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Sandeep Rai*, Kiran V Birari**, Madhur Rai***
 

Abstract

Snoring is not just annoying but could indicate a serious health problem. Many deaths among people in their 40s and older, attributed to heart diseases or road traffic accidents may actually be related to unseen epidemic of snoring and sleep apnoea. If the sleep is disturbed repeatedly by loud snoring, choking in breathing and the person experiences excessive day time tiredness and sleepiness, and then one might be suffering from “Obstructive sleep apnoea syndrome (OSA)” and there could be a danger of losing one’s health, years of productivity and may be life also.

Most patients of OSA are overweight and have a short thick neck and small receding jaw. Because these patients are unaware of repeated arousals during sleep, this condition remains largely undiagnosed. It is a cause of severe cardiovascular morbidity including angina, MI, stroke, arrhythmias and sudden death. Polysomnography is a gold standard for diagnosing this condition. Treatment includes lifestyle changes (weight reduction), CPAP, dental devices that modify position of tongue and jaw and surgical procedures in selected patients. CPAP treatment has proved to be most effective for OSA.

Introduction

OSA is defined as periods of apnoea (cessation of breathing for longer than 10 seconds) or hypopnoea (reduction but not complete cessation of airflow to less than 50% of normal) that occurs throughout sleep.

OSA is overdue for public attention; it is the second leading cause of day time fatigue, after insomnia. Poor sleep caused by sleep apnoea is a major public health problem. Each night lakhs of men over 40 and women after menopause wage a life and death struggle with this little recognized illness. By world statistics nearly 30%-40% of the population snores at any given time. Two international studies have independently shown that 9% of asymptomatic females and 24% of asymptomatic males qualify for the basic criterion of OSA. A total of 2-4% of the population over age of 30 years suffers from significant OSA.1 Thus we might be having nearly 2-4 crores sufferers of OSA in our country, thus making it a major health problem.

There are terrible costs for the family of the person with sleep apnoea syndrome who may experience irritability, mood changes, lowered sexual drive and capacity and a reduction of intellectual ability. Effective medical treatment to overcome this epidemic is available.

The syndrome strikes both sexes, all age groups, all races, socioeconomic strata and ethnic groups. It is less recognized in females before menopause, the reason is being that women are generally silent snorers but suffer from all the effects of snoring. After menopause the prevalence is almost same as in males and females.

Prevalence increases with age, peaking at approximately 60 yrs: obesity is major risk factor for OSA and a 10% increase in weight leads to a six fold risk of developing OSA.2 Other risk factors for OSA include male sex and abnormalities in craniofacial morphology. Frequent alcohol use has been considered a risk factor since it depresses the central respiratory drive and enhances muscle relaxation.3,4

Patients with OSA can present with conditions such as hypertension, CAD, stroke, heart failure, cognitive dysfunctions including multiinfarct dementia,

Pathophysiology

Snoring is just a sign that the upper airway caliber has narrowed to a critical degree and this causes air to speed up as it passes through narrowed area, creating turbulence and noise. If the narrowing becomes too severe it promotes closure of the airway, resulting in apnoea. The collapse occurs in the nose and/or the throat- anywhere from where air enters the nostrils to the back of the tongue. Frequently, this airway collapsibility problem is inherited and starts in childhood. Patients with this disorder are most often overweight, with associated peripharyngeal infiltration of fat or increased size of soft palate and tongue. In daytime it is not a problem because there is a good muscle tone in the airway and the brain monitors breathing. But at night the throat muscles become relaxed and the brain is not as attentive to the airway. So on inspiration the airway walls either completely collapse or significantly narrow. This is a problem because 1) the body must struggle to breathe and 2) the brain has to ‘wake up’ to reopen the airway.

Physiological Changes during OSA

Cyclical oxygen desaturation occurs with each pause in breathing that stimulates arousal from sleep. In REM sleep, muscle tone is most relaxed and apnoea episodes are prolonged with severe desaturation, often 60-70% lower than normal. Following each apnoeic episode a surge of sympathetic activity occurs, stimulating transient increase in blood pressure and heart rate. Over a period of time cardiac hypertrophy, arrhythmias and cor pulmonale can result.

