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Why Treat Iron Deficiency in Sleep-Disordered Breathing? Introduction Adenotonsillectomy for sleep disordered breathing (SDB) is one of the most commonly performed operations in the paediatric group. In the UK approximately 30,000 adenotonsillectomies are performed each year with a complication rate of 5.7%, including potentially life threatening secondary haemorrhage 1. However, there is still little understanding of the aetiology and development of adenotonsillar hypertrophy. The current proposed models for the pathogenesis include allergy, disordered lymphoproliferation and apoptosis and biofilms 2-4, however none of these theories are conclusive. A number of studies in adult sub-populations with SDB have shown that iron supplementation can reduce the clinical incidence and effects of SDB. Zilberman et al noted a relationship between iron deficiency and SDB in patients with chronic heart failure 5. Participants were given intravenous iron and erythropoietin and over the three month study the mean Hb rose from 10.4g/dL to 12.3g/dL. Associated with this rise was a significant reduction in all but one of their measure of SDB. Specifically there was a reduction in episodes of OSA as well as an improvement in the severity of the nocturnal hypoxia. Furthermore, a preliminary study of 10 adult haemodialysis patients by Benz et al showed improvements in day-time sleepiness and periodic limb movements in sleep associated with improving iron status and anaemia 6. Therefore it is worth presenting the developing of evidence of the associations between iron deficiency, adenotonsillar hypertrophy and sleep disordered breathing. Iron deficiency within the North London SDB population. A study of the iron status of 94 children consecutively presenting to the Royal Free Hospital London, between January 2007 and January 2008, for adenotonsillectomy for SDB was performed by the authors. The routine pre-operative blood tests (Table 1) were used to assess iron status in three ages groups; Group A (0-2yr), Group B (3-6yr) and Group C (>6 yrs). Table 1. Pre-operative Routine Blood Tests
The results showed that children undergoing adenotonsillectomy for sleep disordered breathing had a higher incidence of low iron stores when compared to the normal paediatric population. This is most pronounced in the lower age groups but some older children also display higher than expected serological evidence of low iron stores. The WHO states that approximately 2.5% of a normal paediatric population will have evidence of iron deficiency anaemia (Hb <11g/dL) and greater than 5% within a population is considered abnormal 7 . In this study there is a greater proportion of children with anaemia, as defined by the WHO. This is most pronounced in the younger age groups (25% in group A vs. 18% and 9% in groups B and C respectively). The markers of iron status (Table 2 and Graphs 1-4) mirrored the haemoglobin level within each patient group.
Table 2. Markers of Iron Deficiency and Iron Deficiency Anaemia Graphs 1-4. Pre-operative blood results in the groups.
Graph 1. A comparison of haemaglobin concentration ranges and means between the groups and the normal range. Graph 2. A comparison of mean cell volume ranges and means between the groups and the normal range.
Graph 3. A comparison of mean cell haemoglobin ranges and means between the groups and the normal range. Graph 4. A comparison of ferritin ranges and means between the groups and the normal range. Iron deficiency According to the World Health Organisation (WHO), iron deficiency is the commonest nutritional deficiency worldwide 8. In the normal healthy population this is attributable to inadequate dietary intake and increased iron requirement during the rapid development in the child’s early development. The iron requirement in infancy is higher than at any other point is a person’s life. Inadequate dietary intake of iron may also be attributable to diets rich in ‘fast-foods’ and non-fortified formula milk in the paediatric population. Iron and Neurological development Adequate iron stores are important in the developing brain due to the dependence on iron containing enzymes for myelination, synaptogenesis, and neurotransmission 9. Iron deficiency in early brain development can be seen through to adulthood even when the deficiency has been corrected. Dallman et al investigated Iron and Immunity There is some emerging evidence that iron deficiency may increase childhood susceptibility to infection. This may be due to reduced neutrophil and macrophage function and reduced production of pro-inflammatory cytokines, increasing the risk of extracellular infections 13-14. Iron plays a vital role in the generation of immune cells in the bone marrow and in the proliferation of these cells in response to an antigenic stimulus due to its utilisation in DNA production. Laboratory studies have shown a direct correlation between reduced numbers of peripheral blood T-cells and iron deficiency. Clinically iron deficiency has been shown to affect the function of primary lymphoid organs 15. We suggest that altered immunity, due to iron deficiency, may lead to chronic sinonasal inflammation in affected children with resultant adenotonsillar hypertrophy, nasal obstruction and a worsening of SDB. Conversely, iron deficiency may be a resulting outcome of chronic sinonasal infection. SDB Sleep Disordered Breathing (SDB) encompasses a spectrum of clinical presentations from simple snoring to severe obstructive sleep apnoea (OSA). In the UK 3% of the paediatric population has OSA. The causes of SDB can be classified into 3 groups (Table 3). Table 3. Causes of Sleep Disordered Breathing in Children 16
