Obstructive Sleep Apnoea
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Obstructive Sleep Apnoea (OSA) is a pathophysiological disorder that disturbs sleeping, thus, causing recurrent obstruction of the upper airway and brief episodes of stoppages in breathing (referred to as apnoea). This results in effects such as arousal from sleep and a reduction in the normal concentration of oxygen in blood. This description implies that in-depth understanding and effective clinical managing OSA requires a convergence of multiple medical disciplines; this is the primary reason why early studies on sleep failed to understand the causes of OSA and other sleep disorders.
Various Aspects and Perspectives of Obstructive Sleep Apnoea
1.1 Historical perspective
Early in the 19th Century, studies advanced numerous isolated theories to the causes of sleep in a bid to develop clinical practices and pharmacological solutions to manage sleep disorders. For instance, theorized causes of sleep included: increased cranial blood pressure and lack of blood in the brain, accumulation of toxins in the brain, neuron paralysis causing breakdown of nervous communication, and non-stimulation of sensory nerves. These isolated explanations, though currently viewed as inaccurate, covered circulatory and nervous systems and the neuron theory, which collectively provided a base for today’s more accurate diagnosis and management of obstructive sleep disorders.
“The Posthumous Papers of the Pickwick Club”, a novel by Charles Dickens gave the first clinical description of OSA: an overweight, excessively sleepy, snoring boy with possibly a right-sided heart failure. This made way to what is now called the Pickwickian Syndrome, a character trait that took a century to be studied as a clinical disorder. In the late 1900’s, development of Continuous Positive Airway Pressure (CPAP) revolutionized management of OSA. This development led to specialized clinics that dealt with OSA and its widespread awareness, as is presently the case.
Early clinical studies on OSA suffered from methodological drawbacks that mainly focused on case studies and cross-sectional studies, both of which lumped OSA and cardiovascular conditions as a single physiological disorder. This led to assumptions that were significantly inconclusive (Young, Peppard & Gottlieb, 2002). However, recent longitudinal and comparative studies have addressed these shortcomings. In a comparative study on 12 previous studies carried out in western countries, the prevalence of OSA was between 1 to 5% in adults. In three separate cohort studies carried out in Wisconsin, Pennsylvania and Spain, all using two-stage sampling (which required drawing participants from large samples of previous studies) reveal that countries with higher body mass index (BMI) have higher prevalence rates than those with lower BMI. Other inter-racial studies found the prevalence of OSA was higher in African-Americans than whites and Caucasians and more common in adults than in children. This implies that ethnicity and age are among risk factors of developing OSA. While males have a 66% higher chance of developing OSA compared to women, pregnant women have 14% chance compared to 4% chance of non-pregnant women.
All these studies indicate the prevalence rate of OSA. While incidence rates and progression rate are largely unknown, overweight and obese individuals, as well as individuals over the age of 65 years, show a higher incidence and progression rates than the rest of the population.
The amount of airflow into the lungs and neural inputs from the brain are the main indicators that are used to classify sleep apnoea into three broad categories, namely, OSA, central apnoea and mixed apnoea (Gubbi, Khnadoker & Palaniswami 2009). Hypopnea occurs when there is reduced airflow to the lungs. OSA, as stated, occurs when the upper airway is obstructed causing stoppage in breathing, and central apnoea is due to the absence of neural input from the brain causing stoppage in breathing (Gubbi, Khnadoker & Palaniswami 2009). When the upper airway is blocked, and there is no neural input from the brain, that is, OSA and central apnoea occurring together, the condition is classified as mixed apnoea (Mograss, Ducharme & Brouillette 1994).
The human upper airway, the pharynx, is a complex, multipurpose structure that performs a number of fundamental biological functions including speech, swallowing and respiration. The upper airway is made up of more than twenty muscles and soft tissues but lacks a strong bony support. As it can be seen from Figure 1, the anatomy of the upper airway is made up of nasopharynx, oropharynx and laryngopharynx.
The upper airway is akin to a collapsible tube. Two factors that make it susceptible to collapse include; a floating hydroid bone and an indirect air travel route that elongates the airway. Other factors include two opposing forces, one from the weight of soft tissues and bony structures and two, from dilator muscles that maintain pharyngeal patency. Increased collapsibility of the upper airway in individuals with OSA is arguably due to increased pressures from mechanically imposed loads and muscular responses to obstruction of upper airway during sleep.
According to Eckert and Malhorta (2008), individuals with OSA have a narrower cross-sectional area of the pharynx such hat this narrow upper airway is susceptible to collapse than a larger one. This causes an obstruction to the upper airway. Additionally, the arrangement of dilator muscles and soft tissues is altered in individuals with OSA, increasing their susceptibility of a pharyngeal collapse.
