to intubation.

  33. Recognised difficult airway • Inhalational agents. • Laryngoscopy. • If grade 1 or 2,administer short acting muscle relaxant and intubate. • If grade 3 or 4,awaken the patient and go for awake intubation. Awake intubation Asleep intubation

  34. Maintainance

  35. INHALATIONAL AGENTS Inhalational agents should be 1.Insoluble. 2.Resistant to metabolic degradation. 3.Without lipid depot compartmentalization. 4.Rapid return of airway reflexes. Blood Gas Solubility Coefficient of different agents: 1. Nitrous Oxide-0.46 2. Desflurane-0.45 3. Sevoflurane-0.65 4. Isoflurane-1.40

  36. DESFLURANE • Quickest wake up. • Fastest return of airway reflexes. • Lowest solubility as measured by the blood gas solubility coefficient. • Lowest percentage of hepatometabolisation • However ,pungency of the agent is unpleasant for the patient. • When more than 6%inspired Desflurane is administered, it can cause breath holding, coughing or laryngospasm.

  37. SEVOFLURANE • Blood gas solubility coefficient is very near to Desflurane.. • So causes prompt induction,rapid recovery. • Non pungent,does not cause airway irritatio unlike Desflurane. • Liver microsomal enzymes P-450 metabolisesSevoflurane at a rate 25 times that of Des. • Potential nephrotoxicity of the principal degradation product(Compound-A) always remains. • HEPATOMETABOLISATION: • DESFLURANE-0.02% • ISOFLURANE-0.02% • SEVOFLURANE-5%

  38. INTRAVENOUS AGENTS • It should be lipophobic or hydrophilic. • It should spontaneously degrade in vivo. • It should preferably be ultra short acting.

  39. INTRAVENOUS AGENTS

  40. ANALGESIA • OPIOIDS decrease both hypoxic and hypercapnic ventilatory responses. • Possible impairment of sequential neural control mechanism during OSA and failure or delay of pharyngeal opening. • Incidence and significance of hypoxemic episodes related to postoperative OPIOID infusion and respiratory obstruction is documented. • However adequate analgesia in a major surgery is often difficult to achieve without the use of OPIOID.

  41. OPIOIDS-BETTER TO AVOID Pharmacokinetics of Opioid analgesics.

  42. MULTIMODAL ANALGESIA • Epidural analgesia(preferably without opioid supplementation) • NMDA receptor blockade with KETAMINE. • TRAMADOL • PARACETAMOL INFUSION • CLONIDINE. • GABAPENTIN. • Titration of a short acting OPIOID such as half normal dose Remifentanyl using Patient Controlled Analgesia technique. and administering it under supervision with continuous oxygen.

  43. The challenge is to monitor and adjust medications for maximum safety,not to eliminate them at the expense of pain

  44. Extubation Tracheal extubation must not be considered until patients are fully conscious with intact upper airway reflexes and undertaken only under controlled conditions in a monitored environment

  45. Post Operative Complications • Post anaesthetic hypoxemia • Respiratory depression • Early ventilatory failure • Positional ventilatory collapse • Hemodynamic instability • Post operative nausea and vomiting • Venous thromboembolism

  46. Post Anaesthesia Care • Adequate analgesia • Early ambulation is encouraged • Chest physical ambulation & effective coughing is encouraged • Supplementary oxygen at 300 head up position for 24-72 hrs • CPAP or BIPAP • Continuous pulse oximetry and respiration monitoring

  47. Post Anaesthesia Monitoring • ASA recommend OSA patients should be monitored for 3 hrs longer than usual before being discharge from a facility • Monitoring should continue for at least 7 hrs after the last airway obstruction or hypoxemic episodes

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