Common Pediatric ENT Infections: Diagnosis and Management in the ED
Author: Kirsten Bechtel, MD, Assistant Professor of Pediatrics, Section of Pediatric Emergency Medicine, Department of Pediatrics, Yale University School of Medicine, New Haven, CT.
Peer Reviewer: Brian Skrainka, MD, FAAP, FACEP, Medical Director, Pediatric Emergency Department, St. Vincent Children’s Hospital, Indianapolis, IN.
Infections of the ear, nose, and throat (ENT) are common in children. Nearly 75% of all outpatient antibiotic prescriptions in the United States are for otitis media, sinusitis, bronchitis, pharyngitis, or non-specific upper respiratory infection, and children have the highest rates of antibiotic use for these conditions.1 Physicians often report parental pressure to prescribe antibiotics for such conditions, and there currently is a campaign in the United States to improve both physician and parental awareness of the overuse of antibiotics and their attendant risk in increasing the prevalence of drug-resistant bacteria.2-4 The emergency department (ED) physician can be an advocate for the appropriate use of antibiotics in children by becoming familiar with the pathogenesis of common ENT infections and the latest treatment guidelines for some of these entities. This article reviews common ENT infections, diagnostic criteria, and treatment options.— The Editor
Otitis Media
Demographics. After infections of the upper respiratory tract, otitis media is the most commonly diagnosed illness in children in the United States, with a peak incidence during the first two years of life.5,6 Nearly 30 million office and urgent care visits are for otitis media, and there is evidence to suggest that the prevalence of otitis media is increasing in the United States.6,7 Risk factors for the development of acute otitis media (AOM) include male gender; age younger than 6 months; younger maternal age; lower socioeconomic status; the number of household smokers; the number of children to whom a child is exposed, either in the home or in day care; and duration of breastfeeding.8 A child who develops otitis media before reaching 6 months of age has an increased risk of developing subsequent episodes of otitis media within the following 24 months.5
Diagnosis. It is important to make an accurate diagnosis of AOM because AOM will respond to antibiotics, while otitis media with effusion (OME) typically will not.4,5 Symptoms of AOM may include fever and irritability, although more serious infections must be excluded. Verbal children will complain of ear pain or hearing loss. Clinical signs of AOM include a bulging tympanic membrane that is erythematous, opaque with a pale yellow or gray ear effusion, and a displaced light reflex. Children who have OME usually will not have systemic symptoms or signs of infection. They may not complain of much pain, but may complain of hearing loss. A middle ear effusion will be present, but there will not be inflammatory changes of the tympanic membrane, and the tympanic membrane may be in a neutral or retracted position.5
Children with AOM also will have a middle ear effusion. The first step in determining whether there is an effusion is by directly visualizing the tympanic membrane, removing any cerumen with a currette or irrigation, and using pneumatic otoscopy, ensuring that there is a good seal. Tympanometry and acoustic reflectometry are other diagnostic aids tools that may provide objective evidence of a middle ear effusion, but are generally not available in the ED.4,5 Finally, the gold standard by which to diagnose otitis media is tympanocentesis. It can be utilized to culture middle ear fluid and identify the causative pathogen, and especially is useful in cases of AOM that have not responded to antibiotic therapy. Nasopharyngeal cultures are not a substitute for cultures obtained by tympanocentesis, as they do not correlate with the pathogens responsible for middle ear effusions.9 Approximately 70% of children who have been treated for AOM will have a middle ear effusion present two weeks after therapy, and 10% will still have an effusion three months after therapy.4
Microbiology. Streptococcus pneumoniae, (50%) Haemophilus influenzae (30%), and Moraxella cattarrhalis (15%) account for 95% of bacterial cases of AOM, although the prevalence of the predominant pathogen varies geographically.5,10 Other pathogens include Group A beta-hemolytic streptococcus (GABHS), Staphylococcus aureus, and gram-negative bacilli in newborns, immunocompromised children, and those with suppurative complications of AOM, such as mastoiditis.5 Viruses have synergy with bacteria in the pathogenesis of AOM, and may account for up to 40% of cases of AOM.11 From 30% to 60% of isolates of S. pneumoniae are resistant to penicillin and standard-dose amoxicillin.10 Of the strains of penicillin-resistant S. pneumoniae (PRSP), 91% are resistant to trimethoprim-sulfamethoxazole, and 76% are resistant to macrolides.5 In addition, the production of beta-lactamase is high in isolates of H. influenzae (35-40%) and M. catarrhalis (100%).5
Treatment. Selection of appropriate antibiotic therapy for AOM may be challenging, as there has been increasing antibiotic resistance among the pathogens responsible for AOM. A recent report by the Drug-Resistant Streptococcus Pneumoniae Therapeutic Working Group (DRSPTWG) has suggested that there are several antibiotics that have consistent activity against all of these pathogens: amoxicillin (both standard and high-dose [80-90 mg/kg/day]); high-dose amoxicillin-clavulanate (80-90 mg/kg/day); cefuroxime; clindamycin; and intramuscular ceftriaxone.12 Based on surveillance studies, high-dose amoxicillin-clavulanate and ceftriaxone have the greatest activity against all three pathogens responsible for the majority of cases of AOM. While resistance to penicillin can be overcome by using higher doses of amoxicillin, this cannot be achieved by using higher doses of macrolides.5 When the pathogen has been identified by a culture obtained by tympanocentesis, then agents with a much narrower spectrum of activity can be used.
