Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 95. Ear and Nose Emergencies

Hannah Smitherman

Evan J. Weiner


• The diagnosis of otitis media is based on the rapid onset of signs and symptoms of middle ear inflammation in the presence of middle ear effusion. Pneumatic otoscopy is an essential component of the ear examination.

• Worsening otitis media, while on antibiotics, may be a sign of a suppurative complication.

• Sinusitis should be considered in patients with severe rhinitis and in patients with persistent or worsening URI symptoms after 10 days.

• Hospitalization for intravenous antibiotics, sinus imaging, and subspecialty consultation are indicated in patients with sinusitis with orbital or intracranial extension.



The fragile skin of the external auditory canal is easily infected when disrupted by trauma or inflammation, permitting the normal ear flora (Staphylococcus spp., Streptococcus spp., diptheroids, and Pseudomonas aeruginosa) to invade the tissue. Acute uncomplicated otitis externa is diagnosed clinically. A history of local trauma, water exposure (“swimmer’s ear”), and travel to a warm humid climate may be present.1,2 Most patients will present with localized ear pain and itching. The pinna appears normal, the ear canal red and edematous with an exudate, and manipulation of the pinna or tragus usually elicits pain (a hallmark of this condition) (Fig. 95-1). If the infection is due to a fungus (predominantly Aspergillus spp.), white or gray masses composed of hyphae may be seen in the canal. Local lymphadenopathy may be present.


FIGURE 95-1. Picture showing otitis externa.

Malignant or necrotizing otitis externa is most commonly caused by P. aeruginosa and is characterized by a severe cellulitis of the external canal with osteomyelitis of the underlying bone. Hospitalization for intravenous (IV) antipseudomonal antibiotics and otolaryngology consultation are indicated. Imaging with MRI or CT is often necessary to define the extent of any bony and soft-tissue involvement.3Otomycosis and necrotizing otitis externa are predominantly seen among diabetic or immunocompromised patients.1


A furuncle (abscess) may develop at a hair follicle in the lateral canal. Depending on the degree of fluctuance, a combination of antistaphylococcal topical or oral antibiotics and incision and drainage should be employed. Conditions affecting the skin of the ear, such as atopic dermatitis, seborrheic dermatitis, and contact dermatitis, may also lead to itching and inflammation of the external canal. Retained otic foreign body or an acute otitis media with perforation and resultant debris and exudates may be mistaken for an external ear infection.


Treatment of uncomplicated acute otitis externa consists of a combination of topical antimicrobial preparations (targeting P. aeruginosa) and external ear cleaning.4 Options include acetic acid, a combination of polymyxin B and neomycin, quinolones, and aminoglycosides. Antibiotic–steroid preparations may lead to faster and better cure rates (e.g., ciprofloxacin/dexamethasone drops).5,6 Cleaning of the ear canal (with suctioning, irrigation, and dry swabbing) or application of an ear wick left in place for 2 days can help deliver the topical medications if significant edema exists. If one suspects a perforated eardrum, a topical antimicrobial suspension is preferable to a solution that may damage the middle ear. Systemic antibiotics are not routinely recommended. Prevention strategies include reducing water exposure to the ear, using ear plugs, and vinegar/alcohol ear-drying solutions.2


The middle ear is part of a continuous space behind the tympanic membrane that facilitates sound transfer to the inner ear structure and extends from the eustachian tube to the mastoid air cells. The eustachian tube functions to equilibrate middle ear pressure, clear the middle ear of secretions (via the action of ciliated epithelium), and protect the middle ear from the nasopharynx. Eustachian tubes in children are more horizontal in orientation than those of adults, possibly impeding drainage. Any alteration of function from obstruction, inflammation, or excessive compliance can lead to effusion and subsequent infection in the middle ear. Upper respiratory infections (URI), allergic rhinitis, supine bottle-feeding, exposure to tobacco smoke, age younger than 2 years, and attendance at day care increase the risk of otitis media whereas breast-feeding decreases its occurrence.7 Otitis media with effusion refers to a collection of serous fluid in the middle ear, which may commonly occur in a viral URI; acute otitis media indicates superinfection with bacteria. Streptococcus pneumoniae (25%–50%), Haemophilus influenzae (15%–30%), and Moraxella catarrhalis (3%–20%) represent the major bacterial pathogens. The routine use of the heptavalent pneumococcal vaccine is changing the epidemiology of otitis media.7 A large number of H. influenzae and M. catarrhalisisolates produce β-lactamases, which affect therapeutic options; S. pneumoniae resistance is increasingly common (particularly penicillin resistance).


