EARLY DETECTION and INTERVENTION IN CHILDREN DEAFNESS

EARLY DETECTION and INTERVENTION IN CHILDREN deafness
By:
Tutut SRIWILUDJENG T.
Dr. Wahidin Sudiro Husodo Mojokerto

INTRODUCTIONHealth Sense of hearing is an important requirement for improving the quality of human resources because most of the information is absorbed mulalui hearing process is good for the child affect hearing function in speech and language development, socialization and cognitive developments
 Hearing loss is different from other defects where the babies / children who have a hearing loss is often not detected or is not immediately known whether the parents themselves, this disorder also known as "the Invisible disability." The initial symptoms is difficult to know because deafness is not visible. Usually new parents aware of hearing loss in children when there is no response to loud noise or not / too late to talk. Therefore, information from parents is very helpful to know the child's response to the sound environment of the home, the ability of vocalizations and how to pronounce words.Introduction (detection) the existence of early deafness and then treated (intervention) that early would increase the child's ability to speak and spoke. Since the first years of life (0-3 years), is the development of language and speech are the most critical. Research shows that at times the quality of auditory stimulation affects the changes of anatomical, physiological and behavior caused by the development of the auditory system.The delay in diagnosis will also mean there is a delay to start the intervention and will bring serious impact on subsequent developments in the future which will add to burden the family, society and State.Therefore, early detection and intervention is very important to note and should be done immediately.One of the efforts to find cases of infants with hearing loss is to do a hearing in early infancy, mainly contained suspicion of hearing loss and also in groups of infants with high risk.Incidence of hearing loss cases moderate to severe average was detected in 20-24 months. In the case of a mild hearing loss was found the average age of 48 months. Even in cases of unilateral hearing loss which can only be identified at school age.Many researchers argue that early intervention can give better results in speech and language abilities. Handling cases of hearing loss is best done earlier under the age of 6 months.The incidence of hearing loss ranged from 1 to 3 incidents per 1000 live births. That number could increase 10 to 50-fold when it's done a survey on high-risk group.
UNDERSTANDING THE INTERRUPTION OF HEARING and deafnessAccording to the WHO definition of hearing loss and deafness is distinguished beasarkan following provisions.HEARING DISORDERS (hearing impaired): reduced ability to hear well in part or in whole, in one or both ears, either mild or more severe with the average hearing threshold over 26 dB at frequencies 500, 1000, 2000 or 4000 Hz.Deafness (deaf): loss of hearing ability in one or both sides of the ear, is a very severe hearing loss with hearing threshold average of more than 81 dB at frequencies 500, 1000, 2000 or 4000 Hz.WHO also divides the degree of hearing loss into 4 groups as in the following table:Table 1: The distribution of degree of hearing loss





According to WHO hearing loss and deafness problems need to be addressed more seriously considering the amount of losses incurred. Negative impacts such as:1. Interference or obstacle the development of speech, language and cognition in children, especially when it occurs at birth or in infants.2. Difficulty following the lessons in school so that results in lower academic achievement.3. Difficulty obtaining employment or interfere in the work assignment.4. Isolated from social life5. Adverse effects both socially and economically within the environmental community and the State.Classification method that more hearing loss is distinguished from the onset, the genetics, disease progression.In classifying hearing loss need to be considered:1. Type of interruption: type koduktif, sensorineural, mixed.2. Time progress: settled, temporarily, become heavy.3. The degree of hearing loss: rigan, medium, heavy, very heavy.4. The onset of hearing loss: congenital, prelingual period, or postlingual, elderly (presbiakusis)5. Factor: ototoksis, due to noise (GPAB).Auditory function in neonates with a child or adult. The physiology of hearing process is divided into 3 sequence of events, namely the transfer of physical energy in the form of sound keorgan auditory stimulus, conversion or transduction is the conversion of physical energy stimulation to the organ recipient and the delivery of nerve impulses to the auditory cortex.
DEAF congenitalCongenital deafness is deafness which occurs in an infant due to the factors that affect pregnancy or at birth.Deafness can be partially deaf (hearing impaired) or total deafness (deaf). Sebagia Deaf is a state of auditory function is reduced but still can be used to communicate with or without the aid of hearing devices, while the total deafness is a condition that such a disruption of auditory function that can not communicate even if menapat pavement noise (amplification).Deaf kengenital us for a genetic hereditary (adafaktor descent) and non-genetic.Types of deafness that occurs is usually a nerve deafness (sensorineural) degrees of heavy to very heavy on both ears (bilateral)Given congenital deafness have a large enough impact so early on should have no socialization / information to the public and health workers who work in the field for early detection.1. Genesis ScoreThe number of infants suffering from congenital deafness is 1 child in every 1000 live births, while infant being treated in intensive Rungan (Natonal Intensive Care Unit) number is 1 in 50 babies. Then at the age of 2 children under five are growing again in every 1,000 children. Crude birth rate (CBR) in East Java, 22.0 to 24.9 per 1000 population. If the population of East Java 37 million, then the birth rate of approximately 750,000, meaning there are approximately 750 babies are born deaf every year.Prevalence of congenital deafness in Indonesia in the estimate of 0.1%. This will increase each year by 4710 people saw the birth rate of 2.2% in the population of 214.1 million people. It will continue to grow given the risk factors that lead to congenital deafness during pregnancy and childbirth remain high.In developed countries congenital deafness rates ranged from 0.1 to 0.3% of live births .. while in Indonesia based on a survey conducted Dep. Kes in 7 Provinces in the year 1994 to 1996 that is equal to 0.1%.Congenital deafness in Indonesia is estimated as many as 214,100 people when a population of 214,100,000 million (Profile Kesetahan 2005). This amount will increase each year by the existence of population increase due to the high birth rate of 0.22%. This is of course an impact on the provision of educational facilities and employment in the future.WHO estimates that every year there are 38,000 deaf children born in Southeast Asia.WHO meeting in Colombo in 2000 mentapkan congenital deafness as one of the causes of deafness that should lowered prevalence. This of course requires cooperation with other disciplines and society in addition to health tenga.2. CauseCongenital deafness can occur in:Pregnancy (PARENTAL)First trimester pregnancy is an important period for bacterial or viral infection would have caused the deafness. Frequent infections affect hearing include TORCHS infection (Toxoplasmosis, Rubella, Cytomegalovirus, Herpes and Syphilis), in addition to measles and parotitis (mumps).Several types of drugs and teratogenic ototoksik like salicylate, quinine, gentamicin, streptomycin, etc. have pontensi cause disruption tyerjadinya organ formation process and the hair cells in the cochlea (the cochlea). Anatomical structure of ear disorders can also cause the occurrence of deafness among other cochlear aplasia (the cochlea is not formed) and ear canal atresia.At birth (perinatal)The cause of deafness at birth include: premature birth, low birth weight (<1500 g), actions with a tool in the process of birth (vacuum extraction, forceps), hyperbilirubinemia (baby yellow), asphyxia (birth did not burst into tears), and hypoxia brain (the value of Apgar <5 at 5 minutes).According to the Academy of American Joint Committee on Infant Hearing Statement (1994) in infants aged 0-28 days when it was found the following factors should be suspected as a possible cause of hearing loss.1. Family history of deaf since birth2. Prenatal infection; TORSCH3. Abnormalities in head and neck anatomy4. Syndrome associated with congenital deafness5. Low birth weight (LBW <1500 g)6. Bacterial meningitis7. Hiperbillirubinemia (baby yellow) that requires exchange transfusion8. Asfisia weight9. Ototoksik drug delivery10. Using the tool of respiratory / mechanical ventilation for more than 5 days (ICU)
Genetic Hearing LossMost cases of genetic hearing loss is Nonsindromik. Have been identified over 110 loci of chromosome and 65 genes (accessible at http://webhost.ua.ac.be/hhh).More than 300 kinds of syndromes associated with hearing loss, among others, which often Pendred's syndrome, Usher's and Teacher Collins, who is autosomal recessive, Waardenburg's (AD or AR), Mondini malformation, vestibularaqueduct enlargement. Case studies have as many as 20.8% of 810 children with SNHL (Sensory Neural Hearing Loss). Symptoms usually appear after birth and on average about 5.8 years of age referred.The best way to detect cases of prelingual hearing loss that did not appear as sub clinical lahiratau by performing molecular genetic testing of blood samples in infants. Type of inspection that is now available is the test GJB2 deafness and kondria A1555G mutation.The discovery of cases in infants with suspected hearing loss have a genetic cause has been made possible in the present through DNA sequencing techniques. Diperkirkan such an inspection would be a "trend" or stadart future. This progress is an important step in contributing to the handling of cases of deafness, from birth to the better. Infants with congenital deafness who "Late-Onset Hearing Loss Prelingual" depat immediately be identified from birth, either by genetic or environmental causes.
FUNCTION OF HEARING AND SPEAKING SKILLSIn accordance with the child's age, development uditorik as follows: Age 0-4 months: auditory response capabilities are still limited and reflexes. Can be expressed babies keget heard a loud noise while sleeping or awake. Auropalpebral a reflex response or reflex Moro. Age 4-7 months: the response turned his head toward a sound that lies horizontally in the field, although not yet consistent. At the age of 7 months of the neck muscles are strong enough so that the head can be rotated quickly towards the sound source. Age 7-9 months: to identify the precise origin of the sound source and the baby can turn his head firmly and quickly. Age 9-13 months: babies already have a huge desire to seek the source of the sound from all directions quickly. Age 2 years: pemerika should be more careful because children will not respond after several times received the same stimulus. This is because children are able pemperkirakn sound source.Speech development close relation to the stage of development hearing on abayi, so the presence of hearing loss need to be suspected when:Age 12 months: not to rant (babbling) or imitate soundsAge 18 months: not to mention a word that has meaningAge 24 months: vocabulary of less than 10 wordsAge 30 months: can not string 2 wordsTo analyze the early diagnosis of hearing loss is necessary. An easy way to check if there is no means of hearing is to give the sounds at a distance of 1 m behind the child:1. Sound PSS - PSS to describe high-frequency sound2. Beep uh - uh to describe low-frequency3. Sound swipe with a spoon on the edge of the cup (frequency 4 KHz)4. Knocking sound base cup with a spoon (frequency 900 KHz)5. Sound squeezed paper (frequency 6000 KHz)6. Bell sound (frequency 2000 KHz)HEARING EXAMINATIONEarly detection pendengarn disorders can be done by examination of Subjective and Objective. Subjective examination among others, by using acoustic stimuli (noises) that have a certain intensity and value of the response, namely with auropalpebral reflexes. Objective examination conducted by means of electrophysiologic tests of brainstem Auditory Evoked Reponses (ABR) and Otoacoustic Emission (OAE) and tympanometry examination.The important thing to consider before doing this examination is the ear canal should be clean and no abnormalities in the middle ear.Examination important to do is BOA (Behavioral Observation Audiometry), namely by looking at the child's behavior toward a given sound stimulus. Factors that affect the inspection include age, mental condition, will do the test, fear, neurologic conditions associated with motor development and perception.The use of BOA and VRA (Visual Reinforcement Audiometry) in infants and children have limited hearing to determine the valid threshold.