Most children presenting to an ENT out-patient for SDB will have type 1, and will be treated with an adenotonsillectomy, with the risks as described above. The importance of treating this cohort is well described in the literature and is based on the clinical association of SDB. SDB has been associated with failure to thrive and neurological damage 17, as well as the behavioural sequelae of hyperactivity, hypersomnolence, depression and anxiety 18. Conclusion This is still a novel area of research; however it is already opening up interesting avenues. It is not currently clear whether there is a direct relationship between SDB and iron deficiency or if there is an association, which is the cause and which is the effect. Regardless of this the potential consequences of iron deficiency in this young age group should not be overlooked. Berger et al [] demonstrated that 3 month daily oral iron supplementation had a significant positive effect on iron status and some immune factors. If iron deficiency contributes to adenotonsillar hypertrophy, correcting this shortage may reduce the number of young children requiring surgery. If the deficit is a result of chronic upper airway infections or the association is not a direct relationship then supplementing the iron may prevent the other effects of the insufficiency. In conclusion it is felt that being prompted to give iron supplements to children with SDB can be beneficial. References
Progressive Sensorineural Hearing Loss Due to Cytomegalovirus. Case scenario A 12-month-old boy who does not respond to loud sounds. General considerations Progressive sensorineural hearing loss (SNHL) in infants and young children is commonly due to cytomegalovirus, or CMV. Cytomegalovirus is a member of the Herpes virus family- along with the herpes simplex viruses 1 and 2; varicella-zoster virus (chicken pox), Epstein-Barr virus, and the human herpesviruses 6,7,8. CMV is a common virus- over half of all adults have been infected by the age of 40 years. The virus is transmitted through breast milk, and it is secreted in the saliva, tears, and urine. For most people the viral infection causes few symptoms, but once a person is infected the virus lies dormant within the body. For immunocompromised individuals, such as those with HIV, organ transplant recipients, or the unborn, CMV can cause major adverse consequences. It is estimated that approximately 27,000 new CMV infections occur among seronegative pregnant women in the United States each year.1 Approximately 1% of newborns are congenitally infected with CMV. The infection can occur when the mother experiences either a primary or recurrent infection during pregnancy (although the transmission rate to the fetus is considerably higher if it is a primary infection). CMV is the most common intrauterine infection in the United States, and it is the leading cause of damage to the fetus. Only 10% of the babies infected congenitally will have symptoms when they are born- the other 90% are asymptomatic. Up to 15% of those babies with congenital CMV will develop sensorineural hearing loss (SNHL) of some type, and 3-5% will develop bilateral moderate to profound SNHL.2 The children who are symptomatic at birth have a variety of problems. They may be premature, jaundiced, have enlarged livers and spleens, microcephaly, petechiae, cerebral palsy, mental retardation, seizure disorders, vision issues, and SNHL. The presence of petechiae and intrauterine growth retardation have been found to independently predict hearing loss.3 Diagnosing CMV is difficult. It can be cultured from the urine, but to tell if the infection was congenital this must be done during the first few weeks of life. This method is time-consuming (urine needs first to be first collected, then cultured) and expensive. Fortunately, newer, less expensive methods evaluating saliva collected via a buccal swab are on the way. CMV is a major cause of congenital SNHL. Of all children with bilateral moderate to profound SNHL, it is estimated that 15-20% of cases are attributable to congenital CMV infection. The largest prospective studies on CMV and hearing loss are from the southern state of Alabama in the USA. In a study of 651 children with asymptomatic CMV infection, 48 (7.4%) developed SNHL, compared to 85 (40.7%) of the children with symptomatic CMV infection.4 Importantly, many of these children had a delayed onset of the loss, and progressive loss of hearing. In another Alabama study it was found that of the 190 babies with symptomatic CMV, 63% were found to have a progressive hearing loss, meaning that the hearing worsened with time. Newborns with symptomatic CMV may be considered for intravenous ganciclovir (Cymevene) treatment, an intravenous antiviral. In the largest study available, 42 patients with symptomatic CMV were divided into two groups: 25 babies received ganciclovir, and 17 received no antiviral treatment.5 Hearing in the group who received ganciclovir did not worsen, while in 40% of patients in the untreated group the hearing declined. The conclusion was that ganciclovir helps prevent the hearing loss due to CMV. The problem with ganciclovir is that it is quite toxic–at least 2/3 of patients in the study developed neutropenia. Any infant being treated with ganciclovir needs to be hospitalized for two months due to the severity of the side effects. Regarding the above scenario