Acute Otitis Media AOM is defined as a condition with acute inflammation of the ME cleft and the presence of an effusion, and is associated with the onset of the signs and symptoms of acute infection. The pathological definition is straightforward, but the clinical definition can be more difficult. Children can present with specific (otalgia or ear discharge) or more general (fever and irritability) symptoms. In the early stages there is inflammation of the tympanic membrane and the ME mucosa, but there is no ME effusion or fluid. The eardrum is thickened or erythematous, but moves well with pneumatic otoscopy or tympanometry. This early inflammatory stage may resolve or may progress to a full-blown empyema of the ME, which becomes filled with mucopus, often under tension and causing severe pain, sometimes relieved as the drum perforates and pus discharges from the ME ( ▶ Fig. 7.1). Fig. 7.1 Acute inflammation of the left tympanic membrane. The tympanic membrane is bulging and erythematous. Incipient perforation with discharge is evident in the posteroinferior quadrant (arrow). (Reproduced with permission of Probst R, Grevers G, Iro H. Basic Otorhinolaryngology: A Step-by-Step Learning Guide. Stuttgart: Thieme; 2006.) Myringitis is characterized by inflammation of the tympanic membrane alone. This may be associated with either OM or possibly an external ear canal infection, but can occur in isolation due to viral infections with blistering or fluid-filled bullae on the drum—bullous myringitis ( ▶ Fig. 7.2). Fig. 7.2 Bullous myringitis with hemorrhagic blebs (left ear). (Reproduced with permission of Sanna M, Russo A, DeDonato G. Color Atlas of Otoscopy. Stuttgart: Thieme; 1999.) Many children will suffer multiple episodes of AOM. When does this become a separate pathological process and merits the term recurrent acute otitis media (ROM or RAOM), is moot point; but most authors would accept that 3 or more episodes of AOM in a 6-month period, or 4 or more episodes in a 12-month period constitutes RAOM. The ME returns to normal in-between the episodes of AOM, otherwise the child has OME or CSOM, each of which has a different natural history and warrants a different therapeutic approach. There is increasing evidence that ROM in childhood may be associated with hearing loss in adult life. 4 OME is characterized by inflammation of ME with an effusion that is usually serous or mucoid but not purulent, and is not associated with the signs and symptoms of acute infection. OME may follow an episode of AOM or may supervene in children with RAOM; it is discussed in detail in ▶ 8. Teele et al reported that the incidence of AOM is higher in males but other studies have shown little difference between the sexes. 1 AOM is primarily a disease of younger (preschool) children. In the United States, approximately 30 to 60% of children will have an episode in their first year of life, up to 70 to 80% by the time they are 3 years old, and more than 90% by the age of 5 years. The highest prevalence is in the second 6 months of life. 1 A first episode of AOM before 6 months of age does independently make further episodes more likely. This could be due to the inflammatory episode leaving changes, scarring, or residual inflammation in the ME, making recurrent episodes more common, or could suggest that the child has an innate predisposition to AOM. Younger children have short, wide, and immature Eustachian tubes (ETs) associated with aggregates of lymphoid and adenoidal tissue that can harbor bacteria close to the ascending ET, which can infect the ME space. They have immature immune systems and are more prone to upper respiratory tract infections (URTIs). After the age of 7 years, the incidence seems to decrease (see ▶ 8). It appears that there has been an increase in the prevalence of AOM over the last few decades. There is a greater incidence of AOM in native Americans, Canadian Inuits, and Australian Aboriginal children. This may be due to anatomical factors, but also could be related to other factors such as socioeconomic conditions or access to healthcare. In Europe, there seems to be some variation between countries, with Italy seemingly having a lower incidence than average. 