Accordingly, the DRSPTWG has proposed a treatment scheme for the management of AOM.12 For children who have a newly diagnosed episode of AOM, amoxicillin (either standard- or high-dose) may be prescribed, while children who have been previously treated with antibiotics may be prescribed high-dose amoxicillin, high-dose amoxicillin-clavulanate, or cefuroxime. For those who have a clinical failure on day 3 of treatment, previously untreated children can be treated with high-dose amoxicillin-clavulanate, cefuroxime, or a three-day course of once-daily intramuscular ceftriaxone, while those who have been treated previously should have tympanocentesis and then be prescribed a three-day course of intramuscular ceftriaxone or oral clindamycin. For those children who have a clinical failure 10-28 days after initial therapy, both those previously treated and those previously untreated can receive high-dose amoxicillin-clavulanate, cefuroxime, or a three-day course of intramuscular ceftriaxone. Tympanocentesis again would be recommended for children who previously received antibiotics at the outset. Other cephalosporins, such as cefprozil, have less beta-lactamase activity than cefuroxime and cefpodoxime. Cefaclor, lorcarabef, cefixime, and ceftibuten have inadequate activity against PRSP.5
Some practitioners may prefer the use of intramuscular ceftriaxone, using the rationale that the patient is treated before leaving the ED, and the family avoids taking antibiotics for 10 days. However, the injection is painful, and the patient and family do have to travel to a health care facility once a day for the injection. A single dose of intramuscular ceftriaxone probably is insufficient to treat AOM, as there are data to suggest that a three-day regimen is more efficacious than a single dose for patients with AOM who have failed a previous course of antibiotics.13 For those children who are sensitive or allergic to beta-lactam antibiotics, clindamycin would be a good choice to treat S. pneumoniae, but it does not have good activity against beta-lactamase-producing, gram-negative pathogens. Erythromycin-sulfamethoxazole, azithromycin, and clarithromycin would be acceptable alternatives to treat these pathogens, but not to treat penicillin-resistant S. pneumoniae.5
Duration of Treatment and Whom to Treat. Many authors have called for reduction in the use of antibiotics due to evidence that the increased use of antibiotics contributes to the prevalence of drug-resistant bacteria and subsequent infections.1,14,15 In 1997, antibiotic treatment of otitis media accounted for more than 90% of all antibiotic use during the first two years of life in a sample of 2253 children from Pittsburgh.8 Some authors have advocated withholding treatment for AOM, as it may spontaneously resolve, although it may be associated with an increased risk of suppurative complications, especially in children younger than 2 years of age.5,10,14,16 Such suppurative complications include mastoiditis, lateral sinus thrombosis, subdural or brain abscess, and meningoencephalitis.16 A course of antibiotics also may lead to the carriage of resistant organisms. Two groups found that children treated with a course of antibiotics were at higher risk for subsequent nasopharyngeal carriage of drug-resistant S. pneumoniae.17,18
There have been recent clinical studies to support antibiotic therapy for AOM. In each of these trials, antibiotic therapy was significantly associated with clinical resolution, and the duration of therapy did have an impact on success rates. In one study, 453 children 4-30 months of age with AOM were randomized to receive either five days or 10 days of cefpodoxime. The clinical success rate 12-14 days after the initiation of treatment was significantly lower in the five-day group, although at 4-6 weeks post-treatment, there were no differences between groups in the clinical success rate. Poor outcome was associated with day care attendance, a history of OME, and younger age.19 A similar study found that in a group of 385 children 4-30 months of age, a five-day course of amoxicillin-clavulanate led to more treatment failures at 14 days after therapy was initiated than a 10-day course.20
Some authors have recommended that children older than 2 years of age be treated with a five-day course of antibiotics or with a no-therapy, observation-only strategy.4,5 In opting for a short course of therapy for a child older than 2 years of age, the patient should meet the following criteria: the tympanic membrane should not be perforated; the patient should not have a history of recurrent or chronic otitis media; and the patient should not have a craniofacial anomaly or an immuncompromised condition.4 Other authors have not endorsed this idea, instead limiting short-course therapy for children older than 6 years of age in whom the episode of otitis media is mild, occurs during the summer, the response to antimicrobial therapy is prompt, and the child has had only a few previous episodes of otitis media.21-23
Prevention. Heptavalent pneumococcal polysaccharide-CRM 197 vaccine has been shown to reduce by 6% the number of episodes of AOM and to reduce by 9% the number or episodes of recurrent otitis media in two trials.24,25 Though this decrease was not statistically significant, the use of this vaccine has been estimated to prevent up to 1.2 million of the 20 million yearly episodes of AOM in the United States.25
Sinusitis
Definitions. Sinusitis refers to inflammation of the paranasal sinuses that may be viral, bacterial, or allergic in origin. Sinusitis further can be characterized based on the duration and severity of symptoms.