A 12-month-old boy does not respond to loud sounds. In his past medical history he was a 32-week preemie, he was known to have microcephaly and developmental delay, and he was CMV-positive. We hope he has already had an auditory brainstem-evoked response (ABR). He is at high risk for hearing loss due to his CMV-infection, so should have regular hearing evaluations since it is known that he is likely to have hearing loss. An alternative scenario views a similar child, a 12-month old boy who does not seem to be disturbed by loud sounds. This child was a full-term baby, with no health problems. Could this baby have hearing loss due to CMV? The answer is yes, because many of the newborns with CMV are asymptomatic at birth and they can develop hearing loss when they are older. Another similar scenario A 12-month-old boy who does not seem to be disturbed by loud sounds was a full-term baby, no health problems, and he passed a newborn hearing screen. Can the parents be reassured that his hearing is fine because he passed his newborn hearing screen? The answer is no, not until he has another hearing test. CMV can cause a delayed hearing loss, and many of these children are asymptomatic. Even if a baby passes a newborn hearing screen, it does not mean the baby cannot develop hearing loss when he is older. Final scenario A similar 12-month-old boy undergoes a hearing test and is found to have a SNHL. Is it possible to test the child to see if the hearing loss was caused by CMV? Unfortunately, because the testing needs to be done in the first three weeks of life, the answer is no, you cannot tell at a year of age whether the hearing loss was due to CMV. Conclusion CMV is a common cause of congenital hearing loss, estimated at approximately 15-20% of children with SNHL. The hearing loss can be delayed in onset, and is generally progressive. Testing to detect CMV must be done within the first two to three weeks of life. References
Otitis Media: General Considerations. We will discuss some aspects of acute otitis media (AOM), recurrent otitis media (ROM), and otitis media with effusion (OME). Otitis media is so common that it may be called an “occupational hazard” of early childhood. Acute Otitis Media Let us start with AOM by discussing the case of a child with confirmed diagnosis of AOM, a bulging tympanic membrane (TM), and presence of pus and effusion. What are we going to do with this child? Antibiotics? Wait and see? It is important to know that the other ear is normal. It is a recently noted fact, but still important, and we will show you why. The most important element with AOM is diagnosis, to make the correct diagnosis. There is also a scale of intensity of effects in the TM, a scale created in Texas by McCormick.1 It starts with a normal TM, then a TM with hyperemia but without effusion, then AOM itself, and later OME (without infection, only effusion), and little by little, on the advanced level, toward purulent effusion. Is it possible that this child we are considering has AOM or only OME? It really depends on the symptoms. In this specific case, it is AOM with a bulging TM, purulent effusion, and fever. Thus, it is essential to make a precise diagnosis, the most correct possible, right from the beginning. What if there is just one significant finding, otalgia? Almost all nonspecific symptoms in the ear are not significantly associated with AOM, except for otalgia, which is important. I agree with Galen, who said that physicians are nature’s assistants. This is key. It is impossible to manage a disease rationally, manage a condition or effect, without learning first about its natural history or natural course. It is absolutely essential. I published my first study2 of the natural history of otitis media with a meta-analysis. The most interesting fact to me was that spontaneous resolution was observed in over 80% of cases, improvement without antibiotics, only with placebo. This fact was extremely interesting. It certainly shows a minor effect of antibiotics, and the natural history of otitis media as very favorable. Later, a publication from the US Agency for Healthcare Research and Quality3 showed spontaneous resolution in more than 80% of cases, and there are no subsequent complications if the children are followed closely. If they do not seem to improve quickly, then we should start antibiotics. This is an important fact, because in the United States, lawyers are called upon if there are complications. It is good to have a publication by the government saying that we can have “wait and see” management of otitis media, and that it may proceed without further complications. This is a paradigm in the USA: the option simply to follow up, in managing AOM. It is one option. If the physician does not like it, that’s fine: he can then treat the episodes (assuming they are diagnosed properly). But if he starts to wait and watch, this is the paradigm; and I think, it is the best option. We shall start with the child’s age, and then we can consider a definite or an uncertain diagnosis. In cases of an older child, if we cannot clearly visualize the TM, and we are not 100% sure about the diagnosis, we should wait and watch, without a doubt. However, if it is a small child, with an accurate diagnosis of AOM, it is worthwhile to prescribe antibiotics. But we may resort to observation in between the two extremes of the continuum. If the child is over the age of two years and has a moderate infectious episode, this invites observation. Antibiotics have better effect, real benefit, when symptoms