Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Obstructive Sleep Apnea In Pediatric Patients Obstructive sleep apnea is a common disorder. Roughly 2% of the childhood population has obstructive sleep apnea - about 500,000 children in the United States. The peak ages occur between two and five years of age, which corresponds with the peak incidence of adenotonsillar hypertrophy. There is also a second peak that occurs in late adolescence and these patients tend to present in the same way that adults present. In childhood, obstructive sleep apnea occurs in approximately equal numbers of males and females, but as children get older, males begin to predominate. Why do we care about obstructive sleep apnea in children? Because of the complications that we are all familiar with: failure to thrive, developmental delay, behavioral problems, cor pulmonale, polycythemia and arrhythmias, pulmonary complications of chronic aspiration, post obstructive edema, dental abnormalities, bruxism, orthodontic abnormalities and even death can occur in some children. When we think about upper airway obstruction, there is a spectrum of disease ranging from very benign-appearing forms to very severe-appearing forms. Primary snoring is considered the most benign aspect of upper airway obstruction. This is a clinically benign, otherwise asymptomatic condition. Sleep architecture and oxygenation are not altered. Primary snoring is habitual in around 7% to 10% of children and up to 20% of children can have snoring on an intermittent basis. It can be exacerbated by upper respiratory tract infections and the mechanism is felt to be due to an inability of the CNS to maintain muscle tone. Interestingly enough, snoring is not diagnostic of obstructive sleep apnea. However, children who do not snore are unlikely to have obstructive sleep apnea. If you compare children who have primary snoring with children who have true obstructive sleep apnea, there is no difference in the pattern of the their snoring.The next level, if you will, of upper airway obstruction is upper airway resistance syndrome. This is a complex of paradoxical breathing: normally when the abdomen and diaphragm contract, the abdomen and rib cage expand, but in this case the rib cage moves inward secondary to the increased respiratory force. There is also increased respiratory effort and snoring, which occur during REM sleep. This is felt to be due to induced bi-swings in intrathoracic pressure during inspiration. This can cause significant sleep fragmentation, leading to daytime symptoms similar to obstructive sleep apnea syndrome patients. The major difference is that there is no significant decrease in airflow or O2 saturation, and we should probably suspect this in patients who have daytime symptomatology but whose polysomnogram is negative. The exact prevalence of this disorder is unknown, however, many authors feel that it is more common than obstructive sleep apnea. The signs and symptoms of obstructive sleep apnea are snoring, mouth breathing, adenotonsillar hypertrophy, daytime hypersomnolence, obesity, gastroesophageal reflux, change in sleep patterns, behavior changes, cognitive function changes, enuresis and growth impairment. What you will commonly see in the literature is a chart and it will compare adult patients to pediatric patients and it will give you a list; these are common in adults and these are more common in children. I thought I would go through each symptoms and talk about which ones are common in kids or which ones are definitely associated with obstructive sleep apnea and which ones are more myth or common beliefs as opposed to based on well-controlled studies. Adenotonsillar hypertrophy and mouth breathing are perhaps the most common reason for referral to an otolaryngologist and we know that habitual mouth breathing can lead to abnormal facial development and dental malocclusion and lead to, what we call the adenoid face, which is pictured here. When we look at kids with obstructive sleep apnea, around 15% of them do have these features; however, the determinate of habitual mouth breathing are really unknown at this time. If you examine literature critically there is no consistent relationship between mouth breathing, adenotonsillar hypertrophy or obstructive sleep apnea. Daytime hypersomnolence, this picture is of a typical adult patient. We know this is a common feature of adult obstructive sleep apnea. I hope you can recognize that he is asleep in your waiting room, however, this is not a common complaint in children. Some people say that it is common, however, it is difficult to define it because daytime naps are normal and there is no consistent difference between kids who just snore and in the kids who have true obstructive sleep apnea. Obesity, again, is common in adults; however, in children most children with obstructive