The obstructive sleep apnea and anesthesia is a multidimensional problem.The literature indicates that disastrous respiratory outcomes during the perioperative management of patients with OSA are a major and increasing problem for the anesthesia community.The disastrous outcomes are due to failure to secure the airway during the induction of anesthesia,respiratory obstruction soon after extubation and respiratory arrest after the postoperative administration of opiods  to extubated patients.The growing  OSA management problem is almost certainly fueled by the the growing obesity epidemic.Failure to manage  the intubation, extubation and pain of patients with OSA often results in brain damage or death.

PREOPERATIVE EVALUATION:
Preoperative evaluation of a patient for potential identification of OSA includes (1) medical record review, (2) patient/family interview and screening protocol, and (3) physical examination.

            Pertinent patient characteristics associated with OSA  may be available in medical records, such as hypertension, history of stroke, history of myocardial infarction, diabetes mellitus, or abnormal cephalometric measurements. Certain congenital conditions (e.g., Down syndrome, acromegaly) and disease states (e.g., euromuscular disease, cerebral palsy) may also be associated with OSA.

Patient/Family Interview and Screening Protocol :
The patient and family interview should include focused questions related to snoring,apneic episodes, frequent arousals during sleep (e.g., vocalization,shifting position, and extremity movements), morning headaches, and daytime somnolence.
The STOPB-ang questionnaire developed by the ASA to help anaesthetists recognize patients at risk from OSA.If three or more points are positive,OSA is likely
S-Snoring (observed during sleep)
T-Tiredness  (in the daytime)
O-Observed (sleep disordered breathing by sleeping partner)
P-Pressure (hypertension)
B-Body mass index (greater than 35 kg/m)  
a-age (above 50 years)
n-neck(collar size greater than 16.5 inches)
g- gender (male)
ASA,American Society of Anaesthesologists; OSA ,obstructive sleep apnoea.

 A physical examination should include an evaluation of the airway, nasopharyngeal characteristics,neck circumference, tonsil size, and tongue volume. If any characteristics noted during the preoperative evaluation suggest that the patient has OSA, the anesthesiologist and surgeon should jointly decide whether to (1) manage the patient perioperatively based on clinical criteria alone or (2) obtain sleep studies,conduct a more extensive airway examination, and initiate indicated OSA treatment in advance of surgery.

The gold standard for OSA diagnosis is polysomnog- raphy (PSG), which reports an apnea-hypopnea index (AHI) as a measure of severity of disease. OSA is defined by PSG as the occurrence of at least 5 episodes of apnea or hypopnea in 1 hour, or an AHI of 5. Moderate and severe OSA is defined as an AHI greater than 15 and 30, respectively.

The apnea-hypopnea index is an index used to indicate the severity of sleep apnea. It is represented by the number of apnea and hypopnea events per hour of sleep. The apneas must last for atleast 10 seconds and are associated with decrease in blood oxygenation. AHI is calculated by dividing the number of apnea events by the number of hours of sleep.
Normal 0-4
Mild Sleep apnea 5-14
Moderate Sleep apnea 15-29
Severe Sleep apnea 30 or more
Preoperative initiation of CPAP should be considered, particularly if OSA is severe. For patients who do not respond adequately to CPAP, NIPPV should be considered. In addition,the  reoperative use of mandibular advancement devices or oral appliances and preoperative weight loss should be considered when feasible.

INTRAOPERATIVE MANAGEMENT:
Intraoperative concerns in patients at increased perioperative risk from OSA include (1) choice of anesthesia technique,(2) airway management, and (3) patient monitoring.
Virtually all IV and volatile anesthetic agents act as respiratory depressants and muscle relaxants. Therefore, it is prudent to minimize the use of these agents within the parameters of safe anesthetic practice. The anes- thetic technique should prevent intraoperative aware ness, maintain hemodynamic stability, and provide a quiet operative field and optimal postoperative pain con- trol while ensuring the smallest overall cumulative anes- thetic dose.

The use of a short-acting sedative, induction agents, and volatile anesthetics can be helpful. However, the practitioner must keep in mind that the termination of the clinical action of agents such as midazolam, fen tanyl, propofol, and even sevoflurane and desflurane, is based on redistribution of the agent from rapidly per- fused tissues rather than by metabolism of the drugs. The use of high doses of these agents may result in a significant tissue concentration that is only slowly cleared from the body, resulting in prolonged sedation.