Figure 1. Hearing test with the BOA and the response given by infants and neonates.Quoted from: Nothem 1994
Screening for hearing loss in neonates is a process to test a simple and brief, to identify populations with a high probability of occurrence of hearing loss. There is a problem serious enough impact and there is a high prevalence in the community. There is strong evidence that screening a greater benefit than if the case of late caught early and immediate intervention than if the cases are found too late and only realized later. Early treatment should show greater benefits and to change the prognosis of the disease. screening methods have been evaluated, it is stated precisely and can be used in the intended target. Quite sensitive and specific method, the procedure can be applied at 100% of the target population, easily tolerated and free from risk, it can be widely affordable, low cost, easy target, rapid examination of large populations. The availability of diagnostic facilities and the facilities are adequate for the implementation of intervention programs with the aim of correcting the condition is detected during screening.For detection and early intervention programs should be applicable to all infants (target population) not only at high risk.Research has been done if screening is applied only in high-risk groups will only detect 50% of the number of infants with hearing loss. No doubt that early detection and intervention is important for all infants (New Bomb Universal Hearing Screening). Hearing Screening Recommendation dilakuakn since the first months of birth, then in follow-up and the diagnosis is established until the age of 3 months and subsequently included in the intervention program within 6 months of age.With today's technological advances allow for the detection of hearing loss since birth with the result that can be trusted. Currently, OAE (Otoacoustic Emission) and AABR (Automated Auditory brainstem Evoked Response) is the gold standard examination technique (gold standard) with the principle of checks fast, easy, not invasive with a sensitivity approaching 100%. Constraints is that these facilities are not owned by all provincial hospitals.Brainstem Auditory Evoked Response (ABR) recorded Araf auditory responses in areas along the auditory path to acoustic stimuli.ABR examination is an electrophysiologic measurement that assesses the functions and areas along the auditory nerve to the brain stem auditory path. Waves generated on the ABR recording there are 7 waves, as follows:Wave I: eighth nerveWave II: cochlear nucleus (CN)Wave III: superior olivary complex (SOC)Wave IV: The nucleus of the lateral lemnicus (LL)Wave V: inferior colliculus (IC)Wave VI: medial geniculate (MG)Wave VII: auditory cortex (AC)
ABR examination tool based on the clinical use were classified into 2 types namely:a) Automated brainstem Auditory Evoked Response (AABR)The use of AABR is usually done by placing surface electrodes on the upper forehead, mastoid and behind the neck. Stimulus clicks (usually set at 35dBHL) sent into the ear bayimelalui ear phone. Most systems compare AABR waveforms with the mold that formed the sound of a baby ABR normative data. Based on this comparison, it is determined whether the baby responds pass or fail. Is the system commercially available, can be used as an effective screening tool for infants younger than 6 months. AABR give the results of pass / fail without the need for interpretation, but it is not providing enough information on specific frequency.b) Manual brainstem Auditory Evoked ResponseManual ABR is generally known as the Automated Auditory Evoked brainstem response (ABR) course, unlike that caused AABR response to a click which is set at 35 dBHL, ABR stimulus intensity was varied to determine the low level needed to evoke a clear response. The result other than to determine the severity of hearing loss also can determine whether hearing loss is sensorineural or conductive. When using a click to generate ABR, auditory sensitivity is limited information about the limits 1000-4000 Hz. If necessary, an ABR can use the extra low frequency tone (750 Hz) to determine the configuration of hearing loss.By assessing the shape of waves and the time it takes from when the stimulus given to the resulting wave, can provide the clinical significance of the situation in the path of the auditory nerve or the surrounding area that affect the auditory nerve.





Figure 2. Image of ABR waves
Normal ABR recordings must exist a wave I, III and V with a clear peak in both ears. Wave IV is generally one with wave V.Limitations to detect hearing loss at birth is partly due to the occurrence or manifestation of the new hearing loss occurs at age greater, so the "early-onset hearing loss" is not Visible. In this regard the Joint Committee on Hearing has identified 10 risk as an indicator for monitoring the status of pendengaranya, although in a previous examination otherwise normal.For that JCIH determine risk factors for high risk groups with age limit of 29 days served until 2 years.Idikator need for monitoring the risk for progressive-delayed Sensorineural Hearing Loss in infants aged 29 days to 2 years are:1. Attention parents of suspicion of hearing loss, impaired speech, language and developmental delay2. Family history of childhood deafness3. Stigmata or syndrome is known to have a relationship with sensorineural deaf or hard of hearing conduction4. Postnatal infection such as meningitis5. Eg intra-uterine infection and syphilis TORCH6. Indicators such as neonatal hyperbilirubinemia. PPH (presisten pulmonary hypertension), mechanical ventilation disorders.7. Syndrome associated with progressive deafness such as Neurofibromatosis, Osteopetrosis, Usher's Syndrome.8. Neurodegenerative disorders such as Hunter syndrome or neuropathy disorders sensorimotorik or Friedrich's ataxia and Charcot-Marie Tooth syndrome.9. Head trauma.10. Recurrent otitis media or presisten for at least 3 months.
HEARING DISORDERS PREVENTION STRATEGY and PGP RENSTRANAS Sound Hearing deafness for the purpose of 2030 (MOH)WHO - SEARO (South Asia Regional Office) in 2005 has formed an organization: SOUND HEARING 2030 to coordinate the activities of prevention of hearing loss in the WHO - SEARO. Sound Hearing 2030 (SH 2030) has a mission to reduce preventable hearing loss in 2030 through the development of a sustainable health care system.Additionally Sound Hearing 2030 (SH 2030) also aims to reduce hearing loss can be prevented by 50% in 2015 and 90% in 2030. By carrying out activities SH 2030 Indonesia is expected that each resident has the right to have a degree of ear health and hearing 2030.untuk optimal in realizing the above, the sense of hearing health program management efforts directed at combating of hearing loss and deafness. In order to achieve the same perception and increase the ability of managers and implementers (cross-program and cross-sector) required continuous training activities.Until now WHO has not had a specific strategy that is global in the prevention of hearing loss. But at the Bangkok meeting on 4-5 October 2005 WHO - SEARO has formed an organization: SOUND HEARING 2030 to coordinate prevention activities in the area of ​​auditory ganggun WHO - SEARO.At the inaugural meeting SOUND HEARING 2030 (SH 2030) on October 4 to 5 in Bangkok has set the vision, mission and objectives SH 2030. Dr Bulantrisna Djelantik (Indonesia) at the meeting were set as chairman.Vision Sound Hearing 2030Improve health and welfare of Southeast Asia thanks to a better hearing.Mission Sound Hearing 2030Eliminating preventable hearing loss in 2030 through the development of a sustainable health care system.The purpose of Sound Hearing 2030Reduce hearing loss can be prevented by 50% in 2015 and 90% in 2030.
2030 SH conduct expected for each of Indonesia's population has the right to have a degree of ear health and hearing the optima in 2030.To realize the above, the sense of hearing health program management efforts directed at prevention of hearing loss and deafness.Difficulties and obstacles in developing countries is still limited health infrastructure ear and hearing in prevention, early detection, treatment and habilitation / rehabilitation.In 2002 the Central Government, has developed the Guidelines for National Strategy Plan for Hearing Loss and Deafness (Deafness Renstranas PGP). The guidelines contain six Deafness Prevention strategies need to be done in achieving reductions in deafness. Strategy 4 (four), which exists in PGP Renstranas Deafness is to strengthen management and infrastructure services and strategy 5 (five) to increase the quality and quantity of human resources (HR) in the context of prevention of hearing loss and deafness.Results meeting WHO SEARO Intercountry Consultation Meeting (Colombo 2002) in Sri Lanka recommends that priority issues that must ditanggualangi (including Indonesia) are: Deafness due to middle ear infection (otitis media suppurative Khronikal Omsk), congenital Deaf / Congenital, due to exposure to noise Deaf (Noise Induced Hearing Loss / NIHL) and Deafness of old age (presbycusis) and ganggauan another hearing in order to realize the objectives of Sound Hearing 2030. Better Hearing for All (each of Indonesia's population has the right to have a degree of ear health and hearing the optimum in 2030).PDH program aimed at implementing prevention of hearing loss and deafness through the steps of:1. Determining the magnitude of the problem (magnitude) and the main cause of hearing loss and deafness in certain populations.2. Prevent interference Ototoksik drugs freely.3. Lower prevalence of disorders due to exposure to noise pendegaran on high-risk groups.4. Develop basic ear health (basic ear care) as part of Basic Health Services Program in Public Health Centres.5. Improving early detection and treatment of hearing loss.6. Develop appropriate technology (Appropriate Technology) for examination and treatment of hearing loss.7. Entered into technical cooperation with the Government to Develop National Programme in the field of ear and hearing health.8. Having a system of management and administration for a global program.
Lai statement from WHO (Geneva, 2000) also states that 50% of hearing loss can be prevented (preventable Deafness) through the activities of Primary Health Centre (HEALTH). At the meeting the WHO also recommends that each state reduce preventable Deafness by 50% in 2010 (Better Hearng 2010).For this purpose the Ministry of Health of Indonesia has developed the National Strategy Plan for Hearing Loss and Deafness to achieve the goals Sound Hearing 2030, which will guide the activities of prevention of hearing loss and deafness in both the Central and Regional levelVarious health effort ear / hearing loss prevention (UKT / PGP) has been initiated since 1989 with the establishment of Hearing and Speech Center in the centers of Indonesia as the first step to national health program in Indonesia's ear.Since 2002 in Surabaya also has started to follow the program by opening the Center for Hearing and Communication (Hearing and Communication Center) is housed in poly Audiology Dr. Soetomo. It is expected to participate to support the efforts in implementing the detection and early intervention programs and to achieve the goals Sound Hearing 2030.
Visit patients in Dr profound SNHL. SOETOMO











