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Tuesday, April 30, 2013


Which is the most common form of apnea? Perhaps the most common apnea,which causes lot of physiological disturbances due to anatomical alteration of body size or tissues, leading to serious pathological changes in body systems, is Obstructive Sleep apnea.Obstructive sleep apnea syndrome occurs when there are repeated episodes of complete or partial blockage of the upper airway during sleep.

During  episodes of sleep apnea,the diaphragm and respiratory muscles including the accessory muscles work hard to overcome the obstruction and the passage of air through the obstructed airway causes noisy breathing or snoring..Thus instead of getting a sound sleep for the victim, he falls into a "SOUND" sleep disturbing his partner or others.Thus due to obstruction the patient gradually stops his respiration momentarily and breathing usually resumes with a loud gasp,snort,or body jerk.These episodes can interfere with sound sleep[1]The physiological and pathological changes occurring in internal organs are due to relative deficiency of oxygen and retention of carbon dioxide. There is accumulating evidence that OSA is being considered as an independent risk factor for hypertension,diabetes mellitus,cardiovascular diseases and stroke, leading to increased cardiometabolic morbidity and mortality.


An apnoea is defined as the complete cessation of airflow for at least 10 sec.There three types of apnoea found clinically are obstructive,central and mixed.The frequency of apnoeas and hypopnoeas hourly is used to assess the severity of the OSAHS and is called the apnoea/hypopnoea index (AHI) or the respiratory disturbance index (RDI)According to the American Academy of SleepMedicine  recommendations,OSA is defined with AHI>5, and it is classified as mild OSA with AHI of 5 to 15;moderate OSA with AHI of 16 to 30; and severe OSA with AHI > 30.[2]

Respiratory effort–related arousal (RERA) is an event characterized by increasing respiratory effort for 10 seconds or longer leading to an arousal from sleep but one that does not fulfill the criteria for a hypopnea or apnea. The criterion standard to measure RERAs is esophageal manometry[12]


    Daytime sleepiness or fatigue
    Headaches on awakening in the morning.
    Poor concentration,Loss of memory, Depression,or Mental irritability
    Dry mouth or sore throat upon awakening
    Night perspiration
    Restlessness during sleep
    Sexual dysfunction
    Sudden awakenings from sleep with a sensation of gasping or choking

  In Children
    Drooling and often choking
    Excessive perspiration at night
    In drawing of the ribs while inspiration
    Learning and behavioral disorders
    Poor attention sleepiness and poor school performance
    Teeth grinding
    Restlessness during sleep
    Pauses or absence, cheyne stokes pattern of breathing
    Unusual sleeping positions, such as sleeping on the hands and knees, or with the neck hyperextended.

Causes of obstruction:

In adults the causes for obstruction include thick or large necks.They may have a relatively smaller airway with edentulous soft tissues where patency is maintained by active contractions of pharyngeal dilators which are depressed with sleep, alcohol, or sedatives.Babies and small children may have sleep apnea that is caused by swollen tonsils or hypertrophy of the uvula and soft palate.A larger than average tongue can also block the airway in many people as well as a deviated septum in the nose.

Risk factors:  

Age: Prevalence is high in the middle aged reaching a plateau by around 60 years.[3].Older people with OSAS are found have increased fat deposition in parapharyngeal area, lengthening of the soft palate,and
changes in body structures surrounding the pharynx.
Sex: OSAS is more common in men than women.
Obesity: BMI >30,Neck circumference more than 44 cm.The upper airway obstruction during sleep is attributed to increasing adiposity around the pharynx and body. Central obesity has been associated with reduction in lung volume,which leads to a loss of caudal traction on the upper airway, and hence, an increase in pharyngeal collapsibility.[4]
Family history and genetic predisposition: More common in first degree relatives of those with OSAS.
Craniofacial anomalies:Congenital or acquired alterations in the upper airway have been identified as risk factors for developing OSAS.Trauma, congenital anomalies like pierre robins syndrome.
Smoking and alcohol consumption: Cigarette smoking and alcohol have been shown to be risk factors for OSAS.Smoking induced airway inflammation is thought to be the causative factor while alcohol relaxes upper airway dilator muscles, increases upper airway resistance and may induce OSA in susceptible subjects


