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2:  Acute Otitis Media

Aimee Dassner; Jennifer E. Girotto

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Patient presentation.

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Chief Complaint

“Increased irritability and right ear pain.”

History of Present Illness

JL is a 22-month-old female who presents to her primary care provider (PCP) with a 2-day history of rhinorrhea and a 1-day history of increased irritability, fever (to 101.5°F per Mom), and right-ear tugging. Mom denies that JL has had any nausea, vomiting, or diarrhea.

Past Medical History

Full-term birth via spontaneous vaginal delivery. Hospitalized at 9 months of age for respiratory syncytial virus–associated bronchiolitis. Two episodes of acute otitis media (AOM), with last episode about 6 months earlier.

Surgical History

Social history.

Lives with mother, father, and her 5-year-old brother who attends kindergarten. JL attends daycare 2 d/wk, and stays at home with maternal grandmother 3 d/wk.

No known drug allergies

Immunizations

Home Medications

Vitamin D drops 600 IU/d

Physical Examination

Vital signs (while crying).

Temp 100.7°F, P 140 bpm, RR 35, BP 100/57 mm Hg, Ht 81 cm, Wt 23.7 kg

Fussy, but consolable by Mom; well-appearing

Normocephalic, atraumatic, moist mucous membranes, normal conjunctiva, clear rhinorrhea, moderate bulging and erythema of right tympanic membrane with middle-ear effusion

Good air movement throughout, clear breath sounds bilaterally

Cardiovascular

Normal rate and rhythm, no murmur, rub or gallop

Soft, non-distended, non-tender, active bowel sounds

Genitourinary

Normal female genitalia, no dysuria or hematuria

Alert and appropriate for age

Extremities

1. Which of the following clinical criteria is not part of the diagnostic evaluation or staging of acute otitis media (AOM) for this patient?

A. Rhinorrhea

D. Contour of the tympanic membrane

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• Otitis Media
• Author: Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA; Chief Editor: Ravindhra G Elluru, MD, PhD  more...
• Sections Otitis Media
• Practice Essentials
• Pathophysiology
• Epidemiology
• Patient Education
• Physical Examination
• Complications
• Laboratory Studies
• Imaging Studies
• Tympanocentesis
• Other Tests
• Medical Care
• Surgical Care
• Consultations
• Long-Term Monitoring
• AAO-HNSF Guidelines on Tympanostomy Tubes in Children
• AAO-HNSF/AAP/AAFP Guidelines for Otitis Media With Effusion
• AAP/AAFP Guidelines for Acute Otitis Media
• Medication Summary
• Antimicrobial agents
• Vaccines, Inactivated, Bacterial
• Questions & Answers
• Media Gallery

Otitis media (OM) is any inflammation of the middle ear (see the images below), without reference to etiology or pathogenesis. It is very common in children.

There are several subtypes of OM, as follows:

• Acute OM (AOM)
• OM with effusion (OME)
• Chronic suppurative OM
• Adhesive OM

Signs and symptoms

AOM implies rapid onset of disease associated with one or more of the following symptoms:

• Irritability
• Loss of appetite

OME often follows an episode of AOM. Symptoms that may be indicative of OME include the following:

• Hearing loss

Chronic suppurative otitis media is a persistent ear infection that results in tearing or perforation of the eardrum.

Adhesive otitis media occurs when a thin retracted ear drum becomes sucked into the middle ear space and stuck.

See Clinical Presentation for more detail.

OME does not benefit from antibiotic treatment. Therefore, it is critical for clinicians to be able to distinguish normal middle ear status from OME or AOM. Doing so will avoid unnecessary use of antibiotics, which leads to increased adverse effects of medication and facilitates the development of antimicrobial resistance.

Examination

Pneumatic otoscopy remains the standard examination technique for patients with suspected OM. In addition to a carefully documented examination of the external ear and tympanic membrane (TM), examining the entire head and neck region of patients with suspected OM is important.

Every examination should include an evaluation and description of the following four TM characteristics:

• Color – A normal TM is a translucent pale gray; an opaque yellow or blue TM is consistent with middle-ear effusion (MEE)
• Position – In AOM, the TM is usually bulging; in OME, the TM is typically retracted or in the neutral position
• Mobility – Impaired mobility is the most consistent finding in patients with OME
• Perforation – Single perforations are most common

Adjunctive screening techniques for OM include tympanometry, which measures changes in acoustic impedance of the TM/middle ear system with air pressure changes in the external auditory canal, and acoustic reflectometry, which measures reflected sound from the TM; the louder the reflected sound, the greater the likelihood of an MEE.

See Workup for more detail.

Most cases of AOM improve spontaneously. Cases that require treatment may be managed with antibiotics and analgesics or with observation alone.

Guidelines from American Academy of Pediatrics

In February 2013, the American Academy of Pediatrics (AAP) and the American Academy of Family Physicians (AAFP) released updated guidelines for the diagnosis and management of AOM, including recurrent AOM, in children aged 6 months through 12 years. The recommendations offer more rigorous diagnostic criteria to reduce unnecessary antibiotic use.

According to the guidelines, management of AOM should include an assessment of pain. Analgesics, particularly acetaminophen and ibuprofen, should be used to treat pain whether antibiotic therapy is or is not prescribed.

Recommendations for prescribing antibiotics include the following:

• Antibiotics should be prescribed for bilateral or unilateral AOM in children aged at least 6 months with severe signs or symptoms (moderate or severe otalgia, otalgia for 48 hours or longer, or temperature 39°C or higher) and for nonsevere, bilateral AOM in children aged 6 to 23 months
• On the basis of joint decision-making with the parents, unilateral, nonsevere AOM in children aged 6-23 months or nonsevere AOM in older children may be managed either with antibiotics or with close follow-up and withholding antibiotics unless the child worsens or does not improve within 48-72 hours of symptom onset
• Amoxicillin is the antibiotic of choice unless the child received it within 30 days, has concurrent purulent conjunctivitis, or is allergic to penicillin; in these cases, clinicians should prescribe an antibiotic with additional beta-lactamase coverage

In February 2016, the American Academy of Otolaryngology–Head and Neck Surgery Foundation, the AAP, and the AAFP issued updated guidelines for the assessment and management of OME.