2.2 Upper Airway Dilator Muscle Reflex Responsiveness
Patil et al. (2007) demonstrated that, apart from anatomic mechanical loads provided by soft tissues and bony structures in the pharynx, which are insufficient to produce a collapsing effect on the pharynx during sleep, neuromuscular activities play a significant role in the protection of the upper airway. By measuring the activity of genioglossus, the most prominent and extensive pharyngeal dilator muscles, Patil et al. (2007) found out that neuromuscular activity decreased at the onset of sleep and increased during arousal from sleep, during restoration of airway patency. An obstructed upper airway triggers neuromuscular activities, which dilate and elongate the airway to restore patency. Further, neural input is induced by sleep and arousal mechanisms, responses to increased negative pressure, and ventilation mechanisms.
In OSA patients, the activity of genioglossus increases during wakefulness and reduces with application of positive nasal pressure, contrasting to normal individuals whose genioglussus activities recorded negligible reduction. This indicated that in OSA patients, neuromuscular activities increase to compensate for narrow airways, such that, during the onset of sleep, reduced neuromuscular activities may cause obstruction of the upper airway and also due to a greater loss of a stimulus to wake up.
In OSA patients, increased temperature and a disrupted vibration threshold on the repeated opening, and collapse of the pharynx may cause neuromuscular injuries (Adesanya et al. 2010). A disruption of the mechanical receptors slackens neuromuscular response on negative pressure made during obstruction of the upper airway. This is worsened by histopathologic and immunochemical changes in the pharynx of OSA patients. However, these observations are not conclusive and provide room for more studies.
2.3 Pharyngeal Patency and Lung Volume
Studies have linked OSA prevalence to lung volume and pharyngeal patency. When an individual is awake or asleep, there are changes in the lung volume that control mechanisms of the upper airway (Eckert & Malhorta 2008). Between a full lung capacity and lung residual volume, there is a lung volume that depends on the surface area of the pharynx when an individual is awake, which is distinct among OSA patients (Eckert & Malhorta 2008). However, according to Drager (2010) a maximum air intake to a full lung capacity also influences the mechanisms of the upper airway. When an OSA patient is sleeping, lung volume is lowered, which causes a decrease in pharyngeal collapsibility (Drager 2010). Both the thorax and diaphragm move upwards, when lung volume is decreased. This limits pharynx latency causing ease of pharyngeal collapsibility; thus, contributes to OSA pathogenesis.
2.4 Ventilatory Control Stability
Ventilatory control stability is essential to OSA patients because of the cyclic nature of breathing patterns oscillating between arousal and obstructive breathing events, where obstructive events are associated with periods of low respiration levels (Drager 2010). It also plays a part in controlling the collapsibility of the airway when a patient is sleeping. The central nervous system (CNS) coordinates the activities of the pharynx and diaphragm by pre-activating airway dilator muscles before the intake of air (Lyle 2000). Conditions of Hypoxemia and hypercapnia stimulate chemoreceptors to convey signals to the CNS, which subsequently stabilizes dilator muscles of the pharynx to decrease airway collapsibility (Lyle, 2000). Desaturated oxyhemoglobin, long circulatory times and hypercapnia cause low ventilator control stability that in turn results into pauses in breathing (Drager 2010). According to Czeisler (2011), obstructive apnoea takes place at same levels as it is in pharyngeal obstruction. This would imply airflow obstruction in the upper airway which causes OSA such that ventilatory stability could make OSA recurrent.
3.1 Risk Factors
Studies are not clear as to the cause of varying anatomical sizes of the upper airway in individuals. However, there are several risk factors that make individuals susceptible to OSA. A key risk factor, which causes OSA, is obesity. Several studies have indicated that OSA is more prevalent in obese individuals than in individuals within the normal body weight. Obesity is associated with increased fat deposits on and around the upper airway increasing resistance to the passage of air (White 1995). Weight gain is inversely related to the size of the upper airway. Another key risk factor, which causes OSA, is aging. Older individuals have been observed to have anatomically smaller upper airways, which are easily collapsible . A third key factor, which causes OSA, is a genetic and hereditary factor. The position of the jaw, tonsil tissues and the size of the tongue profoundly influences the size of the upper airway. However, these risk factors do not necessarily work in isolation. Instead, they usually act enhanced, in combination, to influence the size and collapsibility of the upper airway.