sleep apnea are not obese. However, the prevalence of obstructive sleep apnea in obese children may be high and, indeed that if you have an obese child who has obstructive sleep apnea their weight will correspond with the severity of their illness. However, if you just take all kids who are obese, it is not a good predictor of obstructive sleep apnea. Again, those kids who are obese and have obstructive sleep apnea, weight loss will reduce the severity of their symptoms. Sleep patterns common in adults are full arousals. Children are more likely to have mini arousals, which are not clinically apparent but they are associated with significant sleep fragmentation. You can also see changes in sleep patterns such as parasomnia, such as sleep walking, bed thrashing, pillow propping, and even some kids will tend to sleep in an upright sitting position.Behavior changes. Depression and anxiety, or other neuropsychiatric disturbances are commonly associated with adult obstructive sleep apnea syndrome. However, those types of symptoms are not as commonly reported in children. What we do see is hyperactivity and aggression. Stradling in 1991 looked at 782 children who happen to snore and had other symptoms suggestive of obstructive sleep apnea and found that a large number of those children were considered hyperactivity, aggressive and had other behavioral problems. Additionally, Gillumont ten years earlier, looked at children who had obstructive sleep apnea and also happened to have symptoms of hyperactivity, aggression, etc. and once the obstructive sleep apnea was treated effectively it was found that those symptoms were reduced. Cognitive functions. Obstructive sleep apnea can lead to learning disabilities. There have been small, uncontrolled studies, and what they found was that kids have impaired school and intellectual performance. It makes sense. We know that sleep is responsible or helps with cognitive functioning and it helps with memory, helps with diligence, it helps with attention. If a kid is not getting enough sleep or has significant sleep fragmentation, we are likely to see the same things that we see in adults, decreased attention, problems with memory, as well as problems with diligence. Growth impairment. This is not a common feature of adult obstructive sleep apnea; however, this is the main feature of pediatric obstructive sleep apnea. The incidences decrease significantly because now we recognize the disorder earlier, and the mechanism is thought to be three fold. First, disruptive sleep architecture leads to chronic CO 2 retention, which leads to chronic acidosis, and that either impairs the release of growth hormone or it impairs the end-organ response to growth hormone. Additionally, adenotonsillar hypertrophy, which is the most common cause of upper airway obstruction in children can lead to difficulty swallowing in and of itself, which can also lead to decreased p.o. intake. Additionally, all children who have obstructive sleep apnea have an increased respiratory effort. This can result in an increased caloric need leading to problems with growth impairment and failure to thrive. Two final things that you will often hear associated with obstructive sleep apnea are one of gastroesophageal reflux. We know that reflux does play a very, very important role in airway disorders of childhood; stridor, laryngospasm, apparent life-threatening events, and it makes some sense that if you have increased intrathoracic pressure as the body tries to compensate to overcome the upper airway obstruction, that then they lead to reflux of gastric contents into the upper airway. Interestingly enough there was a study in 1993 by a gastroenterologist that showed that adults who happen to have gastroesophageal reflux and obstructive sleep apnea, when they were treated, their symptoms for reflux got better. When they were treated for the apnea their reflux got better, however, if you go back and look at all the other studies, there has not been a consistent, conclusive relationship between reflux and obstructive sleep apnea at this time. You will popularly hear that enuresis is commonly associated with obstructive sleep apnea; it is an end-organ affect, if you will. There are even reports that this would cure, or be cured with tonsillectomy and adenoidectomy. This actually is one of the reasons why there was such a big backlash against tonsillectomy in 50’s and 60’s because people were advocating adenotonsillectomy for everything. If you really look at the literature, the studies have all been poorly controlled and there is no indisputable evidence that enuresis is associated with obstructive sleep apnea syndrome. So, once you have gone through the symptoms and you now recognize that snoring, behavioral and cognitive changes, failure to thrive, and disruptive sleep patterns are all the most