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16 Acute Otitis Media andHearing Loss inChildren
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• Being exposed to the same pathogen before, or being vaccinated against it, may
offer some protection by preventing the pathogen’s presence within the
nasopharynx.
• Patients whose immune systems can synthesise immunoglobulins during the
acute phase may not suffer from future episodes, or, if they do occur, attacks may
be less serious. However, the neutralising antibodies against Streptococcus pneu-
moniae and Haemophilus inuenzae target bacterial polysaccharides, and these
develop later than antibodies directed against bacterial proteins or
glycoproteins.
• Mild immunodeciency or immunodeciency of brief duration may cause
repeated middle ear infections.
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16.3 Aetiology
16.3.1 Pathogenic Viruses
Respiratory syncytial virus (RSV) is usually found in bronchiolitis or pneumonia in young children, although it is potentially capable of producing acute respiratory infections in patients at all ages [57]. In northern locales, RSV typically appears in the course of epidemics occurring over winter or in the rst weeks of spring; how­ever, any newborn who appears lethargic, irritable or apnoeic should be suspected of harbouring RSV, regardless of whether a middle ear infection is present. Children who are beyond the neonatal period usually have symptoms that point more clearly to a respiratory infection and are thus more straightforward to diagnose.
It has long been recognised that RSV can cause longer term lung problems in up to 50% of cases of bronchiolitis occurring amongst infants. The usual sequela is asthma. This virus is especially liable to cause death in those born with congenital cardiac disorders, cystic brosis, immune deciencies, dysplasia of the bronchi and lungs or those delivered earlier than 37-week gestation.
The only indication for use of intravenous immunoglobulin targeting RSV is in children at high risk. It is vital that clinical management of children who have otitis media at the same time as pneumonia, or systemic disorders, involves consideration of the whole picture when deciding on treatment. In certain patients, draining the ear through performing tympanocentesis or myringotomy is required, with any aspirate sent for microbiological culture and sensitivity testing. If a newborn is thought to be in sepsis or a child has immunosuppression, draining the middle ear is obligatory [1].
16.3.2 Pathogenic Bacteria
In 50% or more of paediatric cases of AOM, a bacterial pathogen is cultured from a middle ear effusion. In a further 25%, where culture is negative, DNA testing nds bacterial DNA or remnants of the bacterial cell wall. In most patients, except those
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under the age of 6 weeks, four bacterial pathogens are the causative organisms, namely, S. pneumoniae, H. inuenzae, Moraxella catarrhalis and Streptococcus
pyogenes. Certain other pathogens may also be identied in AOM, such as Staphylococcus aureus, alpha-haemolytic Streptococci and Pseudomonas aeruginosa.
Just as with other conditions treated by antibiotics, pharmacotherapy of AOM increasingly needs to take into account the possibility of an antibiotic-resistant organism as the causative pathogen [8]. The mechanisms through which bacteria acquire resistance to specic agents will be discussed in the context of each particu­lar pathogen known to cause AOM [1].
B. Sizer et al.
16.3.2.1 Streptococcus pneumoniae
Infections due to S. pneumoniae are the most common in AOM, as is the case for all invasive infections by bacteria in children, regardless of age [9]. This organism is a diplococcus, which is Gram-positive. Serotyping reveals 90 different variants, which differ in terms of their antigenic polysaccharides. The serotypes occur with different frequencies depending on the age of the patient and where he or she lives. Some 29–40% of cases where a pathogen is cultured are a result of S. pneumoniae, but the number of cases is actually higher, since antigenic components of S. pneu- moniae can be identied in around 33% of culture-negative isolates [1].
Thus, S. pneumoniae potentially causes more than half of cases of AOM.In the United States, the majority of cases where this organism causes invasive infection of any kind can be attributed to the following serotypes: 4, 6B, 9V, 14, 18C, 19F and 23F.In cases of AOM, the most frequently identied serotypes are 19, 23, 6, 14, 3 and 18, with frequencies of 23%, 12.5%, 12%, 10%, 8.5% and 6%, respectively. Being vaccinated with Pneumovax 23 (a polyvalent vaccine) provides immunity to around 85% of the pneumococcal variants that cause AOM [1].