Acute sinusitis can be either nonsevere, lasting 10-14 days but not greater than 30 days, during which the patient has rhinorrhea of any quality, nasal congestion, cough, headache, facial pain, irritability, and low-grade or no fever. Severe sinusitis is characterized by a 3-4 day course in which the patient has mucopurulent rhinorrhea, high fever (> 39° C), facial pain, headache, and periorbital edema. Subacute sinusitis is characterized as persistent cough and rhinorrhea lasting 30-90 days.26,27
Viral and allergic causes can predispose to acute or subacute bacterial sinusitis, and the challenge to the ED practitioner is to make a distinction between these clinical entities. Young children may have up to eight viral upper respiratory tract infections (URTIs) a year normally. Sore throat, sneezing fever, malaise, and myalgias generally occur early in the course of a viral illness and tend to resolve by the sixth day. Cough, nasal discharge, and obstruction may be present in 25% of patients at 14 days.28 Mucopurulent rhinitis does not distinguish URTI from sinusitis, as the color and characteristics of nasal discharge do not predict the likelihood of recovery of a bacterial pathogen. Approximately 10% of URTIs may be complicated by acute bacterial sinusitis.26 Chronic inflammation of the paranasal sinuses may be due to allergy, environmental pollutants, cystic fibrosis, or gastro-esophageal reflux disease.26
Pathophysiology. The maxillary and ethmoid sinuses are present, although small, at birth. The frontal sinus moves to its position above the orbits by age 6. The sphenoid sinuses rarely are infected alone, and usually are involved as part of a pansinusitis.29
Sinus ostial obstruction may occur either from mucosal edema or mechanical obstruction. Mucosal edema can result from viral URTIs, allergic inflammation, cystic fibrosis, immune disorders, immotile cilia, or second-hand smoke. Mechanical ostial obstruction may be due to a deviated septum, choanal atresia, nasal polyps, or intranasal foreign bodies. When there is ostial obstruction, a transient increase in sinus pressure, followed by the development of negative sinus pressure, may facilitate the passage of bacteria from the nasopharynx into the sinus. In addition, sneezing, sniffing, and blowing the nose, associated with negative intrasinus pressure, also may introduce bacteria into the otherwise sterile sinuses.30
Diagnosis. The diagnosis of acute bacterial sinusitis may be made in children who present with URTI symptoms that are either persistent (cough and nasal discharge of any quality for 10-14 days without improvement) or severe (high fever and mucopurulent discharge for at least 3-4 consecutive days).26 Reproducible unilateral sinus pain on percussion or direct pressure may suggest maxillary or frontal sinusitis in older children. Periorbital swelling suggests ethmoid sinusitis. Transillumination of the maxillary and frontal sinuses is helpful at the extremes of interpretation; if transillumination is normal, then sinusitis is unlikely; if transmission is absent, then the sinus likely is filled with fluid. Decreased light transmission has been shown to be poorly correlated with disease.26,30
Diagnostic imaging is not necessary to confirm a diagnosis of acute bacterial sinusitis in children, as the presence of persistent or severe symptoms has a relatively high correlation with abnormalities on plain radiographs. Plain radiographs are helpful only for assessment of maxillary and frontal sinuses and may be considered an alternative if computed tomography (CT) scanning is not available.
In 1981 and 1986, Wald and colleagues studied children ages 2-16 who presented either with persistent or severe symptoms and who had sinus radiographs obtained. If the films showed complete opacification, mucosal thickening of at least 4 mm, or an air fluid level of the maxillary sinuses, aspiration was performed. Of these, bacteria in high density were found in 70-75% of patients.31,32 Plain films of the sinuses may be helpful in children who have vague symptoms, have not responded to antibiotic therapy, or who have antibiotic hypersensitivity that makes antibiotic therapy risky.31 In addition, a normal radiograph is powerful evidence that the patient does not have sinusitis.33 It also should be noted that the common cold often will yield radiographic signs of sinus inflammation, so such studies should be interpreted with caution in the absence of the symptoms and signs of acute bacterial sinusitis.26
CT scans of the paranasal sinuses should be interpreted with caution in children, as many asymptomatic children may have abnormalities. In 1999, Cotter and colleagues studied children undergoing CT scans for severe sinus disease and compared findings with those of children undergoing CT scans for other reasons, such as head trauma. Mucoperiosteal thickening was present in 60% of symptomatic and 46% of asymptomatic children. Early sinus disease, such as mucoperiosteal thickening of the ethmoid or maxillary sinuses, was found in 85% of symptomatic and 96% of asymptomatic children.34 In a similar study, 100% of children undergoing CT scans for reasons other than the diagnosis of sinusitis, who had URTIs in the preceding two weeks, had soft-tissue changes in their sinuses.35 Thus, there is a high prevalence of mucoperiosteal thickening in the paranasal sinuses of children, emphasizing that soft-tissue changes of the sinuses do not necessarily indicate bacterial infection. Therefore, CT scans of the sinuses should be obtained only in children in whom sinus surgery is considered after appropriate antibiotic therapy for sinusitis fails.27 The American College of Radiography has also recommended that the diagnosis of sinusitis be made on clinical grounds alone, as diagnostic imaging can be difficult to obtain in young children, and recommends the use of imaging studies only after the patient does not respond or worsens after antibiotic treatment. CT scans may overestimate the presence of sinus disease, and should be reserved for those patients in whom sinus surgery is being considered, or when there are complications of sinusitis, such as orbital or intracranial involvement.36