Acute otitis media is diagnosed clinically based on the rapid onset of signs and symptoms of middle ear inflammation and middle ear effusion. Symptoms include ear pain or fullness, fever, rhinorrhea, nasal congestion, and fussiness. Otorrhea may be present if the tympanic membrane has perforated. Middle ear effusion is highly suggested by a bulging tympanic membrane with decreased mobility confirmed by pneumatic otoscopy (Fig. 95-2). Redness and dullness of the eardrum can indicate infection but are less predictive,7 especially in a crying or febrile child whose tympanic membrane has normal mobility on pneumatic otoscopy. Routine tympanocentesis or cultures are not necessary for diagnosis.


FIGURE 95-2. Bulging tympanic membrane in acute otitis media. (Used with permission from Glenn Issacson, MD.)


While bullous myringitis is an infection of the tympanic membrane traditionally associated with Mycoplasma pneumoniae, evidence suggests that it is mainly caused by the pathogens causing otitis media, particularly S. pneumoniae.8 It can occur alone or in combination with a middle ear infection and presents with bullae on the tympanic membrane. Effective visualization after suctioning can help distinguish otitis media with perforation from otitis externa. Instillation of anesthetic eardrops may help distinguish between crying due to otalgia from more serious conditions like meningitis.


Complications of acute otitis media include tympanic perforation, cholesteatoma, facial paralysis, and labyrinthitis. Intracranial suppurative complications such as meningitis, brain abscess, encephalitis, and lateral sinus thrombosis, although rare, should be suspected in patients with worsening ear pain while taking antibiotics, persistent headache, intractable emesis, or behavioral changes. Children with acute mastoiditis (an infection of the mastoid bone) usually present with posterior auricular erythema, tenderness, and lateral displacement of the pinna. Computerized tomography (CT) of the temporal bones is crucial to determine the extent of infection and to detect sinus thrombosis or brain abscess (Fig. 95-3).9


FIGURE 95-3. CT scan showing mastoiditis and cholesteatoma.


Most cases of acute otitis media resolve without antibiotics.7 The overuse of antibiotic contributes to increasing bacterial resistance. The American Academy of Pediatrics (AAP) recommends a period of observation for 48 to 72 hours without antibiotics in select patients such as patients older than 6 months with an uncertain diagnosis of otitis media and without severe symptoms; and those older than 2 years with otitis media but without severe symptoms (fever less than 40°C and mild otalgia).7 Delayed initiation of antibiotic therapy after an observation period does not lead to worse outcomes.10

In cases where antibiotics are indicated, high-dose amoxicillin (80–90 mg/kg/d) remains the initial first-line medication.7 For patients with non–type-1 penicillin allergy, cefdinir (14 mg/kg/d in one or two divided doses), cefuroxime (30 mg/kg/d in two divided doses), or cefpodoxime (10 mg/kg/d) may be used. For patients with type 1 allergic reaction to penicillin (urticaria or anaphylaxis), azithromycin (10 mg/kg on day 1 then 5 mg/kg on days 2 to 5 as a single dose), or clarithromycin (15 mg/kg in two divided doses) may be used. For treatment failure after 48 to 72 hours of amoxicillin or for severe otitis media as initial treatment, high-dose amoxicillin-clavulanate (90 mg/kg/d in two divided doses) or a second-or third-generation cephalosporin as outlined above is appropriate (see Chapter 99 for conjunctivitis otitis syndrome). A single dose of ceftriaxone (50 mg/kg) is equal in efficacy to 10 days of oral amoxicillin. Alternatively, patients who fail to improve after 48 to 72 hours can also receive a series of three daily intramuscular doses of ceftriaxone. Patients with persistent treatment failures as well as those with recurrent middle ear infections should be referred to an otolaryngologist due to the potential chronic effects on hearing and development.

