Diagnosis of acute otitis media (AOM) requires (1) a history of acute onset of signs/symptoms, (2) presence of middle-ear effusion, and (3) signs/symptoms of middle-ear inflammation. Accurate diagnosis can be challenging yet is essential for proper management. AOM is considered highly likely if distinct bulging of the tympanic membrane (TM) or acute purulent otorrhea (not caused by acute otitis externa) are seen. AOM is considered possible with mild bulging of the TM with recent onset of otalgia plus opacification, distinct erythema, or reduced mobility (on pneumatic otoscopy). AOM is considered unlikely with findings of middle-ear effusion without bulging or distinct erythema of the TM (eg, otitis media with effusion). Otalgia or other nonspecific symptoms (eg, fever, irritability) without middle-ear effusion or a bulging TM are not consistent with the diagnosis of AOM.
It can be difficult to fully visualize the TM to make the diagnosis; obstructing cerumen can be gently removed with suction or curettage, and AOM should not be diagnosed empirically when the TM is poorly visualized. Instead, refer the patient to otolaryngology for cerumen removal and additional assessment.
Adequate pain relief is an essential part of management, especially in the first 24 hours after diagnosis. Acetaminophen or ibuprofen is recommended; narcotics are rarely necessary and should be avoided. Antibiotics do not reduce pain associated with AOM in the first 24 to 48 hours and should not be used for this purpose. Topical analgesic drops typically containing benzocaine provide mild pain relief for 20 to 60 minutes after administration and may be useful between administration of oral analgesics and onset of pain relief. Topical analgesic drops should not be used if the TM is perforated or a tympanostomy tube is in place.
Choose the antibiotic based on likely pathogens and resistance patterns in the community. Most AOM is caused by Streptococcus pneumoniae (20%–40% penicillin resistant), Haemophilus influenzae (30% β-lactamase producing), or Moraxella catarrhalis (100% β-lactamase producing). Recommended antibiotics include amoxicillin (with or without clavulanate), cefuroxime, cefdinir, and cefpodoxime. Children who are allergic to penicillin or unable to tolerate cephalosporins can receive clarithromycin or azithromycin. Duration of therapy is generally 7 to 10 days, though children aged >2 years may respond to short-course therapy of 5 days. Intramuscular ceftriaxone is appropriate as single-dose treatment for children who cannot tolerate oral antibiotic (eg, severe vomiting) or as a series of 3 consecutive daily injections for children with refractory AOM unresponsive to oral antibiotics.
Initiate antibiotic therapy immediately in infants <6 months of age, in patients with AOM accompanied by otorrhea or bilateral AOM in children <2 years of age. If the above criteria are not met, there is a role for delayed antibiotic therapy in which a safety-net antibiotic prescription (SNAP) is given with an advice to fill the prescription (and begin therapy) only if the child does not improve within 72 hours of diagnosis or begins to worsen at any time. For many children managed with this strategy, the “delay” becomes indefinite so that the antibiotics are never required.
Drainage of pus from the middle ear by aspiration (tympanocentesis) or incision (myringotomy) is not effective for pain relief and should be reserved for (1) complicated infections (mastoiditis, meningitis); (2) severe, refractory AOM that persists despite adequate antibiotic therapy; or (3) when resistant pathogens are suspected and culture is necessary.
Figure 9.4 ▪ Acute Otitis Media Presenting with Otorrhea.
Purulent drainage from the external auditory canal (EAC). Various etiologies of otorrhea include AOM with perforation, otitis externa, drainage through tympanostomy tube, foreign body in EAC, cholesteatoma, chronic suppurative otitis media, or basilar skull fracture (bloody otorrhea). (Photo contributor: Binita R. Shah, MD.)
Consider tympanostomy (ventilating) tubes, which are effective for recurrent or refractory AOM because (1) they ventilate the middle ear, eliminating the pressure gradients that aspirate nasopharyngeal secretions to the middle ear; (2) allow controlled drainage of AOM through the tube, should it recur; and (3) serve as a drug-delivery vehicle (eg, quinolone drops) to the middle-ear, eliminating the adverse effects of systemic antibiotics.
If suppurative complications of AOM are present or suspected, obtain diagnostic imaging, and consult otolaryngology for drainage of the middle ear by myringotomy, tympanocentesis, or placement of a tympanostomy tube.