See Treatment and Medication for more detail.

Otitis media (OM) is the second most common disease of childhood, after upper respiratory infection (URI). OM is also the most common cause for childhood visits to a physician's office. Annually, an estimated 16 million office visits are attributed to OM; this does not include visits to the emergency department.

OM is any inflammation of the middle ear, without reference to etiology or pathogenesis. It can be classified into many variants on the basis of etiology, duration, symptomatology, and physical findings.

Acute OM (AOM) implies rapid onset of disease associated with one or more of the following symptoms:

• Recent onset of anorexia

These symptoms are accompanied by abnormal otoscopic findings of the tympanic membrane (TM), which may include the following:

• Middle-ear effusion (MEE)
• Decreased mobility with pneumatic otoscopy

AOM is a recurrent disease. More than one third of children experience six or more episodes of AOM by age 7 years.

OM with effusion (OME), formerly termed serous OM or secretory OM, is MEE of any duration that lacks the associated signs and symptoms of infection (eg, fever, otalgia, and irritability). OME usually follows an episode of AOM.

Chronic suppurative OM is a chronic inflammation of the middle ear that persists for at least 6 weeks and is associated with otorrhea through a perforated TM, an indwelling tympanostomy tube (TT; see the image below), or a surgical myringotomy.

The most important factor in middle ear disease is eustachian tube (ET) dysfunction (ETD), in which the mucosa at the pharyngeal end of the ET is part of the mucociliary system of the middle ear. Interference with this mucosa by edema, tumor, or negative intratympanic pressure facilitates direct extension of infectious processes from the nasopharynx to the middle ear, causing OM. Esophageal contents regurgitated into the nasopharynx and middle ear through the ET can create a direct mechanical disturbance of the middle ear mucosa and cause middle ear inflammation.

In children, developmental alterations of the ET, an immature immune system, and frequent infections of the upper respiratory mucosa all play major roles in AOM development. Studies have demonstrated how viral infection of the upper respiratory epithelium leads to increased ETD and increased bacterial colonization and adherence in the nasopharynx. [ 1 ]

Certain viral infections cause abnormal host immune and inflammatory responses in the ET mucosa and subsequent microbial invasion of the middle ear. The host immune and inflammatory response to bacterial invasion of the middle ear produces fluid in the middle ear and the signs and symptoms of AOM.

Although interactions between the common pathogenic bacteria in AOM and certain viruses are not fully understood, strong evidence indicates that these interactions often lead to more severe disease, lowered response to antimicrobial therapy, and OME development following AOM.

A multitude of host, infectious, allergic, and environmental factors contribute to the development of OM.

Host factors

Immune system

The immature immune systems of infants or the impaired immune systems of patients with congenital immune deficiencies, HIV infection, or diabetes may be involved in the development of OM. [ 2 ] OM is an infectious disease that prospers in an environment of decreased immune defenses. The interplay between pathogens and host immune defense plays a role in disease progression.

Patel et al found higher interleukin (IL)-6 levels in patients with OM who also had influenza and adenoviral infections, whereas IL-1β levels were higher in patients who developed OM following URI. [ 3 ] In another study, Skovbjerg et al found that middle ear effusions with culturable pathogenic bacteria were associated with higher levels of IL-1β, IL-8, and IL-10 than sterile effusions. [ 4 ]

Familial (genetic) predisposition

Although familial clustering of OM has been demonstrated in studies that examined genetic associations of OM, separating genetic factors from environmental influences has been difficult. No specific genes have been linked to OM susceptibility. As with most disease processes, effects of environmental exposures on genetic expression probably play an important role in OM pathogenesis.

The role of mucins in OME has been described. Mucins are responsible for gel-like properties of mucus secretions. The middle ear mucin gene expression is unique compared with the nasopharynx. Abnormalities of this gene expression, especially upregulation of MUC5B in the ear, may have a predominant role in OME.

Anatomic abnormality

Children with anatomic abnormalities of the palate and associated musculature, especially the tensor veli palantini, exhibit marked ETD and have higher risk for OM. Specific anomalies that correlate with high prevalence of OM include cleft palate, Crouzon syndrome or Apert syndrome, Down syndrome, and Treacher Collins syndrome.

Physiologic dysfunction

Abnormalities in the physiologic function of the ET mucosa, including ciliary dysfunction and edema, increase the risk of bacterial invasion of the middle ear and the resultant OME. Children with cochlear implants have a high incidence of OM, especially chronic OM and cholesteatoma formation. One study described a relation between laryngopharyngeal reflux and chronic OM (COM); the authors concluded that reflux workup should be performed as part of COM investigations and that if reflux is confirmed, reflux treatment should be initiated in addition to treatment of primary disease. [ 5 ]

Other host factors

Vitamin A deficiency is associated with pediatric upper respiratory infections and AOM.

Obesity has been linked to an increased incidence of OM, although the causal factor is unknown. Speculations include alteration of intrinsic cytokine profile, increased gastroesophageal reflux with alterations of the oral flora, and/or fat accumulation; all of these have been linked with an increased incidence of OM. Conversely, OM may increase the risk of obesity by altering the taste buds. [ 6 ]

Infectious factors

Bacterial pathogens

The most common bacterial pathogen in AOM is Streptococcus pneumoniae, followed by nontypeable Haemophilus influenzae and Moraxella (Branhamella) catarrhalis . These three organisms are responsible for more than 95% of all AOM cases with a bacterial etiology. [ 7 ]

In infants younger than 6 weeks, gram-negative bacilli (eg, Escherichia coli, Klebsiella species, and Pseudomonas aeruginosa ) play a much larger role in AOM, causing 20% of cases. S pneumoniae and H influenzae are also the most common pathogens in this age group. Some studies also found Staphylococcus aureus as a pathogen in this age group, but subsequent studies suggested that the flora in these young infants may be that of usual AOM in children older than 6 weeks.