Mastoiditis is a serious complication of otitis media and should be treated aggressively. The most common causative agent is S. pneumoniae with an increasing proportion of isolates showing resistance to penicillin.11 Management strategies consist of IV antibiotics, with or without myringotomy and, in select cases, mastoidectomy to remove necrotic bone.12


Although a wide variety of foreign bodies lodged in the ear or nose have been described in the literature, hair beads, toy parts, eraser tips, food, and insects are commonly encountered. Small disk button batteries have also become more common.13 Most objects are self-inserted in play or as a response to an itch or irritation. Children may report insertion of a foreign body, but many are accidentally discovered by parents and occasionally by physicians during examination.


Foreign bodies are usually apparent on direct visualization. In the absence of a history, helpful clues include epistaxis, pain, discharge, and alteration of sense of smell or hearing. Bleeding and purulent discharge can impede the physical examination. Foreign bodies can masquerade as chronic infections, tumors, recurrent epistaxis, and generalized body odor (bromidrosis).


Blockage of the external auditory canal or nares can interfere with normal function. Aural foreign bodies can predispose to otitis externa, cellulitis, tympanic membrane perforation, or vertigo. Undiscovered nasal foreign bodies may present with recurrent epistaxis, a unilateral foul-smelling discharge, sinusitis, or periorbital cellulitis. During removal, these foreign bodies may be lodged further where it is harder to retrieve and may cause bleeding, laceration, perforation, or aspiration. Button batteries, in particular, can cause tissue necrosis, ossicular disruption, perforation, and facial nerve paralysis.


Refer the patient to an otolaryngologist if there is a low probability of successful removal in the ED (dependent on the material, length of time lodged, and location). To ensure success in the first attempt, appropriate equipment and supplies (Table 95-1) and lighting must be present and the child adequately immobilized. Multiple attempts may cause bleeding, mucosal edema, and movement of the object to a less accessible area. Application of a topical vasoconstrictor on the nasal mucosa may reduce intranasal tissue edema and aid foreign body removal.

TABLE 95-1

Equipment for Examination and Removal of a Nasal or Aural


Forceps removal, irrigation, and suctioning are the three most common techniques used. Insects should be killed with lidocaine, mineral oil, antipyrine/benzocaine drops, or alcohol before removal is attempted. Wood and other vegetable matter tend to swell when wet and are best removed before irrigating the ear canal. When possible, forceps are used to grasp the foreign body. Round, fragile objects may be successfully removed by placing a wire loop curette or a right-angle hook behind the foreign body, or by using superglue-type adhesive on a cotton-tipped applicator. If the canal is traumatized, prophylactic topical antibiotics for acute otitis externa should be considered. Small aural foreign bodies close to the tympanic membrane may be removed with body temperature tap water or saline irrigation using a 60-mL syringe attached to a plastic infusion catheter. A foreign body that completely occludes the nares can be removed by using gentle positive pressure ventilation through a bag valve mask applied to the mouth or by the parent caregiver’s mouth-to-mouth pressure while occluding the noninvolved nare with care given not to induce barotrauma (e.g., ruptured tympanic membrane, pneumothorax). Also, a small balloon-tipped catheter can be passed beyond the foreign body, and the object withdrawn after inflating the balloon. A search for additional objects is advisable after a foreign body is removed.


The majority of nosebleeds in children and adolescents are anterior in location.14 These occur at the nasal vestibule or the plexus of vessels on the anteroinferior portion of the nasal septum (Little area, Kiesselbach plexus). In children, epistaxis digitorum, or “nose picking,” is the most frequent cause followed by mucosal irritation due to decreased humidity, especially during the winter.14 Recurrent URI and allergic rhinitis increase the vascularity of the nasal mucosa and coupled with frequent nose blowing predispose to nosebleeds. Traumatic causes include nasal foreign bodies, chronic inhaled steroid use, cocaine or heroin sniffing, and nasal fractures. Tumors such as pyogenic granuloma or hemangiomas are rare causes. Bleeding disorders from acquired or congenital coagulopathy and platelet or blood vessel abnormalities should be suspected in patients with prolonged nosebleeds with minor trauma, spontaneous and frequent nosebleeds, or a family history of bleeding disorders. The most common bleeding disorder associated with recurrent epistaxis is von Willebrand disease.15