Counsel caregivers about the importance of prompt and regular pain control in the first 24 to 48 hours; a dose of ibuprofen at bedtime will improve sleep.
Topical antibiotic drops are ineffective for AOM and should not be routinely prescribed unless there is a perforated TM or the child has a tympanostomy tube.
Children most likely to benefit from immediate antibiotic therapy for AOM are those younger than age 6 months, younger than age 2 years with bilateral AOM, or of any age with AOM accompanied by otorrhea.
Delayed antibiotic prescribing (observation option) is best for children aged 6 months or older with unilateral AOM or aged 2 years or older with bilateral AOM; there is a substantial role for shared decision making with parents when considering this option.
Do not use delayed antibiotic prescribing for children who appear toxic, are severely ill, or if it cannot be ensured that antibiotic will be begun if the child worsens or there is no improvement within 3 days.
The authors acknowledge the special contributions of Peter Peacock, MD, Mark Spector, MD and Binita R. Shah, MD to prior edition.
Although the use of antibiotics has reduced complications of acute and chronic otitis media, those that do develop can be severe. Complications are intratemporal or extratemporal/intracranial and can develop immediately following an episode of AOM. Some develop within several weeks of the initial infection either despite treatment or when treatment was delayed. Complications resulting from chronic middle ear infections may develop some time after the initial infection. Signs of complications include persistent otalgia, postauricular edema and/or erythema, otorrhea, cranial nerve palsies, orbital pain, nystagmus, vertigo, and hearing loss. Presence of focal neurologic deficits, lethargy, altered mental status, or seizure activity raises concern that an intracranial complication has developed.
Mastoid air cell inflammation generally accompanies simple middle ear infection. Coalescent mastoiditis is defined as bony necrosis and inflammation of the mastoid. Patients present with fever, pain, and tenderness over the mastoid process and persistent otorrhea on the order of weeks. Additional hallmarks include postauricular erythema and edema, and tenderness and edema of the posterior wall of the external auditory canal (EAC). Progression of the infection can lead to abscess formation, with a purulent collection under the periosteum of the mastoid displacing the auricle anteriorly. Extension of an abscess from the mastoid tip and under the sternocleidomastoid muscle into the neck is termed a Bezold abscess. Abscess collection in the zygomatic process of the temporal bone can also develop and presents as a preauricular collection.
Mastoiditis is a clinical diagnosis confirmed by CT imaging, where findings of opacification of mastoid air cells and breakdown of the septations of the mastoid cavity will be seen. Fluid in the mastoid cavity alone is not diagnostic of this complication. Most AOM episodes are associated with fluid in the mastoid but patients usually have a brief duration of symptoms. Petrositis occurs acutely as an extension of mastoiditis into the petrous apex or from spread of OM to the petrous bone via bony erosion, hematogenous spread, or thrombophlebitis. Gradenigo triad (abducens nerve palsy, otorrhea, and retroorbital pain) indicates infection involving petrous portion of the temporal bone. Suppurative labyrinthitis occurs when bacterial infection spreads from the middle ear to the inner ear and presents with sudden sensorineural hearing loss, nystagmus, peripheral vertigo, nausea, and vomiting.
Figure 9.7 ▪ Acute Mastoiditis.
A downward and outward displacement of the auricle associated with erythema and swelling over the mastoid bone in a toddler with purulent otorrhea and tenderness to palpation over the mastoid air cells (postauricular area). (Reproduced with permission from Shah Brand Laude TA: Atlas of Pediatric Clinical Diagnosis. WB Saunders, Philadelphia, 2000, p. 158.)
Figure 9.8 ▪ Chronic Otitis Media with Cholesteatoma and Mastoiditis.