5 A number of environmental factors have been shown in population studies to influence the incidence of AOM, some of which are potentially reversible. AOM has a higher incidence in autumn and winter than in summer. This could be related to the increased prevalence of URTIs and/or the crowding of children inside over these periods. Many studies have shown an increase in AOM in children who attend nursery or day-care facilities especially from an early age. Again, the increased exposure to other children and viral infections is thought to be the cause. Children who are breast-fed compared to those who are artificially fed have a lower incidence of AOM. A number of factors have been suggested to explain this, but the transfer of protective maternal antibodies is probably the most accepted. There is a significant increase in children with AOM who are passively exposed to smoke by parental cigarette use in the home environment. Anatomical changes of the head and neck, or host defense deficiencies have a significant influence on the incidence of AOM. Children with cleft palate, craniofacial abnormalities, and congenital or acquired immune or immunoglobulin deficiencies are all at higher risk for AOM. Adenoidal hyperplasia is also thought to predispose children to AOM, not as previously thought by a direct effect on the ET, but most probably by harboring the bacterial responsible for AOM possibly in the form of biofilms. Some studies have suggested that there may be a genetic predisposition in children with RAOM. The ME cleft is connected to the nasopharynx by the ET, which is responsible for the ventilation of the ME cleft. The ME is not sterile as it is directly associated with the nose and hence the outside world, and there seems to be a balance between the host defenses and the viral/bacterial agents that contaminate the system. When this balance is disturbed, an acute infection and the associated inflammatory response occurs. The balance can be altered by many factors, some of which have been discussed previously. The classic scenario for an episode of AOM is a child who catches a viral upper respiratory tract infection. This leads to mucosal inflammation and functional ET dysfunction, mucociliary stasis, and ME inflammation with effusion formation. Pathologically the stages of AOM are well recognized. It begins with inflammation and hyperemia of the ME mucosa. There may be similar findings in the mucosa of the ET, and these may precede (ascending infection) or follow the changes in the ME. The swollen ME mucosa and dilated capillaries allow exudation of blood products including proteins, inflammatory cells, and mediators into the ME. There is an increase in ME goblet cells that produce more mucous. The bacterial and inflammatory cells produce toxic factors that together with the pressure of the mucopurulent exudate can lead to a perforation of the pars tensa of the drum and discharge into the external ear. AOM is usually benign and often can be self-limiting, with resolution and healing at any point in this process. In a small number of cases, progression of the pathological process occurs, as discussed later in this chapter. Major factors in the pathogenesis of AOM that influence progression in an individual case are the function of the ET, the child’s immune response, and the bacterial or viral load. The biggest contributing factor involved in any one child is difficult to ascertain, and a combination of many factors may well be at work. The ET ventilates the ME. It helps to provide protection by remaining closed for much of the time to prevent microbial ingress and by helping to clear secretions from the ME by the action of its mucociliary lining. In a child, the ET is anatomically different to that in an adult, that is, being shorter and more horizontal, but it can also be functionally immature. It is difficult to know whether AOM may be caused initially by functional tubal obstruction, with a viral upper respiratory tract infection leading to tubal edema and mucociliary clearance breakdown, or by the failure of the tube to stop pathogens ascending into the ME. There have been some studies that have shown reflux from the nasopharynx into the ME in some children during swallowing, and this may predispose to AOM. The nasopharynx naturally carries bacteria, and there is often colonization of the adenoids in children. There is, however, an innate immune defense system in the upper airway and ME that prevents invasion of the pathogens. The mucosa secretes numerous antimicrobial molecules, lysozymes, and antibodies including immunoglobulin M (IgM), and there is systemic production of bacteria-specific immunoglobulin G (IgG). In children, maternal IgG is transferred in the cord blood, but the levels decline after 6 months, before there has been a compensatory rise in the child’s own IgG. This “window” of lower IgG levels probably explains, in part, the rise in the incidence of AOM at 6 months, with the peak age incidence of AOM being 6 to 12 months. Any failure or reduction in the systemic or epithelial immune defense system will make