are more severe. And in cases of uncertainty about the diagnosis, we should prefer the “wait and see” approach. There is a Canadian study4 that compared placebos and antibiotics for AOM. When children were small, below the age of five years, and were treated with placebos, the rate of clinical resolution was high. With amoxicillin, the result was a little better, a statistically significant difference but not very high, not a huge difference, but there was an effect. In that study, most children had moderate and severe AOM. Thus, there was an effect for the placebo. There are three countries worldwide that have policies or guidelines issued by the government on the “wait and see” approach in AOM: The Netherlands, Sweden, and the United States. What about bilateral AOM? This is interesting, again. Is it any different from unilateral AOM? There is a meta-analysis from the Netherlands, by Rovers,5 that shows some interesting facts. It is a somewhat different meta-analysis, analyzing individual patients from many combined studies (individual patient meta-analysis). The study shows that the natural history in bilateral presentation of AOM is worse in children below the age of two years. Moreover, there is an enhanced benefit of using antibiotics in AOM in smaller children, below the age of two years. And I rephrase it: in children below the age of two there is major difference between unilateral and bilateral presentation: 20% of children with bilateral AOM benefit from antibiotics, and 6% of children with unilateral AOM benefit. This is statistically significant, and I think clinically important as well. Another recent study by McCormick from Texas6 showed the same, a difference between bilateral and unilateral AOM, including that bilateral AOM was more frequent in smaller children, with severe presentation and positive bacterial culture. Bilateral and unilateral AOM are different diseases. In Israel, similarly to American researchers, Leibovitz and colleagues7 carried out a secondary analysis of previously published studies and showed similar results: with bilateral AOM the symptoms are more severe (than with unilateral AOM) and the middle-ear culture is more often positive for pathogens. I agree with the recommendation by Leibovitz and colleagues that bilateral presentation is a severity factor in AOM. It may be the case that next time we have an update of American Academy Pediatrics AOM Guidelines, bilateral presentation will be included as an indication of severity. Let us talk about ot There is another study by McCormick in Texas8 that compares “wait and see” with immediate prescription of antibiotics, and “wait and see” and late antibiotics. There are no major differences in results. However, the most interesting thing is that after antibiotics there was a change in the nasopharyngeal flora of the children. After antibiotics, there were more drug-resistant pneumococci, many resistant to penicillin, and of course, more adverse events. Therefore, it is more difficult to treat AOM after the children have received previous antibiotics. If we keep on using more and more antibiotics, it will become more difficult to treat AOM. These microorganisms are known in the USA as killer germs. Summing up the information about AOM 1 – The most important thing is to be sure about the diagnosis. I think that pneumatic otoscopy is useful for that, and examination of the TM as well, to have the most precise diagnosis possible. 2 – Management: which child should only be observed? In which children may we resort to this option? 3 – And finally, which antibiotic should be used? In this case, I consider that the selection of an antibiotic is less important because there are no studies that show major differences among all antibiotics normally used for AOM, at least in the initial therapeutic approach. It may be different after failure of treatment or for relapse of recent infection (within 30 days). Recommendations of the American Academy of Pediatrics9 are: if the patient does not have allergy to penicillin, amoxicillin, amoxicillin/clavulanate, cefdinir, cefuroxime, cefpodoxime, perfect! If there is failure of previous treatment, intramuscular ceftriaxone is indicated. I use three doses, on three consecutive days, or clindamycin. If there is history of allergy to penicillin, I use a macrolide such as azithromycin or clarithromycin. In cases of failure of treatment, clindamycin should be considered. Recurrent otitis media Let us start by considering the case of an 18-month-old child with many episodes of AOM, at least eight episodes in the previous year, with little effusion, without hearing loss, and no developmental delay. First of all, we should identify risk factors that may be modified. To encourage breastfeeding is a good idea. To avoid smoking at home is another one. If the child uses a pacifier it should be discouraged. There are studies from the Netherlands 10 that show that children who use pacifiers have more episodes of otitis media. Daycare centers should be avoided: in these environments there are many cases of AOM. If possible, have the child grow and develop quickly, very quickly (just kidding). But, growth and development are the best–and only long-term–solution to otitis media. Better than that, change genetic material–that is the best way to avoid AOM. Why do I say that? Because studies by Casselbrant,11 in Pittsburgh, showed quite well that AOM has genetic involvement. By studying twins, the author showed that approximately 75% of cases of otitis media were caused by genetic