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Otitis Media withEffusion
17
AyseYaseminGunduz, MahmutTayyarKalcioglu, OzgurYigit, andHaythamKubba

17.1 Introduction

Otitis media with effusion (OME), also referred to as serous otitis media or secre­tory otitis media, as we dene it today, was named and explained by Mawson in the 1970s and is the occurrence of uid accumulation in the middle ear cavity without showing any signs of acute infection [1].
Being one of the most common causes of hearing loss in children, OME stands out as an important public health problem. Language development of these children with hearing losses is impeded, leading to impaired communicative abilities and negatively affected academic lives [2, 3]. For this reason, it is extremely important to recognize OME in the early period and initiate the required treatment and follow­up procedure.
A. Y. Gunduz (*) · M. T. Kalcioglu Faculty of Medicine, Department of Otorhinolaryngology, Istanbul Medeniyet University, Istanbul, Turkey
Goztepe Prof. Dr. Süleyman Yalcin City Hospital, Istanbul, Turkey
O. Yigit Department of Otorhinolaryngology, Istanbul Training and Research Hospital, Health Sciences University, Istanbul, Turkey
H. Kubba Department of Otorhinolaryngology, University of Glasgow, Glasgow, UK e-mail: Haytham.Kubba@ggc.scot.nhs.uk
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 M. T. Kalcioglu et al. (eds.), Otology Updates, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-76173-7_17
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A. Y. Gunduz et al.

17.2 Definition

The lexical meaning of otitis media is middle ear inammation. Otitis media is a range of diseases as different parts of inammatory processes dominate in vari­ous types of otitis media [4]. Acute otitis media (AOM) presents with otalgia and fever and usually accompanies or follows upper respiratory tract infections [5]. When the high-pressure infected uid in the middle ear cavity ruptures the tym­panic membrane, as in acute suppurative otitis media, and the perforation does not heal over time, chronic suppurative otitis media occurs, which is character­ized by persistent or recurrent otorrhea through the tympanic membrane perfora­tion [6].
When uid collection is clinically silent as mentioned before, OME occurs. In this type of otitis media, chronic transformation occurs while the tympanic membrane still keeps its integrity; and when the process lasts longer than 3months, it is called chronic OME [7]. Persistent effusion that remains after AOM even after treatment differs from chronic OME in that it lasts for a maxi­mum of 2months [8].
17.3 Epidemiology andRisk Factors
In the early stages of life, the very rst origin of middle ear effusion is the uid of the amniotic sac. More than two-thirds of term infants were shown to have amniotic uid in their middle ear cavities [9]. The prevalence of OME in children under 2years of age is as high as 60%, and thereafter, middle ear uid begins to dissolve with age [10]. After the age of 7, the prevalence of the disease signicantly decreases and remains below 20% [11].
Children with craniofacial anomalies develop OME more often than their normal peers. OME can be seen in up to 60% of children with Down syndrome and up to 75% of children with cleft lip and palate under 8years of age, [12, 13]. In young girls with Turner syndrome, the prevalence of chronic OME is nearly as twice as that of the general population of their peers [14]. In addition to this increased risk in the preschool age of these girls, problems associated with chronic effusion can often persist or even arise in the school-age period.
Although a direct pathophysiological connection has not been shown yet, it is known that OME is seen more frequently in atopic children. The prevalence increases if a child presents any allergic or asthmatic symptoms [11].
In addition to patient history, socioeconomic environment of the patient has a considerable impact on the development of OME.The child has a higher risk of developing OME if the parents have low education levels and lower status jobs. Apart from that, children with parental secondhand smoke exposure also develop OME more than their peers living in a smoke-free environment [11]. That being said, OME appears as a signicant public health concern and should be considered in this regard.
