Confidently evaluate evidence-based information to make timely and accurate diagnoses and treatment decisions! The second volume features 58 topics with key points and detailed therapies in infectious diseases and dermatologic disorders. Obtain core knowledge needed for medical decision making and evidence-based information to provide insight into diagnostic tests and treatment modalities.Topics include:
- Infectious Diseases
- Bacterial Infections
- Fungal Infections
- Common Infectious Conditions
- Viral Infections
- Parasitic Infections
- Plus much more...
|Publisher:||American Academy of Pediatrics|
|Product dimensions:||6.00(w) x 8.90(h) x 1.20(d)|
About the Author
Leonard G. Feld, MD, PhD, MMM, FAAP is the Professor and Sara H. Bissell & Howard C. Bissell Endowed Chair in Pediatrics, Senior Medical Director and Senior Academic Chair of the Pediatric Specialties Care Division of Carolinas HealthCare System's Medical Group, and Chief Medical Officer at the Levine Children's Hospital at Carolinas HealthCare System in Charlotte, North Carolina, and Clinical Professor of Pediatrics at UNC School of Medicine.John D. Mahan, MD, FAAP is Professor of Pediatrics at the Ohio State University College of Medicine where he is also Assistant Dean for Faculty Development, Vice Chairman for Education in the Department of Pediatrics, Program Director for the Pediatric Residency Program and Program Director for the Pediatric Nephrology Fellowship Program at Nationwide Children's Hospital.
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Succinct Pediatrics Book 2
Evaluation and Management for Infectious Diseases and Dermatologic Disorders
By Leonard G. Feld, John D. Mahan
American Academy of PediatricsCopyright © 2017 American Academy of Pediatrics
All rights reserved.
Acute Otitis Media and Acute Bacterial Rhinosinusitis
Christopher Harrison, MD
* The diagnosis of acute otitis media is objective and relies specifically on physical findings. The diagnosis of acute bacterial rhinosinusitis (ABRS) is more subjective and relies heavily on history or evolution of symptoms.
* Acute otitis media cannot be diagnosed unless there is either a bulging tympanic membrane or otorrhea from a perforated tympanic membrane.
* Sinus opacity on a computed tomographic scan or magnetic resonance image is not sufficient in and of itself to diagnose ABRS because the finding is frequently detected with uncomplicated viral upper respiratory tract infections or in asymptomatic children.
* Radiologic imaging is not warranted or recommended for routine diagnosis or treatment of uncomplicated ABRS, but is useful in defining potential ABRS complications or underlying anatomic abnormalities that cause recurrent ABRS.
* All oral cephalosporins are less active against pneumococcus than high-dose amoxicillin and exhibit less than 50% activity against penicillin-resistant pneumococci.
* Cefdinir is not as active against either pneumococcus or non-typeable Haemophilus influenzae as cefuroxime axetil or cefpodoxime proxetil.
Guidelines from the American Academy of Pediatrics (AAP) for management of otitis media and acute bacterial rhinosinusitis (ABRS) in children focus on specific diagnostic criteria that are relatively easy for clinicians to use. Watchful waiting has become not only acceptable but recommended for certain acute otitis media (AOM) presentations.
Causes and Differential Diagnosis
The 2 most common pathogens in AOM are pneumococcus and non-typeable Haemophilus influenzae. Moraxella catarrhalis and group A Streptococcus are also pathogens, but less frequently (Table 1-1). More than one pathogen can be detected in approximately 8% of AOM episodes. Rarely, Staphylococcus aureus may be isolated from middle ear fluid, usually when other head and neck infectious foci are evident or pressure-equalizing (PE) tubes are in place. Candida species have also been implicated in otorrhea with PE tubes in place, particularly after multiple courses of antibacterial drugs.
The major condition from which AOM must be distinguished is otitis media with effusion (OME). This is important because antibiotics are not indicated for OME, while antibiotics should be considered for AOM. Overdiagnosis of AOM when the condition is really OME is a common scenario for antibiotic overuse.