factors. Thus, the influence of genetics in AOM is very high, more than all other risk factors combined. Otitis media is a disease of the Eustachian tube (ET). As stated quite elegantly by my mentor, Charles Bluestone,12 the “ET in children is too short, too flexible, too horizontal, and doesn’t work.” This is the problem. If parents do not smoke, and mothers breastfeed, otitis media may result from dysfunction in the ET, in addition to genetic causes. The rest is not important. A new interesting study compared children with episodes of AOM to controls with fewer than two episodes. Results showed differences in tumor necrosis factors (TNF), interleukins, and so on, which are more common in children with recurrent AOM. These are factors associated with genetic elements. Is it possible to avoid AOM by using tympanostmy tubes (TT)? Many times, pediatricians state that TTs are not worthwhile in the absence of effusion, if the middle ear is dry. This is not correct. Why do episodes of AOM start from episodes of flu or colds? With negative pressure in the middle ear, all the microbiological “garbage” from the nasopharynx comes up and penetrates into the middle ear, causing a secondary bacterial infection and AOM. However, by using TTs, we can avoid this process because pressure in the middle ear is balanced. With TTs, there is no reason for the garbage, or bacteria and pus from the nasopharynx, to come up, because there will be no difference in pressure between the middle ear and the nasopharynx. A TT lowers the frequency of ROM by approximately 50%, according to several published studies. Biofilms in otitis media, according to studies performed by Hall-Stoodley,13 are present in middle ears without effusion, in dry middle ears, in mucosa of the middle ear. It is possible that biofilms cause the problem of ROM. An advantage of a TT is that it may be a vehicle to deliver medication to the middle ear, through eardrops. It is not only a ventilation tube, but it may serve also as a tube to deliver medication because drug-concentration in eardrops is about 1,000 times higher than concentrations in systemic antibiotics. This is why it is possible to have drops penetrate into the biofilm. The drops are highly concentrated. It would be possible to kill bacteria in the biofilm, but systemic antibiotics are not strong enough to penetrate the biofilm. Eardrops concentrate the drug, and in turn can directly penetrate into the biofilm of affected mucosa of the middle ear. It is an advantage. Another advantage is absence of resistance by using eardrops, because systemic absorption is minimal and the high local concentration limits the emergence of resistant bacterial strains.
Otitis Media with Effusion Let us start with a two-year-old child, visiting the doctor’s office complaining of sore throat, but the physician detects bilateral OME. Apart from that, the child is healthy. I was a consultant in the Committee of Clinical Practice Guidelines for OME 14 in the United States. It is extremely important to differentiate children with risk from healthy children. Children with risk for developmental delay normally benefit from treatment with TTs. The remaining children without developmental delay could be submitted to a “wait and see” managerial approach. If a child comes to our office for the first time and we detect bilateral OME, how many professionals will immediately indicate placement of a TT? How many physicians will prefer to manage by “watch and see”? In my office, when I see a child with bilateral OME, developm When we obtain a type B tympanogram, the main sign of OME, after one month about 50% of cases will improve, but there is no cure. Cure is very rare. Thus, the natural history of OME with a type B tympanogram is worse. Effusion does not quickly disappear. After three months, less than 30% disappears. Within six months, less than 50% disappears. If the child has developmental delay, I think it is harmful to wait, because there is little likelihood that effusion will disappear. Effusion will show up again after an episode of a cold or flu. We may resort to systemic decongestants (antihistamines with vasoconstriction). Would it be a good idea? A meta-analysis made by Cochrane15 showed that there is no benefit in using systemic decongestants. There is also no prolonged benefit in using antibiotics in OME. The benefit is short and temporary. I know that many physicians prescribe systemic decongestants. The American Academy of Pediatrics does not recommend them because of adverse effects. Why don’t we use antihistamines or systemic decongestants to dry effusion of the middle ear? If you like to practice evidence-based medicine, do not use them. But if you prefer fantasy-based medicine, go ahead. There is risk of adverse events for the patient. Cochrane’s review shows the harm caused by systemic decongestants (antihistamines with vasoconstrictors): behavioral problems, cardiac effects. What about autoinflation of the Eustachian tube? There is a Cochrane review 16 that shows that there might be minor benefits in using autoinflation. Poorly designed studies note that there is no damage to the patient. I myself sometimes use this method, because autoinflation is low cost and generally very safe. Finally, let us talk about Paradise’s study17 of TT that did not show benefit to patients. The media love these studies. Parents see it and say: “we don’t want TT; there are no effects/benefits.” This study started more than 20 years ago. In it, children were healthy, without severe problems, no developmental delays.