 REFERENCESAbiratno SFE. Auditory brainstem response (ABR). In the paper "The Grand Opening Hearing and Communication Center Dr. Soetomo "Surabaya 2002: 1-20.Abiratno SF. Handling of hearing dysfunction and developmental disorders in children speak. Handling Seminar on Hearing Loss in Children. Dr Soetomo 26-29 March 2003.Available from http: Http:// www.who.int/ PBD / Deafness / activities / en / Cape Town final report.pdfwww.who.int/ PBD / Deafness / activities / strategies / en / index.htmlDjelantiek B. Deafness and Hearing Impairmentin SEA Region. Strategy formulation of national consultation Gathering prevention of hearing loss and deafness (PGPKT). Bogor in June 2003Future program developments for preventionof Deafness and hearing impairment. 4 Report of the WHO informal consultation, Geneva, 17 - February 18, 2000.Joint Commite on infant hearing. Years 2000 position statement: Priciple and Guidelines for Early Hearing Detection and Intervention Programs. Pediatrics 2000; 106 (4): 798-814.Curriculum and Training Modules Senses Hearing Health Program Management District. Directorate of Community Health. DG Masyarakat.DEPKES Health RI, Jakarta. 2006.Mason JA, Herman KR. Universal Infant Hearing Screening by Automated brainstem Response Measurement. Pediatrics 1999; 101 (2): 221-8.Meyer C, Witte J, Hilman D, Hennceke K, Schunk K, Maul K et al. Neonatal Screening for Hearing Disorders in Infant at Risk: Incidence, Risk Factors, and Follow-ups. Pediatrics 1999; 104 (4): 900-904.Moeler MP. Early intervention and language devwlopment in Children Who Are deaf and hard of hearing. Pediatrics 2000; 106 (3): 45-52.Morton CC, Nance WE. Newborn Hearing Screening - A Silent Revolution. The New England Journal of Medicine 2006; 354: 2151-64.Meyerhoff WL, Carer JB, Scope of the Problem and Fundamental. Ins; Meyershoff WL, Liston S, Anderson RG Eds. Diagnosis and Management of Hearing Loss. Philadelphia: WB Saunders, 1984: 1-24.Northern JL, Downs M. Hearing Behavior Testing of children. In: Hearing in Childern 4th Ed. Baltimore: Williams & Wilkins, 1991: 139-184.Roush J. Screening for Hearing Loss and Otitis Media in Childern. Canada: Singular. Thomson Learning, Inc., 2001.Sirland F, Suwento R (eds). Health Survey Sense of Sight and Hearing 1993 to 1996. MOH RI, 1997.Suwento R, Kadir A, Djelantik B, Zizlavsky S, Hendarmin H: Final Report: WHO Study ON-SEA Helath Sevices And Infrastructure For The Prevention and Control Of Deafness: Indonesian Chapter. Colombo, Dec 17-20, 2002.Suwento, R. Hearing Health infrastructure in Indonesia. In Suzuki J, Kobayashi T, Koga K, Eds. Hearing Impairment: An invisibility. Tokyo: Springer; 2004: 45-8.State-of-Hearing & Ear Care in South East Asia Region. WHO Regional Office for South - East Asia.Smith Aw. Global Perpective On Deafness and hearing impairment. Presentation at Consultation for Preventation and Control of Deafness and Hearing Impairment in the SEA. Colombo, Dec.2002.Yoshinaga-Itano C, Sedey Al, Coulter DK, Mehi al. Language of Early-and Later-Identified Childern With Hearing Loss. Pediatrics 1998; 102 (5): 1161-71.Yoshinaga-Itano C, Gravel JS, The Evidence for Universal Newborn Hearing Screening. Am J Audiol 2001; 10 (2): 62-4.

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DIAGNOSIS and MANAGEMENT Acute bacterial rhinosinusitis CHILDREN

DIAGNOSIS and MANAGEMENT
Acute bacterial rhinosinusitis CHILDREN
By:
Tutut SRIWILUDJENG T.
Dr. Wahidin Sudiro Husodo Mojokerto

