Uncomplicated acute otitis media (AOM) and sinusitis are generally managed in the outpatient setting with excellent outcomes. Occasionally, complications from these infections arise, and a subset of these complications requires immediate intervention and hospitalization (Table 99-1). Children with AOM and sinusitis are predisposed to infectious and inflammatory complications because of their close proximity to orbital and parameningeal structures. The separation between these structures and the middle ear or sinuses may be breached by two main mechanisms: (1) direct extension via communication between the middle ear and the mastoid airspace and thin bony walls separating the sinuses from intraorbital area, and (2) hematogenous spread via penetrating veins from infected sinuses or mastoid spaces to the intracranial region.

AOM is defined as inflammation of the mucoperiosteal lining of the middle ear.¹ An upper respiratory tract infection (URI) precedes most episodes of AOM and causes edema and obstruction of the Eustachian tube, which then impedes drainage of middle ear fluid. One-third of all URIs are complicated by AOM.² By age 3 years, 80% of all children will have had at least one episode of AOM, with the peak incidence occurring between 6 and 18 months of age.³ The high risk in this age group is likely due to a combination of narrower and more horizontal positioning of the Eustachian tubes and a relatively immature immune system, thus making them more susceptible to infection.¹ Most episodes of AOM are treated with oral antibiotics in the outpatient setting. For treatment with parenteral antibiotics, a single dose of ceftriaxone eradicates AOM caused by Haemophilus influenzae and penicillin-susceptible Streptococcus pneumoniae. However, for AOM caused by non-penicillin susceptible S. pneumoniae, ceftriaxone administered intramuscularly successfully treated 52% of cases with a single dose and 97% of cases with three doses.⁴

In the postantibiotic era, complications from AOM have decreased significantly. Serious infectious complications are reported in 0.04% to 0.4% of cases.⁵ The sites of these complications include the surrounding bone, middle/inner ear, and intracranial spaces (Table 99-1).

MASTOIDITIS

Background and Pathophysiology

The mastoid is the inferior posterior portion of the temporal bone and consists of air cells separated by bony septa. Although present at birth, the air cells are not fully pneumatized until 2 to 3 years of age. The mastoid air cells are adjacent to the middle ear, and the two are connected via a narrow opening called the aditus ad antrum. The middle ear and the mastoid share a continuous mucoperiosteum, so the mastoid air cells often become inflamed with middle ear infection.¹ In cases of acute mastoiditis, the aditus ad antrum becomes obstructed and the inflammation within the mastoid air cells progresses to suppuration and necrosis.^1,6

Clinical Presentation

The age-related incidence of mastoiditis mirrors that of otitis media.⁷ Some controversy exists regarding whether infants, whose mastoids are not fully formed, can truly have mastoiditis. However, inflammation and suppuration of the mastoid or antrum, or both, have been observed in this age group.⁸

Children with mastoiditis may present with postauricular erythema, edema, and tenderness in association with fever and ear pain. Symptoms typically develop several days to weeks after an episode of treated or untreated AOM.⁷ The tympanic membrane appears abnormal in approximately 90% of cases. The examiner should look for the presence of a cholesteatoma, because it is frequently associated with subperiosteal abscesses in older children.⁹ If a subperiosteal abscess is present, the area posterior to the ear may be fluctuant and tender. In children younger than 1 year, the fluctuance is typically superior and posterior to the ear with the pinna displaced downward and outward. In children older than 1 year, the fluctuance is most commonly posterior and inferior to the ear with the pinna displaced upward and outward.¹⁰

Differential Diagnosis

The differential diagnosis of mastoiditis includes lymphadenopathy, parotitis, lateral sinus thrombosis, mastoid tumors, and branchial cleft cysts.

Evaluation and Diagnosis

While the diagnosis can be made clinically, computed tomography (CT) of the mastoid/temporal bone with contrast enhancement should be obtained to evaluate for intratemporal or intracranial complications.¹¹ On CT, children with early mastoiditis will demonstrate clouding or opacification of the mastoid air cells. Destruction of the bony septa and empyema formation indicate mastoiditis with osteitis.^1,9,7 Subperiosteal abscess is also readily visualized by CT (Figure 99-1A).

An elevated C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and white blood cell count, with a predominance of neutrophils or band forms, may be observed with mastoiditis; however, these tests are neither sensitive nor specific. A blood culture should be obtained.⁷ Middle ear fluid samples collected after tympanocentesis or placement of a myringotomy tube should be sent for aerobic and anaerobic culture. Culture of fluid in the canal is less reliable than culture of the middle ear or the mastoid because of possible contamination with ear canal flora. Additionally, a lumbar puncture should be considered for patients with findings concerning for meningitis.