Untreated OSA has been strongly implicated in contributing to cardiovascular morbidity by increasing risk of atherosclerosis, ischaemia and strokes.5 The proposed mechanism is increased levels of oxidative stress that contributes to excess free radical production, soluble adhesion molecules6,7 and decreased levels of nitric oxide (NO), a potent vasodilator.5 Apart from cardiovascular damage, cerebral oxygenation and blood flow is hampered by repeated episodes of apnoea/hypopnoea.8 Nitric oxide suppression triggers vasoconstriction, elevates blood pressure and decreases oxygen supply to vital organs like heart and brain tissue. Excess free radicals add to this insult and cause excessive damage to these organs.

Multiple arousals with sleep fragmentation are likely causes of excessive day time sleepiness in patients of OSA.11 In fact patients with sleep apnoea can wake up more than 30 times an hour, and think that they slept uninterrupted through the night. Since sleep must be continuous and consolidated in order to be restorative, a number of cognitive problems can occur with sleep fragmentation: daytime sleepiness, memory problems, concentration difficulties, emotional instability, irritability, slowed reaction time, nocturnal panic attacks.

Due to poor understanding and knowledge about OSA among general public and even the medical practitioners at large this remains widely undiagnosed and thus untreated condition.

OSA and motor vehicular accidents

Patients of OSA perform poorly on driving simulator tests and have 2-7% greater risk of motor vehicle accidents (MVA) caused by driver sleepiness, fatigue and inattention.9 Upto 21% patients who present in casualty with MVA have undiagnosed OSA.9 Emergency department staff should be aware of seriousness of OSA and screen MVA patients for this condition.

The NASA Ames Centre and U.S.Department of transportation warn of the danger of fatigue in the transportation industry, including travel on the highway, in the air, and by sea. Sleep apnoea is a very common cause of daytime sleepiness and the worst hit one third of people with untreated sleep apnoea has an increased auto crash rate and consequent fatalities.10

When should sleep apnoea be suspected?

For many sleep apnoea patients their spouses are the first ones to suspect that something is wrong usually from their heavy snoring and apparent struggle to breathe. Co-workers or friends of the sleep apnoea victim may notice that the individual falls asleep during the day at inappropriate times (such as while driving a car, working or talking.11 The patient also complains of being tired in the morning. The patient often does not know he or she has a problem and may not believe it when told. It is important that a person sees a doctor for evaluation of the sleep problem.

On physical examination most patients with OSA are overweight typically have short thick necks, in fact a neck circumference more than 17 inches in a man correlates with increased risk of this disorder.12 Facial abnormalities may be recognized in patients of OSA. These include small receding chin, small mandible, a large tongue, receding jaw with 2 mm or more of lower lip protrusion may be an obvious finding in some patients of OSA.13 Throat examination may reveal enlarged uvula or tonsillar hypertrophy.12 An elongated soft palate which rests on base of tongue is another cause of airway obstruction seen sometimes.

Diagnosis

OSA can easily be diagnosed by an overnight sleep study in a specialized sleep laboratory or at the home of the patient (home monitoring). Diagnosis of sleep and several tests are available for evaluating a person for sleep apnoea.

Polysomnography (SLEEP STUDY) is the gold standard for diagnosing OSA. It is a technique that records multiple functions during sleep such as the electrical activity of the brain, eye movements muscle activity, heart rate, respiratory efforts, airflow and blood oxygen levels. These tests are used for both to diagnose sleep apnoea and to determine its severity. A diagnosis of mild, moderate or severe OSA is based on one of the three classification criterion: an Apnoea index( number of apnoeic episodes per hour of sleep-more than 5, more than 15, or more than 30); an Apnoea/hypopnoea index, or a Respiratory disturbance index (5-15, 16-30 or more than 30 disturbances).13,14 Typically, a respiratory disturbance index (RDI) is calculated and expressed as the number of abnormal respiratory events per hour of sleep: an RDI of 20 episodes per hour is a cut off point to consider CPAP treatment for OSA, although degree of symptoms is important regardless of RDA score.

The multiple sleep latency test (MSLT) measures the speed of falling asleep. In this test, patients are given several opportunities to fall asleep during the course of the day when they normally are awake. For each opportunity, time to fall asleep is measured. People without sleep problems usually take an average of 10-20 minutes to fall asleep. Individuals who fall asleep in less than 5 minutes are likely to require treatment for sleep disorders. The MSLT may be useful to measure the degree of excessive daytime sleepiness and to rule out other types of sleep disorders. The diagnostic tests are usually performed in the hospital, but now new technology is allowing sleep studies to be conducted at home also, but studies conducted at home do not measure as many physiological parameters as formal laboratory tests. Promising alternative tools for routine mass screening in high risk patients include nocturnal ECG holter monitoring for measuring heart rate increment15 and heart rate spectral analysis of nocturnal pulse oxymetry,16 both of which have equal or higher sensitivity and specificity than polysomnography for diagnosis of OSA. However severe apnoea is associated with significant arterial desaturation and thus a simple pure oximetry can be used at home in night for more severe cases to document sleep apnoea.