commonly consistent reported problems with obstructive sleep apnea we can move on to our diagnostic evaluation. Of course we always start with the physical examination. Overall growth because we want to look for failure to thrive. Cerebrovascular because we are concerned about end-organ damage and pulmonary because, once again, we are concerned about end-organ damage. As well as doing a full comprehensive head and neck exam, taking account tonsil size, also looking at the palate, tongue base, oropharynx size and shape, as well as cranial facial structures.To assist in our diagnostic evaluation you can do nasopharyngoscopy. This can allow you to look at the tongue base, the hypopharynx, the nasopharynx to look for obstruction in that area and you can also use lateral neck radiography to look at the adenoid pad; pictured here you can see an enlarged adenoid pad, as well as a narrow upper airway. CT and MRI can actually show upper airway dimensions, but it is impractical and rarely needed to make your diagnosis. As you go through your physical examination and your history, you also want to keep in mind that there are other things beside adenotonsillar hypertrophy that cause upper airway obstruction, or that can predispose upper airway obstruction; nasal obstruction, polyps, sinusitis, nasal stenosis, undocumented choanal atresia, oropharyngeal and, of course, tonsillar hypertrophy, but also lingual tonsillar hypertrophy, macroglossia, macrognathia, and retrognathia. In the larynx consider subglottic stenosis, true vocal cord paralysis, as well as laryngomalacia and laryngeal webs, and then pharmacologic forms that can predispose, such as sedation and antihistamines.We also want to recognize that there are associated syndromes that put kids at an increased risk of obstructive sleep apnea; kids with Down’s and have other forms of hypertonia, cerebral palsy, Treacher Collins syndrome, Pierre Robin sequence, hemifacial microsomia, etc. There are clinical scoring systems available to help document the likelihood of having obstructive sleep apnea before you move on to polysomnography. Gillumont developed a system, he used it with tonsil size. He looked at the chin size, the degree of retrognathia, the height of the hard palate, the shape of the face, square versus long, with long being more pathologic, the length of the hard palate and the intermolar width and he gave points for each. The highest score that one can achieve is 19 and 13 is considered high, and highly suggestive of obstructive sleep apnea. Carroll, in 1995, came up with a scoring system. I liken this to the Cage Questionnaire when we ask people about alcoholism, “Have you ever cut down?”, “Have you ever been annoyed?” etc. In this case we asked ‘how often does your child snore?’, ‘Does your child ever stop breathing in his sleep?” and “Does your child have difficulty sleeping?”. What they found was the sensitivity if they answered ‘yes’ to these questions the sensitivity was 73%, but more importantly perhaps, is if they answered ‘No’, they probably did not have obstructive sleep apnea.Polysomnography is the goal standard for diagnosis and evaluation. The American Thoracic Society recommends measuring the following; end-tidal CO2, respiratory effort, air flow at the nose and/or mouth, pulse oximetry, electrocardiography, electromyography. They usually put it on the anterior tibial muscle and this is to look for mini arousals or full arousals. Electroencephalography, of course, is to see which sleep stage that the person is in when they have their obstructive event, if any. Some of the definitions that we should be familiar with; obstructive sleep apnea is defined as alveolar hyperventilation caused by upper airway obstruction during sleep; obstructive apnea is the cessation of air flow at the nose and/or mouth; hypopnea is a 50% decrease in nasal air flow for ten seconds or more. This is the predominant way that children will present, with hypopnea as opposed to apnea. In adults apnea for greater than ten seconds is considered significant and in pediatric patients apnea for six seconds or one and one-half to two breaths is considered significant. The apnea/hypopnea index is the number of apneas and hypopneas per hour of sleep. In an adult, greater than five is consistent with sleep apnea, greater than 20 is severe, and in children greater than 1 is abnormal, and severe is once again is greater than 20. Here’s is an example of a polysomnogram. I will not go through it in too much detail, but they are measuring here the abdominal movement and you can see nice breaths and nice breaths, and then you have this hypopnea and shortly thereafter you have an associated dip in pulse oximetry. This is classic for obstructive sleep apnea. When do you get polysomnography? This is an area that is debated quite heavily. People who argue for it say that