Common Pediatric ENT Infections: Adenitis, Otitis Externa, Peritonsillar Disease, and Parapharyngeal Abscess
Common Pediatric ENT Infections: Adenitis, Otitis Externa, Peritonsillar Disease, and Parapharyngeal Abscess
Authors: Jonathan I. Singer, MD, FAAP, FACEP, Associate Program Director for Emergency Medicine, Professor of Emergency Medicine and Pediatrics, Boonshoft School of Medicine, Wright State University, Dayton, Ohio; Andrew Reidy, DO, Resident Physician, Emergency Medicine Residency, Boonshoft School of Medicine, Wright State University, Dayton, Ohio; Michael Crowder, MD, Resident Physician, Emergency Medicine Residency, Boonshoft School of Medicine, Wright State University, Dayton, Ohio.
Peer Reviewer: Jeffrey Linzer, MD, FAAP, FACEP, Associate Professor of Pediatrics and Emergency Medicine, Emory University, Atlanta, Georgia.
Cervical adenitis, otitis externa, and peritonsillar disease are very common diseases that are seen in the emergency department (ED). Early recognition, appropriate treatment and an awareness of potential complications guide the clinician's treatment decisions. Although these disease processes are common, diagnostic and therapeutic evidence has continued to evolve to optimize patient comfort and maximize the potential for an excellent outcome. The authors review the common findings associated with each of these disease processes, current standards for diagnostic testing and evidence-based therapeutic interventions.
- The Editor
Introduction
Pediatric ear, nose, and throat (ENT) infections are common concerns in the ED. Cervical adenitis and otitis externa are examples of superficial ENT infections where the affected patient has complaints that are referable to the location of inflammation. Systemic manifestations are inconstant. Physical examination features reflect alterations of structures impaired by a localized process. Complications are rare, and outcomes are generally favorable. Peritonsillar disease and parapharyngeal abscess are examples of ENT deeper infections where complaints may be subtle and toxicity that is disproportionate to localized inflammation may be seen. Although only a very small number of patients develop a compromise of vital structures; early recognition and aggressive management are needed to optimize patient outcome.
In this article, the clinical manifestations of these selected ENT infections are reviewed, diagnostic testing is outlined, and treatment recommendations are discussed. The article serves as a companion to "Common Pediatric ENT Infections" (Pediatric Emergency Medicine Reports, July 2008).1 The latter discussed pharyngitis, acute otitis media, and sinusitis.
Cervical Adenitis
Definition and Anatomy. The mass of lymphoid tissue is age-dependent, but there are more than 500 lymph nodes in a pediatric patient, with many superficial nodes palpable. About 38%-45% of otherwise healthy children have palpable cervical lymph nodes.2,3 These lymphatic tissues are firm, nontender, and mobile without surrounding erythema or induration of tissues. A normal lymph node measures 1 mm to 1 cm in diameter. Lymphadenopathy implies that a node or multiple nodes have exceeded 1 cm in diameter.4,5 In lymphadenitis, the enlarged lymph node or nodes are inflamed. If lymphadenitis develops over several days, it is referred to as acute lymphadenitis. If the enlargement develops over weeks to months, it is considered to be subacute or chronic lymphadenitis.
The distribution of nodes and lymphatic chains in the head and neck is somewhat variable. However, all individuals possess superficial and intra-connecting deeper chains. Two cervical triangles are formed by the sternocleidomastoid muscle medially and the midline of the neck anteriorly and posteriorly. The anterior triangle contains nodes that assume the nomenclature of the adjacent structure. The anterior triangle contains the preauricular nodes, the jugulodigastric nodes (tonsillar nodes), the submaxillary and submandibular nodes, the salivary nodes, and the submental nodes. The posterior triangle contains mastoid (postauricular), occipital, nuchal, spinal accessory and transverse cervical nodes. (See Figure 1.)
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Nodes receive lymphatic drainage from various structures. The preauricular nodes drain the medial eyelids, forehead, and conjunctival sac. The jugulodigastric nodes drain from the lingual and palatine tonsils. The submaxillary and submandibular nodes receive superficial drainage from the lower lip and vestibule of the nose and cheeks,6 and they will enlarge with infections of the teeth, lips, and gums. The salivary nodes drain from the parotid gland. The submental nodes drain from the lower lip and floor of the mouth. The mastoid lymph nodes drain the parietal scalp and inner surface of the pinna. Occipital and nuchal nodes enlarge in afflictions of the scalp. The spinal accessory chain drains the occipital, mastoid, lateral neck, and scalp regions. The transverse cervical chain drains the deep cervical, supraclavicular, infraclavicular, upper thorax, and anterior neck regions.
Scope of the Problem. Cervical lymphadenitis is a common pediatric problem. Except in neonates, where male dominance has been reported in cases due to group B Streptococcus species, there is no sexual or seasonal predilection. It may affect children of all ages, with the peak age group 1-4 years.7
Pathophysiology. The enlargement of a single lymph node or adjacent lymph nodes results from one of three processes: intrinsic enlargement, extrinsic enlargement, or infectious infiltration. The least common is extrinsic enlargement as a result of a malignant infiltration of the node. Uncommonly, normal but over-proliferative plasma cells, histiocytes, lymphocytes, and monocytes lead to intrinsic enlargement of the lymph nodes. Most commonly, lymph nodes enlarge as a result of an infectious source.
In the cervical region, upper respiratory tract infections result in microorganisms spreading into surrounding tissues. The organisms enter the lymphatic fluid and are carried to the lymph nodes via afferent-collecting vessels. The lymph nodes function as filters hindering or arresting the spread of invading microorganisms. In lymphadenitis, the nodes become infected and inflamed. Histopathologically, this manifests as polymorphonuclear leukocyte infiltration with vasodilatation and edema. If unchecked, microabscess formation and necrosis occur.8
Bacteriology. Knowledge regarding the infectious etiology of pediatric cervical adenitis results from patients who have had percutaneous needle aspiration, incision and drainage, or in rare cases, excisional biopsy.7,9,10 The infectious agents associated with acute adenitis in immunocompetent children include viruses, bacteria, protozoa, and fungi. These causative agents can be divided into common, uncommon, and rare categories. (See Table 1.)