17 Otitis Media withEusion
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17.4 Pathophysiology

The Eustachian tube develops with age and reaches almost adult conguration by the age of 8 [15]. The main reason why OME is seen more frequently in children than in adults is the failure of underdeveloped Eustachian tube to play its part in normal middle ear function. Immature Eustachian tube is shorter, lies more horizon­tally, and dynamically cannot open and close adequately [16]. Consequently, the middle ear begins to be affected by the pressure changes and microorganisms of the nasopharynx. In other words, the immature dysfunctional Eustachian tube provides the predisposition to the development of the disease. Inammatory and infectious phenomena in the nasopharynx are thought to be the triggers of the pathological process that begins in the middle ear. With local inammation arising in the middle ear, vasodilation and cytokine production occur. These inammatory changes, respectively, lead to a decrease in middle ear pressure by increased gas absorption in the middle ear, and accumulation of exudate secretion due to goblet cell and glandular metaplasia in the mucosal epithelium of the middle ear [17]. The uid that starts to collect in the middle ear can be mucous, seromucous, or serous in nature. Excess secretion obstructs the Eustachian tube, and the aeration of the middle ear from the nasopharynx is thus also blocked. As a result, the negative pressure devel­oping in the middle ear starts to damage the structure of tympanic membrane and causes it to atrophy. Eventually, retraction pockets form primarily in the pars ac­cida, which does not have the brous layer. Unless OME is treated and healthy middle ear pressure is achieved, retraction involves the entire tympanic membrane and complicates the development of atelectasis and adhesive otitis. As OME may even lead to the development of cholesteatoma from retraction pockets in the future, which occurs especially in children refractory to treatment, it should be recognized and treated without delay and at a possible earlier age in order to minimize the dura­tion of exposure to negative middle ear pressure [18, 19].
Eustachian tube dysfunction has been the traditional pathophysiological concept in OME for a long time [20]. However, recent studies show that Eustachian tube dysfunction is rather a predisposing factor than being the only and main etiological factor [21]. Healthy middle ear is free of bacteria or viruses [22]; in contrast with this, OME is not a sterile inammatory process. Conventional microscopy and much more sensitive PCR studies have shown that bacteria possibly originating from the nasopharynx are present in the middle ear cavity. Streptococcus pneu- moniae, Haemophilus inuenza, and Moraxella catarrhalis, which are notably abundant in the adenoids [23] and are the main pathogens in the etiology of AOM and acute bacterial sinusitis, are also among the most commonly observed patho­gens in OME [24, 25]. In pathogen reservoir hypothesis, adenoid tissue of the upper respiratory tract serves as a bacterial source initiating infection in the middle ear cavity in susceptible individuals [26]. These pathogens are thought to be involved in the biolm layer formation in the middle ear [27, 28]. These bacteria, which need less oxygen and nutrients and reach the appropriate pH by embedding into the bio­lm layer, are also protected from host phagocytes, antibodies, and systemic antibi­otics by the extracellular matrix in the biolm [29, 30]. The infection becomes
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chronic due to these bacteria that persist in the biolm layer. With novel genetic sequencing techniques, the polymicrobiality of the disease process has been vali­dated and become a well-known fact; moreover, it has been found that these bacteria that dominate and persist in the middle ear effusion actually are not identical to the bacteriome of adenoids [31]. Beyond the three common species of the upper respi­ratory tract mentioned above, Alloicoccus otitis, which is specic to the middle ear, is found to be the most abundant bacterium in the middle ear uid of OME patients [3134]. These most recent ndings reveal the importance of middle ear’s own microenvironment as well as the importance of adenoid microbiome in the forma­tion of OME, thus the need for further studies to investigate the possible patho­physiological processes besides the pathogen reservoir theory [31, 32, 35].
It is thought that some other factors may also be effective in the development of OME.Pepsin and Helicobacter pylori, a microaerophilic bacterium that nds the appropriate pH in the middle ear biolm for its survival, found in the studies per­formed on middle ear effusion samples suggested that gastroesophageal reux may have a role in the etiology of OME [36, 37]. However, studies have not yet shown that a direct cause–effect relationship exists [38, 39]. It has been suggested several times that there may be a relationship between allergic airway diseases and OME [4044], but again, a clear cause–effect relationship has not been demonstrated, and anti-allergic treatment was shown to have no effect on the OME disease process [45]. Allergy screening is recommended in OME patients only in the presence of atopic symptoms suggestive of allergic rhinitis or asthma [46]. Besides all these, the presence of middle ear effusion should be investigated in children with turbinate hypertrophy, allergic rhinitis, or asthma in order not to miss and have a delay in the diagnosis of OME [47].