The severity of the epistaxis is determined by its frequency, duration, estimated amount, and whether the bleeding involves one or both nares. Obtain any history of recent trauma to the face, upper respiratory illness, or exposure to dry air. Ascertain use of any medication such as aspirin, nonsteroidal anti-inflammatory agents (NSAIDs), nasal steroids, recreational drugs, or use of complementary therapies. Inquire about gum bleeding, easy bruising, or other historical factors associated with bleeding diatheses. On physical exam, a foul-smelling odor emanating from the patient’s face may suggest a retained foreign body in the nose. Allergic shiners, allergic salute, and a cobblestoned pharynx suggest allergic rhinitis as the cause of recurrent epistaxis. Pallor, weakness, resting tachycardia, or orthostatic dizziness is indicative of significant blood loss.


Assess the patient for respiratory compromise, hemodynamic instability, or change in mental status that requires airway intervention or fluid resuscitation. In a stable patient, identify the source of nosebleed and apply direct pressure while initiating definitive interventions. Equipment and supplies, including a suction apparatus and suction tips, gauzes, and topical medications, should be ready before attempting evaluation or immobilization of the child (Table 95-1). Positioning small children in their parent’s lap with manual restraint is often helpful. Optimal examination is facilitated by the use of a headlamp and a nasal speculum. Removal of blood with a Frazier suction tip can aid in localizing the bleeding point.

For active anterior nosebleeds, continuous firm compression of the nasal alae for 5 to 10 minutes will usually stop the bleeding. Intermittent compression will not allow sufficient blood clot to form on the Kiesselbach plexus. The child should be sitting up, breathing through his mouth, and leaning forward with his face down to prevent blood from dripping into the hypopharynx or oral cavity. Application of a topical nasal decongestant such as oxymetazoline or phenylephrine prior to compression causes local vasoconstriction and helps stop the bleeding.14

If compression does not control the bleeding, chemical cautery with silver nitrate sticks may be attempted, especially in the cooperative patient. A cotton pledget soaked in phenylephrine (0.125%–0.5%), 1% lidocaine, or cocaine (4%) can be applied to the bleeding area prior to the application of silver nitrate. The tip of the stick should be in contact with the site for a few seconds and repeated as necessary until a grayish-white coloration is noted. Continued bleeding may necessitate the use of an electrocautery device (with caution for nasal ulceration or perforation)14,15 after local anesthesia. The use of topical thrombin, fibrin, or hemostatic sealants was reported to be more effective in controlling bleeding, easier to use, and better tolerated by patients with anterior epistaxis compared to cautery or packing.16,17

If bleeding persists, consider anterior nasal packing in consultation with an otolaryngologist. However, this technique is poorly tolerated by children in the ED. Packing materials include nonresorbable (VaselineTM or XeroformTMgauze, MerocelTM sponge) and resorbable (Gelfoam®, Surgicel) agents. Packing should be removed within 1 to 2 days. A course of antibiotics effective against Staphylococcus and Streptococcus is usually prescribed.14 Posterior nasal packing, balloon catheter insertion, arterial ligation, pterygopalatine fossa block, and embolization are rarely needed in a child. Refractory bleeding necessitates reevaluation of the etiology, otolaryngology consultation, and hospital admission for further workup and management, and consideration for correction of any underlying coagulopathy. In addition, the physician also should provide advice to prevent recurrences: keeping fingernails cut short or keeping the nasal mucosa moist (running a cool mist humidifier at night and application of saline drops, petroleum jelly, or antibiotic cream into the nasal septum and orifice).