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Acute adenitis. Microbiologic techniques may fail to isolate the causative agent in 15%-30% of cases. Viruses alone, such as EBV, CMV, adenovirus, herpes simplex, and HIV, are isolated in a small percentage of children. Bacterial growth is found in more than half of the patients, with the majority of cases having aerobic bacteria alone isolated. The predominant aerobic organisms are methicillin-sensitive Staphylococcus aureus (MSSA), methicillin-resistant Staphylococcus aureus (MRSA), group A beta-hemolytic Streptococcus (GABHS), and Bartonella henselae.7,11,12 Anaerobic bacteria alone or mixed aerobic and anaerobic bacteria infections may be found in roughly 20% of cases. The anaerobic organisms most commonly recovered include Peptostreptococcus species, Peptococcus species, Bacteroides species, Propionibacterium acnes, and Fusobacterium species.13
Nonacute adenitis. Subacute or chronic adenitis is typically not caused by the common viral, aerobic, and anaerobic bacteria that are seen in acute adenitis. The agents most commonly recovered will be the nontuberculous mycobacteria. These include Mycobacterium avium-intracellulare, M. simiae, M. scrofulaceum, M. kansasii, M. fortuitum, M. bohemicum, and M. genavense.14-17 Rarely, M. tuberculosis may be isolated from a cervical gland. Protracted or recurrent adenitis may also be seen with infection from Corynebacterium pseudotuberculosis18 and Actinomyces species.19
Clinical Presentation. The clinical findings of cervical adenitis patients are variable and depend upon the patient's host defenses, the age, the causative agent, and the location of the inflamed node.
History. Adenitis typically develops in previously-healthy individuals who are younger than 5 years of age. The young child develops a subtle illness from an infectious agent in a head and neck location. The organisms extend from the initial site of attachment to a regional node or nodes. Hence, there may be any combination of antecedent coryza, sore throat, painful swallowing, mouth sores, dental pain, or rash on the scalp or face. Fatigue, malaise, and headache are variable. Acute enlargement of the node is often associated with fever. Nodes that enlarge in an indolent fashion are not typically associated with a febrile state.7
The clinician must pursue the possibility of zoonotic disease. Seek a history of insect bite, cat scratch or bite, and exposure to rodents, horses, sheep, or goats. Recent dental extraction or injury to the jaw may be the precipitation of an odontogenic infection. Exclude intrafamilial spread of any infectious disease, including tuberculosis.
Physical Examination. Examination usually reveals a nontoxic child who looks as if he or she does not feel well. With the exception of fever, vital signs are rarely altered. There may be evidence of a skin affliction in the head and neck region, such as atopic dermatitis, seborrheic dermatitis, traction folliculitis, cellulitis, impetigo, boil, or furuncle. There may be evidence of focal infection in regions such as the nares, gingiva, lips, teeth, dental spaces, ears, adenoids, palatine tonsils, lingual tonsils, tongue, or salivary gland. The skin overlying the single affected node or adjacent nodes may be variable in appearance. The skin may be normal without any localized inflammatory response. Often, the skin is discolored with an erythematous hue. A cellulitis appearance (cellulitis-adenitis syndrome) may occur in the buccal or submandibular region over an inflamed node.20 With subacute cases, as is often seen with nontuberculous adenitis, the overlying skin thins out to a parchment-like consistency and develops a distinctive lilac-red color.8 A fibrous skin eruption that is indurated with or without a draining sinus is characteristic of actinomycosis.21
The size of the inflamed node palpable below the subcutaneous tissue may vary, with a range of 2-6 cm. It may be discrete and well demarcated, both visibly and palpably, or be without well-defined margins. Nodes may be mobile or fixed to adjacent tissue and range from nontender to tender and firm to fluctuant. The nodal involvement is occasionally bilateral and typically seen in response to group A beta-hemolytic streptococcal (GABHS) pharyngitis or as part of a systemic infection with a generalized reticuloendothelial response. Unilateral adenitis is caused by staphylococcal organisms or streptococcal organisms in 58%-89% of cases.7,22 The inflamed node may be surrounded by uninvolved nodes, or there may be a cluster of coalescent satellite nodes that are similarly involved.23,24 Other physical exam features may be seen with specific pathogens. A pustular lesion adjacent to the node may be seen with cat scratch. Inflammatory or necrotic tissue may be seen with anthrax. Splenomegaly may be seen with toxoplasmosis and brucellosis. Hepatosplenomegaly may be seen with cytomegalovirus and EB virus infections. Conjunctivitis may be seen with adenoviral-initiated adenitis and in Kawasaki disease.25
Diagnostic Testing. The diagnosis of acute adenitis is established on the basis of history and physical examination. Immunologically-intact children who have mild to moderate constitutional symptoms, who are nontoxic in appearance with either unilateral or bilateral adenitis, may be managed without diagnostic testing.24 Adjuvant testing for other causes should be determined by disease presentation. Patients who have been highly febrile or who are ill appearing should have a blood culture performed.26 Those with a concomitant infection of the skin should have submission of a wound culture. Patients with a fluctuant node or nodes should have a needle aspiration. The latter will identify the causative pathogen in 60%-80% of cases.9 Patients who have progressive or persistent symptoms despite a course of antibiotics may benefit from laboratory evaluation. Prior antibiotic therapy will not alter results from a battery of laboratory tests that have been recommended. These tests include: complete blood count, acute phase reactants, hepatic profile, serologic testing for viral and bacterial pathogens, direct fluorescent antibody, or polymerase chain reaction assays from the lymph node or abscess.12 The frequency of positive results is unknown for subacute, indolent patients. The physician must judge the cost benefit of wide laboratory investigations without knowledge of expected yield for a specific organism.27
In the setting of chronic or subacute lymphadenitis a presumptive diagnosis of a specific pathogen may not be possible from clinical suspicion alone. In the face of uncertainty, diagnostic testing should be performed at the initial presentation. Testing should include an intermediate tuberculin skin test, complete blood count, acute inflammatory markers, and serologic tests for various viruses (EBV, CMV, HIV), bacteria that cause adenitis (cat scratch, tularemia, plague, syphilis, non-tuberculous mycobacterium), protozoan (toxoplasmosis), and fungi (coccidioidomycosis, histoplasmosis, aspergillus, candida, cryptococcus).8,24,28 The frequency with which the serologic tests identify one of these pathogens is unknown. However, the tests are warranted in that an accurate diagnosis is desirable.