Treatment

Snoring and OSA can be very effectively treated. The type of treatment depends upon the severity of the condition. There are four main categories of treatment: Life style changes, Continuous positive airway pressure (CPAP), Dental devices and Surgery.

Lifestyle changes

Weight loss is the simplest treatment for obstructive sleep apnoea in obese patients. Even a modest 10% weight loss may eliminate apnoeic episodes by reducing the mass of the posterior airway. Unfortunately, however, this treatment option is usually not successful because only a small fraction of population can permanently lose weight. Moreover success may be limited, if patients also have anatomic defects in the jaw. Avoidance of alcohol, smoking and sleeping pills are useful measures, because studies have shown that snoring and apnoeic episodes may be worse after patient drinks alcohol or takes sleeping pills, as sedation decreases pharyngeal muscle tone and exacerbates sleep apnoea.

Continuous Positive Airway Pressure (CPAP)

The most effective way to treat sleep apnoea is with CPAP. CPAP is a mask worn over the nose attached by a hose to an air compressor gently and quietly blows room-air into the nose which “stents” the airway open, preventing airway collapse. It is the best treatment option for moderate to severe OSA. This is the most effective way to treat sleep apnoea and all patients diagnosed with sleep apnoea should at least try it before considering other options. Sneezing and rhinorrhoea are mild but common complications of CPAP which can be alleviated with steroid sprays. Dermal irritation by mask and dryness of mucous membranes by continuous positive airflow are other minor complications. Effective CPAP therapy can increase nitric oxide (NO) concentration and rapidly decrease free radical and adhesion molecule release. While it can not reverse all cognitive impairment CPAP therapy has shown to benefit patients with cardiac complications.

Dental Devices

Dental appliance is a device made by a dentist or an orthodontist designed to pull lower jaw forward. By pulling the jaw forward, the tongue is pulled away from the back of the throat. If the airway obstruction is occurring behind the tongue then this can be an effective way to treat sleep apnoea. The treatment of sleep apnoea with oral appliances should be a coordinated effort between the sleep physician, the dentist/orthodontist and the patient.

Surgical treatment

Those who can not tolerate CPAP may be candidates for surgical intervention to alleviate OSA. Uvulopalatopharyngoplasty (UPPP) involves the removal of part of the soft palate, uvula and redundant peripharyngeal tissues, sometimes including tonsils. Patients who undergo UPPP must be hospitalized for a few days. Furthermore they may experience the annoying complication of nasal regurgitation of liquids following the removal of palatal tissues. UPPP is effective in patients of mild to moderate cases of OSA. It reduces symptoms in 90% of patients, decreases number of apnoeic events in 60% patients and achieves a cure in 50% patients.16

Laser assisted uvulopalatoplasty (LAUP) can be performed in series of office treatments (on OPD Basis) and thus has become more popular than UPPP in recent years. The clinical indications for this procedure, as well as its effectiveness, have not yet been clearly defined. Some sleep experts recommend the use of LAUP in patients who have snoring and mild apnoea or patients who have no significant apnoea but want to alleviate snoring.

Why people with sleep apnoea don’t get treated?

Effective medical treatment to overcome this epidemic is available. But people who suffer from this problem usually don’t realize it; after all, they are asleep while the damage is being done.
The importance of this condition also lies in that it can easily be diagnosed and can be effectively treated thus reducing the risk factors, cardiac, respiratory and vascular disease and above all improving the quality life. Since the condition is highly prevalent in the society and is associated with significant morbidity and even some mortality. Family physicians need to be familiar with its clinical presentation and treatment.