bacterial entry and AOM more likely. It has recently been found that bacteria can exist in two states: active or planktonic. In the planktonic state, bacterial activity reduces and the cells congregate in groups surrounded by a matrix termed a biofilm. Biofilms are relatively inert, can lay dormant on the mucosa, and are not well penetrated by antibiotics. Biofilms are found in the nasopharynx and ME and are thought to be reservoirs of infection that can become quickly active if stimulated. They are more resilient in areas of low-oxygen tension, which may exist in the ME when there is ET dysfunction as may often be seen with the immature tube in infants. The persistence of biofilms in the nasopharynx and ME, which are activated by viral inflammation of the area, may be the cause of some episodes of both AOM and RAOM. Knowledge of the potential microbiology of AOM is vital to inform the clinician of the most appropriate antimicrobial treatment. This is discussed further in Chapter ▶ 7.7.3. The role of bacteria in AOM is well recognized, but in many cases, viral infection plays a major part. In approximately 40% of cases of AOM, respiratory viruses are found in the nasopharyngeal secretions. The commonest viruses are respiratory syncytial virus and rhinovirus, but parainfluenza, influenza, and adenovirus are also involved. Viral infection alone is probably the cause of AOM in up to 20% of cases. The clinical features of AOM parallel the pathological process described. Symptoms often start with features of a viral URTI associated with nasal congestion, rhinorrhea, and a sore throat, but symptoms of AOM can occur quite rapidly with no obvious cause. Inflammation of the ME mucosa and tympanic membrane are either preceded by or follow ET dysfunction and ME effusion. Ear discomfort may be present from the start or slowly get worse with the increase in inflammation. The ear feels blocked or pressured, with a conductive hearing loss. There may be no ME fluid, but as the condition continues, the drum becomes dull and the ME mucosa thickens. The pressure of the mucopurulent effusion slowly builds, and at this point, the tympanic membrane is dull, thickened, and bulging. Otalgia at this stage of AOM is usual and is an indicative clinical symptom, but is not present in all children. The toxic effect of the infection and factors released by the bacteria and immune response often give rise to more systemic symptoms with a rising fever, and often, in smaller children, lethargy, malaise, vomiting, and possibly diarrhea. On examination in this early stage, the tympanic membrane is hyperemic with injected vessels over the attic and malleus handle ( ▶ Fig. 7.3). If there is a continued buildup of pressure from the infected effusion in the ME, perforation of the pars tensa may occur ( ▶ Fig. 7.4). Fig. 7.3 Early acute otitis media (right ear) showing a reddened vascular strip along the manubrium. (Reproduced with permission of Wigand ME. Restitutional Surgery of the Ear and Temporal Bone. Stuttgart: Thieme; 2001.) Fig. 7.4 Advanced acute otitis media (left ear) showing a thickened, bulging drumhead. Spontaneous perforation is imminent. (Reproduced with permission of Wigand ME. Restitutional Surgery of the Ear and Temporal Bone. Stuttgart: Thieme; 2001.) This is noticed as a mucopurulent discharge from the ear, often with a reduction in the child’s otalgia. Sometimes, this discharge is blood-stained, and a swab of this otorrhea can be taken for microbiological analysis. The perforation of the drum is often seen as the natural “bursting of the abscess”; the child usually feels better, and the disease process starts to improve. In some cases, possibly more with virulent S. pneumoniae strains, there is not only a pinpoint perforation of the tympanic membrane, but also a degree of necrosis, leaving a much larger perforation. Most small perforations heal spontaneously as the inflammatory process abates. Larger perforations may not heal and can become chronic defects (CSOM; see ▶ 9). If the drum does not perforate, AOM can resolve spontaneously as the child’s immune system regains the upper hand, but AOM can remain active with continuing symptoms or progress with further spread of infection and inflammation outside the confines of the ME and mastoid mucosa ( ▶ Fig. 7.5). Mastoiditis and other complications are discussed later in this chapter. Fig. 7.5 Outcomes of acute otitis media. OME, Otitis media with effusion; CSOM, chronic suppurative otitis media. In older children, the diagnosis of AOM is usually relatively straightforward. They often present with classic symptoms of localized otalgia and are able to describe