Imaging may be warranted in certain circumstances. Ultrasonography may be useful in establishing if a cervical node has a sufficient degree of suppuration such that it would be amenable to needle aspiration.10 A chest x-ray should be considered when the adenitis patient may have pulmonary disease.29 Computerized tomography (CT) with contrast is useful when a deep neck space infection is suspected26 or there is consideration that the inflammatory mass represents a congenital head and neck malformation.30 (See Figure 2.)
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Differential Diagnosis. The differential diagnosis of a mass lesion in the head and neck region includes benign and malignant tumors, congenital neck anomalies, or an inflammatory disease state. (See Table 2.) These conditions, all associated with a regional mass, are distinguishable by their characteristic history and examination features. Of all attributes, their anatomical location is most helpful to distinguish one condition from the other. Midline masses are typically thyroid (goiter, teratoma, papillary carcinoma), dermoid cyst, or thyroglossal duct cyst. Lateral lumps may be unrecognized congenital abnormalities (branchial cleft cyst, cystic hygroma) or tumors (neurogenic, lymphoma). Submandibular masses may be lesions of mandibular origin, such as histiocytosis or osteogenic sarcoma. Preauricular lumps are more commonly inflammatory rather than neoplasia. However, slow-growing tumors may be of vascular or lymphatic origin as well as primary neoplasia of the parotid gland.23 Masses in the posterior triangle or in the supraclavicular region should raise the concern for occult tumor.23,24
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Treatment. It is customary in the ED to initiate antibiotic therapy for adenitis. The optimum duration of antibiotic therapy has not been prospectively studied. However, various authors suggest 10-14 days, or five days after signs of systemic symptoms or nodal inflammation has resolved, whichever is longer.31 The route (parenteral vs. oral) is determined by several factors that include immunologic status, degree of systemic symptoms, the size of the lymph node, the presence of fluctuance, and concomitant cellulitis. Immunologically impaired, toxic patients with severe adenitis or cellulitis, and those who do not tolerate or will not tolerate oral therapy, should be given parenteral antibiotics.
When a primary source of infection likely to be causing the adenitis is identified, antibiotics should be directed empirically against the microorganisms most frequently associated with that source. In the absence of an identifiable primary source, empiric antibiotic treatment is directed against the most common agents - Staphylococcus aureus, GABHS, and anaerobic oral flora. Choices that have good antimicrobial coverage include ceftriaxone, cefazolin, and clindamycin. An immunologically intact, nontoxic patient whose node has not yet become fluctuant can be treated with oral antibiotics. Patients not at risk for MRSA may be treated with cephalexin. Therapeutics at 50 mg/kg/day provide adequate blood and lymph node levels to eradicate methicillin-sensitive Staphylococcus aureus, GABHS, and Peptostreptococcus.7 Augmentin is a suitable alternative. The penicillinase-resistant penicillins, such as oxacillin, cloxacillin, or dicloxacillin, can be used if the patient is able to swallow a capsule. They should not be used in patients unable to swallow a pill, as there is significant taste diversion with the liquid preparations.32 In circumstances where MRSA infection is likely, several empiric regimens are recommended for community-acquired MRSA adenitis. Trimethoprim sulfamethoxazole may be used alone or combined with rifampin. Clindamycin monotherapy is an option for children older than 8 years of age. Doxycycline may also be considered as a suitable treatment.33
Antibiotic therapy is also suitable for patients with fluctuant nodes. However, most authors suggest an aspiration, not only for diagnostic purposes but for therapeutics. Aspiration removes necrotic material from the center of the node, decreasing the inflammation in the area and hastening recovery.9,10
Complications. The overwhelming majority who present acutely with nonfluctuant nodes and are started on antimicrobial therapy have an uneventful resolution of signs and symptoms over a five- to seven-day course. The clinical course may occasionally be more prolonged, or the gland may evolve and develop an abscess.31 Disseminated disease, including bacteremia, septicemia, mediastinal abscess, and purulent pericarditis, have all been reported as rare complications.34
Patients with subacute adenitis may relapse or develop a cutaneous sinus tract.19,35 Disseminated disease has been reported with mycobacterial species and with cat-scratch disease.17,36
Disposition. There are no evidence-based rules established as to the disposition for patients with cervical adenitis. The emergency physician may take the side of caution by admitting marginally ill or obviously sick patients for intravenous antibiotics. Inpatient disposition with continued parenteral therapy would theoretically provide higher blood and tissue concentrations of antibiotic, leading to a prompter resolution of the clinical course. Those patients who appear well can be treated on an outpatient basis and observed. Nontoxic patients treated transiently with what is ultimately determined to be suboptimal therapy suffer little clinical consequences of delayed alternate definitive management.