Sinus puncture and culture of the aspirate is the gold standard by which to diagnose bacterial sinusitis. Clinical scenarios in which to consider maxillary sinus puncture include: severe toxicity; acute illness that does not improve after appropriate antibiotic therapy; suppurative complications, such as intraorbital or intracranial abscess; and underlying immunodeficiency. At present, there is no consensus that middle meatal cultures obtained in a sterile fashion can substitute for maxillary sinus puncture.27
Treatment. The goal of treating acute bacterial sinusitis is to facilitate recovery from the illness, reduce the likelihood of suppurative complications, and prevent exacerbations of underlying disease, such as asthma or cystic fibrosis. However, a recent prospective study called into question whether or not treatment with antibiotics is necessary for sinusitis.37 They conducted a randomized, placebo-controlled study in three community practices in St. Louis. One hundred sixty-one patients age 1-18 years with sinusitis who were diagnosed by pediatric practitioners based on a clinical scoring system were included in the sample and randomized to either amoxicillin, amoxicillin/clavulanate, or placebo for 14 days. Patients were allowed to use other symptomatic treatments. Patients with severe symptoms, such as fever, facial pain, or swelling, were excluded from the study. Patients and their caregivers were interviewed at three, seven, 10, 14, 21, and 28 days for change in symptoms and satisfaction with treatment. No differences were found between the two groups with respect to resolution of sinus symptoms, the use of symptomatic treatments, or secondary outcomes. These researchers concluded that neither amoxicillin nor amoxicillin-clavulanate offered any clinical benefit compared with placebo for children with clinically diagnosed sinusitis. Critique of this article was offered by two authors, who noted that there were no stringent criteria for entry into the study, as children with more severe symptoms such as fever, facial swelling, and pain were excluded, and these patients might have benefitted the most from antibiotic therapy. They also commented that the diagnosis was not confirmed by either radiographs or sinus culture.38,39
The American Academy of Pediatrics recently developed clinical practice guidelines for the treatment of bacterial sinusitis in children 1-21 years of age.26 The consensus opinion was that antibiotics should be used to treat bacterial sinusitis to achieve a more rapid clinical cure. To promote the judicious use of antibiotics, it is important that children meet the criteria of persistent or severe upper respiratory tract symptoms before antibiotic therapy is started. Though nearly 60% of patients eventually will improve without antibiotics, at least 20% more will be cured or improved with the use of antibiotics.26,32
For patients with acute bacterial sinusitis with either persistent or severe symptoms, and for those with subacute disease, the most common responsible pathogens are S. pneumoniae, H. influenzae (non-typeable), and M. catarrhalis.40 In patients with symptoms lasting more than three weeks, anaerobes, such as anaerobic staphylococci and streptococci, and bacteroides species were recovered most often.41
Amoxicillin should be first-line therapy, given its low cost, narrow spectrum, and tolerability. In the absence of risk factors for PRSP, such as day care attendance, antimicrobial treatment within 90 days, or age younger than 2 years, 80% of children with acute bacterial sinusitis will respond to conventional doses of amoxicillin.26 For those who are at high risk for PRSP, then high-dose amoxicillin (90 mg/kg/day in two divided doses) also could be considered as first-line therapy. For patients allergic to amoxicillin, cefdinir, cefuroxime, or cefpodoxime can be prescribed. For patients with suspected cephalosporin allergy, then clarithromycin or azithromycin can be used. If PRSP is suspected and the patient is penicillin and cephalosporin allergic, then clindamycin can be used. A single dose of ceftriaxone can be used in patients who are vomiting and unable to tolerate oral antibiotics. The optimal duration of therapy has not been well studied, with recommendations of 10-28 days, or more conveniently, to continue antibiotic therapy until the patient improves, and then continue for an additional seven days.26 Though erythromycin-sulfisoxazole and trimethoprim-sulfamethoxazole have been used in the past to treat acute bacterial sinusitis, recent surveillance data suggest that bacterial resistance to both drugs is substantial, and thus they no longer are recommended to treat bacterial sinusitis.26,27
Patients who have complications, such as orbital cellullitis or potential central nervous system extension, should be treated with parenteral antibiotics, subspecialty consultation, and surgical drainage when appropriate.26 If PRSP is suspected, then cefotaxime with or without vancomycin should be used. If the patient does not improve, then sinus aspiration should be considered to obtain precise bacteriologic diagnosis.26 For patients who do not improve after two courses of antibiotic therapy, the practitioner either can refer the patient for ENT evaluation for maxillary sinus puncture to obtain culture and sensitivity of the responsible pathogen, or can treat with parenteral cefotaxime or ceftriaxone, and then refer the patient to an otolaryngologist if the patient does not improve.26,27
There are no clear recommendations for adjuvant therapies to treat sinusitis.30 One prospective study randomized children with acute bacterial sinusitis to receive a nasal decongestant-antihistamine or placebo and found no difference in clinical or radiographic resolution.42 Another study evaluated the efficacy of intranasal budesonide spray along with antibiotic therapy in children with acute sinusitis and found there was some modest alleviation of symptoms by the second week of therapy.43 There have been no clinical trials evaluating the effect of mucolytics or saline irrigation in children with acute bacterial sinusitis.