(A) Axial noncontrast CT of temporal bones shows complete opacification of the right EAC and tympanic cavity with nonvisualization of the tympanic membrane and ossicles. This represents a soft tissue mass in the EAC, middle ear, and mastoid with chronic OM with cholesteatoma. Opacification and sclerosis of the right mastoid air cells (compared to left) and bony erosion of the tympanic segment seventh nerve canal is also seen. (B) Axial CT at more superior level demonstrates hypoplastic and sclerotic right mastoid air cells, complete opacification of the right tympanic cavity with nonvisualization of the superior semicircular canal (representing cholesteatoma involving and partially eroding the bone of semicircular canal). (Photo/legend contributors: Sydney C. Butts, MD/Steven Pulitzer, MD.)
| Intratemporal | Extratemporal/Intracranial |
|---|---|
| Coalescent mastoiditis | Meningitis (most common complication) |
| Subperiosteal abscess (postauricular) | Otitic hydrocephalus (elevated intracranial pressure in presence of otitis media and absence of bacterial meningitis) |
| Bezold abscess | Lateral sinus thrombosis |
| Zygomatic abscess | Epidural abscess |
| Petrous apicitis | Subdural abscess |
| Suppurative labyrinthitis | Intraparenchymal abscess |
| Facial nerve paralysis | Temporal lobe, cerebellum |
Acute and chronic OM may also lead to facial nerve paralysis as a result of intratemporal complications. Intracranial infection may also be present or may develop when an intratemporal complication is present. Thrombosis of the lateral sinus (dural sinus that leaves the skull base via jugular foramen and continues as internal jugular vein) can develop and presents with spiking fevers, neck tenderness, papilledema, and paralysis of the lower cranial nerves.
Consult otolaryngology for all cases of suspected OM complications and neurosurgery for intracranial complications. Order a CT scan with contrast of the temporal bones and brain. Obtain a complete blood count (CBC) and blood cultures. Hospitalize such patients for intravenous (IV) antibiotics, and many patients may require operative management.
Include complications of OM in the differential for any patient presenting with facial nerve paralysis. Failing to detect OM as the cause of facial paralysis could result in the patient receiving incorrect treatment.
Maintain a low threshold for brain imaging in patients who have been on antibiotic therapy that can mask more obvious manifestations of spread of the infection from OM.
Figure 9.9 ▪ Facial Palsy; Complication of Acute Otitis Media.
Right-sided peripheral facial palsy associated with right AOM requiring IV antibiotics and myringotomy. Facial palsy results from inflammation directly affecting exposed portions of the facial nerve, which runs through the temporal bone. The facial nerve is usually protected in a bony canal that can either be congenitally absent in portions or eroded by chronic, long-standing OM. (Photo contributor: Binita R. Shah, MD.)
Acute otitis externa (AOE), commonly referred to as “swimmer’s ear,” is an infection of the EAC. Patients typically present with complaints of otalgia, otorrhea (often foul smelling), and pruritus and physical examination often reveals swollen, tender, and erythematous skin in the EAC. Purulent discharge can be thick to watery. Bacterial infections are most common, though fungal infections also occur. The most common etiologic organisms are bacteria including Pseudomonas and Staphylococcus species. However, otomycosis can result from fungal otitis externa. Susceptibility is related to local factors such as swimming or minor trauma of the ear (including use of cotton swabs). Immunocompromised patients, including those with diabetes, are more vulnerable to OE.
Figure 9.10 ▪ Acute Otitis Externa (Swimmer’s Ear).
White-yellow discharge from the external auditory canal (EAC) associated with excoriation of the surrounding skin were seen in this child who was swimming daily during summer camp. His EAC was very edematous and filled with dried debris. Other etiologies of otorrhea from otitis externa (OE) include fungal OE, eczematous OE, and furunculosis (hair follicle infection usually due to S aureus). (Photo contributor: Binita R. Shah, MD.)
The differential includes otitis media with a perforated TM (as purulent discharge from the middle ear fills the EAC), foreign body with secondary infection, and, rarely, EAC malignancy in patients who complain of longstanding infection. A careful history and physical examination will provide indications, such as unsuccessful prior treatments, of disease beyond routine AOE.
AOE is a clinical diagnosis. Appropriate therapy and counseling will alleviate symptoms and lead to resolution of OE in the overwhelming majority of patients. Treat with antibiotics or antifungals as well as topical agents that both dry the EAC and restore the normal pH. Monotherapy with topical otic drops is the recommended, first-line treatment for uncomplicated AOE. Systemic antibiotics are not indicated in most cases and should be utilized only in the immunocompromised or if cellulitis has extended to the outer ear. If edema or debris prevents adequate delivery of topical drops, use an ear wick in the EAC. Otic drops are selected empirically based on coverage of suspected organisms and include neomycin/polymixin B/hydrocortisone suspension or one of the quinolone preparations. Combined antibiotic/steroid drops are chosen based on the degree of edema present. In mild cases, acidifying drops that restore the normal pH of the ear canal may be used alone. Acetic acid drops are prescribed and preparations containing hydrocortisone are also available.