Otitis Externa
Definition and Anatomy. Otitis externa (OE) is a diffuse inflammation of the external auditory canal (EAC). Also known as swimmer's ear, this inflammatory process involves the tympanic membrane and pinna in uncomplicated cases. In acute otitis externa (AOE), the skin-lined cul-de-sac becomes abruptly inflamed.37 In circumstances where symptoms and signs are noted for weeks to months, the condition is referred to as chronic otitis externa (COE).38 Malignant otitis externa (MOE) occurs when the inflammatory process extends into structures outside the auditory canal. Cartilaginous, osseous, deep soft tissue, and intracranial extension is facilitated by neurovascular tissues that pass through fissures at the anterior cartilaginous portion of the auditory canal. These fissures allow potential spread of ear canal disease to the parotid gland, temporomandibular joint, and soft tissues of the upper neck. Venous drainage of the external ear is to the superficial temporal and posterior auricular vein. The latter connects to the sigmoid sinus, providing a route for extension of infection into the intracranial cavity.39
Scope of the Problem. The lifetime incidence of AOE is as high as 10%.40 AOE affects approximately four of every 1,000 children and adults per year.41 In a majority of cases, AOE is unilateral. Symptoms are disabling enough to cause patients to interrupt their daily activities for a median duration of four days. AOE is found in early childhood, with a peak of 7-12 years of age. COE affects 3%-5% of the population38,42 and has no age predilection. MOE is a rarity that has no age predilection.39
Pathophysiology. Any alteration of the natural physiology or barriers of the external auditory canal predisposes to a localized inflammatory process. The inflammation leads to edema of the skin, which leads to obstruction of the apocrine glands and pruritus results. Itching commonly leads to self-instrumentation, which may create further injury. Any inflammation of the EAC changes the quality and amount of cerumen produced. This results in reduced epithelial migration, and the ear canal pH changes. The resulting warm, alkaline, moist canal becomes an ideal place for colonization with pathogens.43
The greatest risk factor for the development of AOE is moisture. Continuous contact with water, related to swimming or bathing in hot tubs, pools, or freshwater lakes, results in pathologic alterations in the EAC. Warmth and humidity are environmental factors leading to increased canal moisture with disruption of the canal physiology. Devices that trap moisture, such as swimming caps, hearing aids, or headphones, are causative factors.44 Excessive disimpaction of cerumen may support growth of bacteria and fungi.45 Insertion of foreign objects, such as cotton tip applicators, fingernails, and earplugs, may create localized injury, predisposing to secondary invasion by pathogens.46
A risk factor for the development of COE includes inadequate treatment of AOE. COE may also be precipitated by a reaction to a component of an ototopical used to treat AOE.38,47 Food sensitivity is a potential origin of COE, particularly in patients who have an associated atopic dermatitis.48 Allergic hypersensitivity to metal earrings, plastic of hearing devices, and chemicals from shampoos also predispose to COE.38,47
Immunosuppression as a result of therapy for malignancy is the greatest risk factor for MOE. Other underlying conditions predisposing to MOE are diabetes mellitus, malnutrition, anemia, and leukemia.49
Bacteriology. The ear canal is normally colonized by both aerobic and anaerobic organisms. In AOE, the majority of infections are aerobic. The organisms cultured are most commonly methicillin-sensitive Staphylococcus aureus, methicillin-resistant Staphylococcus aureus, and Pseudomonas aeruginosa. Other gram-negative organisms cause no more than 2%-3% of cases.48,50,51 Anaerobic bacteria are isolated in exclusion from 4%-25% of AOE. Bacteroides species and Peptostreptococcus species predominate.46 In approximately one third of cases, polymicrobial bacterial infection occurs.52 Pure fungal AOE (otomycosis) accounts for 2%-10% of cases. Fungal disease is more common in patients with diabetes or other immunocompromised states. Candida species are more prevalent in temperate climates, and Aspergillus species tend to be the offending pathogens in tropical regions.53
Clinical Presentation. The severity of the clinical presentation is variable and largely dependent upon the timing of the patient encounter. The disease has been striated into four classifications: mild, moderate, advanced, or severe. (See Table 3.)
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History. More than 50% of the patients present in the early stages of inflammation. Their chief complaint is largely earache. Other symptoms include pruritus, ear canal tenderness, a sense of fullness in the ear, and hearing loss.48,54 Pain intensifies and becomes more disabling with longer-standing disease. With more prolonged disease, the pain is constant, felt in and about the ear. Pain is aggravated by any motion of the jaw or external ear.
Physical Examination. Patients with mild to moderate disease are afebrile and are not ill-appearing. They have pain, but they are easily distracted. The pre- and postauricular skin is not inflamed. There is no retroauricular mass and no percussion tenderness over the mastoid air cells. Inward pressure on the tragus or pulling the auricle backwards elicits discomfort. In mild disease, the external auditory canal is completely visualized and displays edema. The tympanic membrane may be minimally erythematous. In moderate disease, there is swelling and tenderness of the canal. The canal may be partially occluded with debris, which will present in various colors including yellow, brown, white, and gray. The tympanic membrane remains at least partially visualized. The outer circumference will appear red, thick and covered by inflammatory vascularization. There is an absence of middle ear fluid. In advanced disease, there may be low-grade fever. The patients are poorly distracted from their pain. They are nontoxic in appearance. In advanced disease, the canal is completely occluded by a cheesy discharge. The tympanic membrane cannot be visualized. Patients with severe disease have debilitating pain. They are febrile and toxic appearing. With severe disease, erythema and edema have spread to the preauricular tissues, the parotid gland, or the retroauricular region.47,48,55 The presence of fever and a toxic appearance should suggest systemic spread or MOE.56
There are several clues to the presence of otomycosis. Itching is more prominent than pain. As the fungi multiply, they fill the canal with a mycelial mat containing epithelial debris and cerumen, mixed in a mass with a consistency of wet blotting paper. This accumulation of white debris with sprouting hyphae is typical for Candida species.53,57 When caused by Aspergillus species, a fine layer of filamentous mycelia and spores can be seen extending from the debris. It appears as a moist, white plug dotted with black debris.