Course of Illness

Acute mastoiditis is defined as the presence of symptoms for less than a month. Although most cases of mastoiditis are isolated, a small percentage may be complicated by extension of the infection. The possibility of extension of the mastoiditis necessitates frequent assessment of the patient’s neurologic status and neck examination.

A subperiosteal abscess may occur if the infection extends to and penetrates the external cortex of the mastoid.^12,13 A Bezold abscess occurs if the infection progresses inferiorly and extends into the deep tissues of the neck. It results in a collection beneath the sternocleidomastoid with swelling and tenderness.¹ The facial nerve courses through the middle ear, thus making it susceptible to both direct infectious injury and mechanical compression from surrounding structures.¹⁴ Facial nerve palsy is usually unilateral, and paresis of the lower part of the face, as well as the forehead, would be seen, as expected with this peripheral neuritis. CT can identify the bony erosions and is important to assess for the possibility of cholesteatoma or other middle ear tumor.¹⁵ The facial nerve palsy generally improves as the infection is treated, usually with intravenous antibiotics and surgical drainage with placement of myringotomy tubes.⁵ If the infection extends into the petrous portion of the temporal bone (petrositis), Gradenigo syndrome, a triad of pain behind the eye, ear discharge, and abducens nerve palsy, may develop.¹

Intracranial complications occur either by hematogenous spread or by bony erosion leading to direct extension. Children with these complications frequently present with headache, fevers, and vomiting and may or may not demonstrate neurologic impairment. If intracranial complications are suspected, CT with contrast or magnetic resonance imaging (MRI) of the brain should be performed immediately, and neurosurgical consultation should be sought.¹

Lateral sinus thrombosis is a rare but well-described intracranial complication of AOM. While more often described in areas of the world with limited healthcare access, cases still occur in developed countries despite effective antibiotic therapy for AOM. Sinus wall inflammation resulting from middle ear infection can result in thrombosis, most typically in the sigmoid sinus given its position within the mastoid bone (Figure 99-1B).^16,17 Children with lateral sinus thrombosis may present with spiking fevers (often called “picket fence” fevers), neck pain, headache, emesis, neurologic signs and symptoms, or any combination of these findings.^1,18 They may also demonstrate evidence of distant septic thromboemboli. A recent case series described signs and symptoms of elevated intracranial pressure (ICP) and cranial neuropathies (specifically 6th and 7th nerve palsies) as being more often reported than symptoms of otalgia and fevers, despite most patients having recent AOM. Thrombosis may also occur in the mastoid emissary vein as a complication of AOM or mastoiditis. This results in edema or bogginess over the posterior mastoid, known as Griesinger sign.¹⁴

Treatment

Medical Management

Antibiotic coverage should target the most common pathogens with cognizance of local resistance patterns. The microbiology of mastoiditis and AOM differs to some degree. As in AOM, S. pneumoniae is the most common pathogen. However, whereas Moraxella catarrhalis and nontypeable Haemophilus influenzae are the second and third most common organisms responsible for AOM, Staphylococcus aureus and group A β-hemolytic Streptococcus (GABHS; Streptococcus pyogenes) are the next most common bacteria found in mastoiditis.¹ Anaerobes are isolated in up to 10% of cases. Pseudomonas aeruginosa (usually with chronic mastoiditis), and Proteus species, in addition to M. catarrhalis and nontypeable H. influenzae, also have been implicated.

Empirical antibiotic regimens typically include a third-generation cephalosporin with clindamycin. Ampicillin-sulbactam provides similar coverage except that it is not effective against methicillin-resistant S. aureus (MRSA). Patients should receive vancomycin in lieu of clindamycin if they are seriously ill or are known to be colonized with clindamycin-resistant MRSA. Patients with intracranial involvement should receive a third-generation cephalosporin (e.g. ceftriaxone, cefotaxime) in combination with vancomycin and metronidazole. Antibiotic therapy can be modified based on intraoperative culture results. Most children require 4 weeks of antibiotics, though children with severe illness or intracranial complications may require 6 or more weeks of antibiotic therapy. Patients with mastoiditis with or without mastoidectomy can receive oral antibiotic therapy at discharge; patients with intracranial complications should receive parenteral antibiotics for the entire treatment course.

Surgical Management

Consultation from otolaryngology should be sought in the management of children with mastoiditis. Neurosurgical involvement should be considered if intracranial complications exist.