INTRODUCTIONRhinosinusitis is a condition which is a manifestation of the inflammatory response paranasalis sinus mucous membranes, which are usually associated with infection that can cause thickening of the mucosa and accumulation of mucus secretions in the sinus cavity paranasalis. So great is rinogen paranasalis sinus infections and rhinitis is often accompanied by changes in the sinuses, the term rhinosinusitis is now a term that is more sidukai for sinusitis, especially in children where the disease is seen as one of the same diseases (Bachert and Verhaeghe, 2002; Mulyarjo, 2002).Rhinosinusitis is an inflammatory disease with a high prevalence and likely will continue to rise. Due to quality of life of patients with this condition can be severely disrupted, it is important for doctors to be able to cope with having the correct knowledge about the definition, symptoms and methods of diagnosis rhinosinusitis.CRS is widespread and is estimated to about 10% hinga 30% of individuals in Europe. In the United States nearly 15% of the population have suffered from at least one episode of rhinosinusitis in his life (bachert and Verhaeghe, 2002; mulyarjo, 2002). In Indonesisa rhinosinusitis morbidity is not known with certainty.Rhinosinusitis generally starts from a viral infection, namely acute rhinitis, which often attack children. According to O'Brien (1998), 0.5 - 5.0% upper respiratory tract infections can suffer from complications of a bacterial rhinosinusitis acute (RSBA).RSBA treatment principle is to eliminate bacterial infection, reduce inflammation and symptoms of clogged nose and restore clearance mukosilier (mulyarjo, 2002). Rhinosinusitis is a disease of "medical" meaning medical therapy is the main treatment modality especially pda children. Act of surgery aimed at cases that are not responsive to maximal medical therapy or in case of orbital or intracranial complications.In this referat will be explained about the diagnosis and management of rhinosinusitis in children.1. AnatomySinus paranalis is a series that surround the nasal cavity. There are four pairs of sinuses paranasalis, namely the frontal sinus, sinus sfenoidalis, etmoidalis sinus and maxillary sinus. Maxillary sinus and sinus etmoidalis began to develop during the 3rd month of pregnancy until the 4th and already formed at birth. Maxillary sinus grew very rapidly until age 3 years later at age 7 years to 18 years of growth to happen again as it grows teeth. At the time of birth sinus air cells etmoidalis grow from 3-4 cells and develop into 10-15 cell precision at the age of 12 years, and became 30-40 when an adult cell. Sinus sfenoidalis grow at the age of 3 years and fully formed at age 12. Frontal sinuses started there at age 8 years and fully formed at age 18. Up to 5% in adults may get one or two sine frontalisnya not fully developed. Therefore, the absence of the frontal sinus which teraerasi well on radiological examination of young people do not need to be considered as a pathological condition (Rachelefsky, 1984; Rohr and Spector, 1984; Josephson and Roy, 1999).Although the anatomy of the sinuses in children is similar to the sinus in adults, the sinuses in children is much smaller so often makes clinical evaluation difficult. On examination of the nasal cavity appears the three projections of the lateral wall of the nasal cavity called konkanasalis. Drainage of the maxillary sinus, frontal sinuses and sinus etmoidalis (sinus - sinus anterior) is through Konka nasalis medius, while drainage of the sinuses and sinus etmoidalis sfenoidalis posterior (sine - sine the posterior) is through Konka nasalis superior (Josephson and Roy, 1999 .)The area is called the complex osteomeatal regarded as a place of major blockages that cause stasis of secretions and recurrent sinus disease. The anatomical area bordered by the anterior edge of Konka nasalis medius in the medial and leteral wall on the lateral nasal cavity.
2. Rhinosinusitis2.1 DefinitionRhinosinusitis is defined clinically as a condition which is a manifestation of the inflammatory response paranasalis sinus mucous membranes are usually associated with infection that can cause thickening of the mucosa and accumulation of mucus secretions in the sinus cavity paranasalis (Bachert and Verhaeghe, 2002).Most sinus infections are rinogen paranasalis and rhinitis is often accompanied by changes in the sinuses. The term rhinosinusitis as a combination of rhinitis and sinusitis seems appropriate to use in children, because both are ongoing disease, where the sinusitis is a continuation of rhinitis and rarely stand alone. Besides the clinical symptoms of rhinitis and sinusitis similar to each other so it looks as a whole the same disease (Mulyarjo, 2002; Bachert and Verhaeghe, 2002).
2.2 IncidentsRhinosinusitis is a common disease encountered in everyday practice. CRS is widespread and is estimated to about 10% to 30% of individuals in Europe. In the United States nearly 15% of the population have suffered from at least one episode of rhinosinusitis in his life (Mulyarjo, 2002; Bachert and Verhaeghe, 2002).Actual incidents of child rhinosinusitis may be very high and largely unknown. If a CRS is an inflammation of the mucous lining of the nose and sinuses paranasalis, it can be said that CRS can occur at any upper respiratory tract infection (Saragih, 1985 quoted by Jonathan B, 1991). But in children where the sinus cavity is relatively small paranasalis with paranasalis sinus ostium size is relatively large, then there is no retention of secretions, so that despite the rhinitis due to viruses that can spread to the mucous layer paranasalis mukosasinus contained in the sinus cavity will be quickly removed by cilia movement. Therefore, in children aged 2-3 years clinical problems rarely arise. Infection of the sinuses paranasalis more likely in older children, however this does not mean that the incident paranasalis sinus infections in children less frequently than adults because children are more often exposed to upper respiratory tract infections than adults (Climent, 1981 quoted Jonathan B, 1991, Rockville, 2000).Menururt Ballenger (1985) rhinosinusitis in children often occurs at the age of 40-10 years. Medium Becker, et al (1989) states that CRS increases in children above the age of 4 years and the majority between the ages of 7-12 years.According to Hayes (2001) upper respiratory tract infections in children caused by viruses do not always develop into RSBA, but RSBA ranks fourth disease is diagnosed in children aged 15 years or younger in age.2.3 PathogenesisSinus ostium paranasalis plays an important role in the pathogenesis of rhinosinusitis. Normal ostium diameter less than 2.5 mm. Acute rhinitis that occurs because of a viral infection caused edema of the mucosa and this can cause pembuntuan ostium in 80% patients (Roos K, 1999 cited Mulyarjo, 2000). Pembuntuan this will cause a decrease of oxygen in the sinus cavity and occurs hypoxia. Hypoxia causes dysfunction of cilia that inhibits drainage of the sinus cavity. When the healing of acute rhinitis, pembuntuan darainase ostium will disappear and return to normal. If there are predisposing factors such as anatomical abnormalities, pembuntuan ostium will settle and drainage disruption lasts longer (Rohr and Spector, 1984; Mulyarjo, 2002).Mucus produced by the normal sinus mucosa contain antimicrobial and very few nutrients so that will complicate the growth of germs. This mucus will always be excluded from the sinus cavity by cilia movement through the sinus ostium. When the ostium deadlock will occur so that the flow resistance of mucus to accumulate in the sinus cavity. Hypoxia also causes mucus gland dysfunction resulting in changes in the quality and quantity of mucus in the sinus cavity. Secretions become more viscous as well as changes in pH so that it becomes a fertile medium for bacterial growth (Roos K, 1999 cited Mulyarjo, 2002).Accumulation of thick secretions also cause damage to the mucosa and ulceration and damage to cilia. Because they served cilia push the mucus out of the sinus cavity lining, the damage to some of cilia would interfere with the task due to the increased accumulation of secretions. In this condition there was an acute bacterial rhinosinusitis (RSBA) is fulminant. Germs breed and many proteolytic enzymes released by leucocytes which became more severe mucosal damage. Metabolic acidosis occurs because tertimbunya lactic acid, and the defense declined antimokrobial. Colonization of bacteria increases and so the damage becomes more severe. These changes occur grandual (Mulyarjo, 2002).When pembuntuan ostium and the ongoing buildup of secretions within the sinus cavity is not resolved, then the process into sub-acute and chronic phase. This occurs when handling RSBA inadequate or there are other factors that cause sinus drainage and ventilation, especially in complex osteomeatal (Mulyarjo, 2002).Maxillary sinus is the most frequently affected by rhinosinusitis is mainly caused by anatomical structures. Maxillary sinus ostium is a winding canal with a length of several millimeters. This canal connects with the meatus medius maksial antrum to form a complex osteomeatal. In addition, maxillary sinus base is lower than the base of the nasal cavity, so that the maxillary sinus ostium is in the superior part of the maxillary antrum. Secretions can terdrainase spontaneously from maxillary sinus into the nasal cavity when the head in an upright position, drain secretions cilia must work out with the superior direction against the force of gravity. It is not surprising that most cases of rhinosinusitis on maxillary sinus, and after that etmoidalis sinus, frontal and sfenoidalis (Slavin, 2002).Factors that may predispose the occurrence of rhinosinusitis are: (Rachelefsky, 1984, Rockville, 1999; Slavin, 2002).2.3 Udem nasal mucosa: upper respiratory tract infection allergic rhinitis, non-allergic rhinitis, smoking, swimming.2.3 mechanical obstruction: hipertofi adenoids, septal deviation rice, Konka bullous, rice polyps, trauma, foreign bodies, neoplasms.
Common factor is the upper respiratory tract infection by the virus allergic rhinitis. Nasal mucosal edema are characteristic of acute infections or allergic rhinitis resulting ostium obstruction, decrease work paranasalis cilia in the sinuses and increased mucus production and viscosity. Ritis non-allergic may experience similar effects with allergic rhinitis.Physiological factors may be predisposing factors affected rhinosinusitis. For example, a cigarette that has a profound effect because it can increase production mukusdan slow cilia movement.This is based on the fact that shows that children who live in the wild house where one or both parents smoke, have an increased incidence of respiratory disorders and chronic rhinosinusitis. Swimmers also have a high incidence of rhinosinusitis may be caused by contaminated water entry of chemicals or bacteria into the sinuses (Slavin, 2002).Mechanical obstruction also can be a predisposition for individuals to get rhinosinusitis. Some circumstances, such as adenoid hypertrophy, septal deviation rice, Konka bullous, rice polyps, trauma, foreign bodies, and neoplasms should be ruled out by endoscopic examination in patients with recurrent rhinosinusitis (Slavin, 2002).