Diagnostic Testing. The diagnosis of AOE is established on the basis of history and physical examination. No diagnostic investigations are warranted, as expectant therapy is generally efficacious. In COE, where there has been incomplete recovery or persistent symptoms and signs, submission of the suppurative canal debris for bacterial and fungal culture may be of assistance to the longitudinal caretaker. When MOE is suspected, cultures should be obtained from the purulent drainage in the ear canal. A needle aspirate of inflamed or pre- or postauricular tissue and a culture of blood should be obtained.56 If central nervous system invasion is suggested, perform a lumbar puncture. Regional imaging is necessary to determine the extent and nature of tissue invasion. CT, magnetic resonance imaging (MRI), and radionucleotide imaging are the three modalities of utility.58 Radionuclide technetium and gallium scans are most reliable in identifying osteomyelitis of the temporal bone and base of the skull. These scans may be positive well before bone demineralization is apparent by other imaging techniques.59 Contrasted CT and MRI both provide information on inflammatory changes in the soft tissue surrounding the auditory canals. Some feel MRI is superior in delineating soft tissue disease.60
Differential Diagnosis. The differential diagnosis for AOE includes conditions which cause earache, and diseases that distort the normal anatomy of the tympanic membrane, external auditory canal, and periauricular tissues. Ear pain that is poorly localized may occur with many disease processes. These include dental pathology, including apical abscess, pharyngitis, tonsillitis, uvulitis, retropharyngeal abscess, parotitis, preauricular adenitis, mastoiditis, sinusitis, bullous myringitis, and temporomandibular joint disorders.1,61 An abnormal-appearing tympanic membrane may occur with several disease states. Erythema of the tympanic membrane may be present in crying infants and in children with upper respiratory tract infections. Vesiculation of the tympanic membrane may occur in the course of chickenpox and Ramsey-Hunt syndrome. Many diseases may cause edema or erythema of the external auditory canal, including eczema, seborrhea dermatitis, psoriasis, foreign bodies, mite infestation, and reactions to ototopical agents.62-64 Suppurative otitis media (OM) with perforation may lead to otorrhea that may be easily mistaken for AOE. Additionally, both acute suppurative OM with perforation and a secondary inflammatory AOE may coexist.
The differential diagnosis of COE includes an allergic reaction to a solvent/preservative (i.e., propylene glycol), a singular ototopical agent (i.e., benzocaine), or a component of a multiple-active ototopical (i.e., neomycin).634 The generalized dermatoses (seborrhea, psoriasis, neurodermatitis) are associated with recurrent ear drainage. Wegener's granulomatosis, histiocytosis, cholesteatoma, and rhabdomyosarcoma may present with a mass or inflammatory discharge from the ear.65 Recurrent ear drainage may be caused by congenital brachial cleft abnormalities.30
The differential diagnosis of MOE includes facial cellulitis, preauricular adenitis, mastoiditis, cervicofacial necrotizing fasciitis and, in addition, lymphomas, soft tissue sarcoma, and leukemia that rarely present in an inflammatory fashion.49
Treatment. While in the ED, the patient with AOE should have cleansing of the external auditory canal. A clean, dry canal facilitates healing and penetration of ototopicals. Debris is removed with a small tuft of cotton attached to a wire applicator passed under direct visualization. Gentle suctioning may be required if the canal is occluded with debris, and/or the canal is edematous. Various devices have been used for débride removal, including urethral swabs, cotton swabs, a trimmed infant feeding tube attached to a DeLee suction device, or suctioning with a 5 or 7 French FRAZIER tip suction. In circumstances of severe edema of the canal, an ear wick should be placed. The wick rests against the lining of the external auditory canal and holds the ototopical agent in contact with the skin. Other options include ribbon gauze covered with an ototopical agent or compressed cellulose ear wicks. These can be placed deep into the external auditory canal with an alligator forceps and the topical solution applied.
Topical otic or ophthalmic preparations delivered to the external auditory canal are the mainstay of treatment. (See Tables 4 and 5.) These ototopical products may be self-prepared or marketed pharmaceuticals. Acetic acid-containing solutions have historically been used with moderate success. Their efficacy is based upon their ability to reduce the pH of the canal environment, which restricts the growth of bacteria and fungi.66 Isopropyl alcohol can be mixed with equal parts of a 5% vinegar solution. Following its instillation, gentle heat can be used to dry the canal. Two percent acetic acid solutions are commercially available in an aqueous or propylene glycol base. They are suitable alternates with an intact ear drum. These acetic acid solutions may require prolonged treatment in contrast to topical antibiotics, which cause less irritation than acetic solutions. High concentrations of antibiotics are delivered to the infectious site; there is negligible systemic absorption of the antibiotics. Ototoxicity is rare.67 Therefore, topical antibiotics are the preferred approach when the integrity of the tympanic membrane (TM) is unknown, or if there is a known TM perforation or pressure-equalization (PE) tubes. Ofloxacin is the only preparation available without corticosteroids. Ciprofloxacin and polymyxin/neomycin are combined with hydrocortisone. The addition of hydrocortisone implements a modest reduction in the duration of symptoms and an equal cure rate.68 Ophthalmic antibiotics are off-label alternatives for administration in the external ear canal. Their slightly higher pH than ototopicals may cause less stinging and burning in the face of an active inflammatory process. Additionally, they are less viscous and penetrate into a narrow, edematous canal with less difficulty.69
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Patients who are prescribed ototopical agents should have specific instructions to avoid dizziness. The ototopical should be warmed to room temperature before application. Another individual should apply the ototopical, as self administration provides inadequate therapy in 40% of patients.70 The caretaker should apply the ototopical with the patient lying in a decubitus position. The patient or the administrator should pump the tragus after application of the drops in order to disperse the medication into the ear canal.47,54
Oral antibiotic agents are not efficacious for uncomplicated AOE. Oral antibiotics may be added to ototopicals when suppurative OM with perforation has led to secondary AOE, or the child with PE tubes has developed supperative OM and a secondary AOE. Parenteral antibiotics should be administered when the diagnosis of MEO is considered.71
Complications. A majority of patients with AOE have reduction in pain, itching, and discharge within a 48-hour period of initiating treatment. The most common cause of failure to improve is noncompliance with the therapeutic regimen. Rarely, the offending organisms may be resistant to the chosen ototopical agent and predisposed to COE. If Staphylococcus species are the cause of infection, microabscesses or furunculosis of the lateral canal may occur. Soft tissue infection from any organism may extend, creating a facial cellulitis, perichondritis, or chondritis. Malignant infection may destroy the tympanic membrane. In MEO, the infection may extend along fascial planes and invade the vascular system and bone, causing vasculitis, necrosis, and osteomyelitis. Extension into the styloid and jugular foramina has been known to affect the facial and cranial nerves. Meningitis and brain abscess are rare complications of MEO.49
Disposition. The majority of patients with acute or chronic otitis externa are treated as outpatients. Mild and moderate cases are treated from 5-10 days, or for three days after the last symptoms. Patients with moderate or severe cases typically require insertion of a wick. Repeat examination in 24-48 hours is suggested, at which time the wick is removed. Patients who have failed to respond to a chosen ototopical within 48-72 hours may be changed to a different ototopical agent. Inpatient admission is warranted for any patients who develop expanding soft tissue or suspected deep-plane infections, as well as patients suspected of MOE.