Many experts had proposed that the MEE associated with OME was sterile because cultures of middle ear fluid obtained by tympanocentesis often did not grow bacteria. This view is changing as newer studies show 30-50% incidence of positive results in middle ear bacterial cultures in patients with chronic MEE. These cultures grow a wide range of aerobic and anaerobic bacteria, of which S pneumoniae, H influenzae, M catarrhalis, and group A streptococci are the most common.

M catarrhalis –induced AOM differs from AOM caused by other bacterial pathogens in several ways. It is characterized by higher a proportion of mixed infections, younger age at the time of diagnosis, lower risk of spontaneous perforation of the tympanic membrane, and an absence of mastoiditis. [ 8 ]

Further evidence for the presence of bacteria in the MEE of patients with OME was provided by studies using polymerase chain reaction (PCR) assay to detect bacterial DNA in MEE samples that were determined to be sterile with standard bacterial culture techniques. In one such study using PCR assay, 77.3% of the MEE samples had positive results for one or more common AOM pathogens (eg, S pneumoniae, H influenzae, M catarrhalis ).

In chronic suppurative OM, the most frequently isolated organisms include P aeruginosa, S aureus, Corynebacterium  species, and Klebsiella pneumoniae . An unanswered question is whether these pathogens invade the middle ear from the nasopharynx via the ET (as do the bacteria responsible for AOM) or whether they enter through the perforated TM or a TT from the EAC.

The role of Helicobacter pylori in children with OME has been increasingly recognized. [ 9 ] Evidence that this agent might be responsible for OME comes from its isolation from middle ear and tonsillar and adenoidal tissue in patients with OME.

Alloiococcus otitidis is a species of gram-positive bacterium that has been discovered as a pathogen associated with OME. [ 10 , 11 ] This organism is the most frequent bacterium in AOM, as well as in OME. It has also been detected in patients who had been treated with antibiotics, such as beta-lactams or erythromycin, suggesting that these agents may not be sufficiently effective to eliminate this organism. Further investigation is needed to reveal the clinical role of the organism in OM.

Viral pathogens

Because acute viral URI is a prominent risk factor for AOM development, most investigators have suspected a role for respiratory viruses in AOM pathogenesis.

Many studies have substantiated this suspicion by showing how certain respiratory viruses can cause inflammatory changes to the respiratory mucosa that lead to ETD, increased bacterial colonization and adherence, and, eventually, AOM. Studies have also shown that viruses can alter the host-immune response to AOM, thereby contributing to prolonged middle ear fluid production and development of chronic OME.

The viruses most commonly associated with AOM are respiratory syncytial virus (RSV), influenza viruses, parainfluenza viruses, rhinovirus, and adenovirus. Human parechovirus 1 (HPeV1) infection is associated with OM and cough in pediatric patients. [ 12 ] OM developed in 50% of 3-month follow-up periods that yielded evidence of HPeV1 infection but in only 14% of the HPeV1-negative periods; in recurring OM, the middle ear fluid samples were positive for HPeV in 15% of episodes.

Factors related to allergies

The relation between allergies and OM remains unclear. In children younger than 4 years, the immune system is still developing, and allergies are unlikely to play a role in recurrent AOM in this age group. Although much evidence suggests that allergies contribute to the pathogenesis of OM in older children, extensive evidence refutes the role of allergies in the etiology of middle ear disease.

The following is a brief list of evidence for and against the etiologic role of allergy in OM:

• Many patients with OM have concomitant allergic respiratory disease (eg, allergic rhinitis, asthma)
• Many patients with OM have positive results to skin testing or radioallergosorbent testing (RAST)
• Although mast cells are found in the middle ear mucosa, most studies fail to show significant levels of immunoglobulin E (IgE) or eosinophils in the MEE of patients with OM
• OM is most common in the winter and early spring, yet most major allergens (eg, tree and grass pollens) peak in the late spring and early fall
• Most patients with concomitant OM and allergy show no marked improvement in middle ear disease with aggressive allergy management, despite marked improvements to nasal and other allergy-related symptoms

Environmental factors

Infant feeding methods

Many studies report that breastfeeding protects infants against OM. The best of these studies indicates that this benefit is evident only in children who are breastfed exclusively for the first 3-6 months of life. Breastfeeding of this duration reduces the incidence of OM by 13%. The protective effects of breastfeeding for the first 3-6 months persist for 4-12 months after breastfeeding ceases, possibly because delaying onset of the first OM episode reduces recurrence of OM in these children.

Passive smoke exposure

Many studies have shown a direct relation between passive smoke exposure and risk of middle ear disease. [ 13 ] A systematic review of 45 publications dealing with OM and parental smoking showed pooled odds ratios of 1.48 (95% confidence interval [CI], 1.08-2.04) for recurrent OM, 1.38 (95% CI, 1.23-1.55) for MEE, and 1.3 (95% CI, 1.3-1.6) for AOM. [ 14 ]

Group daycare attendance

Daycare centers create close contact among many children, which increases the risks of respiratory infection, nasopharyngeal colonization with pathogenic microbes, and OM.

Many researchers have used meta-analysis to confirm that exposure to other young children (including siblings) in group daycare settings is a major risk factor for OM. [ 15 ] A meta-analysis reported that care outside the home conferred a 2.5-fold risk for OM. Other critical reviews of studies on OM and group childcare show heightened odds ratios of 1.6-4.0:1 for center care versus home care.

Children who attend daycare centers frequently acquire antibacterial-resistant organisms in their nasopharynx, leading to AOM that may be refractory to antibacterial treatment. American Academy of Pediatrics (AAP) and American Academy of Family Physicians (AAFP) guidelines recommend high-dose amoxicillin-clavulanate as the antibiotic of choice in the treatment of AOM in children who attend daycare.

Socioeconomic status

Socioeconomic status encompasses many independent factors that affect both the risk of OM and the likelihood that OM will be diagnosed. [ 16 ]

In general, lower socioeconomic status confers higher risk for environmental exposure to parental smoking, bottle-feeding, crowded group daycare, crowded living conditions, and viruses and bacterial pathogens. Compared with children from middle-income and high-income families, children from lower socioeconomic groups use health care resources less frequently, which decreases the likelihood that OM cases will be diagnosed.