If the TM is perforated or tympanostomy tubes are present, use fluoroquinolone drops (avoid potentially ototoxic drops) and provide appropriate pain control as associated otalgia can be debilitating.
Maintain a high index of suspicion for temporal bone osteomyelitis in patients who are diabetic or immunocompromised. This typically causes development of granulation tissue in the EAC and can present with several lower cranial neuropathies. Evaluate patients with temporal bone imaging and consult otolaryngology.
In uncomplicated cases of otitis externa, instruct patients to maintain dry ear precautions until infection resolves and not to put anything (including cotton tip swabs) except drops in their ear, symptoms should improve within 72 hours and typically resolve over 10 to 14 days. Any patient with an ear wick placed will need it changed within 24 to 48 hours and should have follow-up with an otolaryngologist at that time.
Perichondritis is inflammation of the perichondrium of the external ear, usually caused by a break in the skin barrier, including auricular trauma (blunt or sharp object), piercing of the cartilaginous portions of the external ear, and postoperative wound infections. Progression to chondritis or abscess may follow and the cartilage may quickly become devitalized and necrotic. Perichondritis is marked by thickening of the perichondrium, making the well-defined shape of the ear less discernible. The skin is often erythematous, and palpation results in marked tenderness. An early auricular abscess may have many of these clinical findings. It is critical to determine if abscess collection has formed so that prompt drainage is done. Edema from a contusion of the ear can usually be distinguished by a history of recent blunt trauma and the appearance of ecchymosis. Other conditions to be excluded include erysipelas, eczema or other dermatitis, otitis externa, and relapsing polychondritis.
Order a CBC in all and blood cultures in those with high spiking fevers. Select empiric antibiotic therapy with a quinolone, extended spectrum penicillin or cephalosporin, which offers both antipseudomonal and gram-positive bacterial coverage. Quinolones are not approved for use in young children because of concerns about cartilage and bone growth. Admit those with severe infections for IV antibiotic therapy to ensure clinical response followed by oral therapy. Patients with obvious cartilage necrosis or abscess collection require operative management for drainage and/or cartilage débridement. Those who are treated as outpatients need close monitoring by an otolaryngology. Consult dermatology in complicated cases where an underlying skin condition may be the contributory cause. Appropriate analgesia is also paramount given the significant pain that can be experienced by patients.
Severity of pain can be a guide to which tissue is involved as perichondritis is often more painful and associated with more tenderness than cellulitis.
Treatment failure has significant consequences (eg, chondritis, cartilage necrosis with permanent auricular deformity); thus obtain an otolaryngology consult in the emergency department (ED).
An assortment of foreign bodies (FBs) may be found in the external auditory canal (EAC), including plastic beads, cotton swabs, food particles, insects, and button batteries. Patients may be asymptomatic, but more likely they will report symptoms including otalgia, itching, aural fullness, tinnitus, hearing loss, otorrhea, and bleeding. Even though many auricular FBs have a straightforward presentation and successful outcome, several serious clinical presentations warrant prompt attention. Foreign bodies in place for days or weeks can be associated with significant edema of the EAC and frank otitis externa. Sharp FBs can result in injury to the TM or other middle ear structures.
Successful removal depends on the type and location of the object, and patient cooperation. Take a careful history focused on the type of FB, when and how it entered the ear, and if and how removal was attempted. Carefully inspect the auricle, EAC, and TM, and also look for potential FBs in other orifices. If it appears that the TM has been damaged or if the patient complains of hearing loss, consult otolaryngology before attempting removal.
It is best to use an otoscope with an operating head that will allow adequate visualization. If the FB can be visualized well and is in the proximal EAC, attempt removal with wax curettes, right-angled hooks, alligator forceps, or Frazier tip suctions (nos. 5 or 7). It is important to avoid iatrogenic trauma, which may cause edema of the EAC, bleeding, distal displacement of the object, or TM perforation; consult otolaryngology if the FB is difficult to remove. Worsening anxiety of the child and parents results from multiple unsuccessful attempts at removal. When possible, use a microscope that allows adequate lighting and magnification with the patient awake. However, some patients will need to be taken to the operating room for removal.
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