People with sleep apnoea have a smaller pharyngeal airway than do matched controls.Also there will be alteration in bony structure and soft tissue surrounding the lumen.Due to the anatomical compromise,OSAS patients are susceptible to pharyngeal collapse during sleep or anaesthesia.Patients with OSA have increased pharyngeal dilator muscle activity which keep the airway patent during awake.Healthy individuals experience a loss of upper airway muscle tone at sleep onset (alpha-theta transition in the electroencephalogram) and experience some degree of breathing instability, an individual reliant on muscle tone due to an anatomical vulnerability will be particularly susceptible to apnoea when the dilator effect of pharyngeal muscles are lost.[5]Although pharyngeal dilator muscle responsiveness is likely impaired during NREM and REM sleep[6], the genioglossus can respond to both sustained mechanoreceptive (negative pressure) and chemo receptive stimuli, particularly when combined stimuli are present[7] The physiological response to this effect is a raise in CO2 due to respiratory obstruction and raise in negative intrathoracic pressure.The intrathoracic pressure appears to be a potent stimulus for genioglossal activation  and maintaining airway patency.Elevated endexpiratory lung volume may lead to increased caudal traction on the diaphragm which may keep the airway stable and patent.

Thus the sequence is airway obstruction, hypoxia, increase CO2,increased EMG activity causing genioglossus and other pharyngeal muscle activation,negative intrathoracic pressure and chemoreceptor activation causing arousal.The pharyngeal muscle patency may be restored even before arousal.The mechanism of arousal is thought to be activation of parabranchial nucleus of pons due to neurohumoral activation by hypoxia and hypercarbia.A deeper stage of sleep, central nervous system depressants, prior sleep fragmentation, and the presence of obstructive sleep apnea (OSA) have been observed to increase the arousal threshold to airway occlusion.[8]

Systemic effects:

Neurobehavioral and social:  Excessive daytime sleepiness, impaired vigilance, mood disturbances, and cognitive dysfunctions are the features of OSAHS. The sleepiness may interfere with efficiency in work and may worsen interpersonal and social relationships. The sleepiness may be  dangerous when driving and causes increase in road traffic accidents or  injuries when operating machinery. Partners of patients with OSAS experience poor sleep,and will be the first one who takes the patient to a doctor for evaluation of his sleep disorder.[9]
Cardiovascular: The intermittent hypoxia, Chronic hypercarbia, frequent negative intrathoracic pressure variations,and sleep disturbance and arousals lead to increase in blood pressure and lead on to sustained hypertension via chronically heightened sympathetic nervous system activity and arterial baroreceptor dysfunction.Myocardial infarctions are also common.The cerebrovascular system is also affected making the patient prone for CVAs and intracranial hypertension.Cardiac arrhythmias and cor pulmonale are commoner in these patients.[9]
Diabetes mellitus: OSAS is an independent risk factor for development of  Diabetes,associated with insulin resistance,Obesity further increase the risk. Obesity associated changes in pharyngeal muscles may also contribute to OSAS.[9] 
Liver: Hepatic dysfunction marked by  raised liver enzymes,fatty liver and fibrosis are also associated with OSAS [9]

Perioperative and postoperative considerations:

Patients with OSAHS may have increased perioperative risks.There is frequent prevalence of undiagnosed obstructive sleep apnea.Loss of control over airway, inability to mask ventilate, difficulty in intubation, intraoperative hypoxemia,abnormal raise in ETCO2 causing arrhythmias, intraoperative hypertension etc. are the problems anaesthesiologists face.The patients should be taken to OT adequately fasted and after acid aspiration prophylaxis.Fastrach LMA and fiberoptic bronchoscope are ideal for intubation and must be kept ready.It is advised to control the ventilations to match preoperative SPO2 and ETCO2.Spontaneous ventilations with LMA may cause hypoventilation and hypercarbia due to high rate of metabolism and increased thoracic mass.Whenever possible regional anaesthetic techniques or nerve blocks may be tried..Pre operative CPAP may be continued intra operatively also and extubation should be done when neuromuscular block is completely reversed and once the patient is fully conscious,communicative and able to generate adequate tidal volume.Semi sitting position or ramped position may be used to aid extubation, and the ETT may be pulled over a bougie or exchange catheter. Post operative respiratory depression is common and repetitive apnea may occur if the patient is somnolent.Monitor ETCO2 and SPO2 post operatively and if needed RBS and ABG may be performed frequently.Caution should be exercised when prescribing narcotics for post operative pain relief.