In the study, there was almost no difference between children in whom tubes were placed earlier or later. Those who received tubes earlier had a 10% reduction in prevalence and duration of OME. There was almost no difference between the two groups. And it is no surprise. Children were assessed at two years and at 3, 4, 5, 6, and 11 years of age. Every year there was a new publication of this study in a distinguished medical journal. The problem is that Dr. Paradise, a very astute physician, included the wrong children in the study, children who did not necessarily need surgery, because most had unilateral or intermittent effusion (very few had chronic, bilateral OME). Importantly, all children with delays, disorders, or at high risk for OME were excluded. The remaining children might be called “innocent bystanders,” who only had effusion without any other problems in their lives. Unfortunately, they lived in Pittsburg and joined the OME study. But normally these children would never be recommended to have surgery because they were problem-free. Most children are expected to have some episodes of OME in early childhood, and this is no reason to indicate surgery at every episode of OME. Given that there were no symptoms, it was impossible to make the patient feel better. Impossible. Thus, who needs TTs? There is no doubt that some children occasionally need tubes. I think there are three types of children who do: first, susceptible children, who have cleft palate, facial disorders, Down syndrome, many episodes of AOM and/or OME. Second, high-risk children do (e.g., those with underlying hearing loss, severe visual impairment, speech or language disorders, autism-spectrum, or developmental delays). Third, children who suffer from otitis media, who do not sleep, have constant otalgia, balance disorders also benefit from TTs. Apart from these three types, there are innocent bystanders, who do not need management. In children with cerebral palsy, should we place TTs? What is the level of evidence? The problem is there is no evidence, given that there are no studies in this population of patients. All studies have some innocent bystanders, and we do not know about the benefits of TTs to this population. There is a study that I presented at the Otitis Media Symposium in Florida, in June 2007 18 that checks the benefits and effects of TTs, comparing children without developmental problems and children with problems. I enrolled children aged six months to 13 years, using audiometry, and used the validated modified Glasglow Benefit Questionnaire to check the effects of TTs. The questionnaire has questions about changes in quality-of-life, hearing, speech, language, expectations, progress in voice and language therapy, and overall improvement after placement of TTs. There were children with different effects: 50% had developmental delay, and more than 50% had speech and language deficits, some developmental delay, and many episodes of otitis media between the ages of two months and one year. Most children in the study had hearing loss. There was 73% response to the questionnaire, on average, two years after placement of TTs. The results showed that most reported a beneficial effect on quality-of-life. Children could do more things, had better hearing. Unfortunately, the study had no control group, but at least parents did realize beneficial effects of the use of TTs. Concerning hearing loss, parents of children with developmental delay reported benefits/effects. The same occurred with children who had speech and language problems, which were improved, as was school performance, much better after placement of tubes. Children were matched by age, gender, and level of hearing when included in the study. In cases of OME or recurrent AOM, is surgery to place TTs the only surgery to be considered? The first surgery would be TT-placement. Adenoidectomy is not recommended as a first procedure except if there is specific indication. However, if a second set of TTs is required, adenoidectomy may be considered in children older than two or three years of age. Tonsillectomy does not have any benefit to otitis media and should not be considered an important procedure in otitis media. References
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