Sinusitis refers to inflammation of the paranasal sinuses. Allergic versus bacterial etiologies may be difficult to distinguish.18 Persistent URI symptoms suggest sinusitis.19 Children average two to seven viral URIs per year, of which approximately 13% are complicated by bacterial sinusitis.20 In addition to viral infection of the nasal passages and sinuses (viral rhinosinusitis), allergic rhinitis and atopy are the two most common predisposing factors for bacterial sinusitis.21 Other risk factors include day-care attendance, mucosal irritants such as tobacco smoke, foreign bodies, craniofacial abnormalities, septal deviation, adenoidal hypertrophy, and polyps secondary to allergies or cystic fibrosis (Fig. 95-4). Conditions that cause ciliary dysfunction and atmospheric pressure changes can also cause sinusitis.


FIGURE 95-4. Nasal polyp.


While maxillary and ethmoid sinuses are present at birth, sphenoid sinuses become pneumatized after 5 years of age. Frontal sinuses appear by 6 to 8 years and complete development at adolescence. Sphenoidal and posterior ethmoidals drain into the ostium of the superior meatus on the lateral wall while the maxillary, frontal, and anterior ethmoidals drain into the middle meatus. Normal function of the paranasal sinuses depends on patency of the sinus ostia, the nature of sinus secretions, and function of the ciliary apparatus; abnormalities promote conditions for bacterial growth.22


Acute bacterial sinusitis presents in one of three manners22: (1) rhinorrhea (any quality) and cough (any quality, but usually more at night) >10 days and <30 days; (2) severe symptoms at onset marked by high fever lasting 3 to 4 days (longer than a typical viral infection) and mucopurulent rhinorrhea; (3) a biphasic pattern whereby symptoms worsen after a period of improvement. Headache, facial pain, and halitosis is variable and less common in children while fatigue, malaise, chronic cough, and decreased appetite are sometimes noted by parents.

On physical examination, there is anterior or postnasal drainage and swelling of the nasal mucosa. Signs of allergic rhinitis (e.g., allergic shiners, allergic salute, and cobblestoning of the posterior pharynx) may be present. Periorbital swelling suggests ethmoidal sinusitis. There may be frontal or facial tenderness to palpation, but transillumination is of limited value in children.


Acute uncomplicated bacterial sinusitis in children younger than 6 years can be diagnosed clinically.18,19,21 Although controversial, plain radiographs of the sinuses (anteroposterior, lateral, and occipitomental views) may be obtained in children older than 6 years to confirm the diagnosis or in those who do not improve after a course of antibiotics. Contrast enhanced CT may be indicated in the setting of treatment failures and complications (orbital or intracranial).23 Radiographic findings are often found even in patients with rhinosinusitis alone and cannot distinguish inflammation caused by viruses from that caused by bacteria leading to the variable reliability of radiographic evaluation, especially in the younger age group.22 However, normal studies are helpful in ruling out sinusitis.23 Findings in plain films or CT consistent with sinusitis include complete opacification of the sinus, mucoperiosteal thickening of more than 4 mm, and presence of air–fluid levels (Fig. 95-5).


FIGURE 95-5. CT scan showing pansinusitis.


Recurrent rhinitis, enlarged adenoids, and allergic rhinitis have similar symptoms to bacterial sinusitis. Foreign bodies, neoplasms, or polyps more commonly present with unilateral drainage and obstruction but may predispose to the development of sinusitis. Other causes of persistent cough such as gastroesophageal reflux, pertussis, and reactive airway disease should be considered. Over suctioning or too vigorous of nasal washes and the abuse/overuse of nasal decongestants (rhinitis medicamentosus) are iatrogenic causes of chronic nasal symptoms.


Direct extension from the sinuses can result in facial cellulitis, facial abscess, periorbital and orbital cellulitis, cavernous sinus thrombosis, epidural abscess, subdural empyema, meningitis, and brain abscess.18,22 Potts’ puffy tumor, a subperiosteal abscess or osteomyelitis of the skull, is a rare complication of frontal sinusitis that presents with fever, headache, and forehead tenderness or swelling.24 Rarely, sinusitis may seed the systemic circulation resulting in bacteremia or septicemia.