United States statistics

OM, the most common specifically treated childhood disease, accounts for approximately 20 million annual physician visits. Various epidemiologic studies report the prevalence rate of AOM to be 17-20% within the first 2 years of life, and 90% of children have at least one documented MEE by age 2 years. OM is a recurrent disease. One third of children experience six or more episodes of AOM by age 7 years.

International statistics

Incidence and prevalence in other industrialized nations are similar to US rates. In less developed nations, OM is extremely common and remains a major contributor to childhood mortality resulting from late-presenting intracranial complications. International studies show increased prevalence of AOM and chronic OM (COM) among Micronesian and Australian aboriginal children.

Age-related demographics

Peak prevalence of OM in both sexes occurs in children aged 6-18 months. Some studies show bimodal prevalence peaks; a second, lower peak occurs at age 4-5 years and corresponds with school entry. Although OM can occur at any age, 80-90% of cases occur in children younger than 6 years. Children who are diagnosed with AOM during the first year of life are much more likely to develop recurrent OM and chronic OME than children in whom the first middle ear infection occurs after age 1 year.

Sex-related demographics

Several studies have now shown equal AOM prevalence in males and females; many previous studies had shown increased incidence in boys.

Race-related demographics

For some time, the prevalence of OM in the United States was reported to be higher in black and Hispanic children than in white children. However, a study that controlled for socioeconomic and other confounding factors showed equal incidence in blacks and whites. Hispanic children and Alaskan Inuit and other American Indian children have higher prevalence of AOM than white and black children in the United States.

US mortality is extremely low in this era of antimicrobial therapy (< 1 death per 100,000 cases). In developing nations with limited access to primary medical care and modern antibiotics, mortality figures are similar to those reported in the United States before antibiotic therapy. A study that examined the causes of death in Los Angeles County Hospital from 1928-1933, years before the advent of sulfa, showed that 1 in 40 deaths was caused by intracranial complications of OM.

Morbidity from this disease remains significant, despite frequent use of systemic antibiotics to treat the illness and its complications. Intratemporal and intracranial complications of OM are the two major types.

Intratemporal complications include the following:

• Hearing loss (conductive and sensorineural)
• TM perforation (acute and chronic)
• Chronic suppurative OM (with or without cholesteatoma)
• Cholesteatoma
• Tympanosclerosis
• Mastoiditis
• Labyrinthitis
• Facial paralysis
• Cholesterol granuloma
• Infectious eczematoid dermatitis

Intracranial complications include the following [ 17 ] :

• Subdural empyema
• Brain abscess
• Extradural abscess
• Lateral sinus thrombosis
• Otitic hydrocephalus

The prognosis for almost all patients with OM is excellent [ 18 ] ; the exceptions are patients in whom OM involves intratemporal and intracranial complications (< 1%).

Data on cognitive and educational outcomes of OM in the literature are limited. [ 19 ] The impact of OM on child development depends on numerous factors. OM in infants younger than 12 months predisposes to long-term speech and language problems. OM has also been reported to negatively affect preexisting cognitive or language problems. Careful follow-up and early referral are key to management.

Patient education topics should include the following:

• Avoiding risk factors
• Appropriate use of antibiotics
• Understanding the implications of antibiotic-resistant bacteria in OM

Education for health care providers should focus on the following topics:

• Antibiotic-resistant bacteria and the need to avoid overprescribing antibiotics
• Importance of pneumatic otoscope examination to distinguish AOM from OME
• Treatment differences between AOM and OME

For patient education resources, see the Ear, Nose, and Throat Center , as well as Earache .

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• Diagram of the normal tympanic membrane anatomy.
• Healthy tympanic membrane.
• Acute otitis media with purulent effusion behind a bulging tympanic membrane.
• Chronic otitis media with a retraction pocket of the pars flaccida.
• Cholesteatoma of the pars flaccida.
• Central/pars tensa tympanic membrane perforation with a healthy middle ear membrane.
• Central/pars tensa tympanic membrane perforation with a tympanostomy tube in place.
• Various tympanostomy tube styles and sizes.
• Initial presentation of a young girl with chronic right ear pain and multiple untreated middle ear infections.
• Acute coalescent mastoiditis with a Bezold abscess in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
• A young girl who presented with chronic right ear pain and multiple untreated middle ear infections on the operating table for mastoidectomy and drainage of Bezold abscess.
• Aspirating pus from the Bezold abscess for Gram staining, culturing, and sensitivity testing in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
• Surgical incision to aspirate pus in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
• Freer elevator demonstrating extension of an abscess cavity from the mastoid into the neck in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
• Incision is closed and a drain is placed in the abscess cavity in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
• Postoperative bandage in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
• The wound now appears clean and dry on postoperative day 4. This young girl initially presented with chronic right ear pain and multiple untreated middle ear infections.
• Postoperative day 4: Mom is smiling. This young girl initially presented with chronic right ear pain and multiple untreated middle ear infections.

Contributor Information and Disclosures

Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA Professor of Emergency Medicine and Clinical Pediatrics, Weill Cornell Medical College; Attending Physician, Departments of Emergency Medicine and Pediatrics, Lincoln Medical and Mental Health Center; Adjunct Professor of Emergency Medicine, Adjunct Professor of Pediatrics, St George's University School of Medicine, Grenada Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA is a member of the following medical societies: American Academy of Pediatrics , American Academy of Urgent Care Medicine, American College of Emergency Physicians , American Heart Association , American Medical Association , Association of Clinical Research Professionals , Public Responsibility in Medicine and Research , Society for Academic Emergency Medicine , Society for Simulation in Healthcare Disclosure: Nothing to disclose.

Muhammad Aslam, MD Professor of Pediatrics, University of California, Irvine, School of Medicine; Neonatologist, Division of Newborn Medicine, Department of Pediatrics, UC Irvine Medical Center Muhammad Aslam, MD is a member of the following medical societies: American Academy of Pediatrics Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Nothing to disclose.