Peritonsillar Disease
Definition and Anatomy. Peritonsillar infection develops when oropharyngeal bacteria invade the peritonsillar space. The peritonsillar space is located lateral to the fibrous wall of the tonsillar capsule and medial to the pharyngeal fascia.72 Patients who develop infection in this space suffer a disease continuum from peritonsillar cellulitis (PTC) to peritonsillar abscess (PTA). In PTC, pus is not demonstrated by CT, MRI, or ultrasound imaging, nor by needle aspiration or incision.73 In PTA, pus collects and an abscess forms. The abscess is most commonly restricted to the superior pole of the tonsillar fossa, but may extend superiorly to the hard palate and inferiorly to the level of the piriform sinus.74
Scope of the Problem. Untreated or inadequately treated childhood tonsillitis is on occasion associated with PTC, but the true incidence is not known. Similarly, there is little information on published population-based incidence rates of PTA in childhood. In the pediatric emergency medicine literature, the incidence rate of PTA in children younger than 18 years has been reported as 14 per 100,000 person-years at risk.73 PTA has been reported in children as young as 2 years of age. There are multiple case reports of PTA in children in their first decade of life.75 However, the incidence rate is highest in late adolescence. The incidence rate was reported as 40/100,000 person-years in children 14-17 years.73 In the ENT literature, surveyed otolaryngologists reported an overall rate of 30 cases per 100,000 person-years in both children and adults in the United States.76 Peritonsillar disease accounts for half of hospital admissions for all patients with deep neck infections.77,78
Pathophysiology. Patients ultimately diagnosed with peritonsillar disease have pharyngitis at onset. Patients who have had tonsillectomy remain at risk for peritonsillar disease. Patients with intact tonsils typically have a pharyngitis that advances to tonsillitis. Tonsillitis, if severe, may be associated with peritonsillar cellulitis. Cellulitis is the precursor to PTA. This spectral shift to more severe inflammation and abscess formation may occur in previously healthy, immunologically intact individuals. Several predisposing conditions to PTA have been reported. They include mononucleosis and Kawasaki disease. Infectious mononucleosis, as confirmed by a positive heterophile antibody screen, has been found in 6%-18% of PTA patients.73 A small percentage of PTA patients have been concurrently diagnosed with Kawasaki disease.73,79 Immunodeficient patients are at risk for "deep infection," of which PTA is an example.
Bacteriology. Studies of the microbiology of PTA are limited, but most report polymicrobial infection. There is typically a mixture of aerobic and anaerobic oral bacteria florae. The dominant aerobic pathogens isolated are alpha-hemolytic streptococci and GABHS. Recovered anaerobes include Bacteroides species, Peptostreptococcus species, and Fusobacterium species.80
Clinical Presentation. In peritonsillar disease, the severity of the clinical presentation is characteristically out of proportion to that expected from a routine episode of pharyngitis. Both PTC and PTA share many of the same symptoms and signs.
History. The typical complaint for peritonsillar disease is sore throat that has worsened over days despite symptomatic care and/or oral antibiotic therapy for pharyngitis. The throat pain is moderate to severe, occasionally radiating to an ear. The child may be unable or unwilling to open the mouth. This leads to reduced oral intake. There may be an inability to swallow fluids or an inability to swallow saliva, leading to drooling. Fever of all ranges is near universal. Chills may occur. A parent may perceive a change in the quality of their child's vocalization.