Although at one time S. pneumoniae could generally be successfully eradicated using any of the antibiotics in frequent use, in particular penicillin G, erythromycin or the majority of sulfonamides. These antibiotics targeted the penicillin-binding protein located on the bacterial cell wall. This target has now mutated in some vari­ants, with the result that multidrug-resistant S. pneumoniae (MDRSP) are no longer sensitive to beta-lactam type agents, macrolides or the sulfonamides. Indeed, up to 40% of pneumococci may now withstand treatment with antibiotics of beta-lactam, macrolide or sulfonamide type. The serotypes most likely to be insensitive to peni­cillin are 6B, 9V, 14, 19A, 19F and 23F [1].
16.3.2.2 Heamophilus İnfluenza
H. inuenzae occupies the second rank in the list of bacterial pathogens most com­monly identied in aspirated uid from cases of AOM.It accounts for around one in ve of cases in children under school age [10]. This organism may be more com­mon in paediatric cases where otitis recurs and the child is somewhat older or in adults vaccinated against streptococci [1].
Martin et al. examined cases of AOM, which occurred from 1991 to 2014 in children over the age of 6 months but under 2 years. They ascertained that S.
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pneumoniae was less prevalent in the nasopharynx following introduction of the pneumococcal conjugate vaccine, but the number of individuals colonised with H. inuenzae then went up for some time before falling to the original level recorded at a time when the heptovalent pneumococcal vaccine (PCV7) was not routinely given. For this study, four different paediatric cohorts were examined. In each case, the study looked at culture of swabs obtained from the nasopharynx. The initial cohort dated to 1999–2000, at a time when PCV7 was not routinely provided. The second and third set of cultures dated from 2003–2005 and 2006–2009, respec­tively. At the time of the second set, 93% double vaccination levels applied, whereas by the time of the third set, this gure was 100%. The nal set came from 2012 to 2014, when at least double vaccination with a triskaideka-valent conjugated vaccine (PCV13) was universal. Colonisation of the nasopharynx with H. inuenzae was proven in 26% of the initial cohort, 41% of the second, 33% of the third and only 29% of the fourth [11].
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16.3.2.3 Moraxella catarrhalis
Fifty years ago, the organism now called M. catarrhalis was not considered a patho­gen causing otitis media, despite it being identied in around one in ten cases where an aspirate was cultured. The bacterium was also believed at that point to be within the Neisseria genus. In the 1970s, it was rare for M. catarrhalis to exhibit resistance to ampicillin and related penicillin. Since then, not only has the organism been twice reassigned to different genera (rst to Branhamella and now to Moraxella), it has become virtually invariably resistant to beta-lactam antibiotics that resemble ampicillin and is recognised as a pathogen in approaching 25% of paediatric cases of AOM.
M. catarrhalis is a normal component of the bacteria ora within the upper respira­tory tract. It is Gram-negative and is a diplococcus. Its ability to withstand beta- lactam arises from possession of several isoenzymes performing a lactamase function. The genes coding for these enzymes may reside on the chromosome or on plasmids. Furthermore, they may only be expressed at signicant levels when an antibiotic is used. Possession of more than one lactamase by the bacterium is possible [1].
16.3.2.4 Anaerobes
Although anaerobes are found in some paediatric cases of AOM where the contents of the middle ear are cultured, it appears that they do not act as signicant pathogens responsible for otitis media, especially in the acute form. It is possible that anaer­obes are of greater signicance where adenoiditis becomes chronic and a biolm is secreted. It is unusual for an aspirate to yield only an anaerobe when cultured. Usually, another pathogenic species is also grown [1].
16.3.2.5 Frequently Noted Pathogenic Bacteria inNeonates
Around the time of birth, the usual pathogens, which cause sepsis or meningitis, are Escherichia coli, Enterococci or Group B streptococcal organisms. It is not unusual for a middle ear aspirate to yield one of these pathogens, but they likely constitute no more than one in ten of the pathogens causing AOM in newborns.
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The single pathogen most frequently identied in AOM, regardless of age, is still S. pneumoniae. In second place come H. inuenzae organisms lacking a capsule or the untypeable variants, which may cause invasive infections in newborn infants [1].
B. Sizer et al.
16.4 Risk Factors
There is evidence to conrm all of the following are risk factors for the develop­ment of middle ear infections [1]
• Premature birth and low body weight on delivery
• Extreme youth
• A rst episode occurring early
• Family history
• Ethnic inheritance. Native Americans, Inuits and Australian aborigines are at
increased risk
• Immunodeciency
• Abnormal development of skull or face
• Neuromuscular disorders
• Allergic conditions
• Attending childcare facilities
• Overcrowding at home
• Socioeconomic disadvantage
• Being exposed to smoking or other air pollution
• Using a dummy
• Sleeping face down
• Seasonal—infections are more common in winter and autumn
• Not breastfed or bottle feeding continued for longer than usual
16.5 Epidemiological Aspects
Seven out of ten American children have at least one episode of AOM before they reach the age of 2 years. Researchers based in Pittsburgh who prospectively tracked a cohort of children living in the city or countryside up to the age of 2 years found that 48% of children had had a middle ear effusion by the age of 6months, 79% by the rst birthday and, by the second birthday, 91% had suffered a middle ear effu­sion [12].