Complications. Orbital cellulitis is the most frequent serious complication of acute sinusitis and is a potentially life-threatening infection.16,30,44 The orbit is susceptible to contiguous infection from the ethmoid sinus, as it is separated from the ethmoid only by the thin lamina papyracea. The ophthalmic veins have no valves and have direct communication with the cavernous sinus and the intracranial venous system.44 One must make the distinction between preseptal or periorbital cellulitis and orbital cellulitis. In the early stages of orbital cellulitis, it may be difficult to distinguish from preseptal cellulitis, as there is inflammatory edema of the medial and lateral upper eyelids that may be tender or indurated. This will progress to inflammatory edema of the orbital contents, with proptosis, chemosis, and limited and painful extraocular muscle movements. There also may be some degree of vision loss. If a subperiosteal abscess develops, the eye will be proptotic and will be positioned down and laterally. If an orbital abscess develops, there will be complete ophthalmoplegia and moderate to severe vision loss. This is why it is imperative that children with preseptal cellulitis be followed closely to mointor for the early stages of orbital cellulitis. CT scans of the orbits can be helpful in cases where the clinical distinction between preseptal and orbital cellulitis is not clear. (See Figure 1.)
Fifty percent of all brain abscesses are due to acute bacterial sinusitis and most often involve the frontal lobe.45 Meningitis also can be due to frontal, ethmoidal, or sphenoid sinusitis. Infection may affect the brain by direct extension through necrotic areas in the posterior wall of the frontal sinus, and then may involve the dura, leading to an extradural abscess.44 The infection may extend through the dural vessels, resulting in a subdural abscess that may extend to the subarachnoid space, as well. Another means is by spread of infection within the sinuses through its valveless venous network, leading to a diffuse cortical thrombophlebitis. Finally, brain abscesses may develop from a necrotic, thrombosed region of a cerebral blood vessel, which would provide a good environment for the growth of micro-aerophilic or anaerobic organisms.44 Treatment of intraorbital and intracranial complications of sinusitis includes antibiotics, drainage, and aggressive intensive care.
Pharyngitis
GABHS is the most common bacterial cause of pharyngitis, responsible for up to 15% of all cases of pharyngitis.46 Other rare bacterial causes include Mycoplasma pneumoniae, Neisseria gonorrhoeae, Chlamydia pneumoniae, and Arcanobacterium haemolyticum.47 While viruses make up the majority of pathogens responsible for pharyngitis, GABHS, due to its propensity for suppurative and non-suppurative sequelae, will be the focus of this section.
Diagnosis. The gold standard for diagnosis of GABHS pharyngitis is a culture obtained by a pharyngeal swab. Clinical differentiation between viral and GABHS often is not possible.48 Several investigators have attempted to devise a scoring system by which to prospectively identify those patients most likely to be infected with GABHS.49-51 These scoring systems rely on the presence of specific clinical criteria, such as the patient’s age; presence of pharyngeal edema, erythema, or exudates; fever; and absence of URTI (i.e., rhinorrhea, cough, or conjunctivitis). Such scoring systems have been shown to have sensitivities ranging from 17-24% to 51-75%. Some authors have surmised that the streptococcal scoring system could be used to direct which children should have a rapid antigen test and culture done. Those with scores of 5 or 6 are most likely to have a positive antigen test, and if the antigen test is positive, then a throat culture need not be done. Those children with lower scores can have only a throat culture done, and treatment should be based on the results of the throat culture.50 It has been estimated that such a system would reduce the use of antibiotics by 52.3% and reduce the use of throat cultures by 35.8%.51
Rapid antigen kits also have been evaluated to determine if they could aid in the more rapid identification of patients with GABHS pharyngitis. Two groups prospectively evaluated the sensitivity of an optical immunoassay (OIA) for the rapid detection of GABHS. (Strep A optical immunoassay-OIA by Biostar Inc., Boulder, CO).52,53 One group evaluated 2113 adults and children with acute pharyngitis at several different office practices in Connecticut and Chicago. Each had an OIA kit and culture done. The authors reported that the OIA’s sensitivity and specificity were 84% and 99%, respectively. These authors proposed that with clinical personnel who were properly trained in interpreting the OIA kit, a negative result from the OIA may not need to be confirmed with a culture.52 Another group prospectively studied 233 children ages 1-18 years who presented with a sore throat at an urban children’s hospital. All patients had a rapid antigen kit and throat culture done. The authors reported a sensitivity and specificity of 79.5% and 96.9%, respectively, and the positive and negative predictive values were 92.1% and 91.2%, respectively. There were five false positive interpretations that, when later independently reviewed by a representative of Biostar, were interpreted as negative. These five false positives were left in the final statistical analysis, as these conditions may reflect those in the urgent care setting. These investigators also stated the sensitivity and specificity of this kit was not high enough to justify omitting a throat culture.53