their pain and hearing loss. Examination of the larger ear canal, with a better view of the drum, makes confirmation of the bulging, reddened tympanic membrane far easier ( ▶ Fig. 7.3, ▶ Fig. 7.4). Contrary to much traditional teaching, the diagnosis of AOM in young children is neither easy nor certain. In 1990, a study in the British Medical Journal 6 found that the self-reported diagnostic certainty in a group of general practitioners of their diagnosis of AOM in the under 12-month age group was only 58%. In children under the age of 2 years, the symptoms can be vague, and they often cannot give a meaningful history. A child may pull at their ear, but pain is not always present, and nonspecific systemic symptoms such as fever, vomiting, loss of appetite, and even diarrhea may be the only signs of AOM. The most important sign is the state of the eardrum, and in a crying and upset 12-month-old child with a small ear canal and a little wax, getting an adequate view of the tympanic membrane may not be possible. The peak age for the incidence of AOM is 6 to 18 months, so there can be diagnostic uncertainties in this largest group of children with AOM. Not all ear pain in these children is necessarily AOM, so a careful history and examination is essential in an unwell child, especially if he/she is “pulling an ear,” with the potential for AOM as a diagnosis being borne in mind at all times. The presence of ear discharge with a history consistent with AOM certainly helps to confirm the diagnosis. The ME, and not the external ear, contains mucous secreting glands, so the presence of mucopus in the external canal confirms that the drum has perforated. In the absence of mucopurulent otorrhea, the only true way of absolutely confirming the diagnosis of AOM is to perform a tympanocentesis, taking a small aspirate of ME fluid for microbiological diagnosis. This is generally not practical in the awake child and is rarely done in routine clinical practice. Tympanometry can sometimes be used to assist with the diagnosis, but it can only give an indication as to the presence or absence of ME effusion and does not distinguish between the infected bulging effusion of AOM and the chronic noninfected effusion seen with OME. It should be used only as an aid to the clinical history and examination. AOM is a painful and distressing condition for the parents and the child, and adequate symptom control, particularly analgesia, is essential. Pain may be controlled by simple analgesia such as paracetamol, with the addition of a nonsteroidal anti-inflammatory drug such as ibuprofen, if needed. In younger children, systemic symptoms such as fever and vomiting may occur, and it is important that hydration is maintained in this age group. There is no evidence base for the use of decongestants and antihistamines in the treatment of AOM. Sometimes, topical decongestants when used in the short term can relieve the nasal symptoms caused by the viral nasal infection that preceded AOM, but they are not an effective treatment for AOM itself. The natural history of AOM in many cases is that of a relatively benign self-limiting condition that resolves without major sequelae. It can progress to cause a chronic perforation, hearing loss, or the serious complications discussed later. A study from the preantibiotic era reported mastoiditis in 17% of cases of AOM, 7 and many older ear, nose, and throat (ENT) surgeons remember wards full of children needing surgery for AOM and its complications. In the postantibiotic era, the use of antimicrobial drugs has made the more serious sequelae of AOM fortunately very uncommon, but they are still seen, and some data suggest that possibly with the reduced use of antibiotics for AOM, these complications are being seen more often. The difficulty for the treating clinician is that currently there is no predictive test that can determine whether AOM affecting the child in front of them will resolve spontaneously or whether the infection if left untreated will progress. The use of antibiotics is therefore still the mainstay of treatment, but the clinical decision about how to treat a child with suspected or definite AOM may be finely balanced. There have been a number of studies including a Cochrane review 8 that have shown that antibiotics have only a small effect on the resolution of AOM in many children. The role of early antimicrobial therapy is uncertain. 9 Most published guidelines emphasize that the great majority of children will recover from AOM without antimicrobial treatment, but compliance with guidelines is highly variable. 