The age at which AOM is most common in paediatric patients is between 3 and 18months. A child who has an initial episode of AOM as a neonate is at elevated risk of recurring middle ear infections. When Megged etal. compared paediatric patients with a rst episode of AOM in the neonatal period with those where the episode occurred later, they found the incidence was raised three times (30% vs 10%) [13].
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16.5.1 Demographic Characteristics—Age, Sex andEthnicity
There is an increased tendency to develop AOM between the ages of 6–11months, and the incidence falls at the time the child reaches the age of approximately 18–20months. Male children are at somewhat greater risk than females. The onset of AOM in some children begins after the age of 3 or 4 years. Once the permanent dentition has erupted, the number of episodes greatly decreases, albeit certain patients remain susceptible to recurrent attacks up to when they turn adult. On rare occasions, adults who are suffering with acute viral infections of the upper respira­tory tract but have not had middle ear infections before present with a de novo epi­sode of AOM [1].
There are also clear ethnic differences in the rate of AOM, with Native American or Inuit individuals prone to a highly elevated incidence of ear infections, both acute and chronic. By contrast, African American children are somewhat less prone to ear infections than their Caucasian peers [1].
16.6 Signs andSymptoms
Despite some variability in presentation at different ages, during the time when children are most likely to develop ear infections, there are several features that tend to be consistent, such as the following [1]:
• The sole sign of an infection in many newborns is irritability or difculty feeding.
• Older children typically present with pyrexia and earache, or keep pulling at
their ears.
• Auditory impairment is usually present in cases of AOM or OME in older chil-
dren or adults. The ear may feel blocked prior to any demonstrable uid in the
middle ear cavity.
Adults who present with earache but neither auditory impairment nor pyrexia are likely to have otitis externa, a tooth abscess or a temporomandibular joint problem causing referred pain. It is common for dental prostheses to cause referred pain on account of their changing how occlusion occurs.
16.7 AOM andAuditory Impairment
AOM and OME is invariably accompanied by auditory impairment in an older child or adult. Prior to uid accumulating in the middle ear patients complain of ear blockage. If a patient complains of earache but has neither loss of hearing nor pyrexia, the cause may be otitis externa, a tooth abscess or a temporomandibular joint problem causing referred pain. It is common for dental prostheses to cause referred pain on account of their changing how occlusion occurs.
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In its acute stage, AOM causes auditory impairment of conductive type [14]. It has also recently been shown that auditory loss of sensorineural type also occurs in cases where AOM is acute or recurring. The loss particularly affects higher pitched sounds in the range 2–8kHz [15, 16]. There is a paucity of research on the effects of auditory loss of high frequencies, but there does appear to be an association with difculty hearing the difference between musical notes, problems working out where a sound is coming from, comprehending speech (particularly where back­ground noise exists) and tinnitus [1720]. One study that followed up a cohort of adults prone to repeated episodes of AOM as children found these adults were sig­nicantly more likely to suffer from tinnitus than controls who had not suffered from acute middle ear infections [20, 21].
Given the fact that high-frequency hearing loss is the most likely decit in AOM, it appears useful to screen hearing when the illness is acute, to identify as soon as possible the likelihood of future auditory impairments and other compli­cations of the acute phase, for example, suppurative infection of the labyrinth [15,
2224]. This procedure may enable early therapeutic intervention and protect
against future hearing loss. The evidence base for using hearing tests during an acute attack of AOM is slender, and further research is called for to establish exactly what changes in the auditory thresholds occur, both for conduction through air and bone [14].
B. Sizer et al.
16.8 Diagnosis
16.8.1 Physical Examination
A careful and complete physical examination is essential. In cases of both acute and chronic middle ear infections, the ear should be examined with the pneumatic otoscope. Patients with AOM present with an inamed eardrum, which starts as mucosal erythema and goes on to involve a pus-lled effusion in the middle ear and a less mobile eardrum. There may be bulging of the eardrum in the posterior quadrant, whilst the supercial epithelium may look as though a scald has been sustained [1]. It is fairly common for the eardrum to become perforated during the course of AOM.This generally occurs in the posterior or lower quadrant. In some cases, rather than perforating, there is sometimes seepage of an opaque exudate with the viscosity of serum. This seepage occurs over the whole surface of the drum [1].
