Can Prednisone contribute to Sleep Apnea?

Answer 1

Prednisone is used for the treatment of sleep apnea by some doctors. For a complete explanation and treatment plans, visit : http://www.emedicine.com/ped/topic2114.htm Good luck !

Answer 2

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Answer 3

This Site Might Help You.

RE:
Can Prednisone contribute to Sleep Apnea?

Answer 4

Stop Snoring Sleep Apnea Forever : http://Snoring.neatprim.com

Answer 5

Don't ever take the sleeping pills route!!

1. They will damage your liver big time and you can get into serious health problems.

2. You will get hooked up on them and you won't be able to have a normal life any more if you don't take your pills everyday.

The sleeping pills industry is damaging our health by capitalizing on our ignorance, and by distracting people from effective and natural ways to deal with this problem. I had been taking prescription sleep medications [Ambien] for over 5 years. It stopped working and I simply took more. Still did not work. Nights were very difficult - medication put me to sleep but I would wake up after 2–3 hours with a strong sympathetic response (fast pulse, pounding heartbeat, wide awake alert). It was a very difficult cycle to break. I was really in bad shape due to lack of sleep.

After years of struggling I was able to cure my insomnia naturally and pretty fast. I followed the Sleep Tracks sleep optimization program, here is their official web -site if you want to take a look: http://www.insomniacure.net

Ohhh..and Good Luck!

Answer 6

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Answer 7

Background: Childhood obstructive sleep apnea (OSA) syndrome is characterized by episodic upper airway obstruction that occurs during sleep. The airway obstruction may be complete or partial. In contrast to simple snoring, OSA is accompanied by varying degrees of oxygen desaturation, hypercarbia, autonomic stimulation, and sleep fragmentation. Sleep disruption leaves some children with daytime somnolence, difficulty waking in the morning, and disturbed concentration. Other children develop paradoxical hyperactivity during the day rather than hypersomnolence; attention deficit hyperactivity disorder may be diagnosed. Common symptoms include restless sleep and loud nightly snoring, sometimes with audible pauses followed by gasping or snorting. Complaints of nocturnal enuresis, nightmares, and morning headaches may occur. Long-standing severe OSA may result in failure to thrive, neurobehavioral disorders, pulmonary hypertension, and, ultimately, cor pulmonale.


Pathophysiology: Disordered breathing during sleep is a hallmark of OSA syndrome. Breathing abnormalities include apnea (cessation of air flow) and hypopnea (decreased air flow). In addition, in contrast to adults, some children exhibit a variation of OSA termed obstructive hypoventilation (OH). Children with obstructive hypoventilation demonstrate periods of hypercarbia that occur in the absence of discrete respiratory events that fulfill criteria for apnea or hypopnea.

Physiologic recording methods can differentiate the types of apnea. During obstructive apnea, an individual makes respiratory efforts, but no airflow occurs because of upper airway obstruction. Central apnea is an interruption in both airflow and breathing effort. Mixed apneas have both central and obstructive components to them. A typical mixed event begins with a central apnea, which is followed immediately by one or more obstructed breaths.

Hypopneas are episodes of shallow breathing during which airflow is decreased by at least 50%. They are usually accompanied by some degree of oxygen desaturation, which can be minor and transient. Like apnea, hypopnea is subdivided as being obstructive, central, or mixed. Obstructive hypopneas are episodes of partial upper airway obstruction. Respiratory efforts occur, but airflow is reduced. In central hypopnea, breathing effort and airflow are both decreased. Mixed hypopneas have both central and obstructive components.

In adults, episodes of disordered breathing must last 10 seconds or more before being considered an apnea or hypopnea. Normal resting respiratory rates in children are faster than those in adults. The child has a smaller functional residual capacity and a more compliant chest wall. As a result, children undergo oxygen desaturation more rapidly than adults whenever airflow is interrupted. A definition of apnea or hypopnea requiring that an event last 10 seconds or more before it is considered significant is somewhat arbitrary and does not take into account the physiologic differences between adults and children. Consequently, pediatric sleep centers use different duration criteria for labeling events such as apnea or hypopnea. In children, if obstruction occurs with 2 or more consecutive breaths, the event can be called an apnea or hypopnea, even if it lasts less than 10 seconds.

Individuals with OSA syndrome have pathologic degrees of obstructive apnea, obstructive hypopnea, or both. Severity is quantified using a polysomnographic-derived index known as the apnea-hypopnea index (AHI). The AHI is the total number of apneas and hypopneas that occur divided by the total duration of sleep in hours. An AHI of less than or equal to 1 is considered to be normal by pediatric standards. An AHI of 1-5 is very mildly increased, 5-10 is mildly increased, 10-20 is moderately increased, and greater than 20 is severely abnormal.