17.5 Diagnosis

17.5.1 Clinical Evaluation
Most OME patients are diagnosed clinically. Hearing loss is the main symptom of middle ear effusion. The anamnesis given by the parent is extremely important to suspect a hearing loss and the presence of OME in children. The most commonly stated complaints are not responding when called out and watching TV or videos on tablet/phone with the volume turned up high. It is also very valuable and should not be overlooked when the parents share their observations on their child such as a drop in school success, deterioration in friendship relations and social behavior, arising behavioral problems such as irritability and restlessness, and emerging sleep problems [48, 49].
A clinical diagnosis is made with an ear examination performed after the anam­nesis that arouses suspicion of OME.The presence of dullness, opacity, air-uid level, air bubbles, or retraction pockets in the tympanic membrane in otoscopic examination conrms the clinical diagnosis (Figs.17.1 and 17.2). Pneumatic oto­scope is the main examination tool recommended to be used in the diagnosis of
ab
ab
17 Otitis Media withEusion
Fig. 17.1 Image of a right (a) and the left (b) tympanic membrane of a 5-year-old child with OME.The right tympanic membrane has the typical opaque appearance of OME, and an image of a concomitant bullous myringitis can be seen. The left tympanic membrane has lost its translu­cency and looks dull due to the uid behind the membrane
351
Fig. 17.2 Preoperative image of the right (a) and the left (b) tympanic membrane of a 6-year-old child with adhesive otitis. Air bubbles within the uid are visible through the tympanic membrane
OME, as it also provides the ability to evaluate the tympanic membrane movement against pressure changes. Diagnosis of chronic OME is made when the same nd­ings persist at the end of 3months. Endoscopic or microscopic tympanic membrane examinations could also be performed as alternative methods.
Nasal endoscopy and nasopharyngeal examination should especially be performed in adults in the presence of unilateral OME.It should be kept in mind that a possible nasopharyngeal mass or tumor may present only with OME in the early period. In children, however, nasal endoscopy is not routinely required if the child does not have
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a nasal complaint. As will be discussed further in this chapter, in most of the cases, adenoidectomy will be included in the treatment protocol whether there is a hypertro­phy or not. When there is an accompanying complaint of nasal congestion or in the presence of resistant OME, nasal endoscopic examination should be performed, and the nasopharynx should be viewed for the diagnosis of a possible obstructive adenoid vegetation as well as for the differential diagnosis of the other etiologies of nasal con­gestion such as turbinate hypertrophy or nasal septal deviation [5052].
Recognizing craniofacial malformations is important as they predispose to resis­tant or recurrent OME [53]. In the absence of apparent phenotypic anomalies, a careful oropharyngeal and oral cavity examination should be performed to deter­mine whether there is an accompanying nding of a palatal defect, such as a bid uvula, submucous cleft palate, or incomplete cleft palate. In the presence of these palatal disorders in which resistant and recurrent OMEs can be seen, if there is a presence of concomitant adenoid vegetation, extreme caution should be exercised during adenoidectomy surgery due to the risk of velopharyngeal insufciency.
17.5.2 Audiological Workup andHearing Evaluation
Tympanometry testing is the gold standard investigation to conrm the diagnosis in the presence of clinical OME.In the tympanometry test that assesses the mobility of tympanic membrane, Type B tympanogram indicating a static tympanic compli­ance is the typical response and the curve with the highest specicity for OME [54,
55] (Fig.17.3).