 1)A sleep test or polysomnogram( PSG): may be used for confirmation.Sleep testing is performed in a sleep lab and is supervised by a trained technologist. The test will measure various body functions, including:

    Air flow
    Blood oxygen levels
    Breathing patterns
    Electrical activity of the brain
    Eye movements
    Heart rate
    Muscle activity
For more information about polysomnography visit:  http://classes.kumc.edu/cahe/respcared/cybercas/sleepapnea/trenpoly.html

                                                          The plysomnograph, Ref:[10]

                                                               UARS: upper airway resistance syndrome

2)Nocturnal sleep pulse oximetry:  The oxygen desaturation index (ODI) measures the mean number of episodes of oxygen desaturation per estimated sleep hour and is sometimes used as a surrogate for the
3)Epworth sleepiness scale (ESS):  Used to measure excessive day time sleepiness[10].


1) Continuous positive airway pressure: 
Continuous positive airway pressure:(CPAP) is the preferred treatment of choice for OSAHS.[9] The required CPAP is titrated to a level that eliminates snoring, usually 5–20 cm Hg. A randomized placebo-controlled trial showed that CPAP can improve breathing during sleep, sleep quality, blood pressure,vigilance, cognition, and driving ability as well as mood and quality of life in patients with OSAHS.The drug Modafinil is found to be effective in treating OSAS along with CPAP.It was also observed that CPAP therapy improves hypertension usually by about 10mmHg.[11]
2) Mandibular repositioning splint:
Mandibular repositioning splints (MRSs)or oral devices work by holding lower jaw and the tongue forward, thereby increasing the pharyngeal airway.
3) Surgery:
Bariatric surgery is useful and often curative in patients with morbid obesity. Tonsillectomy is highly effective in children. Tracheostomy carries high morbidity and  may be curative but rarely used.[9]. Jaw advancement surgery, especially maxilla-mandibular osteotomy, is effective in patients with retrognathia.Somnoplasty uses radiofrequency energy to tighten the soft palate at the back of the throat.
Nasal surgery may be considered for correction of nasal obstructions, such as a deviated septum.
Uvulopalatopharyngoplasty: A procedure that  increases the width of the airway at the throat by removing soft tissue in the back of the throat and palate.
 Mandibular/maxillary advancement surgery : The procedure involves surgically moving the jaw bone and face bones forward to make more room in the back of the throat, done in severe cases of OSAS and in patient with facial anomalies.
1). http://www.webmd.com/sleep-disorders
2).AASM,Sleep 1999; 21 : 667-89.
3).Young T, Skatrud J. Peppard PE. Risk factors for obstructive sleep apnea in adults. JAMA 2004; 291 : 2013-6.
4).Schwartz AR, Patil SP, Laffan AM, Polotsky V, Schneider H,Smith PL. Obesity and obstructive sleep apnea – pathogenic mechanisms and therapeutic approaches. Proc Am Thorac Soc 2008; 5 : 185-92.
5). Pathophysiology & genetics of obstructive sleep apnoea,Lisa Campana, Danny J. Eckert, Sanjay R. Patel† & Atul Malhotra.Indian J Med Res 131, February 2010, pp 176-187
6).Shea S, Edwards J, White D. Effect of wake-sleep transitions and rapid eye movement sleep on pharyngeal muscle responseto negative pressure in humans. J Physiol 1999; 520 : 897-908.
7).Stanchina ML, Malhotra A, Fogel RB, Ayas N, Edwards JK,Schory K, et al. Genioglossus muscle responsiveness to chemical and mechanical stimuli during non-rapid eye movement sleep.
Am J Respir Crit Care Med 2002; 165 : 945-9.
8).Respiratory arousal from sleep: mechanisms and significance.Berry RB, Bleason, Department of Medicine, Long Beach VA Medical Center, CA, 90822, USA.Sleep1997 Aug;20(8):654-75.
9). GC Mbata and JC Chukwuka1,Obstructive Sleep Apnea Hypopnea Syndrome Ann Med Health Sci Res. 2012 Jan-Jun; 2(1): 74–77.
11)Shiomi T, Sasanabe R, Ohtake K, et al. Cardiovascular complications,Obesity-induced hypertension and obesity heart failure accompanying obstructive sleep apnea. Journal of the Japanese Society of Internal Medicine. 2004;93(6):1114–1119.
Image courtesy:
1.Image header :evelyngarone.wordpress.com 
2. Image on diagnostic criteria and pathophysiology from Advances in Diagnosis and Treatment of Sleep Apnea Syndrome in Japan JMAJ 52(4): 224–230, 2009,Toshiaki and Ryujiro. 
3.The multicolour circular flow chart..http://www.dentonsleepdisorderlab.com/obstructive-sleep-apnea.html

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