2.4 Classification and Clinical Symptoms2.4.1 ClassificationClassification of rhinosinusitis is based on the long duration of disease on clinical symptoms. According to The American Academy Of Pediatrics (AAP), 2001, CRS classification is as follows:• Acute bacterial rhinosinusitis (RSBA): infection lasts less than 30 days, with mild symptoms or beratdan a continuation of a viral infection (acute renitis).• RSBA recurrent (recurrent rhinosinusitis): several episodes of bacterial infections, each of which less than 30 days and separated by asymptomatic intervals of at least 10 days.• Chronic rhinosinusitis (CRS): inflammation lasting more than 90 days and there are residual symptoms of cough, rinore and clogged nose.
2.4.2 Clinical Symptoms• RSBARSBA Symptoms often preceded by upper respiratory infections (ARI) because firus with rinore clear. ARI symptoms generally improved itself in 5-7 days. If symptoms do not improve after 7 days RSBA diagnosis should be considered (Josephson and Roy, 1999; Mulyarjo, 2002).RSBA clinical symptoms can be classified into major and minor symptoms symptoms. Major symptoms: clogged nose, purulent nasal mucus, pain in the region face (cheeks, forehead, nose), disruption of smell. Minor symptoms are: cough, febrile, slimy throat, headache, sore teeth, halitosis (Josephson and Roy, 1999; Bachert and Verhaeghe, 2002; Mulyarjo, 2003).• SSRSSR is defined as a sinus infection that settled in paranasalis for 90 days or more. Often this becomes a challenge for physicians to make the diagnosis of rhinosinusitis due bervariasidan symptoms are often nonspecific (Josephson and Roy, 1999).The signs and gelaja SSR in children generally include nighttime cough, rinore, clogged nose, postnasal drip, headache. According to Josephson and Roy, (1999), a number of other symptoms may dapt not mislead doctors in ensuring the diagnosis of rhinosinusitis (Table 1).
Chronic rhinosinusitis Acute rhinosinusitisPurulent nasal mucus RinoreCough recurrent facial painFebrile headacheCough postnasal dripUdem poriorbita nose CoughingSore throatMild febrileAsthmaPain in the face / eyes / teeth
Table 1. The symptoms of rhinosinusitis (Josephson and Roy, 1999).
2.5 DiagnosisDiagnosis of acute rhinosinusitis or chronic rhinosinusitis with a diagnose clinically established a careful and complete physical examination. Many common diseases that have similar symptoms of rhinosinusitis. ARI because of viruses and adenoiditis are the two most common diseases that may be difficult to distinguish from patients with rhinosinusitis in children. It is difficult to distinguish acute respiratory infection with rhinosinusitis in the early stages of disease. ARI is the emergence Often predisposisiuntuk rhinosinusitis (Josephson and Roy, 1999).According to Cohen R, 1999 cited Mulyarjo (2002), rhinosinusitis in children is often controversial. Often there is over diagnosis thereby increasing the use of unnecessary antibiotics. Kadan difficult to distinguish viral infections with bacterial rhinosinusitis. ARI is a disease that most children receive, but only less than 5% only which is a bacterial rhinosinusitis.Based on the latest pedoamn from AAP (2001), the diagnosis of rhinosinusitis based only on clinical criteria for both mild and severe radiological examination only to confirm the diagnosis.• Clinical featuresRSBA in children suspected when: O'Brien, 1998; Hayes, 2001) Colds> 10 days Mucus thick yellow / green cough continues, especially at night Gejal Other: fever, headache (on a weight) and halitosisAccording Mulyarjo (2002), the diagnosis is established based RSBA: Colds persist or worsen> 7 days, especially after treatment with free drug The combination of major and minor symptoms. According to Bachert and Verhaeghe (2002) obtained 2 or more major symptoms or 1 major symptom and 2 minor symptoms Rinoskopi anterior: presence of mucosal edema, hyperemia and the presence of secretions mukopurulen Symptoms that may be of particular sinus (maxillary sinus: pain in cheek or graham, sinus etmoid: pain between the two eyes, the frontal sinuses: pain in the forehead, sinus sfenoidalis: severe pain in the center of the head or occipital)
• Physical ExaminationPhysical examination RSBA in children are found: (Suyitno, 1996) nasal mucosa edema and hiperemis purulent discharge in the meatus medius mucosa, nasal cavity or nasopharynx breath smelled but not found signs of pharyngitis, abnormal teeth and foreign bodies in the nasal cavityPhysical examination is less describe RSBA specificity in children, especially children under the age of 10 years• transilluminatesThis examination helps lift maxillary rhinosinusitis diagnosis in children with the shadow of differences between right and left maxillary sinus where the sick sinus provide more gloomy shadow. This examination is only to help the diagnosis, especially in children over the age of 10 years (Suyitno, 1996).
• RadiographyWith Waters position we can evaluate the maxillary sinus. X-ray picture is often found on maxillary rhinosinusitis in children are: Thickening of the mucosa of more than 4mm dim or dark picture on the maxillary sinus Air fluid levelsHowever sometimes the picture mucosal thickening, a grim picture of the sinuses do not always describe rhinosinusitis, especially in children younger than 1 year. Because the form is still small maksilia sinus and soft tissue shadow on the cheek gives grim / dark (Suyitno, 1996).
• CT-ScanWith the CT-scan obtained more detailed information about sinus paranasalis and abnormalities in complex osteomeatal. Thus CT scan can diagnose more precisely, only the higher cost and not smua hospitals have CT-scan devices (Josephson and Roy, 1999).• MRIMRI is superior to menggambartakan examination of soft tissue abnormalities in the sinus paranasalis. However, because the examination is limited to disorders of bone structure. MRI is not is not an option a survey tool to evaluate acute rhinosinusitis and chronic rhinosinusitis (Josephson and Roy, 1999).
2.6 MicrobiologyThe actual picture rhinosinusitis microbiology obtained from studies where taken from the sinus by way punksi antrum or by direct sampling of the affected sinus during surgery (Slavin, 2002)In a study of 76 adults who experienced failure with medical treatment of rhinosinusitis and scheduled for surgery, aerobic bacteria found in 76.3% of cases and anaerobic bacteria in 7.6% cases. Similar results were also obtained in children. Wald et al, 1989 quoted by Slavin (2002), conducted a study of 40 children with non-allergic chronic rhinosinusitis. The results obtained positive sinus aspirates in 58% of the sample, with the dominant bacteria Streptococcus pneumonia, Haemophilus influenzae, and Moraxella Catarrhalis. There is no anaerobic bacteria were isolated in children who do not have this allergy. Similar results were obtained in the study of chronic rhinosinusitis in children with respiratory allergy.According to the AAP (2001), Lippincott (2002), Slavin (2002), and Lampl (2003), bacteria that commonly cause acute bacterial rinoinuitis is Streptococcus pneumonia (30-40%), Haemophilus influenzae (20-30%), Moraxella Catarrhalis (12-20%) and Streptococcus pyogenes β Hemolyticus (3%). These germs are bacteria that are commonly found in cultured bacteria, in addition to the germs that are rarely encountered such as Staphylococcus aureus and anaerobic germs. Anaerobic germs into play when the sinus cavity oxygenation dwindle. The more progress in the process increasing the population of anaerobic bacteria. In chronic rhinosinusitis is more dominant role anaerobic (Lampl, 2003).
2.7 TherapyThe principle of management of rhinosinusitis include the treatment and prevention of infection, improved patency otium sine, repair and menkan mucociliary airway mucosa inflammation. Medical management of rhinosinusitis is a phased approach. Once the diagnosis rinosinuitis established, therapy with antibiotics is generally a first-line therapy (Moesges, 2002). Ostium Pembuntuan inus needs to be eliminated with decongestants for sinus drainage back to normal.According Moesges (2002), treatment with antibiotics is often times based on experience because of the difficulty of obtaining reliable specimen for culture. Most importantly, the selection of antibiotics should be based on the prediction of its effectiveness, potential side effects, and price. To RSBA recommended antibiotic therapy 14 days diving.Lately a number of studies published stating that the need for antibiotic therapy is still uncertain. Effects greater damage can occur by the emergence of side effects from drugs that balanced with the beneficial effect of oral antibiotic therapy. Therefore, some researchers estimate the end of antibiotic therapy (Moesges, 2002).According to the Rockville (1999) RSBA potential to become a serious illness sehigga needed antibiotics to prevent complications. But the excessive use of antibiotics can increase the incidence of side effects, bacterial resistance to antibiotics and treatment costs (Watson et al, 1999; Rockville, 1999; Garbutt et al, 2001; Lampl, 2003).Based on the bacteria that often cause RSBA, then the first-line antibiotic is amoxicillin (Josephson and Roy, 1999; Clients, 2001; Lampl, 2003). According to the AAP (2001), the election is because the antibiotic amoxicillin are relatively safe and affordable price. This option is done mainly to attack the pertaman RSBA which have never been treated with antibiotics. To RSBA a history of recurrent or maybe day after amoxicillin antibiotics less effective, for the second-line antibiotics may be an alternative. If the suspected existence of germ-producing β-lactamase enzymes, the combination of amoxicillin and klavulanat acid can be used. For patients hypersensitive to penicillin can be used katrimoksazol, makrolid or doxycycline, but the latter drug is not recommended in children. Antibiotics are given 10-14 days ahrus (Mulyarjo, 2002).According to the AAP (2001), about 80% of children with RSBA improved with amoxicillin treatment. Lippicott (2002) reported the same thing at 90% of cases, and Hayes (2001) melapoekan 91.2% of cases.Fenilpropanolamin or systemic decongestants pseudoephedrine may improve ventilation and restore sinus mucociliary function. While topical decongestants may be useful in the early stages of the disease process rinosinuitis, but the use of this topical decongestants should be limited to three smapai 5 days (Josephson and Roy, 1999; Lampl, 2003).Surgical therapy in patients with rhinosinusitis children aimed at recurrent rhinosinusitis and chronic rhinosinusitis who are not responsive to maximal medical therapy and when there are complications such RSBA orbital or intracranial complications (Josephson and Roy, 1999; Mc Clay, 2001).