Alan D Murray, MD Pediatric Otolaryngologist, ENT for Children; Full-Time Staff, Medical City Dallas Children's Hospital; Consulting Staff, Department of Otolaryngology, Children's Medical Center at Dallas, Cook Children's Medical Center; Full-Time Staff, Texas Pediatric Surgery Center, Cook Children's Pediatric Surgery Center Plano Alan D Murray, MD is a member of the following medical societies: Alpha Omega Alpha , American Academy of Otolaryngology-Head and Neck Surgery , American Society of Pediatric Otolaryngology , Society for Ear, Nose and Throat Advances in Children , American Academy of Pediatrics , American College of Surgeons , Texas Medical Association Disclosure: Nothing to disclose.

Ravindhra G Elluru, MD, PhD Professor, Wright State University, Boonshoft School of Medicine; Pediatric Otolaryngologist, Department of Otolaryngology, Dayton Children's Hospital Medical Center Ravindhra G Elluru, MD, PhD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery , American Academy of Pediatrics , American Bronchoesophagological Association , American College of Surgeons , American Medical Association , Association for Research in Otolaryngology , Society for Ear, Nose and Throat Advances in Children , Triological Society , American Society for Cell Biology Disclosure: Nothing to disclose.

Orval Brown, MD Director of Otolaryngology Clinic, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center at Dallas

Orval Brown, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery , American Academy of Pediatrics , American Bronchoesophagological Association , American College of Surgeons , American Medical Association , American Society of Pediatric Otolaryngology , Society for Ear, Nose and Throat Advances in Children , and Society of University Otolaryngologists-Head and Neck Surgeons

Disclosure: Nothing to disclose.

Michael Jones, MD Consulting Staff, Department of Emergency Medicine, Brooke Army Medical Center

David Malis, MD Assistant Chief, Otolaryngology Service, Brooke Army Medical Center, Clinical Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, The University of Texas Health Science Center at San Antonio

Leslie A Wilson, MD Chief, Well-Baby Clinic and Chronic Ear Clinic, Department of Pediatrics, Wilford Hall Air Force Medical Center

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• Complications of Otitis Media
• Otitis Media With Effusion
• Acute Otitis Media
• Chronic Suppurative Otitis Media
• Acute Otitis Media Empiric Therapy
• Emergent Management of Acute Otitis Media
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Otitis Media

Otitis media is a common and frequently encountered ear infection that affects individuals of all ages, particularly young children. This condition involves inflammation and infection of the middle ear, often resulting from viral or bacterial pathogens. Otitis media can lead to various symptoms, including ear pain , fever , hearing difficulties, and fluid buildup behind the eardrum .

This article aims to serve as a comprehensive nursing guide to otitis media, diving into its causes, clinical manifestations, diagnostic methods, medical management, and nursing interventions .

Table of Contents

• What is Otitis Media? 

Pathophysiology

Statistics and incidences, clinical manifestations, assessment and diagnostic findings, pharmacologic management, surgical management, nursing assessment, nursing diagnoses, nursing care planning and goals, nursing interventions, documentation guidelines, what is otitis media.

Otitis media is very common among children.

• Otitis media is an inflammation of the middle ear without reference to etiology or pathogenesis.
• It can be classified into many variants based on etiology, duration, symptomatology, and physical findings.

In children, developmental alterations of the eustachian tube, an immature immune system, and frequent infections of the upper respiratory mucosa all play major roles in AOM development.

• The most important factor in middle ear diseases is eustachian tube dysfunction, in which the mucosa at the pharyngeal end of the ET is part of the mucociliary system of the middle ear.
• The eustachian tube in an infant is shorter and wider than in an older child or adult.
• The tube is also straighter, thereby allowing nasopharyngeal secretions to enter the middle ear more easily.
• Interference with the mucosa by edema , tumor , or negative intratympanic pressure facilitates the direct extension of infectious processes from the nasopharynx to the middle ear, causing otitis media.

Otitis media is one of the most common infectious diseases of childhood.

• Two of every three children have at least one episode of otitis media by the time they are 1 year old.
• Otitis media accounts for approximately 20 million annual physician visits.
• Various epidemiologic studies report the prevalence rate of acute otitis media to be 17-20% within the first two years of life.
• One-third of children experience six or more episodes of otitis media by age 7 years.
• Peak prevalence of otitis media in both sexes occurs in children aged 6 to 18 months.

A multitude of host, infectious, allergic, and environmental factors contribute to the development of otitis media.

• Immature immune system. Otitis media is an infectious disease that prospers in an environment of decreased immune defenses.
• Genetic predisposition. Although familial clustering of otitis media has been demonstrated in studies that examined genetic associations of otitis media, separating genetic factors from environmental influences has been difficult.
• Anatomic abnormality. Children with anatomic abnormalities of the palate and associated musculature have a higher risk for otitis media.
• Physiologic dysfunction. Abnormalities in the physiologic function of the ET mucosa increase the risk of bacterial invasion of the middle ear and the resultant otitis media.
• Bacterial pathogens. The most common bacterial pathogen is Streptococcus pneumoniae, followed by Haemophilus influenzae , and Moraxella catarrhalis .
• Infant feeding methods. Many studies report that breastfeeding protects infants against otitis media.

Otitis media should be suspected in children with a history of characteristic head-neck and general symptoms.

• Otalgia . Young children may exhibit signs of otalgia by pulling on the affected ear or ears or pulling on the hair ; otalgia apparently occurs more often when the child is lying down.
• Otorrhea . Discharge may come from the middle ear through a recently perforated tympanic membrane , or through another perforation.
• Headache. An older child may complain of a headache.
• Symptoms of upper respiratory infection. Concurrent or recent symptoms of URI, such as cough , rhinorrhea or sinus congestion is common.
• Fever. Two-thirds of children with otitis media have a history of fever, although fevers greater than 40°C are uncommon.
• Irritability. Irritability may be the sole early symptom in a young infant or toddler.