10 With the growing concerns over the number of bacteria that are becoming antibiotic-resistant, a policy of a “watchful waiting” period is being increasingly used by many clinicians in a number of countries, notably in the Netherlands, in the treatment of AOM. A child seen with early AOM who is otherwise systemically well is prescribed analgesia to control any otalgia, but not antibiotics at the initial consultation. If the ear pain subsides, then no further treatment at that stage is suggested as it would seem AOM has resolved. However, if the pain continues for more than 24 to 48 hours, the child becomes systemically unwell, or there are other worrying symptoms, then the child should be returned to the doctor for review and antibiotics. Topical antimicrobial therapy may be indicated, especially if the drum has perforated. 11 The decision to adopt a “watch and wait” policy for AOM should be carefully considered by the clinician and discussed with the child’s parents. It is not suitable for children with other underlying medical conditions, for those that are systematically unwell, when follow-up care at 24 to 48 hours cannot be guaranteed, or when the child is under the age of 2 years. In these cases probably antibiotics should be the mainstay of treatment. Children under the age of 2 years have the highest incidence of not only AOM, but also the complications of AOM, and as exact diagnosis is difficult, antibiotics should be used as the first line of treatment if there is any suspicion of complications. All antibiotics carry the risk of allergic reactions, gastrointestinal disturbance, and other reactions. Their use is not without unwanted side effects. The benefit of treatment need always be weighed against the risks. The antibiotic used to treat AOM should take into account the three main bacteria involved: S. pneumoniae, H. influenzae, and M. catarrhalis. If there are microbiological data available, for example, from a swab of otorrhea post-AOM, then this information should be used to inform which antimicrobial is used. The three main organisms are generally sensitive to amoxicillin, which is a broad-spectrum penicillin, and so this is usually the antibiotic of choice. It is safe, well tolerated in children, available as a liquid, and inexpensive. In children who are allergic to penicillin, a good alternative is one of the macrolide group, for example, azithromycin, or a cephalosporin, which again are usually well tolerated. There is a growing problem of bacterial resistance to antibiotics, especially with the emergence of β-lactamase-producing bacteria. Approximately 20 to 30% of H. influenzae and up to 100% of M. catarrhalis are now found to produce β-lactamase, and in certain parts of the developed world, 30 to 50% of S. pneumoniae are penicillin-resistant. A growing number of S. pneumoniae and H. influenzae species are showing growing resistance to macrolides. Where there are great concerns about such bacterial resistance, amoxicillin–clavulanate or a cephalosporin is probably the first-line antibiotic of choice. Treatment with antibiotic therapy should continue for at least 5 days (5–7 days usually) in uncomplicated cases of AOM. There is usually an improvement in the child’s symptoms over the first 1 to 2 days, with a slow resolution of the ME inflammation. Many children continue to have a noninfective effusion in the ME for up to 6 weeks after an episode of AOM, and the ear should be examined at 4- to 6-week intervals to make sure of full resolution. If the eardrum has perforated, the child will need to keep the ear dry until it has healed. Healing usually occurs rapidly once the infection has resolved, but the eardrum needs to be checked when the child is reviewed at the follow-up appointment. The majority of children with AOM will have symptomatic improvement within 24 to 48 hours of antimicrobial therapy. If symptoms are ongoing or worsening after 48 to 72 hours, then this represents a failure of response to the antibiotics used.
7.2.2 Recurrent Acute Otitis Media
7.2.3 Otitis Media with Effusion
7.3 Epidemiology, Prevalence, and Risk Factors
7.3.1 Gender and Age
7.3.2 Geographical and Ethnic Factors
7.3.3 Environmental Factors
7.3.4 Anatomical Factors and Comorbidity
7.4 Pathophysiology of Acute Otitis Media
7.4.1 Eustachian Tube Function
7.4.2 Immune Response
7.4.3 Bacterial or Viral Load
7.5 Flora
7.6 Clinical Features
7.6.1 Symptoms and Signs
7.6.2 Otoscopic Findings
Perforation of the Pars Tensa
7.6.3 Diagnostic Uncertainty
7.7 Treatment
7.7.1 Analgesia and Symptom Control
7.7.2 Antimicrobial Therapy
7.7.3 Choice of Antibiotic
7.8 Treatment Failure
7.8.1 Antimicrobial Therapy Modification
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