Fig. 17.3 Preoperative tympanogram of a 4-year-old child diagnosed with bilateral chronic OME.This is a Type B tympanogram of both ears with the at lines on the graph indicating very limited or no compliance of the tympanic membrane due to the uid accumulated in the cavity behind it and blocks its movement
17 Otitis Media withEusion
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As OME is most commonly seen in children during the language development period, it is important to determine the degree of hearing loss after the diagnosis before any treatment intervention. Tonal audiometry and speech audiometry with measurement of air and bone conduction thresholds are the audiometric tests ide­ally recommended to be performed (Fig.17.4). Half of the children with OME have hearing loss greater than 20dB, and one-fth of them have hearing loss greater than 35dB between 500 and 4000Hz [56]. In cases which are left without any treatment for a long time and there is a moderate or severe hearing loss of more than 45–50dB, it should be considered that the inner ear also starts to get affected and damaged. It should also be noted that the degree of hearing loss may be higher in children with OME and craniofacial anomalies compared to their normal peers with OME [13].
It is recommended to obtain auditory brainstem response or auditory steady-state response recordings before any intervention, particularly in cases where audiomet­ric tests cannot be performed due to patient incompatibility especially in very young age or when very high free-eld thresholds are obtained [57].
Fig. 17.4 Preoperative pure-tone audiogram of the same 4-year-old child, whose tympanogram was shown in Fig.17.3, diagnosed with bilateral chronic OME.In both right and left ears, air–bone gaps can be noted clearly along with the normal bone conduction thresholds. Pure-tone averages between 500 and 4000Hz show that the child had mild conductive hearing loss in his left ear, whereas he had moderate conductive hearing loss in his right ear before the intervention
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17.6 Treatment

17.6.1 Medical Treatment
Various maneuvers developed to mechanically resolve Eustachian tube dysfunction, and negative middle ear pressure should be included as the rst-line treatment. Toynbee and Valsalva maneuvers, which do not need any equipment, are self­administered maneuvers instructed to the patient. In Toynbee maneuver, the patient swallows after pinching his or her nose. In Valsalva maneuver, a deep breath is taken, the nose is pinched again, and a strong expiration is performed while the mouth is closed. Even 1week of successful Valsalva maneuver has been shown to lead to signicant improvements in hearing [58]. Both maneuvers provide similar improvements in middle ear pressures [59], are of very low cost, and have no side effects. Therefore, they are recommended to be used either alone or as an adjunct to medication treatment.
Intranasal corticosteroids are agents that suppress the local inammation in the Eustachian tube and the middle ear. These molecules also help restore normal func­tion in these anatomic regions by decreasing the viscosity of the middle ear effusion uid, increasing the secretion of surfactant, and reducing the volume of lymphoid tissue at the orice of Eustachian tube [60]. As topical steroids have short-term benets in the resolution of effusion and OME symptoms, they may be preferred for having early symptomatic relief [61]. Having no benets on OME in the long term, topical steroids should only be included as an essential part of treatment in atopic children [62]. Oral steroids do not have a place in the treatment of OME, as they have not been shown to provide a signicant gain on hearing, besides having sys­temic side effects which is the most important handicap of using these medica­tions [63].
Mucolytic agents indirectly alleviate inammation by decreasing mucus produc­tion and increasing excretion of secreted mucus. With these effects, they can pro­vide relief in OME symptoms in the short term and can even omit the need for ventilation tube (VT) insertion surgery in one out of every 5 children [64]. However, since studies on mucolytics have not been able to clearly demonstrate their benets in terms of cost-effectiveness, these agents are not recommended in the treatment of OME in international guidelines [65].