Physical Examination. Examination reveals a potentially drooling, febrile, fretful child who looks uncomfortable and has a blunted affect, lack of engagement with caregiver or examiner and decreased motor activity. The child does not seek airway-preserving posturing, and there is no increased work of breathing or respiratory distress. Regional lymphadenopathy may occur in the anterior cervical chain. Lymph nodes are discrete and nontender. The vocalization is abnormal, classically depicted as "hot potato" hoarseness is not present. The breath is fetid and trismus may preclude an optimal oropharyngeal evaluation. However, a tongue blade facilitated examination reveals bilateral tonsillitis with or without exudate. In both PTC and PTA, there is edema and erythema of the peritonsillar tissue, typically in the superior portions, adjacent to the lateral aspect of the palate. With PTA, there are usually two additional features: these include a unilateral, erythematous mass lateral to the enlarged tonsil and a medial deviation of the uvula away from the infected abscess.74,81,82
Diagnostic Testing. As there is clinical overlap of PTC and PTA, an imaging technique can be of diagnostic utility in equivocal cases. Three imaging techniques equally discriminate between PTC and PTA. Both contrasted CT and MRI exquisitely demonstrate normal and morbid anatomical structures in the head and neck. (See Figures 3 and 4.) Both are sensitive in assessing alterations in the peritonsillar space and can accurately discriminate PTC from PTA.83 Intraoral ultrasound has the distinct advantages of being less expensive, readily accessible, and free of ionizing radiation. It is amenable to cooperative patients. It has proven to be of utility in the adult population, who are provided analgesia to overcome trismus. With a sheath-endocavity transducer, PTC exhibits enlarged tonsils with a homogenous or striated appearance, whereas PTA exhibits tonsillar enlargement with a heterogenous or cystic appearance.81
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Ultrasound-guided aspiration or a "blind" aspiration of the most pointed peritonsillar mass, if productive of pus, confirms the diagnosis of PTA. The sample can be sent for aerobe and anaerobic culture. However, peritonsillar abscess culture in non-immunocompromised patients may not be cost effective, as most patients respond to intravenous penicillin therapy.76
Differential Diagnosis. The differential diagnosis for a child with severe sore throat, dysphagia, and impaired vocal quality with or without either drooling or frank upper airway obstruction includes uvulitis, epiglottitis, retropharyngeal abscess, parapharyngeal abscess, and prevertebral abscess. A noninvasive oropharyngeal examination may be all that is necessary to discriminate these disease processes. Careful intraoral examination will uncover uvulitis and potentially epiglottitis. Neck stiffness may be seen with retropharyngeal abscess and prevertebral abscess. An upright lateral radiograph of the neck may discriminate between these entities.
Treatment. Antibiotics remain the mainstay of treatment for PTC and PTA. The clinician may obtain a culture or empirically treat with penicillin or aminopenicillin, with or without a beta-lactamase inhibitor or clindamycin. These individual antibiotic agents have been used with equal success in peritonsillar disease.77 Parenteral ED loading-dose therapy may be used before the initiation of oral antibiotics.84 No specific route of administration or treatment duration has been established for peritonsillar disease by prospective study.
Dexamethasone as an adjuvant for severe tonsillitis may improve the time to onset of throat pain relief.85 Corticosteroids have been given to many patients with peritonsillar disease, but no studies have proven a significant benefit. They are not suggested as routine for peritonsillar disease.73
Surgical management of PTC is unnecessary. Patients with PTC are successfully treated with antibiotic therapy alone. Surgical management of PTA can be performed prior to antibiotic administration or delayed and utilized only in those patients who have failed 48-72 hours of intravenous antibiotics. The surgical options for PTA are needle aspiration and incision and drainage. Ultrasound-guided needle aspiration is the preferred management. A meta-analysis of multiple published studies of needle aspiration for PTA has demonstrated a success rate of 94%.76 Patients may be cured with one aspiration or require additional aspirations. Incision and drainage or acute "quinsy" tonsillectomy are additional surgical options for otolaryngologists.
Complications. Serious complications with peritonsillar disease are uncommon. Airway compromise is a potential concern, particularly for those younger than 8 years of age. (See Figure 5.) PTA runs the risk of rupture. If it ruptures, the airway can be occluded, aspiration of pus can lead to secondary pneumonia, lung abscess, or empyema. Suppurative thrombophlebitis of the internal jugular vein with peritonsillar disease can lead to multiorgan distal abscesses (Lemierre's syndrome).86
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Disposition. No convention has been established for the disposition of patients with peritonsillar disease. There is a greater tendency for adults to be managed as outpatients. Pediatric patients with peritonsillar disease are more often managed as inpatients.73 Patients with newly diagnosed with peritonsillar cellulitis who have not received antibiotics can be treated and followed on an outpatient basis as long as reliable follow-up is available. Those patients newly diagnosed with peritonsillar abscess who have not been treated with antibiotics may be managed in conjunction with an ENT specialist. All pediatric patients with PTC or PTA who continue to have moderate to severe symptoms despite outpatient ambulatory treatment should be admitted to the hospital. Admission would further be warranted for individuals with dehydration, concern for compromise of airway, or management of systemic complications, such as distal abscess formation.
Parapharyngeal Abscess
Definition and Anatomy. Parapharyngeal abscess develops when bacteria from oral, tonsillar, adenoidal, mastoid, parotid regions, or deep cervical lymph nodes gain access to the lateral pharyngeal space. The lateral pharyngeal space has an inverted pyramidal shape. The apex of the inferior border is the submandibular glands at the level of the hyoid bone. The superior border is the petrous portion of the temporal bone at the base of the skull. The lateral wall of the pharynx is its medial border, which extends posteriorly to the prevertebral fascia and laterally to the mandible, parotid gland, and medial pterygoid muscles. It can be divided into two compartments by the styloid process. The anterior compartment is adjacent to the muscles of mastication. The posterior compartment is traversed by the carotid sheath, cranial nerves (IX-XII), and the jugular vein.
Scope of the Problem. Parapharyngeal abscess is the fourth most common deep neck abscess in childhood. It is far less common than the other three (peritonsillar, retropharyngeal, and submandibular).77 Parapharyngeal abscesses occur with the greatest frequency in children age 2-12 years.
Pathophysiology. The pathogenesis of abscess is unclear in many patients who lack a history of trauma to the oral cavity or its contents, and who have no antecedent symptoms to suggest focal infection anywhere within the head and neck region. The mechanism is clear in patients who have a history consistent with palatine tonsillitis, lingual tonsillitis, dental infection, or parotitis. It is postulated that bacteria from these focal infections invade lymph nodes in the lateral pharyngeal space. Adenitis leads to necrosis and local rupture of the lymph node with a secondary abscess formation.72,74
Bacteriology. Many parapharyngeal abscesses are polymicrobial and contain both gram-positive and gram-negative aerobic and anaerobic organisms.87,88
Clinical Presentation. Patients with parapharyngeal abscess share common denominators of infectious symptoms and signs of all deep space infection.