Medical complications

People with sleep apnoea have a higher rate of death than normal population, an increased rate of hypertension and stroke, depression and death in sleep or car accidents. Cardiovascular diseases are common in patients with OSA. Apart from hypertension which is more common accompaniment of OSA, there is increased risk of nocturnal cardiac arrhythmias, including severe bradycardia during apnoeic episodes and also increased incidence of sudden death. OSA has also been shown to cause delayed cardiomyopathy, Myocardial infarction and angina. It has been shown that during episodes of apnoea oxygen supply to heart decreases and chances of MI increase in already compromised hearts. Incidence of stroke also increases in patients of OSA. It has been hypothesized that severe oxygen desaturation and decreased blood flow velocity to brain tissue may cause cerebral infarction (lacunar) after several years of untreated OSA. The impact may become clinically evident as multi-infarct dementia. Apart from this patients can present with difficulties in usage of core language skills, visual/perceptual abilities, and remote memory capacity. After CPAP treatment some but not all cognitive deficits improve. These cognitive deficits may be related to irreversible structural damage from chronic hypoxia in frontal cortex.

Do you have sleep apnoea

There are recent reports which show significant number of patients of OSA have associated type II diabetes also.

If majority of the answers to the above questionnaire are yes then one has a very high probability of having OSA. This questionnaire should also be given to bedroom partner.

References

  1. Strollo PJ Jr, Rogers RM. Obstructive sleep apnoea. NEJM 1996; 334 : 99-104.
  2. McGowen AD, Makker H, Elwell C, et al. Measurement of changes in cytochrome oxidase redox state during obstructive sleep apnoea using near infrared spectroscopy. Sleep 2003; 26 (6) : 710-16.
  3. Quinell TG, Smith IE. Obstructive sleep apnoea in elderly: recognition and management consideration. Drugs Aging 2004; 21 (5) : 307-22.
  4. Bradley TD, Floras JS. Sleep apnoea and heart failure, I: obstructive sleep apnoea. Circulation 2003; 107 (12) : 1671-78.
  5. Ip MS, Lam B, Chan LY, et al. Circulating nitric oxide is suppressed in obstructive sleep apnoea and is reversed by nasal continuous positive airway pressure. Am J Respir Crit Care Med 2000; 162 (6) : 2166-71.
  6. El-Solh AA, Mador MJ, Sikka P, et al. Adhesion molecules in patients with coronary artery disease and moderate to severe obstructive sleep apnoea. Chest 2002; 121 (5) : 1541-47.
  7. Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecule expression and production of reactive oxygen species in leukocytes of sleep apnoea patients. Am J Respir Crit Med 2002; 165 (7) : 934-39.
  8. Valipour A, McGown AD, Makker H, et al. Some factors affecting cerebral tissue saturation during obstructive sleep apnoea. Eur Respir J 2002; 20 (2) : 444-50.
  9. Fuchs BD, McMaster J, Smull G, et al. Underappreciation of sleep disorders as a cause of motor vehicular crashes. Am J Emerg Med 2001; 19 (7) : 575-78.
  10. Aldrich MS. Automobile accidents in patients with sleep disorders. Sleep 1989; 12 : 487-94.
  11. Wittig R. Clinical evaluation of excessive daytime sleepiness. In:Victor LD, ed. Clinical pulmonary medicine. Boston:Little, Brown, 1992; 439-60.
  12. Davies RJ, Strandling JR. The relationship between neck circumference, radiographic pharyngeal anatomy and the obstructive sleep apnoea syndrome. Eur Respir J 1990; 3 : 509-14.
  13. . Victor LD. Obstructive sleep apnoea in primary care. Dearborn, Mich:Oakwood Hospital,1997.
  14. Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnoea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med 2000; 162 (2 pt 1) : 566-70.
  15. Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecule expression and production of reactive oxygen species in leukocytes of sleep apnoea patients. Am J Respir Crit Med 2002; 165 (7) : 934-39.
  16. Victor LD. Treatment of obstructive sleep apnoea in primary care. Am Fam Physician 2004; 69 (3) : 561-68.


Corrigendum

In our July Issue of Bombay Hospital Journal (2007; 49 (3) : 439-42) inadvertent mistake have remained.
Please read as follows:

Abstract : Pg. 439, 2nd para 4th line Bupivacaine 12 ml of 25% while group II received Sufentanil 25 µg.

Material and Methods : Pg. 440, 3rd para Bupivacaine 12 ml of 0.25% epidurally.
and 4th para glycopyrrolate 4 µg/kg. 6th Para 6th line Bupivacaine given to group I and 25 µg Sufentanil is added to the above drug and given to group II.

Discussion : Pg. 441 2nd column 5th line of 3.5 to 4.5 hours with doses of 40-55 µg (Fig. 1). Pg. 442, 2nd para 6th line 40,55 and 70 µg respectively.

Conclusion : Ist line We conclude that epidural sufentanil 25 µg.....

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