2.8 Complications of Acute Bacterial rhinosinusitisSinus paranasalis limited by the brain and cavum orbit in lateral, superior and posterior, so that the spread of infection can cause intracranial or orbital complications of life-threatening. Orbital complications are usually caused by direct spread of infection from the sinuses through the lamina papiracea etmoidalis.
Orbital ComplicationsSelusitis preseptalSelusitis orbitalSubperiosteal abscessOrbital abscessCavernous sinus thrombosisBlindness

Intracranial complicationsMeningitisEpidural abscessSubdural abscessBrain abscessAnterior wall of frontal sinus osteomyelitis
Systemic ComplicationsToxic shock syndromeSepsis
Table 2. complications of rhinosinusitis (Josephson and Roy, 1999).
SUMMARYRhinosinusitis is a common disease encountered in everyday practice. anatomical factors cause children vulnerable to obstruction of sinus ostium, causing ketidaklancaran nasal secretion and increases bacterial growth.Diagnosis of acute and chronic rhinosinusitis, especially Diagnosis based on clinical history and clinical examination. Medical treatment plays an important role in the handling RSBA, with the aim to kill the germs that cause, opening the sinus ostium and restore the function of cilia. Surgical therapy is intended for cases that are not responsive to medical therapy or if there is intracranial or orbital complications.


 LiteratureAmerican Academy of Pediatrics, 2001. Clinical PracticeGuidelme: Management of Sinusitis. Pediatrics: 108 (3): 798-808.Bachert C, Verhaeghe of Pediatrics, 2002. Differential Diagnosis of Rhinosinusitis. Enhancing the Treatment of Rhinosinusitis Family Practice Recertification. 24 (1) 8-13.BallengerJJ, 1995. Infectio paranasal sinuses. In Ballenger JJ. Deseases of the Nose, Throat, Ear, Head and Neck. 13 Ed. Philadelphia Lea & Febiger. 205-217.
 W. Becker Nouman HH. Pfaltz CR, 1989. Ear, Nose and Throat Siseases 3rd Ed. New York. Theme Medical Publishers. 224-253.Garbut JM et al, 2001. A randomized, Plaeebo Antimierobial-Controlled Trial of Treatment for Children with Clinical Diagnosed Acute Sinusitis. Pediatrics, 107 (4): 619-625.Hayes RO, 2001. Pediatrics Sinusitis: When it's Not Just a Cold. Clinician Reviews: 1 (10) :52-59Jonathan B, 1991. Comparative Test maxillary sinusitis treatment in children with Diathermy and Irrigation. End of Work Pathology Laboratory SMF Dr ENT Medical Faculty Airlangga University. Soetomo.Josephson G, Roy S. 1999. Pediatrics Rhinosinusitis: Diagnosis and Management. International Pediatrics, 14 (1): 15-21.Klein GI, 2001. Treatment Guidelines for Acute Rhinosinusitis Infect Med, 15 (10F): 26-33.Lampl KL. 2003. The Role of OTC decongestants in the Treatment of Rhinosinusitis. http://www.medscape.com/viewprogram2685. Download date 09/26/2003.I. Lippincott, 2003 Sinusitis Pediatrics. Medical Treatment http://www.emedicine.com/ent/topic/612.htm 144 k10.11.03 Download date 11/10/2003.McClay JE, 2001. Sinusitis Pediatrics, Surgical Treatment http://www.emedicine.com/ent/topic/612.htm 144 k10.11.03 Download date 11/10/2003.Mosges R, 2002. Medical and Surgical Management of Rhinosinusitis. How Much Treatment Is Required?. Enhancing the Treatment of Rhinosinsitis. Family practice Recertification; 24 (1): 14-18.Mulyarjo, 2002. Rhinosinusitis and Penatalaksanannya. Symposium management of rhinosinusitis and otitis media. Surabaya. 1-8.Mulyarjo, 2003. Diagnosis and management of rhinosinusitis in children. Rhinology Symposium Abstract Update. Bali. 56.O'Brien KL, et al 1998. Acute Sinusitis-Principles of Judicious Use of Antimicrobal Agents. Pediatrics, 101 (1): 174-177.Rachelfsky GS, 1984. Sinusitis in Children. Diagnosis and Treatment. Clin Rev Allergy, 2: 397-408.Rockville, 1999. Diagnosis and Treatment of Acute Bacterial Rhinosinusitis summary, Evidence Report / Technology Assesement (9). http://www.ahrg.gov/clinic/epcsums/sinussum.htm.download dated 02/22/2004.Rohr A.S and Spector SL. 1984. Paranasal Sinus Anatomy and pathophysiology. Allergy Rev Clin 1984; 2: 387-395.Slavin RG, 2002. Rhinosinusitis Epidemilogy and Pathology. Enhancing the Treatment of Rhimosinusitis Family Practice Recertification, 24 (1): 1-7.Suyitno S, 1996. Maxillary sinusitis in children at Dr. Manuscript Collection Semarang Kariadi annual Scientific 

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DIAKNOSIS AND MANAGEMENT Otitis media effusion in CHILDREN

DIAKNOSIS AND MANAGEMENT
Otitis media effusion IN CHILDREN
By:
Tutut SRIWILUDJENG T.
Dr. Wahidin Sudiro Husodo Mojokerto

INTRODUCTIONOtitis media effusion (Ome) is a disease often suffered by babies and children. Outside the country, particularly in countries that have 4 seasons of this disease were found with the incidence and prevalence rates are high. From some literature can be concluded Ome average incidence by 14% - 62%, while other researchers have reported an average prevalence rate Ome 2% - 52% .1In Indonesia, are still rarely found in the literature that reported the incidence of this disease, this is caused because there has been no specific research on this disease, or not detected due to minimal complaints in children who suffer OME.1Ome is an inflammation of the middle ear of the mark in the presence of fluid in the pleural cavity of the middle ear with intact tympanic membrane without the signs of acute ifeksi. Ome included in the class of non-suppurative otitis media. There are many synonyms of this Ome. But the most widely accepted terminology is otitis media based efusi.4The presence of fluid in the middle ear resulting in hearing loss. Parents complain their children listen to television with the volume too loud, often re asking for the answers given his parents and did not immediately ignored when on call. Some children may not get complaints. The fluid in the middle ear in children can be many months and only recently recognized when the examination was held rutin.5The children need the ability to hear to learn to speak. The presence of hearing loss because of fluid in the middle ear resulted in delays bicara.6-8 diagnosis and early treatment can prevent children from hearing barriers Ome. This paper will be delivered the diagnosis and management of Ome.
1. DefinitionOtitis media effusion is middle ear inflammation characterized by the accumulation of fluid in the middle ear effusion with intact tympanic membrane without the signs and symptoms of inflammation akut.2, 9.102. Anatomy and physiologyTo understand the occurrence of Ome, anatomy and function of the fallopian Eustachius plays an important role. Tuba Eustachius is part of the system which best corresponds including the nose, nasopharynx, middle ear, and the cavity mastoid.2, 4 Tuba Eustachius not just a tube but an organ that contains lume with mucosa, cartilage, surrounded by soft tissue, such as Veli Palatine muskulus peritubular , Levator Veli Palatine, salpingofaringeus, and tensor tympanic and bone in the superior support. Differences tuba Eustachius in children and adults who cause increased incidence of otitis media in children anak.4The length of half the length of the fallopian tubes in young adults, making it easier reflux of nasopharyngeal secretions into the middle ear through the tube is short. The direction of the tube varies in children, the angle between the tubes with a horizontal plane is 100. While in adults 450. The angle between the tensor Veli Palatine with cartilage varies in children but relatively stable in adults. These differences may help explain the opening of the tubal lumen (contraction tensor Veli palatini) which are not efficient in children. Period of cartilage to grow from infancy to adulthood. Density of elastin in cartilage in infants less but greater density of cartilage. Ostmann fat pad is smaller by volume in infants. In children many Mucosal folds in the lumen of the fallopian Eustachius, this may explain the increased tubal compliance in children-anak.2, 4