History. Patients with parapharyngeal abscess may have insidious prodromal events, such as nasal congestion, rhinorrhea, cough, or sore throat. They may present without prodromal symptoms or have a brief history of a sore throat that has escalated rapidly. Pain is severe, and there is difficulty with swallowing, occasionally with drooling. Children may experience pain with neck movement, and neck stiffness may be an observation of the parent. Parents may also perceive a change in the quality of their child's vocalization.
Physical Examination. Examination reveals a highly febrile, toxic-appearing child who has neck stiffness. The head may be maintained in a neutral position or rotated away from a unilaterally, diffusely brawny, indurated neck region. The neck may exhibit a true mass. The mass obliterates the inferior border of the mandible and lateral neck. Intense spasm is noted of the sternocleidomastoid muscles. Discrete lymphadenopathy, often palpable in peritonsillar disease, is absent. The child resists mouth opening, as there is trismus. If visualization of the oropharynx is possible, disrupted anatomy of the tonsillar pillars is present with anterior compartment abscess. The findings are similar to peritonsillar disease. However, with parapharyngeal abscess, the whole lateral pharyngeal wall is involved, not just the tonsil.72 With posterior compartment abscess, the tonsillar tissue has no distorted anatomy.
Diagnostic Testing. Imaging of the neck is warranted for suspected parapharyngeal abscess. The potential modalities include plain radiographs, ultrasonography, CT, and MRI. An upright lateral neck film is of utility only for excluding the other diseases on the differential diagnosis. The anatomic boundaries of parapharyngeal abscess are not apparent on plain radiographs. Ultrasonography through the neck externally can identify the location and internal characteristics of a parapharyngeal abscess.89 CT is a suitable imaging modality for defining the boundaries of a parapharyngeal abscess. Additionally, CT with intravenous contrast can assess vascular structures. MRI is equally useful to delineate the soft tissue planes of an abscess. MRI is warranted if CT scans have not been successful in defining abscess extension.74
Imaging of the chest with plain radiographs or CT is warranted if there is concern for pulmonary involvement or mediastinal spread.
Blind aspiration of parapharyngeal abscess for diagnostic culture is contraindicated due to the complexities of the regional anatomy. Ultrasound-guided aspiration of the abscess is optional.
Differential Diagnosis. On the basis of history, it may be difficult to differentiate parapharyngeal abscess from uvulitis, epiglottitis, peritonsillar disease, retropharyngeal abscess, and prevertebral abscess. All are associated with fever, dysphagia, odynophagia, drooling, and potential changes in the quality of the voice. Torticollis, when present, is distinctive of parapharyngeal abscess. Several other deep neck space infections are associated with soft-tissue swelling and mass effect. These include sublingual space, submental space, and masticator space infection. In sublingual or submental space infection, the mass effect is in the midline. With masticator space infection, the mass is lateral. The disease is associated with pain and soft tissue swelling that may be preauricular, overlying the zygoma, and extends inferiorly to the mandible. However, parapharyngeal space infection is distinguishable as its mass obliterates not only the angle of the mandible, but any indentation normally present below the ear to the midpoint of the neck. Branchial cleft anomalies may create an inflammatory mass effect similar to parapharyngeal abscess. An infected second or third branchial cleft anomaly, if unassociated with an external draining tract, may simulate parapharyngeal abscess with a mass in the anterior, inferior neck.30
Treatment. Patients with parapharyngeal abscess should be empirically started on broad-spectrum intravenous antibiotics. A single intravenous antibiotic agent, such as meropenem, can be administered. Alternately, several antibiotic combinations may be used, which include penicillin plus clindamycin, a beta-lactamase inhibitor plus clindamycin or metronidazole. A small percent of patients will recover on antibiotics alone. Most authorities suggest that drainage be instituted.
With anterior compartment parapharyngeal abscess, ED intraoral aspiration or incision and drainage are potential options. However, even a sedated older pediatric patient is unlikely to tolerate the procedure, which requires upright posturing, mouth gags, suctioning equipment, and instruments for blunt dissection. Further, as ED procedures, aspiration and incision/drainage carry risks of airway obstruction and bleeding. If drainage is attempted, it is perform by an otolaryngologist, with the patient under anesthesia. For posterior compartment disease, intraoral drainage is not possible. External needle-directed or incision and drainage procedures are performed under general anesthesia by otolaryngologists.
Complications. Parapharyngeal abscess in either the anterior or posterior compartment poses a danger of upper airway obstruction, mediastinal dissent, metastatic abscess, and septicemia. Posterior compartment involvement can lead to multiple problems. These include arteritis and aneurysm formation leading to carotid artery rupture. Septic thrombophlebitis can occur in the internal jugular vein. Patients may develop Horner's syndrome or palsies of cranial nerves IX-XII.72,74
Disposition. Patients with parapharyngeal abscess in either compartment should be admitted to the hospital for observation. All complications can develop rapidly. Patients require close monitoring while under treatment.
Conclusion
Pediatric ENT infections are common in the ED. Fortunately, the majority are easily diagnosed, and early appropriate management makes an optimal outcome likely. The clinician must be aware of clinical findings associated with more significant infections and evidence-based diagnostic testing and therapeutic choices to ensure the best outcome for each patient.
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Cervical adenitis, otitis externa, and peritonsillar disease are very common diseases that are seen in the emergency department (ED). Early recognition, appropriate treatment and an awareness of potential complications guide the clinician's treatment decisions.Subscribe Now for Access
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