OH in children is a sleep-related breathing disorder that is considered a variation of obstructive sleep apnea. Children with OH may have a normal ranged AHI, but they have episodic periods of hypercarbia, as identified based on end-tidal (ET) CO2 monitors. Peak ET CO2 measurements of greater than 53 mm Hg are considered abnormal. The percentage of sleep time spent with ET CO2 measurements greater than 50 mm Hg should not be more than 9%.

Most physicians who treat children with sleep apnea generally recommend specific interventions when the AHI is greater than 5 or respiratory events are associated with oxygen desaturations of less than 85%. When the AHI falls between 1 and 5, other clinical factors must be taken into account to determine whether to pursue adenotonsillectomy or other therapy.

Obstructive apnea and hypopnea are related to upper airway obstruction. Upper airway obstruction may occur at one or more levels, including nasopharynx (area from the nose to the hard palate), mouth, velopharynx (space behind the palate), retroglossal region (area behind the tongue), hypopharynx (region between the tongue base and larynx), and larynx.

The upper airway is a pliant tube whose sidewalls consist of muscle and other soft tissues. During wakefulness, neural input to a number of small muscle groups in the pharynx maintains muscle tone and airway patency. With sleep, an increased resistance to airflow normally accompanies muscular relaxation of these muscle groups. Although most people compensate for these changes, individuals with certain anatomic problems have repeated episodes of partial or complete upper airway obstruction when they sleep.

Childhood differs from adult OSA. Adults with sleep apnea frequently present with hypersomnia, while children often demonstrate short attention spans, emotional lability, and behavior problems. Among adults, obesity is a major risk factor for OSA. Fatty infiltration of the pharyngeal soft tissues narrows the caliber of the upper airway and contributes to airway resistance. Although obesity plays a role in some cases of childhood sleep apnea, the airway obstruction is usually related to tonsillar hypertrophy, adenoid hypertrophy, or craniofacial abnormalities. Children with some types of neuromuscular disease (eg, Duchenne muscular dystrophy, spinal muscular atrophy, cerebral palsy) may also have a higher risk of developing sleep apnea.


Frequency:


In the US: Obstructive apnea is believed to affect approximately 4% of men and 2% of women in the United States. The disorder is most commonly recognized in middle-aged individuals, although symptoms usually predate diagnosis by years.
Prevalence of OSA in US children is estimated to be 2%. In comparison, 7-9% of children snore habitually.

Internationally: In the United Kingdom, approximately 1.75-2.25% of children aged 4-5 years are thought to have OSA. Unfortunately, very few epidemiologic studies of childhood OSA exist.
Mortality/Morbidity: Major morbidities associated with childhood OSA include failure to thrive, difficulty concentrating and/or developmental delay, behavioral problems, hypertension, pulmonary hypertension, and, ultimately, cor pulmonale. Some pulmonologists theorize that chronic upper airway obstruction with labored breathing may result in the development of a pectus excavatum deformation in a compliant immature chest wall. Concomitant gastroesophageal reflux is likely to be exacerbated by OSA.

Children with OSA syndrome, as well as children with a history of loud habitual snoring, appear to be at risk for developing deficits of executive function. According to the model by Beebe and Gozal, sleep fragmentation, intermittent hypoxemia, and hypercarbia contribute to dysfunction in the prefrontal areas of the brain. Executive functions include behavioral inhibition, regulation of affect and arousal, ability to analyze and synthesize, and memory. Executive dysfunction interferes with cognitive abilities and learning.

Children with severe OSA may develop postobstructive pulmonary edema within a few hours of surgery undertaken to relieve upper airway obstruction. Furthermore, such patients are at risk for postoperative respiratory compromise, which is characterized by severe upper airway obstruction and may require endotracheal intubation or the use of noninvasive respiratory support such as continuous positive airway pressure via a nasal mask. Surgical treatment of severe OSA warrants an overnight observation, especially if the child is younger than 3 years, has concomitant cardiopulmonary disease, morbid obesity, hypotonia, or craniofacial anomalies.

Obesity-related hypoventilation, commonly known as the pickwickian syndrome, occurs in some children who have obesity and OSA. These individuals respond abnormally to both hypercarbic and hypoxemic stimuli to breathe; they have repetitive obstructive events with sleep and marked daytime sleepiness, daytime hypoventilation, and hypercarbia.

The incidence of cor pulmonale and death due to OSA is unknown. Once pulmonary hypertension has developed, it is usually reversible if the underlying OSA is effectively treated.

Race: OSA occurs more commonly among African American and Hispanic individuals than among white adults and children. In patients younger than 18 years, African Americans are 3.5 times more likely to develop OSA than whites.