Figure 1. The difference degree angle in children and tuba Eustachius dewasa.2
3. Etiology and PathogenesisEtiology and pathogenesis is multifactorial Ome include viral or bacterial infections, tubal dysfunction Eustachius, immunologic status, allergy, environmental and social factors. However a negative middle ear pressure, immunological abnormalities, or a combination of both factors is estimated to be a major factor in the pathogenesis of Ome. Other factors including adenoid hypertrophy, chronic adenoiditis, palatoskisis, nasopharyngeal tumors, barotrauma, radiation therapy, and inflamed comorbidities such as sinusitis or rhinitis. Smoking can induce lymphoid hiperplasi nasopharynx and adenoid hypertrophy is also an emergence pathogenesis OME.2
3.1 Impaired function of the fallopianTubal dysfunction causing aeration mechanism into the middle ear cavity is interrupted, the drainage from the ear cavity into the nasopharynx cavity disturbed and impaired middle ear cavity protection mechanisms against reflux of nasopharyngeal cavity. Due to the disorder of the middle ear cavity will experience a negative pressure. Negative pressure in the middle ear causes increased capillary and subsequently occurs permaebilitas transudation. In addition, populations occur infiltration of inflammatory cells and glandular secretion. As a result there is accumulation of secretions in the middle ear cavity. Chronic inflammation in the middle ear will cause the formation of granulation tissue, fibrosis and bone destruction.Tubal obstruction Eustachius ytang lead to a negative pressure in the middle ear tympanic membrane retraction will be followed. Adults will usually complain of discomfort, a feeling of fullness or feeling depressed and consequently incurred a mild hearing loss and tinnitus. Children may not show symptoms like this. If this situation lasts for a long time the liquid will be drawn out of the mucous membrane of the middle ear, causing a state which we call the serous otitis media. These events often occur in children associated with upper respiratory tract infections and some hearing loss mengikutinya.7, 12


3.2 InfectionsBacterial infection is an important factor in the pathogenesis of Ome since reported the existence of bacteria in the middle ear. Streptococcus pneumonia, Haemophilus influenzae, Moraxella Catarrhalis known as the most pathogenic bacteria found in ear tengah.7, 13.14 Although the results obtained from a lower culture. The cause of the low figure is expected karena13: The use of long-term antibiotics prior to pemakian ventilation tube would reduce the proliferation of pathogenic bacteria, Secretion of immunoglobulins and lysozyme in middle ear effusions inhibits the proliferation of pathogens, Bacteria in middle ear effusion acts as a biofilm
3.3 Status of ImmunologyAdequate immunological factors play a role in Ome is secretory Ig A. immunoglobulin is produced by glands in the mucosa of the tympanic cavity. Secretory immunoglobulin A is mainly found in the effusion mukoid and is known as an active working surface immunoglobulin respiratory mucosa. It acts to block germ that is not to direct contact with the surface apitel, by forming the complex bond. Direct contact with the epithelial cell wall is the first stage of the penetration of bacteria to tissue infection. Thus, Ig A actively prevent infection kuman.14

3.4 AllergiesHow allergic factors play a role in causing Ome is still unclear. However, the clinical picture in believing that allergies play a role. The idea is embriologik analogy, where the tympanic mucosa were similar to the nasal mucosa. At least manifestation of the fallopian Eustachius lergi is a cause of chronic grafting and subsequently cause the effusion. However, IgE levels of research that became the criteria of atopic allergy, both levels in effusions and in serum does not fully support the allergy as penyebab.15Etiology and pathogenesis of otitis media because of allergies may be caused by one or more of the following mechanisms: 15 middle ear mucosa as the target organs (target organs) swelling due to inflammatory processes in the mucosa of the fallopian Eustachius nasopharyngeal obstruction due to inflammatory processes, and nasopharyngeal aspiration of bacteria contained in allergic secretions into the middle ear space.
4. Clinical symptomsOme Patients rarely give symptoms so that the children are often late known. Ome symptoms marked by a feeling of fullness in the ear, you hear a buzz that intermittent or continuous, hearing loss and mild pain. Dizziness also felt patients Ome-sufferers. Symptoms often are asymptomatic, so the Ome known by people close to the child such as parents or guru.2, 16Children with Ome also sometimes be seen pulling at their ear or feel like his ears tersumbat.17In advanced cases often found the existence of speech disorders and language development. Sometimes the situation is also encountered difficulties in communicating and backwardness in pelajaran.18, 19
5. DiagnosisOme diagnosis in children is not easy and there are significant differences in accordance with clinician skill, particularly at primary care level or pediatrician who diagnosed it. Symptoms no sensitive or specific, in fact many children without symptoms. Physical examination on children with Ome potentially inaccurate picture because the subjective impression of the tympanic membrane difficult to assess. Not to mention the children who are uncooperative during examination. However enamnesis and physical examination still plays an important role in diagnosing OME.6
5.1 AnamnesisIn diagnosing Ome required carefulness of the examiner. This is due to complaints that are not typical, especially in children. Parents usually complain of hearing loss in children, teachers reported that the child has hearing problems, setbacks in lessons at school, even in speech and language disorders. Ome often discovered accidentally during ear examination and hearing screening in school-sekolah.5, 11In children with Ome of history's most frequent complaints were hearing loss and sometimes felt ears feel full up with ear pain. And in children with Ome usually they are also often found with a history of cough, runny nose and sore throat berulang.3 In children greater difficulty they usually complain menengarkan lessons at school, or have to raise the volume while watching television in rumah.18 People Parents also often listened to his ears feel uncomfortable or often saw her son pulling the leaves telinganya.20
5.2 Physical examinationTo diagnose Ome on physical examination should be done otoskopi examination, timpanogram, audiogram and sometimes miringotomi action to ensure there is fluid in the ear tengah.5, 7,8,11,21
5.2.1 OtoskopiOtoskopi examination done for the condition, color, and translusensi tempani membrane. Various kinds of changes or abnormalities that occur in the tympanic membrane can be seen as berikut.21, 22:a) The tympanic membrane is dull and yellowish translucent menggati description other than that where the triangle of light reflex in the inferior quadrant Antero shortened, perhaps also showed that increased blood vessel kapier on the tympanic membrane. In the case with liquid mukoid or tympanic membrane mukupurulen younger colored (beige).b) retraction of the tympanic membrane when the manubrium malei look shorter and more horizontal, looked haggard and membrane retracts the light reflex. The color may change slightly yellowish.c) atelectasis, tympanic membrane is usually thin, atrophy and may stick to the incus, stapes and promontium, especially in cases that have been advanced, usually cases like this because of tubal dysfunction and otitis media effusion Eustachius longstanding.


Figure 2. Otitis media adesiva (atelectasis) 23d) the tympanic membrane with sikatrik, bleak until severe retraction accompanied by the atrophy was found in otitis media due adesiva by fibrotic tissue middle ear as a result of previous inflammatory process that lasted long.e) The description of water or fluid level bubles usually found in liquid-filled Ome serus.






Figure 3. Serous fluid in the cavity Figure 4. Multiple water bubbletimpani23 on Ome 23
f) tympanic membrane dark blue or purple hematotimpanum shown in cases caused by temporal bone fractures, leukemia, tumor vascular middle ear. While the younger blue color may be caused by barotraumas.




Figure 5. Tympanic cavity with fluid which is mixed darah.23g) Another description is found sikatrik and spotting kalisifikasi.
On examination Ome otoskopi pointed suspicion if found mark-tanda21:a) There were no signs of acute inflammation.b) There is a change in color of the tympanic membrane due to reflection from the fluid in the tympanic cavity.c) tympanic membrane appear more prominent.d) tympanic membrane retraction or atelectasis.e) There were water or bubble fluid levels, orf) The mobility is reduced or modifying membrane.
5.2.2 Otoskop pneumatic / otoskop SieglePneumatic Otoskop was first introduced by Siegle, relatively unchanged since its first introduction in 1864. Examination otoskopi pneumatic but can see the type of perforation, tissue pathology, and to an intact tympanic membrane can also be viewed gerakanya (mobility) by giving positive pressure then the tympanic membrane will move to the medial and when given a negative pressure then will move to the tympanic membrane leteral. Examination otoskopi pneumatic is standard on OME.6 diagnostic physical, 21





Figure 6. Otoskop Siegle23
5.2.3 tympanometryTimpanometer is a tool to determine the condition of the middle ear system. This measurement gives an overview of tympanic membrane mobility, hearing bone stock condition, including circumstances in the middle ear air pressure in it, so useful in knowing conduction disorders and tubal function Eustachius.14, 21Graph the results of measurements or timpanogram timpanometeri can to find a picture in the middle ear abnormalities. Although found a huge variation in timpanogram but in principle there are only three types, namely type A, type B, and type C.6, 21In patients Ome timpanogram picture that is often found is type B. Type B is relatively flat shape, it shows the movement of the tympanic membrane is limited due to the fluid or adhesions in the tympanic cavity. The graph is very flat may occur due to perforation of tympanic membrane, a lot of wax on the outer ear canal or fault on the appliance that is clogged channels.