Otitis media may be revealed through the following:

• Laboratory tests. Laboratory evaluation is usually unnecessary, although many experts recommend a full sepsis workup in infants younger than 12 weeks who present with fever and otitis media.
• Tympanocentesis. The criterion standard in the diagnosis of otitis media is tympanocentesis to determine middle ear fluid, followed by culture of fluid to identify causative pathogens.

Medical Management

In 2013, the American Academy of Pediatrics (AAP) and the American Academy of Family Practice published updated guidelines on the medical management of otitis media.

• Antibiotic therapy. Among other recommendations, the guidelines recommended antibiotics for bilateral and unilateral otitis media in children aged at least 6 months with severe signs and symptoms.

The FDA has approved more than a dozen antibiotics to treat otitis media.

• Antimicrobial agents. These agents remove pathogenic bacteria from the middle ear fluid.

From the beginning, it is essential to integrate surgical management of otitis media with medical treatment.

• Myringotomy and TT placement. Myringotomy or the incision of the eardrums may be performed to establish drainage and to insert tiny tubes into the tympanic membrane to facilitate drainage.
• Adenoidectomy. The performance of adenoidectomy to treat patients with otitis media has generated extensive discussion and research, though potential benefits are controversial.

Nursing Management

Most infants and children with otitis media are cared for at home; therefore, a primary responsibility of the nurse is to teach the family caregivers about prevention and the care of the child.

Assessment of a child with otitis media include the following:

• Physical examination. The infant’s ear is examined with an otoscope by pulling he ear down and back to straighten the ear canal.
• History. Assess if there is a history of trauma to the ears, affected siblings, a history of cranial/facial defects or any familial history of otitis media.

Based on the assessment data, the major nursing diagnoses are:

• Acute pain related to the inflammation of the middle ear.
• Anxiety related to health status.
• Impaired verbal communication related to effects of hearing loss.
• Disturbed sensory perception related to obstruction, infection of the middle ear, or auditory nerve damage.
• Risk for injury related to hearing loss, decreased visual acuity.
• Infection related to presence of pathogens.

Main Article: 4 Otitis Media Nursing Care Plans 

The major goals for the child with otitis media are:

• The child or parent will indicate absence of pain .
• The child will be free of infection.
• The parents will state understanding of preventive measures.
• The child will have normal hearing.

Nursing care for the child with otitis media include:

• Positioning . Have the child sit up, raise head on pillows, or lie on unaffected ear.
• Heat application. Apply heating pad or a  warm hot water bottle.
• Diet. Encourage breastfeeding of infants as breastfeeding affords natural immunity to infectious agents; position bole-fed infants upright when feeding .
• Hygiene . Teach family members to cover mouths and noses when sneezing or coughing and to wash hands frequently.
• Monitoring hearing loss. Assess hearing ability frequently.

Goals are met as evidenced by:

• The child or parent indicated absence of pain .
• The child is free of infection.
• The parents stated understanding of preventive measures.
• The child has normal hearing.

Documentation in a child with otitis media include the following:

• Individual findings, including factors affecting, interactions, nature of social exchanges, specifics of individual behavior.
• Cultural and religious beliefs, and expectations.
• Plan of care.
• Teaching plan.
• Responses to interventions, teaching, and actions performed.
• Attainment or progress toward desired outcome.

5 thoughts on “Otitis Media”

This was very useful..thank you

One tip I always share with parents is to make sure their child is up to date on their pneumococcal vaccinations, as pneumococcal bacteria are a common cause of ear infections. Another important tip is to encourage frequent hand washing, especially after being in crowded or public places, to help prevent the spread of infections. It’s also important to monitor for signs of an ear infection, such as pain, redness, or discharge, and to seek prompt medical attention if these symptoms occur. Thank you for bringing attention to this important topic!

I have this and It absolutely sucks! I started getting Eustachian tubes put in when I was 18months old, and still to this day I am having Estuation tubes put in every other year or so. I am currently, 24. I got my first set of hearing aids when I turned 17, bilateral. I hope one day in the future we can have an answer to permanently treat this instead of creating more and more scar tissue on my eardrums every single surgery I get. Scar tissue gets worse and worse every surgery I have. It’s building up on my eardrum, so it’s just decreasing my hearing every single time.

Hello Skyler M,

I’m really sorry to hear about your ongoing struggle with otitis meida and hearing loss. It sounds incredibly tough, especially with the impact on your hearing. It’s totally understandable to hope for a better, more lasting solution.

Have you explored any new treatment options lately? Sometimes specialists in audiology or advanced otology might have different approaches worth considering.

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Case Report

The connection between acute otitis media and the acute abdomen, imran masood.

Touro University California, Vallejo, California, USA

Tami Hendriksz

A female aged 9 years with a recent episode of acute otitis media (AOM) presented to her primary care physician with complaints of severe abdominal pain with right lower quadrant rebound tenderness, suggestive of an acute surgical abdomen. Neurological examination was normal on presentation. She was transferred to the local children’s hospital for workup of appendicitis, during which she began exhibiting ataxia and slurred speech. Further evaluation revealed mastoiditis, venous sinus thrombosis and subdural empyema. Appendicitis was ruled out. We describe the first documented case of neurological complications of AOM presenting as an acute surgical abdomen without initial neurological findings.

Our case highlights many important lessons that primary care physicians will encounter. First, we present an example of when prematurely focusing on one diagnosis may distract the clinician from the true diagnosis and lead to diagnostic delay. Moreover, we illustrate an example of the interplay between distant body systems; connecting abdominal pain to a neurological infection. We believe that this case provides a fund of knowledge for other primary care physicians.