Treatment. There is some controversy over the effectiveness of penicillin in treating GABHS pharyngitis. The American Academy of Pediatrics and the American Heart Association recommend penicillin as first-line therapy in patients with GABHS pharyngitis who are not allergic to penicillin.48,54 However, there have been several studies that have demonstrated improved efficacy of cephalosporins, such as cefadroxil, cefixime, ceftibuten, cefpodoxime. and cefprozil, as well as azithromycin, in treating GABHS pharyngitis.55-60 Recently, some authors have reported failure rates of penicillin to eradicate GABHS from the pharynx to be as high as 30%.47,61 There have been several hypotheses to explain this failure rate. One is copathogenicity, in which bacteria susceptible to one class of antibiotics are protected from those antibiotics by strains of bacteria that are resistant to that class of antibiotics.62 A second postulated factor may be the eradication of normal nonpathogenic bacteria, which produce bacteriocin that may prevent the pharynx from being colonized by GABHS.62,63 However, these two hypotheses have been refuted by one group, which demonstrated that the success rates of either cefadroxil or penicillin were not dependent on the presence of beta-lactamase or bacteriocin produced by normal non-pathogenic pharyngeal flora.64 A third hypothesized factor is penicillin resistance, which rarely has been observed, although resistance to erythromycin recently has been reported.65,66 Finally, patient non-compliance with 3-4 times-per-day dosing of penicillin could be a factor in the failure rate.67
One critique of studies demonstrating the superiority of antibiotics other than penicillin is the possible inclusion of patients who are streptococcal carriers with an intercurrent viral pharyngitis, which may have skewed these results to favor cephalosporins, as cephalosporins are more effective in eradicating GABHS from the pharynx in those with chronic streptococcal carriage.68 One group found that when patients were classified as more likely to have acute infection with GABHS, the efficacy of penicillin and cefadroxil was similar.68 Streptococcal carriers need not be treated if they are asymptomatic, unless the following is present: an outbreak of acute rheumatic fever or post-streptococcal acute glomerulonephritis; an outbreak of GABHS pharyngitis in a closed community; a family history of acute rheumatic fever; multiple episodes occurring in a family despite appropriate treatment; excessive family anxiety about GABHS infections; when tonsillectomy is considered; or when a case of GABHS toxic shock syndrome or necrotizing fasciitis occurs within a family.48
What is clear is that there are many treatment options for acute GABHS pharyngitis, from once-daily amoxicillin, to twice-daily penicillin, to the oral cephalosporins and macrolides for the penicillin-allergic patient.55-60,69,70 In this era of increasing prevalence of antibiotic resistance, it is probably most prudent to use the most narrow spectrum agent when possible. If there is concern about penicillin allergy, compliance with taking the medication properly, or adequate follow-up when the patient fails to improve, then cephalosporins or macrolides may be the better choice.70
Adjunctive Therapy. Studies evaluating the use of glucocorticoids in alleviating symptoms in patients with pharyngitis have been done in adult populations. No similar study has yet been done in children.
One group evaluated 58 patients ages 12-58 years with exudative pharyngitis. Half the patients received intramuscular dexamethasone (10 mg/dose) or intramuscular placebo. All patients were empirically treated with antibiotics.The onset and duration of pain relief was significantly better in the dexamethasone treated group.71 In a similar study by one group, patients treated with betamethasone had improvement in pain scores when compared with placebo.72 Finally, another group found, again with a similar study design, that oral and intramuscular betamethasone were equivalent in the relief of pain from acute exudative pharyngitis.73
Complications of Pharyngitis. Pharyngitis, whether due to viral or bacterial causes, may be complicated by contiguous abscesses.74-76 Retropharyngeal abscess is most often a complication of pharyngitis due to GABHS.76 It is most often seen in preschool age children, as the prevertebral fascia contains lymph nodes that are present until 4 years of age.77 These nodes drain the nasopharynx and can become superinfected and suppurate, leading to abscess formation. These nodes also can become infected by penetrating wounds to the retropharyngeal space, or extension of infection from cervical vertebral osteomyelitis.
On physical examination, a bulge in the posterior pharynx may be evident. If the infection extends to the nasopharynx, a bulge of the soft palate may be noted.76 Frequently, these children may be difficult to examine, and often these findings may not be present or may be difficult to appreciate. Lateral radiographs of the neck in extension will demonstrate a bulging of the retropharyngeal space, the width of which will be greater than the width of one vertebral body. If an abscess is present, an air fluid level may be noted. CT scans also may demonstrate the abscess, but sometimes are more difficult to obtain than plain radiographs, as sedation may be required and the patient may need to remain motionless for a longer period of time.