In cases of both acute and chronic middle ear infections, the ear should be exam­ined with the pneumatic otoscope. The potential physical ndings in cases of AOM are as follows [1]:
• The eardrum appears inamed
• The posterior quadrant of the eardrum may bulge outwards. The supercial epi-
thelium has the appearance of a scald
• Perforation of the eardrum, usually in the posterior or inferior quadrant
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• Seepage of an opaque exudate with the viscosity of serum. This seepage occurs
over the whole surface of the drum
• Earache, with or without a discharge from the ear
• Pyrexia
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16.8.2 Auditory Tests
It is usually not benecial to test hearing in children during an acute attack of AOM, since the effusion in the middle ear cavity invariably produces auditory impairment of conductive type. Tympanometry is potentially benecial to diagnose the presence of an effusion but is rarely necessary if the clinician can utilise pneumatic otoscopy correctly [1].
If the ear has recently perforated or tympanocentesis has been performed, send­ing aspirate for microbiological culture and susceptibility testing may be bene­cial [1].
16.8.3 Imaging Investigations
Unless complications occur, imaging investigations are not routinely required in cases of AOM.Nonetheless, CT imaging may be needed if there are suspected com­plications. If the complication may be intracranial, MRI may be a more suitable modality [1].
16.8.4 Operative Interventions
Tympanocentesis refers to a procedure whereby the eardrum is pierced with a nee­dle and any effusion aspirated for laboratory analysis.
The indications for tympanocentesis in cases of AOM are as follows [1]
• Newborn infants less than 6weeks old, who are at risk of infection by unusual
pathogens or of more invasive illness
• Cases where immunosuppression or immunocompromise is present
• Cases where there is ongoing evidence of AOM, either local infection or sys-
temic signs, in spite of appropriate antibiotic pharmacotherapy
• Cases where complications are present and culture is necessary to guide treatment
16.9 Clinical Management
16.9.1 Medication
The only pharmacotherapeutic intervention that has been shown to be effective in treating AOM is antimicrobial pharmacotherapy. Accordingly, antibiotics are the
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rst-line management. The choice of agent depends on the most probable pathogen, any allergies, degree of tolerability, previous treatment, cost and resistance pattern in the area where the child is living. It may also be important to consider the length of treatment [25].
The following agents are all antibiotics, which may be considered in AOM [1]
• Amoxicillin
• Co-Amoxiclav
• Erythromycin base/sulsoxazole
• Co-trimoxazole
• Cexime
• Cefuroxime axetil
• Cefprozil
• Cefpodoxime
• Cefdinir
• Clindamycin
• Clarithromycin
• Azithromycin
• Ceftriaxone
B. Sizer et al.
16.9.2 Surgical Interventions
The options for surgery in AOM involve the following techniques [1], which have a degree of overlap:
• Tympanocentesis
• Myringotomy
• Myringotomy and grommet placement
Choice of surgical intervention depends on various factors, including the indi­vidual patient, the experience of the surgeon, the resources that may be accessed and the degree of emergency involved.
16.10 Complications
The extent of the spread of infection is the basis for classifying complications in AOM.Infection may extend beyond the middle ear cavity in the following pat­terns [1]:
• Intratemporal. This includes cases where the eardrum perforates, and there is
acute mastoid osteitis, involvement of the seventh cranial nerve, acute inamma-
tion of the labyrinth, infection of the petrous temporal bone, acute otitis causing
necrosis or chronic otitis media.
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• Intracranial. This includes meningitis, encephalitis, central nervous system
abscess, otitis hydrocephalus, subarachnoid abscess, subdural abscess or a
thrombotic event within the sigmoid sinus.
• Systemic. Bacterial spread to the bloodstream, infected joints or bacterial
endocarditis.
References
1. Donaldson JD.Acute otitis media. In: Meyers AD, editor. Medscape; 2021. https://emedicine.
medscape.com/article/859316- overview. Accessed 10 Feb 2022.
2. Rettig E, Tunkel DE.Contemporary concepts in management of acute otitis media in children. Otolaryngol Clin N Am. 2014;47(5):651–72.