only 55% of kids, if you get polysomnography one, will have obstructive sleep apnea. That would help limit unnecessary interventions. You will not have kids on CPAP and you will not have kids undergoing adenotonsillectomies when they do not need to. Cost and convenience are arguments against. The cost at Texas Childrens’ Hospital for an overnight sleep study is $1300. Of course, that is staying in the hospital overnight, time away from work, and is just not convenient. A perhaps indication that we should considered is first if they do not snore they probably do not have obstructive sleep apnea. If they have another indication for adenotonsillectomy, you do not have to get the study, however, in anyone else you would not be faulted for getting a sleep study for definitive diagnosis. You should probably get it in anyone who has severe CNS disease, a medical illness that would increase the risk of surgery, or age less than two. In other words, anyone who the morbidity of the surgery or treatment is so great that you went to make absolutely certain that you are doing the right thing. Alternatively you can use other studies. Overnight pulse oximetry and observation at Texas Childrens’ Hospital this happens quite often. A kid gets admitted for gastroenteritis or some other problem, they happen to be on pulse oximetry and in the middle of the night all of the alarms starting going off, nurses run in the room and they find that the patient is not breathing. The next thing you know you get a consult the next day, saying, “hey, we think we got a kid with sleep apnea.” I’m sure everyone has had a parent who has brought in an audio tape of their child, saying listen to how my child snores and that is actually a reasonable thing. You can get a good idea of whether or not there is apnea events just based on an audio recording. There are also some studies that show sleep videotape analysis is very sensitive but this is probably outside the realm of what we would do. So, now that you have made your diagnosis what are we going to do about it? With any patient observation is a reasonable option, especially if it is mild disease. You can also approach it medically, mechanically and surgically. We would want to keep in mind that a step-wise approach is the best approach. You want to look at the severity of the disease, the other comorbidity, as well as what the family wants. Medical therapy, if they happen to have obesity-induced obstructive sleep apnea, weight loss will improve their symptoms. Acute tonsillar hypertrophy of a child who has 2+ tonsils and develops mono or acute tonsillitis and now they have sort of tipped over the edge, you can try steroids and antibiotics to get them back to their baseline. There are some studies that show that kids with adenoid hypertrophy, if you use nasal steroids that can help shrink the adenoid pad. Of course, once you stop the steroids the adenoid pad comes back. And, also if they have significant nasal obstruction, decongestants can also help. Mechanical therapy, CPAP, is the mainstay of therapy. In adults this is the treatment of choice. The continuous positive airway pressure stents open the airway, but from via a tight-fitting mask, pictured here, and it has been shown to be a good alternative for children. Waters reported he had a 90% success rate and he was able to reduce, on average, the apnea hypopnea index, AHI, from 27 to 3 in those patients. Then there are other studies shown that you can get anywhere from 86 to 97% success rate. The problem is noncompliance and comfort. As you can see, this is a tight-fitting mask. It creates problems with comfort, nasal congestion, crusting, nosebleeds, you can have rashes around where the mask fits on the face, and it also does not allow for the different kinds of sleep patterns; some people like to sleep on their stomach, some people like to sleep on their side, and it is a very uncomfortable object for most adults, let alone children. You can also consider, beside nasal CPAP, if the kid only has significant hypoxemia at times during the night, supplemental oxygen often will be enough to get them over the hump. Oral splints have been shown to be effective in adults, however, there is no study showing effectiveness in children as of yet. Surgical therapy, this is the mainstay of treatment for kids, mostly because adenotonsillectomies are the most common site of obstruction. Hence, this is the most common procedure performed. There are treatment failures, kids who have smaller tonsils, kids who have maxillary mandibular protrusions, children younger than one year of life. It has been considered advanced obstructive sleep apnea surgery for children; UPPP, septoplasty, hyoid advancement, expansion, tongue reduction, lingual tonsillectomy, maxillary mandibular surgery, as well as tracheotomy, of course being the common final