3.2 Impact on Individual
OSA has an impact on the life of an individual. The most common effect of OSA is sleep deprivation. A recurrence of an obstructed upper airway causes arousal from sleep of an individual to enable him or her to breathe (Beebe et al. 2003). This repeated arousal from sleep throughout the night causes interruptions of sleep, which an individual diagnosed with OSA does not easily notice. Sleep deprivation is symptomized by daytime sluggishness, a lack of concentration, irritability, migraine and forgetfulness. In addition, individuals with OSA are more susceptible to motor accidents and are not highly productive at the workplace (Beebe et al. 2003). OSA has also been shown to cause a strain in familial relationships. Disgruntled spouses may opt to sleep in another room due to the inconvenience caused by snoring, which eventually causes drifts in the couple. There are also co-morbidities due to OSA, which includes increased chances of individual getting hypertensive, cardiovascular diseases, stroke and depressions.
3.3 Modes of Diagnosis
There are two main modes of diagnosing OSA: laboratory testing and physical examination. However, laboratory testing done through overnight polysomnography in a sleep laboratory is the preferred standard mode of diagnosing OSA. In a laboratory setting, a patient sleeps overnight while measurements of key psychological variables are taken (Lyle 2000). The variables measured include rapid eye movement (REM) during sleep, incidences of sleep arousals, movements during respiration, air flow through the nasal cavity, and movements of limbs that may result in sleep arousal and saturation of oxyhemoglobin. These variables are used to calculate the respiratory disturbance index (RDI), defined as the number of abnormal respiratory episodes in each hour of sleep. An index of 20 or more episodes indicates a severe OSA. Still, in a laboratory setting, daytime sleep latency could be measured to indicate OSA. A normal individual takes ten minutes or more to sleep; thus, sleep latency of five or fewer minutes indicates an abnormality and most likely indicates OSA.
On the other hand, physical examination seeks to identify physical factors that affect and make the airway easily collapse. Studies indicate that OSA patients are obese and have thick, wide necks, as a rule (Patil et al. 2007). A wide neck measuring 40.6cm and 43.1cm or greater in women and men respectively indicates a higher risk for OSA (Patil et al. 2007). Other physical features that increased risks for OSA include a large tongue, enlarged tonsils and an arched palate (Lyle 2000).
4- Prognosis and Treatment
4.1 Non-Surgical Treatment
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An easy non-surgical treatment for OSA among obese individuals is weight loss. Even a minimal weight loss of about 10% effectively reduces RDI count by widening upper airway. However, weight loss is not reliable because it is difficult for patients to lose weight perpetually, or there may be causes other than obesity that would persist after weight loss.
Another non-surgical treatment of OSA is Continuous Positive Airway Pressure (CPAP). In CPAP, patients are fitted with a nasal mask where a fan blows air to keep the airway open (Beebe et al. 2003). This method, however, assumes patients sleep with their mouths shut. In the circumstance that they do not close their mouths, the chin is then fastened with a strap, so as to stop the outflow of air through the mouth. However, CPAP is associated with complications such as rhinorrhea, dermal irritation and nasal dryness, which usually leads to noncompliance.
Devices, which hold tongue movement, could also be used to mitigate obstruction of upper airway during sleep, as a form of non-surgical treatment (Lyle 2000). However, these devices are not as effective as CPAP. Nonetheless, patients with mild OSA or those who snore heavily and, however, do not like CPAP or surgery may use these devices (Beebe et al. 2003).
4.2 Current Management Practices/Therapies
Currently effective management of OSA requires some form of surgery. In younger patients, uvulopalatopharyngoplasty (UPPP) is performed. This surgical procedure involves removal of tissues that are redundant in the pharynx, at times including the tonsils, uvula and the soft palate (Lyle 2000). While UPPP eliminates snoring, it does not cure OSA since, apart from the soft palate, other pharyngeal tissues also collapse and obstruct the airway (Lyle 2000). Another limitation of UPPP is post surgery hospitalization and recurrent rhinorrhea. Still, UPPP has an initial success rate of 80% that decreases to 46% in twelve months, implying its effectiveness decreases with time. Recently, laser-assisted uvulopalatoplasty is becoming common. However, it is suited to OSA patients who snore heavily or who have mild apnoea.
Another surgical procedure is gastric surgery. While this procedure is most suited to obese patients where adipose levels of palatal tissues are significantly reduced, it is not conclusive how weight loss or reduction of adipose levels of the palatal tissues minimise OSA.
Jaw surgery is yet another surgical procedure mostly used when other procedures are not highly effective. It refers to nudging the tongue forward or moving both the maxilla and mandible. This procedure is rarely performed alone; instead, it is used to increase the efficacy of the other methods. Its key limitation is aesthetic facial changes that most patients are uncomfortable to obtain.
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