3. Minovi A, Dazert S.Diseases of the middle ear in childhood. GMS Curr Top Otorhinolaryngol Head Neck Surg. 2014;13:Doc11.
4. Danishyar A, Ashurst JV.Acute otitis media. Treasure Island (FL): StatPearls Publishing; 2022.
5. American Academy of Pediatrics. Respiratory syncytial virus. Red book: report of the commit­tee on infectious diseases. 27th ed. Itasca: American Academy of Pediatrics; 2006. p.560–6.
6. Arola M, Ruuskanen O, Ziegler T, et al. Clinical role of respiratory virus infection in acute otitis media. Pediatrics. 1990;86(6):848–55.
7. Arola M, Ziegler T, Ruuskanen O.Respiratory virus infection as a cause of prolonged symp­toms in acute otitis media. J Pediatr. 1990;116(5):697–701.
8. Block SL.Causative pathogens, antibiotic resistance and therapeutic considerations in acute otitis media. Pediatr Infect Dis J. 1997;16(4):449–56.
9. American Academy of Pediatrics. Pneumococcal infections. Red book: report of the commit­tee on infectious diseases. 27th ed. Itasca: American Academy of Pediatrics; 2006. p.525–37.
10. American Academy of Pediatrics. Haemophilus inuenzae infections. Red book: report of the committee on infectious diseases. 27th ed. Itasca: American Academy of Pediatrics; 2006. p.310–3318.
11. Martin JM, Hoberman A, Shaikh N, etal. Changes over time in nasopharyngeal colonization in children under 2 years of age at the time of diagnosis of acute otitis media (1999–2014). Open Forum Infect Dis. 2018;5(3):ofy036.
12. Paradise JL, Rockette HE, Colborn DK, etal. Otitis media in 2253 Pittsburgh-area infants: prevalence and risk factors during the rst 2 years of life. Pediatrics. 1997;99(3):318–33.
13. Megged O, Abdulgany S, Bar-Meir M. Does acute otitis media in the rst month of life increase the risk for recurrent otitis? Clin Pediatr (Phila). 2018;57(1):89–92.
14. Kasemodel ALP, Costa LEM, Monsanto RDC, Tomaz A, Penido NO.Sensorineural hearing loss in the acute phase of a single episode of acute otitis media. Braz J Otorhinolaryngol. 2020;86(6):767–73.
15. Park JH, Park SJ, Kim YH, et al. Sensorineural hearing loss: a complication of acute oti­tis media in adults. Eur Arch Otorhinolaryngol. 2014;271:1879–84. https://doi.org/10.1007/
s00405- 013- 2675- x.
16. Cordeiro FP, da Costa MR, Kasemodel ALP, de Almeida GL, de Oliveira PN. Extended high-frequency hearing loss following the rst episode of otitis media. Laryngoscope. 2018;128:2879–84.
17. Moreno-Gómez F.N. , Véliz G. , Rojas M. , Martínez C. , Olmedo R. , . Panussis F, etal. Music training and education slow the deterioration of music perception produced by presbycusis in the elderly. Front Aging Neurosci 2017; 9: 149
18. König O, Schaette R, Kempter R, Gross M.Course of hearing loss and occurrence of tinnitus. Hear Res. 2006;221:59–64.
226
https://t.me/medicina_free
19. Nondahl DM, Cruickshanks KJ, Wiley TL, Klein R, Klein BEK, Tweed TS.Prevalence and 5-year incidence of tinnitus among older adults: the epidemiology of hearing loss study. J Am Acad Audiol. 2002;13:323–31.
20. Aarhus L, Tambs K, Kvestad E, Engdahl B. Childhood otitis media: a cohort study with 30-year follow-up of hearing (the HUNT study). Ear Hear. 2015;36:302–8.
21. Aarhus L, Engdahl B, Tambs K, Kvestad E, Hoffman HJ.Association between childhood hear­ing disorders and tinnitus in adulthood. JAMA Otolaryngol Head Neck Surg. 2015;141:983–9.
22. Bluestone CD.Clinical course, complications and sequelae of acute otitis media. Pediatr Infect Dis J. 2000;19:S37–46.
23. Klein JO.The burden of otitis media. Vaccine. 2000;19:S2–8.
24. Leskinen K. Complications of acute otitis media in children. Curr Allergy Asthma Rep. 2005;5:308–12.
25. Sakulchit T, Goldman RD. Antibiotic therapy for children with acute otitis media. Can Fam Physician. 2017;63(9):685–7.
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