Due to the fact that OME is a nonsterile inammatory process, oral antibiother­apy has occasionally been prescribed, especially more commonly by non­otorhinolaryngology specialists [66, 67]. However, none of these antibiotic drugs given for varying durations have a benet on OME symptoms, hearing loss, or VT application rates in the long term [68]. Middle ear effusion regressed in only 10% of children who received antibiotics, whereas spontaneous resolution can be seen at similar or even higher rates in patients who do not receive antibiotics [69]. The inef­fectiveness of antibiotics is due to the sheltering effect of the biolm layer on the pathogenic bacteria, as discussed before [29, 30, 70]. Therefore, the use of agents from any antibiotic class is not recommended in the treatment of OME in interna­tional guidelines [65]. Macrolide group antibiotics can be preferred in the treatment
17 Otitis Media withEusion
355
of rhinosinusitis with accompanying OME due to their anti-inammatory effects in addition to their antimicrobial effects [71].
It should be known that the use of antihistamines or decongestants in oral or nasal form does not make a clinical contribution in OME treatment, and in addition, side effects related to these drugs can be seen at a substantial rate [72]. However, in the presence of concomitant atopy or upper respiratory tract infection, these agents should be included in the prescription as the part of treatment protocols of these conditions.
As argued above, there is no specic medical treatment for OME, and both American and European guidelines recommend surgical treatment for chronic OMEs that persist after a 3-month watchful waiting period [7, 73].
17.6.2 Surgical Treatment
In management of persistent OME, key treatment according to the global guidelines is VT (or also referred to as tympanostomy tube) insertion [65]. VT insertion is an effective treatment both in OMEs that have begun to develop tympanic membrane damage and in OMEs that have caused hearing loss and thus affected the quality of life. VT insertion is indicated in cases when atrophy or retraction of the tympanic membrane starts to emerge when there is an objective hearing loss between 25 and 40dB on audiometry, or when the quality of life is affected for that individual in milder hearing losses [74]. Signicant improvements are seen in hearing and quality of life during the rst 9months after VT insertion [2, 7, 10, 75]. The long-term benecial effect of VT insertion on language development has not been clearly demonstrated yet [76]. However, rapid surgical treatment is recommended in order not to allow the possible devastating effect of additional hearing loss in children who are in the risk group for speech or learning disorders (children with autism spectrum disorder, developmental dysphasia or speech delay, perception deafness, craniofacial malformations, cleft palate) [77].
Ventilation tubes placed in the tympanic membrane allow the passage of air from the external auditory canal to the middle ear cavity which cannot be ventilated via the Eustachian tube, thus allowing the middle ear pressure to equalize with atmo­spheric pressure. There are several different types of VTs used in the surgical treat­ment of OME.Shepard-style grommet tubes that are generally used in Europe and Asia stay in place for around 6months (Figs. 17.5, 17.6, 17.7, and 17.8), while Armstrong-style grommet tubes that are more commonly used in America have bev­eled inner anges providing a relatively long lifetime of up to 1 and a half year [77]. Paparella-type grommet tubes are silicone tubes with a notched inner ange to aid the insertion. Type I Paparella tube has a small inner ange as of Shepard style grommet, which are both short-term tubes thus showing similar clinical features. Type II Paparella tube, however, has a wider inner ange which makes it a long­lasting tube [78, 79]. Apart from grommet tubes, there are also T-tubes for perma­nent middle ear aeration that stay in place for a much longer time and are not expected to exhibit a spontaneous fall out into the external ear canal [80] (Fig.17.9).
356
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Fig. 17.5 Postoperative follow-up view of a 13-year-old 1week after a Shepard style grommet tube insertion to a tympanic membrane with a large retraction pocket
A. Y. Gunduz et al.
Fig. 17.6 Postoperative images of a 5-year-old child at 1year follow-up of VT insertion surgery. The Shepard-style grommet tube stays in place in the right ear (a), whereas the tube is expelled into the external ear canal in the left ear (b). Note the healthy appearance of both tympanic membranes
Grommet tubes, which are expected to fall off between 6 and 18months, are pre­ferred in the rst line in primary OME surgery. Since grommet tubes are short-term VTs, except Type II Paparella tubes, their complication rates are also relatively low [81]. Although complication rates are higher, T-tubes that are long-term tubes that remain in place for more than 2 years are indicated in patients with chronic Eustachian tube dysfunction and patients with resistant or recurrent OME who have not beneted from a grommet tube.