If the abscess has not reached a fluctuant stage, then parenteral antibiotics that cover GABHS, S. aureus, and anaerobes, such as a semisynthetic penicillin or first-generation cephalosporin should be administered to avoid progression to fluctuance. If the abscess is in a fluctuant stage, or if the patient has considerable compromise of the airway, a definitive airway should be obtained and an incision and drainage should be performed under general anesthesia by the appropriate subspecialist.74,76
Peritonsillar Abscess. Peritonsillar abscess is another complication of bacterial pharyngitis, and most often is due to GABHS or oral anaerobes. It is seen most commonly in preadolescent and adolescent patients. The abscess typically forms in the space between the superior pole of the tonsil and the superior constrictor muscle.76 Patients typically will have an antecedent pharyngitis, and then develop severe pain with swallowing. There may be spasm of the ipsilateral neck muscles, resulting in torticollis. The voice may become thick and muffled. On physical examination, there will be tonsillar asymmetry, with the affected tonsil crossing the midline and displacing the uvula. The involved tonsil will be erythematous, edematous, and occasionally may have exudates. The gold standard for diagnosis is needle aspiration, but occasionally, if the abscess is in the prefluctuant stage, CT scanning may be helpful to distinguish this stage from an abscess.75 The treatment of a peritonsillar abscess is the adminstration of appropriate antibiotics and removal of the abscessed material, when appropriate. If the patient can swallow without great difficulty and has no airway compromise, oral antibiotics can be prescribed, with the provision that the patient comply with close follow-up. If neither is present, the patient should be hospitalized for administration of parenteral antibiotics. Similar to that for a retropharyngeal abscess, antibiotic coverage should include coverage of GABHS and oral anaerobes, and thus, a semi-synthetic penicillin or first-generation cephalosporin should be administered. For penicillin-allergic patients, clindamycin would be appropriate.75
Nonsuppurative Complications of Group A Beta-hemolytic Strep Infection. Acute rheumatic fever (ARF) follows non-cutaneous infection with GABHS and is characterized by inflammatory lesions in the heart, skin, central nervous system, and joints. Children ages 5-15 years most often are affected. Major criteria for the diagnosis of ARF include carditis such as valvular heart disease (mitral and aortic valves primarily); arthritis; chorea; and skin lesions such as subcutaneous nodules and erythema marginatum. Minor criteria include such physical examination findings as fever, arthralgia, first-degree heart block, and the elevated presence of acute phase reactants, such as the erythrocyte sedimentation rate. ARF usually is a self-limited disease, although recurrences can occur, and permanent heart disease, such as mitral or aortic insufficiency, may result. Even though pharyngitis with GABHS is a self-limited illness, antibiotic therapy is recommended to prevent the occurrence of ARF and should be started within one week of the development of pharyngitis. If the initial episode of ARF does not include carditis, the likelihood of full recovery is good. Risk of recurrence of ARF is greatest in the first several years after the initial episode. Prevention of ARF is dependent on eradication of GABHS from the pharynx.48,74
Acute glomerulonephritis (AGN) is an inflammatory disorder affecting the renal glomeruli that follows both cutaneous and non-cutaneous infection with nephritogenic strains of GABHS. Approximately 10-15% of patients infected with these strains will develop AGN.74 AGN develops due to deposition of antigen-antibody complexes within the renal glomeruli and can occur approximately 10 days after the initial infection with GABHS. Patients commonly will develop edema, hypertension, and most often, macroscopic hematuria. The long-term prognosis is good, with a low rate of recurrence.74
Croup
Definitions. The croup syndrome refers to a constellation of symptoms and signs that includes hoarseness, brassy cough, difficulty breathing, and varying degrees of inspiratory stridor of sudden onset. The most common cause of the croup syndrome is viral laryngotracheitis. Viral laryngotracheitis most often is due to parainfluenza types 1, 2, and 3, but also can be due to respiratory syncytial virus, adenovirus, and influenza virus.78,79 Typically, infection starts in the nasopharynx, and children most often will have antecedent cough and coryza. The virus then invades the tracheal walls and vocal cords, leading to inflammatory edema and impaired movement of the vocal cords. Laryngotracheitis typically occurs in children up to 6 years of age, with the peak incidence during the second year of life.79 Laryngotracheitis typically is a benign, self-limited illness, and most children do not require hospitalization, nor do they progress to upper airway obstruction. Spasmodic croup is very similar to laryngotracheitis, except that its etiology is unclear.78 Children will awaken in the middle of the night with hoarseness, cough, and difficulty breathing, but will not have an antecedent URTI.