There is limited and conflicting evidence to determine whether the use of antihistamines, decongestant, or nasal irrigation is efficacious in children with acute sinusitis.25 Nasal irrigation along with adjunct therapy may alleviate some symptoms (but not radiographic findings) in acute sinusitis in atopic children. A suspected viral etiology suggests supportive measures (bulb suctioning, limited use of vasoconstrictors). Saline nose drops may be useful in liquefying nasal secretions. Although some children with sinusitis will improve gradually, antibiotic therapy is indicated to hasten resolution of symptoms and to prevent complications.18,26 The pathogenesis and microbiology of acute bacterial sinusitis are similar to acute otitis media because the middle ear is contiguous with the paranasal sinuses.

Although S. pneumoniae, nontypeable H. influenzae, and M. catarrhalis have been the most common causes, a decrease in the incidence of S. Pneumonia and a corresponding increase in nontypeable H. influenzae, may be attributable to the introduction of the pneumococcal conjugate vaccines.27 Prior to the era of beta-lactamase resistance, amoxicillin was once thought to be the mainstay of treatment. However, the Infectious Diseases Society of America has recently published recommendations for the management of acute bacterial sinusitis which includes the prompt treatment with high-dose amoxicillin-clavulanate (90 mg per kilogram per day, administered in two doses) as first-line therapy for children.26 This is particularly where penicillin resistance S. pneumoniae strains are endemic and resistance is 10% higher, those in day care, those younger than 2 years of age, and those who have been hospitalized or treated with antibiotics in the last 30 days.26 Alternatively, although not FDA approved, Levofloxacin is recommended for children with a history of type 1 hypersensitivity reaction to penicillin.22,26 Cefdinir (14 mg/kg/d in one or two doses), cefuroxime (30 mg/kg/d), or cefpodoxime (10 mg/kg/d) may be used in conjunction with clindamycin (30–40 mg/kg/d in three divided doses).18,19 Macrolides and trimethoprim–sulfamethoxazole are not recommended because of high rates of resistance in the United States.26 For patients who are vomiting, a single dose of ceftriaxone (50 mg/kg/d intramuscularly or intravenously) can be used with initiation of oral antibiotics 24 hours later once vomiting has subsided. Oral antibiotics can be given for a minimum of 10 to 14 days and extended depending on the clinical response. However, most patients will have improvement in their symptoms within 48 to 72 hours. Patients with severe symptoms, clinical deterioration while on oral antibiotics, immunodeficiency, or orbital or intracranial involvement, should be hospitalized for IV antibiotics, sinus imaging studies and consultation with an otolaryngologist. Parenteral antibiotic coverage against resistant pneumococci, H. influenzae, and M. catarrhalis includes cefotaxime (100–200 mg/kg/d divided every 6 hours) or ceftriaxone (100 mg/kg/d divided every 12 hours) with consideration for adding clindamycin.19


1. Hirsch BE. Diseases of the external ear. In: Bluestone CD, Stool SE, Kenna MA, eds. Pediatric Otolaryngology. Philadelphia, PA: W. B. Saunders; 1996:378.

2. Centers for Disease Control. Estimated burden of acute otitis externa—United States, 2003-2007. MMWR Morb Mortal Wkly Rep. 2011;60(19):605–609.

3. Handzel O, Halperin D. Necrotizing (malignant) otitis externa. Am Fam Physician. 2003;68(2):309–312.

4. Kaushik V, Malik T, Saeed SR. Interventions for acute otitis externa. Cochrane Database Syst Rev. 2010;CD004740.

5. Van Balen HAM, Smit WM, Zuithoff NPA, Verheij TJM. Clinical efficacy of three common treatments in acute otitis externa in primary care: randomized control trial. BMJ. 2003;327(7325):1201–1205.

6. Pistorius B, Westberry K, Drehobl M. Prospective, randomized, comparative trial of ciprofloxacin otic drops, with or without hydrocortisone, vs. polymyxinB-neomycin-hydrocortisone otic suspension in the treatment of acute diffuse otitis externa. Infect Dis Clin Pract. 1999;8:387.

7. Subcommittee on Management of Acute Otitis Media. Diagnosis and management of acute otitis media. Pediatrics. 2004;113(5):1351–1365.

8. Palmu AAI, Kotikoski MJ, Kaijalainen TH, Puhakka HJ. Bacterial etiology of acute myringitis in children less than two years of age. Pediatr Infect Dis J. 2001;20(6):607–611.