Sex: The male-to-female ratio of obstructive apnea in children is approximately 1:1. At puberty, the male-to-female ratio starts to increase. By adulthood, symptomatic men outnumber women by 2:1 or more.

Age: OSA is observed in children of all ages and may develop even in infancy. Retrospective studies note that a large number of parents with children in whom OSA is diagnosed recall that their child's snoring began within the first months of life. Most children with OSA are aged 2-10 years. Children with severe obstructive apnea are likely to present when aged 3-5 years. The mean age at diagnosis has been reported to be 14 months, plus or minus 12 months.




CLINICAL Section 3 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography



History: Not only do manifestations of OSA differ between children and adults, they also frequently vary from one child to another. Not every child with OSA has the exact same constellation of symptoms. Keeping this in mind, perform a careful interview to explore the following issues when OSA is suspected:

Abnormal breathing during sleep: Parents should describe their child's breathing in detail. Some children snore loudly and have audible intermittent gasps. Some demonstrate paradoxical chest and abdominal wall movements, labored breathing with retractions, cyanosis, sweating, and restlessness. Often, children prefer sleeping in unusual positions, with their head and neck extended and their mouth wide open.
Frequent awakenings or restlessness: Recurrent obstruction leads to restlessness, and parents may report that the child wakes frequently or falls out of bed. Ask families about the child's sheets and blankets. Constant tossing and turning during the night often causes the child's bedcovers to be in wild disarray by morning.
Frequent nightmares: Obstructive apnea and hypopnea tend to worsen during rapid eye movement (REM) sleep, which is associated with dreaming. Frequent wakening with nightmares or vivid dreams is common in children. Occasionally, the dreams may include imagery about suffocation or drowning. Adults or children with OSA may describe choking sensations during the night.
Enuresis: Bedwetting is common among children with OSA, although no well-controlled studies have been performed to date. Always consider the possibility of OSA in children who have histories of snoring and develop enuresis after they have already been successfully toilet trained. Older children need to be asked specifically about whether they wet the bed because often they are too embarrassed to bring up the subject on their own. In addition to questioning the family about enuresis, ask about nocturia. Many children and adults with obstructive apnea report frequent awakenings to use the bathroom at night.
Difficulty getting up in the morning: Morning complaints may include dry mouth, grogginess, disorientation, fatigue, and an unrefreshed feeling after an overnight sleep. Some children are very difficult to arouse in the morning and require multiple interventions by the family before they get out of bed.
Excessive daytime sleepiness: Adolescents and adults with OSA frequently report feeling sleepy during the day and may fall asleep at inappropriate times. They have difficulty staying awake in quiet situations and can have problems focusing their attention. Ask children whether they struggle to stay awake in class or while watching television, reading, or sitting in a car. Daytime somnolence may lead to falling grades, mood changes, and inattentiveness. Young children appear much less likely to develop excessive daytime sleepiness.
Hyperactivity and/or behavior problems: Paradoxically, some children with OSA develop signs of hyperactivity rather than daytime somnolence. Patients may exhibit aggressive behavior, discipline problems, decreased attention span, emotional withdrawal, and bizarre behaviors.
Daytime mouth breathing: Most children with OSA have tonsillar hypertrophy, adenoid hypertrophy, or both. Parents frequently describe these children as mouth breathers, even during the day while they are awake.
Sleep patterns: Daytime somnolence may be due to any number of factors in addition to OSA. Many children and teenagers have poor sleep habits, irregular sleep schedules, and unrealistic views regarding how much sleep they need. Often, having families keep a sleep diary for 2 weeks to document bedtimes, rise times, and naps can be very informative to both the physician and the family.
Historical features suggestive of OSA syndrome are typically absent from children without OSA syndrome but poorly distinguish between OSA and primary snoring. Therefore, to differentiate between OSA syndrome and primary snoring, overnight polysomnography is essential.
Physical: Children with suspected OSA should undergo a complete physical examination with special attention to structures of the upper airway. Obtain accurate vital signs, including measurement of blood pressure; plot the child's height and weight on a standard growth chart.

Determine whether the child's growth is normal. Recent rapid weight gain or obesity may predispose a school-aged child or adolescent to developing OSA. Severe OSA in the younger child may lead to failure to thrive and stunted growth.
Determine if the child's face appears normal, or if craniofacial anomalies are present. Inspect for midfacial hypoplasia, a flat nasal bridge, or facial asymmetry. Determine if the jaw abnormally small (micrognathia) or jaw recessed (retrognathia). Look for adenoid facies with mouth breathing, nasal speech, and periorbital swelling, which may be present in as many as 15-20% of younger children with OSA.
Assess nasal patency. Evaluate for signs of allergic rhinitis, nasal polyps and growths, and septal deviation. Determine if the child can breathe through the nose.