Other, much less common causes of the croup syndrome include epiglottitis and tracheitis, which have a bacterial origin. Epiglottitis is a rare entity since the adminstration of H. influenzae type B vaccine, and S. pneumoniae and GABHS now have been reported as etiologic agents.79,80 Epiglottitis is a cellulitis of the supraglottic tissues, and typically affects children 2-4 years of age. It can have a rapid onset, like laryngotracheitis, but typically children appear quite toxic within several hours of the onset of symptoms. Children often will drool and prefer to sit forward in the sniffing position. Tracheitis is a bacterial infection that results in ulceration and necrosis of the tracheal mucosa. It most often is due to S. aureus, and can be a complication of laryngotracheitis.78 Again, tracheitis may have a rapid onset, and children can become toxic and require intensive airway management within hours of the onset of symptoms. It is important to distinguish laryngotracheitis from epiglottis and tracheitis, as the two conditions can rapidly progress to upper airway obstruction.
Diagnosis. Viral laryngotracheitis most often is diagnosed based on clinical symptoms and signs. In children who appear toxic and have signs of significant upper airway obstruction, direct laryngoscopy and endoscopy may be needed to distinguish it from epiglottitis and tracheitis. This should only be done in a controlled setting, where definitive airway management, such as orotracheal intubation and possibly cricothyroidotomy, can be rapidly done.
Radiographs occasionally may be helpful in making the diagnosis of laryngotracheitis and excluding other causes of the croup syndrome, but should be done only in children who are stable and do not have signs of imminent airway obstruction. They are helpful in cases when foreign body aspiration is suspected. In children with laryngotracheitis, the lateral view of the neck will demonstrate widening of the hypopharynx and haziness of the subglottic trachea. The anteroposterior view may demonstrate narrowing of the laryngeal air column for 5-10 mm below the vocal cords, which is known as the steeple sign.78 However, the reliability of this sign to diagnose laryngotracheitis is questionable, as it may be present in children who do not have croup and may be present in children who have epiglottitis.81 Thus, the diagnosis of laryngotracheitis, epiglottitis, and tracheitis best can be made on clinical grounds.
Treatment. Typically, laryngotracheitis is a self-limited illness, and many patients do not seek emergent medical care. There are, however, several treatment modalities for this illness. Cool mist long has been a mainstay of therapy, though its efficacy is unclear. Mist therapy has been utilized since the 19th century for the treatment of croup, as it was noted that steam from teapots and hot baths alleviated the symptoms of croup.78 Cool mist then replaced warm, as it reduced the risk of airway burns and because cool night air ameliorated children’s symptoms. A 1994 study demonstrated a statistically significant improvement in croup symptoms with the administration of cool mist, though there was no comparison to a placebo control group.82 Subsequent studies of saline nebulization with nebulized glucocorticoids did not demonstrate any improvement in symptoms.83,84 It is possible that children spontaneously improve with time, as the course of this illness typically is benign. It should be noted that cool mist may intensify bronchospasm in children who present with both stridor and wheezing.85
The efficacy of racemic epinephrine in treating laryngotracheitis has been well documented since the 1970s. In one series, 30% of outpatients treated with racemic epinephrine were discharged.86 The beneficial use of racemic epinephrine in the ED has since been well documented.87-89 One group demonstrated that l-isomer form of epinephrine was similar to the racemic form in terms of efficacy and adverse effects.87 Two others demonstrated that children treated with one racemic epinephrine nebulization treatment and oral steroids safely could be discharged from the ED within 3-4 hours, provided that symptoms did not recur and close follow-up could be guaranteed.88,89
Various forms of glucocorticoids have also demonstrated efficacy in treating both inpatients and outpatients with laryngotracheitis. Nebulized budesonide has been shown to lead to significant clinical improvement in both mild and moderate-severe laryngotracheitis.83,84,90 Where budesonide is not available, nebulized dexamethasone has not been shown to lead to clinical improvement when compared to nebulized saline in children with moderate croup.91,92 Oral dexamethasone may be the most cost-efficient means by which to deliver glucocorticoids in children with croup. One group compared oral dexamethasone (0.6 mg/ kg/dose), nebulized budesonide (2 mg/dose), and both treatments in children presenting to the ED with mild to moderate croup. Since all three groups had similar, improved clinical outcomes, these investigators concluded that a single oral dose of dexamethasone should be the preferred method of administering glucocorticoids, given its easy administration, lower cost, and widespread availability.93 Oral and intramuscular dexamethasone also have been shown to be equal in their efficacy.94
Finally, helium-oxygen (Heliox) therapy has been shown to be as efficacious as nebulized racemic epinephrine in treating children with moderate-to-severe croup. One group studied children age 6 months to 3 years with moderate to severe croup who were randomized to receive either Heliox therapy or nebulized epinephrine after having received intramuscular dexamethasone. The two treatment groups were similar at the end of the treatment period in the amount of clinical improvement.95 Heliox therapy is limited in its duration of action when compared to racemic epinephrine, and probably is used best in the inpatient setting.
Summary
Children commonly present to the ED with ENT-related illnesses. There are practice guidelines for otitis media and sinusitis that are helpful to prevent the injudicious use of antibiotics. Clinical scoring systems and rapid antigen testing may be helpful in identifying patients most likely to have pharyngitis from GABHS. Finally, glucocorticoids are a mainstay of treatment for children with viral laryngotracheitis.
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