Complications of acute otitis media (AOM) are varied and can result in significant harm. Of these, most notable are intracranial disease such as venous sinus thrombosis (VST) and cerebral abscess, and extracranial disease such as mastoiditis. VSTs among children most commonly present as isolated, gradual-onset, localised headaches. 1 Although less likely, ‘thunderclap’ and migraine-type headaches may occur. 2–5 Focal neurological findings, encephalopathy and seizures are possible findings as well. Intracranial abscesses are associated with the classic triad of headache, fever and focal neurological findings; however, less than half of cases present with this triad. 6 Common findings for intracranial abscesses also include lethargy, nausea and vomiting. 7 Mastoiditis is characterised by postauricular tenderness, erythema, fluctuance, auricular displacement or protrusion and ear pain. 7 8

In the case of our patient, she presented with a primary concern of acute onset abdominal pain in the setting of an episode of AOM. Her presentation has never been reported in the literature as the presenting complaint for VST, mastoiditis or subdural empyema.

Case presentation

Our patient is a female aged 9 years with no significant past medical history who presented to her primary care provider on 21 January 2016 with the complaint of 5 days of fever, bilateral ear pain, anorexia, non-bloody and non-bilious emesis and 2 days of generalised abdominal pain. Two days prior to presentation, she was seen at an outside emergency department for AOM. Because of a penicillin allergy, she was given azithromycin 500 mg for 1 day, followed by 250 mg for 4 more days. However, after the first dose, she began to vomit, and did not complete her antibiotic therapy. The remaining review of systems were negative. On arriving to the primary care paediatrician, initial physical examination revealed that she was tired and ill-appearing with purulent drainage from her left ear and acute tenderness in the right lower quadrant of her abdomen. She exhibited rebound and guarding. Her urinalysis in the outpatient clinic was negative, and due to concern for acute abdomen and serious bacterial infection she was sent to the emergency department of the local Children’s Hospital.

Investigations

Initial labs at the emergency department showed a white blood cell count of 23 x 10 3 /µL and a C reactive protein of 28.6 mg/L. Chemistry was within normal limits. Her left ear was again noted to have purulent drainage, and her abdomen continued to be very tender to palpation with guarding. She was initially admitted to the surgical service given concern for appendicitis. On her first day of admission, she received a limited abdominal ultrasound, which was negative for appendicitis. During the ultrasound, the patient was noted to have slurred speech and right-sided weakness. Neurology was then consulted, and felt that her symptoms were more consistent with a seizure disorder, therefore, they recommended an electroencephalogram (EEG) which showed focal left paracentral slowing. After receiving the results of the EEG, neurology recommended a brain MRI and magnetic resonance venography (MRV). These studies were done the same day, and they revealed meningeal enhancement of the frontal and parietal lobes consistent with meningitis, as well as left venous sinus thrombosis and left mastoiditis. Haematology was then consulted. They recommended a hypercoagulable workup, which was negative. Due in part to her persistent right-sided weakness, a subsequent brain MRI was obtained, 6 days after the first, which showed a subdural empyema. The patient’s venous sinus thrombosis, subdural empyema, meningitis and cerebritis were attributed to a complicated otitis media and mastoiditis. Blood culture drawn at the time of admission grew coagulase-negative staphylococcus at 24 hours, which was thought to likely be a contaminant. A lumbar puncture revealed cerebral spinal fluid (CSF) with a white blood cell count of 153 cells/µL, with 59% neutrophils and 41% monocytes. The CSF protein level was 71 mg/dL and glucose 67 mg/dL. CSF culture had no growth. CSF was positive for Streptococcus pneumoniae by PCR (negative PCR for Neisseria meningitides and Haemophilus influenzae type b). Subdural empyemic fluid culture had no growth, and culture of her ear drainage grew scant coagulase-negative staphylococcus.

Studies completed during this hospitalisation:

Hospital day 1—ultrasound abdomen limited

Hospital day 1—EEG

Hospital day 1—MRI and MRV brain with contrast

Hospital day 3—CT orbit, ear, temporal bone with and without contrast

Hospital day 3—CT neck with contrast

Differential diagnosis

• Mesenteric adenitis (working diagnosis).
• Lemierre’s syndrome with otogenic variant.
• Mesenteric ischaemia and cavernous sinus thrombosis secondary to hypercoagulable state induced by serum inflammation.
• Primary otitis media with spread to adjacent tissues causing central nervous system infection with secondary bacteraemia/fungaemia, leading to hematogenous spread to the abdomen.
• Abdominal pain secondary to recurrent vomiting in the setting of elevated intracranial pressure.

The patient was started on vancomycin and ceftriaxone empirically on admission. Infectious disease consultants recommended adding metronidazole on day 2 of hospitalisation given the unclear aetiology of her infection and her persistent fevers. She was treated with intravenous ceftriaxone and metronidazole for 2 weeks inpatient, followed by an additional 4 weeks outpatient (via a peripherally-inserted central catheter (PICC) line). On discovery of the venous sinus thrombosis, the patient was started on a heparin drip and later in her hospital course transitioned to enoxaparin and heparin XA (low molecular weight heparin). She also underwent tympanostomy tube placement and left mastoidectomy on day 2 of hospitalisation, followed by burr hole irrigation of the subdural empyema 5 days later. The patient was followed by neurology, haematology, neurosurgery, otolaryngology, infectious disease and physical therapy during the course of her stay.

Procedures completed during this hospitalisation:

Hospital day 2—bilateral myringotomy tubes, and mastoidectomy with wash out

Hospital day 4—single lumen PICC line placement in left brachial vein

Hospital day 7—burr hole irrigation of subdural empyema

Outcome and follow-up

The patient’s abdominal pain resolved within the first 2 days of her hospital stay. Patient was discharged from the hospital after 22 days. Follow-up brain MRI 3 weeks after hospital discharge showed resolution of the subdural empyema and the venous sinus thrombosis, with resolving cerebritis, and evolving postsurgical changes of the left mastoid process. Her antibiotics were discontinued at that time, and her PICC line was removed the following day. By her follow-up appointment with haematology 7 weeks after discharge, patient had ‘returned to her baseline normal activity without any evidence of ongoing infection’ or sequelae.

On recent follow-up, now 11 months after initial presentation, the patient exhibits a full recovery. She has graduated from physical therapy, and is back to practicing competitive gymnastics. Our patient is no longer on any medications, and has been discharged from the haematology, infectious disease, neurosurgical and neurology specialists. She does continue to see the otolaryngologist and audiologist for follow-up care while her tympanostomy tube remains in place.