Because opioids have the strongest respiratory depressant effect of all anesthetic agents, the use of remifentanil, which is rapidly metabolized by blood and tissue esterases, may be preferred over other relatively short-acting alternatives. The sedative dexmedetomi dine has a narcotic-sparing effect, causes minimal respiratory depression, and may be a useful adjunctive agent.

The potential for postoperative respiratory compromise should be considered in selecting intraoperative medications. General anesthesia with a secure airway is preferable. Unless there is a medical or surgical contraindication, patients at increased perioperative risk from OSA should be extubated while awake. Full reversal of neuromuscular block should be verified before extubation.

POSTOPERATIVE MANAGEMENT:
The primary challenge during the immediate post-operative period in the postanesthesia care unit (PACU) is the balance between pain control and adequate res- piration. The initial use of short-acting IV narcotics for rapid pain control must ultimately shift to the use of longer-acting IV narcotics. If appropriate, non- narcotic analgesics such as ketorolac should be used early in the course of PACU treatment.During the titration of pain control, the PACU staff should carefully observe the patient for respiratory events such as bradypnea, apnea, arterial oxygen desaturation, inability to wean from supplemental oxy- gen, and pain-sedation mismatch (ie, concurrent high pain and sedation scores.

Risk factors for postoperative respiratory depression may include the underlying severity of the sleep apnea, systemic administration of opioids, use of sedatives, site and invasiveness of urgical procedure, and the potential for apnea during rapid eye movement (REM) sleep on the third or fourth postoperative day (i.e., “REM rebound”), as sleep patterns are reestablished. Postoperative interventions to manage OSA patients who may be susceptible to the above risks include the topics of (1) postoperative analgesia, (2) oxygenation, (3) patient positioning,and (4) monitoring.Supplemental oxygen should be administered continuously to all patients who are at increased perioperative risk from OSA until they are able to maintain their baseline oxygen saturation while breathing room air.

CPAP or NIPPV (with or without supplemental oxygen)should be continuously administered postoperatively to patients who were using these modalities preoperatively, unless contraindicated by the surgical procedure. patients at increased perioperative risk from OSA should be placed in nonsupine positions throughout the recovery process.OSA should have continuous pulse oximetry monitoring.Frequent or severe airway obstruction or hypoxemia occurs during postoperative monitoring, initiation of nasal CPAP or NIPPV should be considered.

UVULOPALATOPHARYNGOPLASTY:
Oropharyngeal obstruction Obstruction at the level of the soft palate, pharynx, and tonsillar ordermany of the surgical procedures traditionally labelled phase I therapies. The goals of surgery here are to expand and open the oropharyngeal airway and to remove obstructing or redundant tissue leading to a reduction in the resistance to airflow. Uvulopalatopharyngoplasty (UPPP), initiallydescribed by Fujita & collegues10-12, is used to correct obstruction at the oropharyngeal level by modification of the uvula, removal of redundant pharyngeal and palatal tissue, and primary closure of the posterior and anterior pillars to enlarge the retropalatal airway. Numerous experts have subsequently attempted to modify the initial procedure, with proposed changes aimed at enlarging the pharynx and reducing the redundancy and collapsibility of hypopharyngeal tissues. These modifications include complete removal of the uvula and distal soft palate, removal of part of the palatopharyngeus muscle and the use of an uvulopalatal flap13-20.Laser also has been used to reduce the vertical height of the uvula or remove the elongated or enlarged tissues in the oropharynx. Kamami, a French surgeon,first described laser-assisted uvulopalatoplasty (LAUP) in the 1980s to reduce the uvula and distal portion of the soft palate without total excision of the muscle uvulus21. A laser was used to vaporize the uvula and a specified portion of the palate in a series of small procedures. He suggested that scar contracture would lead to a reduction in the redundancy of the soft palate andlto dilatory effect on the pharynx.

OBSTRUCTIVE SLEEP APNEA:
Worldwide,obstructive sleep apnoea(OSA) is the most common medical disorder of sleep,affecting 4-5% of middle aged men and 2-4% of middle aged woman. Anesthetists are frequently involved with patients presenting either for surgergy to treat the condition itself ,or for unrelated surgery.

Airway obstruction may arise from a number of discrete anatomical features in the upper airway but, in the absence of abnormal anatomy, it is relaxation of the genio- and pharyngeal constrictor muscles during sleep that allows collapse of the airway. There is evidence that these muscles are hypertonic during wakefulness, unmasking fatigue during sleep with excessive relaxation. Physical associations with OSA include being male, a collar size of 17 inches (43 cm) or greater, a wide tongue base and often some degree of retro-ghathia. The association with a high body mass index (BMI) means that these patients are potentially difficult to intubate. Medical associations include hypothyroidism, acromegaly glycogen storage diseases, whereas congenital causes include Down’s syndrome, Pierre-Robin sequence and other facial anomalies. Obstruction from hypertrophied tonsils should always be considered.             There is now good evidence that OSA is associated with the development of metabolic syndrome.