Figure 7. Overview timpanogram.25 type
Tympanometry examination can predict the existence of fluid in the tympanic cavity better than saja.6 otoskopi examination, 7,21,25

5.2.4 audiogramFrom examination audiometrik obtained pure tone threshold value of bone and air.Hearing loss is more frequently found in patients Ome with a viscous fluid (glue ear). Nevertheless some studies say there is no significant difference between the liquid and viscous serus against hearing loss, while the volume of fluid found in the middle ear is more berpengaruh.21Patients with Ome found deafness conductive hearing loss with mild to moderate so as not very influential in everyday life. Persistent bilateral deafness more than 25 dB can interfere with intellectual development and ability to speak anak21. If this could be allowed to gain weight deafness is bad for patients. Ill-effects may include local disorders of the ear as well as the more common disorders, such as disorders of language development and decline in school lessons. Patients with more severe conduction deafness may have been obtained fixation or break the chain osikel.26Ome guidelines prepared jointly by the AAFP, and AAP AAOHNS states that audiology is one component of patient examination Ome. Audiometrik examination is recommended in patients with Ome for 3 months or more, language delay, learning disorders or suspicion of significant hearing impairment. Based on several studies, conduction deafness is often associated with Ome and influential in the process of hearing both ears, sound localization, speech perception in noise. Hearing loss caused by Ome will start blocking the ability of language that didapat.7, 27
5.2.5 RadiologyMastoid radiology examination images previously used for screening effective Ome, but now rarely done. Anamnesis of disease history and physical examination to help diagnose disease much month.7CT scans are very sensitive and is not required for diagnosis. Although CT scan is important to get rid of the complications of otitis media eg mastoiditis, sigmoid sinus thrombosis or any kolesteatoma. CT scan is important especially in patients with unilateral Ome which must be ensured that the mass in the nasopharynx has disingkirkan.7
6. ManagementThe diagnosis and treatment as early as possible play an important role. The success of treatment is determined by finding the causes and overcome in order to prevent further due to the disease. Tubal blockage and infection of upper respiratory tract of chronic and recurrent is one important factor diperhatikan.16But Ome own management is still a debate, is caused by either conservative treatment or surgery, each has advantages and disadvantages. Ome conservative treatment is not yet proven to cure patients with Ome, but in principle can reduce morbidity when conservative therapy fails or is not considered memuaskan.28Treatment of Ome include conservative treatment and surgery. Conservative treatment locally (nose drops or spray) and systemic broad spectrum antibiotics among others, an antihistamine, decongestant, with or without corticosteroids. Treatment and control of allergies can reduce or cure otitis media efusi.16Operative treatment be done in cases where conservative treatment after diving more than 3 months did not recover. To give good results against the drainage done miringotomi and vent pipe installation. Ventilation pipes installed in the area quadrant Antero Antero inferior or superior. Vent pipe will be maintained until this paten.16 tubal function in the operative management include mirigotomi with or without ventilation pipe installation and adenoidektomi with or without tonsilektomi.2, 4The objective is to eliminate the ventilation pipe installation in the middle ear fluid, hearing loss happens, preventing recurrence, preventing disruption of cognitive development, speech, language and psikososial.2, 4






Figure 8. Figure 9 Installation of vent pipe. Ome with a hole(Grommet) .23 ex parasitesis.23
Otitis media effusionOme (otitis media effusion)Full flavor ears / hearing loss / otofoni








Figure 10. Scheme of the diagnosis and management OME297. ComplicationDue to continued Ome may result in loss of auditory function that will affect the development of speech and intellectual. Changes that occur in the middle ear can lead to disease progression to otitis media and chronic otitis media adesiva maligna.2, 4.30
8. SummaryOme often occurs in infants and children so it is quite difficult in diagnosing illness. Nearest and many interact with the child would be a good source of information. Attention parents and teachers are very helpful in making the diagnosis.Etiology and pathophysiology is multifactorial Ome, mutual support and inter-related. In infants and children, immunological status is very important to maintain resistance to infection.History and physical examination is necessary in the diagnosis Ome. The use of pneumatic tools otoskopi, tympanometry, audiometric for physical examination is helpful in establishing the diagnosis.Treatment of Ome include conservative treatment and surgery. Conservative treatment includes antibiotics, antihistamines, dekogestan, with or without corticosteroids. Treatment is operative include mirigotomi with or without ventilation pipe installation and adenoidektomi with or without tonsillectomy.Piñatalaksanaan a fast, accurate and adequate essential role in inhibiting the process of hearing loss and other complications.REFERENCES1. Tamim S, Djafar ZA, Soetirto I. The prevalence of otitis media effusion in children nursery school - and elementary school children in kindergarten and elementary school of Al-Azhar Jakarta. Manuscript collection of PIT attention. Batu Malang 27 to 29 October 1996; 215.2. Bluestone CD, Client JO Otitis media in infants and children In bluestone et al eds. Otolaryngology Pediatrics 2nd ed Philadelphia, WB Saunders Co., 1995.3. Paparella MM, Jung TTK, MV Goycoolea Otitis media with effusion In Paparella MM, eds DA Shumrick Neurootology Otolaryngology and Otolaryngology 3rd ed, WB Saunders Co, 1991: 1325-1330.4. Rosenfeld RM and bluestone CD. Evidence-based media Stephen Berman, MD eds. Canada BC Decker Inc. 1999.5. Lavenson MJ, MD, FACS. Fluid in the middle ear (serous otitis media) http://www.earsurgery.org.serous.html. Acces on February 16, 2008.6.accuracy of clinical diagnosis of otitis media with effusion in children, and significance of myringotomy: Diagnostic or therapeutic? J Korean Med Sci 2004; 19: 739-43.7. Thraher RD, Allen GC. Middle ear, otitis media with effusion. http://www.emedicine.coom/ent/topic209.htm. acces on February 16, 2008.8. BRM Pereira, Pereira BR, Canterlli V, Sady SC. Prevalence of bacteria in children with otitis media with effusion. J Pediatry (Rio J). 2004; 80 (1): 41-8.9. MT Johnson, Ph.D. Otitis media: A Desease presentation, Indiana University school of medicine. http://web.instate.edu/theme/micro/otitis/otitis/htm. acces on February 16, 2008.10. Kim S.C. Pediatric Clinical Guidelines, Editor: Schwartz M.W. EGC kedokeran book publishers, p.: 299-300.11. Restuti, R. Sosialisman. Otitis media effuse relation to allergic rhinitis. Collection of manuscripts of national symposium on the latest developments in the management of several allergic rhinitis comorbidities. Malang; August 2006: 1-9.12. Courchane M, Essen J. Serous otitis media. http://www.med.umn.edu/otol/library/serous.htm. acces on February 16, 2008.13. Chul-Won Park at all. Detection rates of bacterian in chronic otitis media with effusion in children. J Korean Med Sci 2004; 19: 735-8.14. Koivunen P. Otitis media in children: detection of otitis media effusion and influence on hearing. Oulu university library. Oulu, 1999.15. Doner F. Yariktas M, Demirci M. The role of allergy in recurrent otitis media with effusion. J Inverst Allergol Clin Immunol 2004; Vol. 14 (4): 154-158.16. Djafar ZA, Effendi G. Management of serous otitis media in children. XI Congress manuscript collection intently: Yogyakarta, 1995; 621-31.17. K.J Lee, MD, FACS. Otitis media with effusion. In: Lee K.J, MD, FACS eds. Essential Otolaryngology Head & Neck surgery. 8th Edition. Nc Graw-Hill medical publishing division. 479-95.18. Maw AR: otitis media with effusion (glue ear). In: Kerr, A.G, Groves eds. Scott Brown's deseases of the ear, nose and throat. 4th ed. Vol 2. London. Butterworths. 1979: 159-76.19. Patient health library. Children surgeries ear - otitis media. http://www.kkh.com.sg/PatientHealthLibrary/ChildrensHelath/ChildrensSurgeries/. Access on February 18, 2008.20. E.N Myers, MD. Otitis media with effusion. In: Myers E.N, MD eds. Operative Otolaryngology Head & Neck surgery. Vol. II. W.B. Saunders company.: 1237-39.21. The Johns Hopkins University School of Medicine and the Institute for Hopkins nursing. A view through distinguishing acute otitis media from otitis media with effusion. The Otoscope: 2004.22. Bluestone CD. Gates AG, Client OJ. Lim recent advances in otitis media: I. definition, terminology, and classification of otitis MADIA. Ann Otol Rhinol 2004; 111: 18-8.23. Irwan AG. Lewis. Atlas bewarna examination techniques ear nose throat disorders. FK UNSRI. EGC medical book publisher, 2008: 75-78.24. Pollart S. M. Common ENT problems. http:///www.aafp.org/.../aafp_org/documents/cme/courses/board/ent.Par.0001.File.dat/Common% 20ENT% 20Breakout.pdf. Access on February 16, 2008.25. Wilmot J.F, Cable H.R. Following Persistent acute otitis media effusion: tympanometry and pneumatic otoscopy in diagnosis. The Royal College of General Practitioner. 1998; 38:149-5226. Djaafar ZA. Abnormalities of the middle ear. In health science textbook head neck ear nose throat. Editor: dr. H. Efiaty Arsyad Soepardi, SpTHT, Prof. Dr. H. Nurbaiti Iskandar, SpTHT. FKUI, Jakarta, 2003: 49-62.

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