We present the case of a female aged 9 years with multiple sequelae of AOM demonstrating an atypical clinical presentation. VSTs are considered exceptionally rare, with the incidence reported at 0.67/100 000 in children. 9 Studies also show that VSTs are more common in neonates and infants, rather than children or adolescents. 9 Furthermore, while mastoiditis is more common than VSTs, the incidence of mastoiditis is exceedingly rare in a child aged 9 years. Various studies have demonstrated that mastoiditis occurs most often in children <2 years of age, with one report of a median age of 48 months. 10–12 Moreover, as mentioned above, the clinical presentation for these particular sequelae largely present with neurological findings. Our patient did not initially exhibit any of the aforementioned neurological findings.

Demographically, statistically and clinically, our patient exists as an anomaly to the current literature. Our case highlights the essential nature of acknowledging the connection between distinct organ systems. Additionally, focusing on the possibility of an acute emergency can be a distraction from investigating its aetiology, and may lead to diagnostic delay.

In an attempt to connect otitis media with abdominal pain, we propose the diagnosis of mesenteric adenitis. Mesenteric adenitis is associated with group A streptococcal (Streptococcus pyogenes) pharyngitis, which is also present in cases of AOM. 13 14 Mesenteric adenitis has been shown to present very similarly to appendicitis. 14 A potential cause of our patient’s severe abdominal pain with rebound and guarding may have been her S. pneumoniae otitis media contributing to the development of mesenteric adenitis. It is possible that the mesenteric lymph node enlargement was missed on the limited abdominal ultrasound, as the ultrasound focused primarily on the appendix. Along with this theory, we also postulate that a primary otitis media may have occurred, with spread into contiguous tissues causing mastoiditis, subdural empyema and venous sinus thrombosis. This infection may have then become haematologically disseminated, with resultant seeding of the infection in the abdomen, which prompted the need for intravenous antibiotics. Interestingly, her ear fluid culture grew coagulase-negative staphylococcus, an organism also found in her blood culture, which correlates this theory. However, this was considered to be a contaminant, and not a true infection. This theory is less likely considering the bacteria that was isolated in her CSF was S. pneumoniae , and that her blood cultures were presumably negative. Furthermore, we considered the link between elevated intracranial pressure and repetitive vomiting to be a potential explanation for her abdominal pain. However, abdominal pain due to vomiting would not typically present as severe right lower quadrant pain with rebound tenderness and guarding.

Another potential explanation to connect these symptoms include the otogenic variant of Lemierre’s syndrome. Lemierre’s syndrome is a suppurative thrombophlebitis involving the internal jugular veins, most often caused by Fusobacterium necrophorum . Thrombosis of the jugular veins occur, followed by septic emboli to the lungs. 15 A case reported by Masterson et al revealed an otogenic variant of Lemierre’s syndrome, in which a young girl suffered bilateral mastoiditis with subsequent internal jugular vein thrombosis. 16 While this explanation is plausible, it is weakened by the fact that she did not present with pulmonary symptoms, which is a classic finding in Lemierre’s syndrome. Chest X-ray was not performed during the course of this illness.

Moreover, considering her elevated CRP suggesting serum inflammation, she may have been in a hypercoagulable state. This hypercoagulable state could have presented with two separate infarctions, one being her documented venous sinus thrombosis, and the other being a thrombus in a mesenteric vessel. This theory is supported by her improvement while on anticoagulants and decreased abdominal pain with bowel rest (a hallmark aspect of managing mesenteric ischaemia). However, considering her otitis media, mastoiditis and subdural empyema, it is more likely that the thrombus in her cerebral sinus was due to contiguous spread of infection with vascular insult, rather than primary vascular thrombosis.

Unfortunately, due to the high morbidity associated with appendicitis, it is likely that the clinician will narrowly focus on this diagnosis, at the expense of a broad diagnostic workup. In this scenario, focusing on the diagnosis of appendicitis resulted in a distraction away from the patient’s ear infection and its potential sequelae. Had neurological symptoms not developed, she may have suffered from a higher morbidity, due to delayed diagnosis. Luckily she had been admitted to a Children’s Hospital, under the care of multiple specialists, where she was able to have an EEG and then subsequent brain MRI with MRV with little time delay. It is interesting to note that this patient had an EEG performed prior to any imaging of her brain. At the time, the patient had been admitted to the surgical service for a likely appendicitis, and the recommendation to obtain an EEG by the consulting neurology team had been followed without consideration of prior emergent brain imaging. Also interesting to note is that no further workup (beyond the initial limited ultrasound) or discussion regarding the cause of her acute abdominal pain is apparent in review of her medical records. There appears to have been a somewhat myopic focus on the symptom that was most severe at a given time (initially abdominal pain, later the neurological symptoms), without much effort to search for connections or provide more holistic care.

In conclusion, our unique case provides important teaching points for any physician treating patients in the ambulatory clinic. We found in this case, that prematurely focusing on one diagnosis led to diagnostic delay. Furthermore, we highlighted that distant body systems may be unsuspectingly related, requiring a ‘whole-body’ approach for accurate diagnosis. An important lesson to be taken away from this case is that one unifying diagnosis is more likely than two separate, unrelated diseases. Fortunately, our patient is healing appropriately and remains well overall.

Learning points

• Prematurely locking onto a diagnosis may distract a clinician from the true diagnosis.
• Distant body systems may be unsuspectingly related, therefore, clinicians should always exercise a ‘whole-body’ approach.
• For a set of signs and symptoms, one unifying diagnosis is more likely than two separate aetiologies.
• There is a potential connection between abdominal pain and neurological infections that is not well-defined by our current literature. Mesenteric adenitis may be one possible explanation.

Contributors: This manuscript has not been published previously and is not under consideration for publication elsewhere. Both authors participated in the concept and design, analysis and interpretation of the data, drafting and revising of the manuscript and have approved the manuscript as submitted. The authors have no conflicts of interest to disclose.

Competing interests: None declared.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.