Tympanocentesis (with middle ear fluid culture) should be performed, preferably with tympanostomy tube placement. Indications for mastoidectomy include (1) osteitis or subperiosteal abscess, (2) poor response to medical therapy within 48 hours, or (3) evidence of intracranial complications.^1,18 Treatment of petrositis involves intravenous antibiotics, placement of myringotomy tubes, and surgical drainage of the petrous portion of the temporal bone.⁵ Surgical decompression of the facial nerve is considered in some cases of facial nerve palsy associated with AOM/mastoiditis.^5,7 Surgical drainage may also be indicated for a Bezold abscess that does not respond to antibiotic therapy.

Other Considerations

For lateral sinus thrombosis, diagnosis is made with MRI with angiography/venography. Treatment should involve culture-directed antibiotic therapy and otolaryngology consultation for consideration of myringotomy tube placement and mastoidectomy. Additionally, if deemed safe after head imaging, lumbar puncture with measurement of opening pressure may be both diagnostic and therapeutic for otic hydrocephalus (benign increased ICP secondary to infectious process of the inner ear, not related to brain abscess or meningitis); repeat lumbar puncture may be necessary to manage increased ICP, and acetazolamide may be helpful by reducing production of cerebrospinal fluid.^5,18 Anticoagulation should be considered, especially for patients with high risk for thrombus, clot extending beyond the sigmoid sinus, or neurologic changes.¹⁷ Consultation from hematology and neurosurgery is also warranted.

On completion of therapy, an audiogram should be considered for all children with mastoiditis.¹

Admission and Discharge Criteria

Children with suspected mastoiditis, with or without evidence of further complications, should be hospitalized for intravenous antibiotics, definitive diagnosis, and, if needed, surgical management.

Discharge criteria include:

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  Afebrile for 48 hours with an improving overall clinical picture

  
  
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  No evidence of further complications (normal or improving neurologic findings)

  
  
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  Ability to tolerate oral nutrition

  
  
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  Compliance with oral antibiotic regimen or home parenteral therapy, if necessary

  
  
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  Reliable follow-up with a generalist and otolaryngologist

Prevention

The extent to which antibiotic therapy for AOM prevents complications of AOM, such as mastoiditis, is controversial. Up to 80% of children with untreated AOM will have resolution of symptoms within 7 to 14 days. A Cochrane review concluded that 20 children with AOM would need to receive antibiotic treatment to improve the clinical outcome (pain at 2-7 days) in one of the children.¹⁹ This evidence has led to the wait-and-see approach that asks caregivers to start the antibiotic if the patient is not improved in 48 hours; in these circumstances, the family receives a prescription for the antibiotic but does not obtain the medication unless symptoms have not improved. This approach significantly decreases antibiotic use and is not associated with differences in subsequent fever or ear pain at follow-up.²⁰ Additionally, a systematic review concluded that if 100 children were treated with immediate antibiotic therapy for AOM, 12 more would improve than if none had received antibiotics, but up to 10 would develop a rash and 10 would develop diarrhea.²¹

In their clinical guidelines, the American Academy of Pediatrics concluded that a “watch and see” approach to antibiotic use did not increase the risk for mastoiditis, and concluded that this approach is acceptable for children older than 2 years with a definite diagnosis of AOM but without severe illness (moderate to severe otalgia, otalgia lasting >48 hours, or fever >39 ^OC) or in children between 6 months and 2 years of age without severe illness and without a certain diagnosis of bilateral AOM.²² This age-stratified recommendation was based on evidence indicating higher risk for severe illness and poor outcomes in children younger than 2 years of age.^22,23 Further, a study in the United Kingdom examined records of over 2 million children and found risk of mastoiditis was halved by use of antibiotics but that almost 5000 episodes of AOM would need to be treated to prevent one case of mastoiditis, which was felt to preclude the use of antibiotic treatment of AOM as a method of preventing mastoiditis.²⁴

Sinusitis develops in 6% to 8% of episodes of URI, and typical cases can be diagnosed clinically.^2,25 The peak incidence is in children age 2 to 6 years; by 3 years of age, 10% of children will have had sinusitis. Sinusitis can be classified into one of three categories: symptoms persisting beyond 10 days, severe symptoms with purulent rhinorrhea, and fever >38.5°C for at least 3 to 4 days or worsening after initial improvement.^25,26 URIs facilitate the development of sinusitis by causing mucosal edema with subsequent obstruction of the ostia and by impairing ciliary clearance of bacteria.