            Physiologically, there is mounting evidence that cyclical alterations in arterial oxygen saturation caused by OSA lead to hypoxia/reperfusion injury. This causes excessive release of oxygen radicals, which outstrips the ability of naturally occurring intracellular anti-oxidants with consequent lipid peroxidation in the cell membrane. There is evidence that this leads to cellular damage and the development of endothelial damage and atheroma formation. Thus, recurrent night-time hypoxaemia can lead to several cardiovascular complications, including arterial and pulmonary hypertension, cor pulmonale and an increased incidence of heart disease and cerebrovascular events.

            To meet the criteria for diagnosis of OSA, complete obstruction of the airway should occur repeatedly during sleep for more than 10 seconds in the presence of the continued movement of the diaphragm, leading to a reduction of more than 4% in arterial oxygen saturation (SaO2) from the baseline. Attempted inspiration becomes more vigorous as arterial oxygen desaturation progresses, finally leading to partial arousal from sleep with sudden reopening of the airway. This causes an explosive intake of breath, which is usually accompanied by some movement of the body or twitching of the limbs as partial arousal from sleep occurs. Hyperventilation follows for a short time, but as sleep deepens again airway obstruction returns, causing the cycle to restart. The worst cases may have up to 60 of these cycles per hour (apnoea index) giving 400-500 episodes in a sleep period of 8 hours, with each dip in oxygen saturation as low as 60%.

CLINICAL PRESENTATION:
The symptoms of snoring, apnoea and Excessive Daytime Sleepiness usually lead to consultations.

            A full examination of the upper airway should be undertaken with attention to the collar size, mallampati score, dental occlusion and pharyngeal volume. Tonsillar hypertrophy should be recorded because this may be the underlying problem. Any retrognathia should be recorded. The tongue may have crenulations at the side-small indentations on the lateral borders made by the teeth-which indicate that it is being squeezed inwards and backwards into the pharyngeal space when the mouth is closed. The pharyngeal volume is often reduced with reduntant mucosal folds limiting the lateral diameter.

            Ability to sublux the jaw forwards should be measured because  good degrees of movement of greater than 5mm may allow treatment with mandibular advancement devices rather continuous positive airway pressure devices.

Investigations:
Investigations include blood tests to exclude other causes of EDS such as hypothyroidism and narcolepsy, but the diagnosis is readily confirmed by carrying out a sleep study called a polysomnogram. Full polysomnography includes monitoring of the chest movement, airflow dynamics, heart rate and blood pressure, arterial oxygen saturation and the electroencephalogram(EEG), all during sleep. EEG monitoring is used to assess the stage of sleep (stages I, II, III, IV non-rapid eye movement (NREM), or REM sleep).

Treatment of OSA:
The gold standard treatment for OSA is to submit the patient to nasal continuous positive airway pressure (nCPAP) while asleep. Throughout the breathing cycle, CPAP is applied to the pharynx to overcome the obstructive forces due to pharyngeal collapse. CPAP is best initiated in hospital for one night under supervision while the correct level of airway pressure measured in centimeters of water (cmH2O) is set for the individual, although there are now machines that detect reduced airflow and adjust the pressure automatically. While the pressure energy, should be high enough to overcome the pharyngeal collapse, it should not be so high as to reach the lower airway and raise the functional residual capacity, because this in itself disrupts sleep. Pressure requirements range from as low as 5 cm H2O to as high as 15-20 cm H2O depending on severity.

            Although the most noticeable effect of nCPAP is to reduce daytime sleepiness, physiological benefits also occur. Hypertensive patients treated with nCPAP show a beneficial reduction in both systolic diastolic blood pressure, the effect of which appears to increase with time.  Some patients can be treated for mild OSA with mandibular advancement devices, which posture the mandible forwards, pulling the tongue away from the posterior pharyngeal wall via the suprahyoid muscles.

            More recently, radiofrequency coagulation of the palate (somnoplasty) and ablation of the base of the tongue have been used with some success in the treatment of palatal snoring, having replaced the unpleasant operation of uvulopalatopharyngplasty (UPPP).

            Select patients may benefit from bimaxillary osteotomy which advances the mid-face and mandible to increase space in the nasopharynx and oropharynx.