pathway. So adenotonsillectomy, let’s say this is the treatment of choice for kids. It is because the tonsils and adenoids tend to be the most common source of obstruction and if you look at the studies, most studies will report anywhere from 84 to 100% cure rates. Indications should be compelling history or a child with polysomnography, documented obstructive sleep apnea, or a kid who does have the compelling history as well as the adenotonsillar hypertrophy. Some people will argue any kid with obstructive sleep apnea should undergo adenotonsillectomy even if they do not have very large tonsils. Because, like I said, it has also been shown to be beneficial in children who do not have polysomnography-proven obstructive sleep apnea, just kids with large tonsils and difficulty swallowing and obstructive airway resistance syndrome. One of the big areas of controversy is whether or not all of these children should be admitted and has post-op monitoring overnight. Uvulopalatopharyngoplasty can be applied in children with obstructive sleep apnea. This, of course, is the most common way to treat adults with obstructive sleep apnea surgically. It is indicated if you think the palate is the likely source of obstruction. You want to consider it in anyone who has severe obstructive sleep apnea, if they have small tonsils, if there is obesity involved, and interesting enough if there is hypotonia commonly associated with kids with Down’s. There has been well-documented success in adults, roughly 60%. In kids it is roughly 50% or less. There is an increase of uvulopharyngeal insufficiency with this procedure in children, so you want to keep that in mind.Tongue base surgery. If the tongue base happens to be the source of obstruction, there are some case reports and studies showing that this does work for some kids; kids who have Down’s, other kids who have hypotonia, kids who have micrognathia and macroglossia, you can consider tongue-base surgery. What I saw was that the indications are nebulous but if tracheotomy is the only option left and the tongue is the site of obstruction, you should strongly consider it. The proof of efficacy is limited at this time and there are various procedures you can try. Here, I am showing a classic laser lingual tonsillectomy. Maxillofacial framework surgery. This has shown some efficacy in adults who have failed conservative procedures. It is considered advanced sleep apnea surgery. There are several reports that it works in kids as well. Cohen is plastic surgeon, who in 1998 looked at 16 patients, half of which had tracheotomies and the other half were on their way toward tracheotomy. All had severe retrognathia and he performed maxillofacial framework surgery, and only one patient at the end of that study required tracheotomy to overcome the air obstructive apnea. Indeed, they did not even do interim tracheotomy on patients who did have tracheostomies, they simply left them intubated to allow the surgical wound to heal for approximately two weeks or ten days to two weeks, extubated them and those patients were able to go home without difficulty. Growth consideration is what makes this decision the most difficult and it has to be kept in mind. Like I said, children with marked retrognathia are probably the best patients to have this kind of surgery, and it is an alternative to tracheotomy or long-term nasal CPAP. Tracheotomy is the common final pathway; it is the most reliable means of treating recalcitrant diseases. The indications are for patients who have severe polysomnography-documented obstructive sleep apnea and select patients as previously mentioned (i.e, Pierre Robin sequence, kids with severe cerebral palsy, severe glossoptosis, as well as children who have other indications for tracheotomy aspiration, pulmonary disease, etc.) There is an increased risk of postoperative morbidity. You can create a central apnea as you drive down the CO2 content and accidental dislodgement is always a problem. As Dr. Donovan always tells us, sometimes the tracheostomy becomes the new problem. In conclusion, obstructive sleep apnea syndrome in kids is a common disorder. The manifestations have both similar and disparate features when comparing children to adults. Serious complications can still occur without appropriate evaluation and treatment. Adenotonsillectomy remains the most common and successful surgical means of therapy and more studies are needed to examine the efficacy of advanced sleep apnea surgery in children with recalcitrant disease. Case Presentation: JM is an 11-year-old boy who presents with persistent mouth breathing, loud snoring at night, as well as breath holding spells during sleep. He is obese and according to his parents, seems especially tired during most days and falls asleep easily. They deny any problem with academic performance or overall behavior. On