9. Smith JA, Danner CJ. Complications of chronic otitis media and cholesteatoma. Otolaryngol Clin North Am. 2006;39(6):1237–1255.

10. Tahtinen PA, Laine MK, Ruuskanen O, Ruohola A. Delayed Versus Immediate Antimicrobial Treatment for Acute Otitis Media. Pediatr Infect Dis J. 2012;31(12):1227–1232.

11. Kaplan S, Mason E, Wald ER, et al. Pneumococcal Mastoiditis in children. Pediatrics. 2000;106(4):695–699.

12. Talor MF, Berkowitz RG. Indications for mastoidectomy in acute mastoiditis in children. Ann Otol Rhinol Laryngol. 2004;113(1):69–72.

13. Sharpe SJ, Rochette LM, Smith GA. Pediatric battery-related emergency department visits in the United States, 1990-2009. Pediatrics. 2012;129(6):1111–1117.

14. Massick D, Tobin E. Epistaxis. In: Flint P, Haughey B, Robbins KT, Thomas JR, eds. Cummings Otolaryngology: Head and Neck Surgery. Philadelphia, PA: Mosby Elsevier; 2005

15. Sandoval C, Dong S Visintainer P, Ozkaynak MF, Jayabose S. Clinical and laboratory features of 178 children with recurrent epistaxis. J Pediatr Hematol Oncol. 2002;24(1):47–49.

16. Vaiman M, Segal M, Eviatar E. Fibrin glue treatment for epistaxis. Rhinology. 2002;40(2):88–91.

17. Mathiasen RA, Cruz RM,. Prospective randomized clinical trial of a novel hemostatic sealant in patients with acute anterior epistaxis. Laryngoscope. 2005;115:899–902.

18. American Academy of Pediatrics. Sinusitis. In: Pickering LK, Baker CJ, Kimberlin DW, Long SS, eds. Red Book: 2012 Report of the Committee on Infectious Diseases. Elk Grove Village, IL: American Academy of Pediatrics; 2012.

19. Wald ER, Applegate KE, Bordley C, et al. American Academy of Pediatrics, Subcommittee on Acute Sinusitis. Clinical practice guideline for the diagnosis and management of acute bacterial sinusitis in children aged 1 to 18 years. Pediatrics. 2013;132(1):e262–e280.

20. Revai K, Dobbs LA, Nair S, Patel JA, Grady JJ, Chonmaitree T. Incidence of acute otitis media and sinusitis complicating upper respiratory tract infection: the effect of age. Pediatrics. 2007;119(6);e1408–e1412.

21. Chen CF, Wu KG, Hsu MC, Tank RB. Prevalence and relationship between allergic diseases and infectious diseases. J Microbio Immunol Infect. 2001;34(1):57–62.

22. DeMuri GP, Wald ER. Acute Bacterial Sinisitus in Children [Review]. New Engl J Med. 2012;367(12):1128–1134.

23. Setzen G, Ferguson BJ, Han JK, et al. Clinical consensus statement: appropriate use of computed tomography for paranasal sinus disease. Otolaryngol Head Neck Surg. 2012;147(5):808–816. doi: 10.1177/0194599812463848.

24. Parida PK, Surianarayanan G, Ganeshan S, Sacena SK. Pott’s puffy tumor in pediatric age group: retrospective study. Int J Pediatr Otorhinolayrngol. 2012;76(9):1274(7). doi: 10.1016/j.ijporl.2012.05.018.

25. Shaikh N, Wald ER, Pi M. Decongestants, antihistamines and nasal irrigation for acute sinusitis in children. Cochrane Database Syst Rev. 2012;9:CD007909.

26. Chow AW, Benninger MS, Brook I, et al. IDSA clinical practice e guidelines for acuter bacterial rhinosinusisits in children and adults. Clin Infect Dis. 2012;54(8):e72–e112.

27. Casey JR, Pichichero ME. Changes in frequency and pathogens causing acute otitis media in children. 1995-2003. Pediatr Infect Dis J. 2004;23(9):824–828.