physical examination, he is noted to have 3+ tonsils. Lateral neck films show an enlarged adenoid. Polysomnography is consistent with moderate obstructive sleep apnea. Patient is also noted to have left ventricular hypertrophy on electrocardiogram. Patient was started on nasal CPAP, which reduced his AHI from 22 to 3. He also underwent an uneventful adenotonsillectomy. He is currently tolerating his nasal CPAP and the parents report significant improvement in his original presenting problems. Bibliograhpy: Al-Ghamdi SA, Manoukian JJ, Morielli A, Oudjhane K, Ducharme FM, Brouillette RT. Do systemic corticosteriods effectively treat obstructive sleep apnea secondary to adenotonsillar hypertrophy? Laryngoscope 1997;107:1382-1387. Ali N, Pitson D, Stradling J. Natural history of snoring and related behaviour problems between the ages of 4 and 7 years. Arch Dis Child 1991;71:74-76. Arnold J, Allphin A. Sleep apnea in the neurologically-impaired child. Ear Nose Throat J 1993;72:80-81. Bate T, Price D, Holme C, McGucken RB. Short stature caused by obstructive apnea during sleep. Arch Dis Child 1984;59:78. Bower C, Richmond D. Tonsillectomy and adenoidectomy in patients with Down syndrome. Int J Pediat Otolaryngol 1995;33:141-148. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr 1982;100:31-40. Cohen SR, Simms C, Burstein FD. Mandibular distraction osteogenesis in the treatment of upper airway obstruction in children with craniofacial deformities. Plast Reconstr Surg 1998;101:312-318. Cohen SR, Suzman K, Simms C, Burstein FD, Riski J, Montgomery G. Sleep apnea surgery versus tracheostomy in children: An exploratory study of the comparative effects on quality of life. Plast Reconstr Surg 1998;102:1855-1864. Fry J. Are all “T’s and A’s” really necessary? BMJ 1957;1:124-129. Gozel D. Sleep-disordered breathing and school performance in children. Pediatrics 1998;102:616-620. Grundfast K, Berkowitz R, Fox L. Outcome and complications following surgery for obstructive adenotonsillar hypertrophy in children with neuromuscular disorders. Ear Nose Throat J 1990;69:756-760. Guilleminault C, Eldridge F, Simmons F, Dement WC. Sleep apnea in eight children. Pediatrics 1976;58:23-30. Guilleminault C, Lorobkin R, Winkle R. A review of 50 children with obstructive sleep apnea syndrome. Lung 1981;159:275-297. Guilleminault C, Pelayo R, Leger D, Clerk A, Bocian RC. Recognition of sleep-disordered breathing in children. Pediatrics 1996;98:871-882. He J, Kryger MH, Zorick FJ, et al. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest 1988;94:9-14. Hultzcrantz E, Svanholm H, Ahlquist-Rastad J. Sleep apnea in children without hypertrophy of the tonsils. Clin Pediatr (Phila) 1988;27:350-353. Klein J. Nasal respiratory function and craniofacial growth. Arch Otolaryngol Head Neck Surg 1986;112:843. Leach J, Olson J, Hermann J, Manning S. Polysomnographic and clinical findings in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992;118:741-744. Loughlin G, Brouillette R, et al. Standards and indications for cardiopulmonary sleep studies in children. Am J Respir Crit Care Med 1996;153:866-878. McBride J. Snoring Pediatr Rev 1993;14:445-446. McColley S, April M, Carroll J, Naclerio RM, Loughlin GM. Respiratory compromise after adenotonsillectomy in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992;118:940-943. Messner A. Evaluation of obstructive sleep apnea by polysomnography prior to pediatric adentonsillectomy. Arch Otolaryngol Head Neck Surg 1999;125:353-356. Potsic S, Pasquariello P, Baranak C, Marsh RR, Miller LM. Relief of upper airway obstruction by adenotonsillectomy. Otolaryngol Head Neck Surg 1986;94:476-480. Stewart MG, Friedman EM, Sulek M, deJong A, Hulka GF, Bautista MH, Anderson SE. Validation of an outcomes instrument for tonsil and adenoid disease. Arch Otolaryngol Head Neck Surg 2001;127:29-35. Stool S, Eavey R, Stein N, Sharrar WG. The “chubby puffer” syndrome: Upper airway obstruction and obesity with intermittent somnolence and cardiorespiratory embarrassment. Clin Pediatr (Phila) 1977;16:43-50. Tom LW, Templeton JJ, Thompson ME, Marsh RR. Dexamethasone in adenotonsillectomy. Int J Pediatr Otorhinolaryngol 1997;37:115-120. Wang RC, Elkins TP, Keech D, Wauquier A, Hubbard D. Accuracy of clinical evaluation in pediatric obstructive sleep apnea. Otolaryngol Head Neck Surg 1998;118:69-73. Weissbluth M, Davis A, Poncher J, Reiff J. Signs of airway obstruction during sleep and behavioural, developmental and academic problems. Dev Behav Pediatr 1983;4:119-121. Wiet GJ, Bower C, Seibert R, Griebel M. Surgical correction of obstructive sleep apnea in the complicated pediatric patient documented by polysomnography. Int J Pediatr Otorhinolaryngol 1997;41:133-143. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2005 Baylor College of Medicine
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