Otitis media with effusion is differentiated from AOM mostly by AOM having a bulging tympanic membrane (TM) while OME does not. The TM in OME is usually retracted but may sometimes be in a neutral position. Most OME occurs when pressure in the middle ear is lower than atmospheric yet middle ear fluid is also present. This occurs predominantly from 2 mechanisms, both due to eustachian tube dysfunction. The first is caused by the eustachian tube failing to equalize pressure while the normal physiologic daily process of approximately 1 cm of air in the middle ear is being absorbed by the mastoid bone. Mostly this is itself because of post-viral, smoke-induced, or allergic inflammation in the posterior nasopharynx and eustachian tube. The second mechanism is a residual from a prior AOM episode despite there no longer being viable bacteria. In this scenario, residual inflammation and retained bacterial antigens impede absorption or clearance of the residual effusion from the AOM. This inflammation, however, is not sufficient to increase middle ear pressure as is seen with AOM.
Less common conditions in the differential diagnosis of AOM are hemotympanum, traumatic hemorrhage into TM, or cerumen impaction. Hemotympanum is usually associated with basilar skull fracture and can produce bulging of the TM as well as opacity and color changes. Color change of the TM is often blue-purple or deep red (blood). Pneumatic otoscopy will reveal limited motion of the TM because of blood filling the middle ear cavity. Traumatic hemorrhage into the TM itself can occur with direct trauma (eg, insertion of cotton-tipped applicator too deep into external ear canal or post-barotrauma or an explosion causing pressure that overstretches the TM without rupturing it). The TM is rarely bulging with traumatic hemorrhage, but there can be an intense erythema. Pneumatic otoscopy will usually reveal near-normal movement, or possibly excessive movement if the middle ear ossicles have been disrupted. Cerumen impaction seems unlikely to be confused with AOM, but if the visible surface of the impaction is deep in the canal and has been molded to have a concave surface by cleaning attempts with cotton-tipped applicators, such a misdiagnosis has occurred.
Acute otitis media can be more common in patients with altered immune states (ie, less defenses) or anatomic conditions that impair eustachian tube function.
Immune-altered states associated with AOM are wide ranging. The simplest and most common is a temporary condition (ie, the immature immune capabilities of children <2 years). Immune systems of young children fail to recognize and respond to polysaccharide antigens in the capsules of pneumococci. Repeated AOM episodes can therefore occur from the same serotype because protective antibody is not produced. Recent use of pneumococcal conjugate vaccines (PCVs) has helped overcome this problem. Any congenital or acquired immunodeficiency that has a B-cell deficiency, with or without a T-cell deficiency, also makes a host more susceptible to AOM. Examples of this are X-linked agammaglobulinemia (also called Bruton agammaglobulinemia), common variable immunodeficiency, severe combined immunodeficiency, or uncontrolled HIV infection.
Anatomic predispositions to AOM include anomalies such as cleft palate, malformed or floppy eustachian tubes (eg, any young child or any with Down syndrome), or congenital absence of cilia. Mucosal-disrupting conditions also increase risk of AOM. Examples of this are viral upper respiratory tract infections (URTIs). Acute otitis media is more frequent in children attending day care or living in a household with more than 3 children, or after passive smoke exposure.
Acute otitis media is an acute purulent inflammatory condition of the middle ear cavity. It has an expanding volume of purulent material that bulges an intact TM, or causes otorrhea if increased middle ear pressure perforates the TM. The presence of shiny mucous in otorrhea or in external ear canal secretions indicates a connection between the canal and middle ear via a TM perforation and differentiates otorrhea caused by a perforated TM from that caused purely by acute otitis externa. Pain from pressure on the tragus most often indicates otitis externa.
Other clinically associated symptoms/signs may include recent onset of otalgia or intense erythema/opacity of the TM. Fever, irritability, sleep disturbance, and reduced appetite and activity may also occur.
Acute otitis media usually occurs coincident with or following a viral URTI. Acute otitis media is most often exclusively caused by bacterial pathogens. Less often it is caused by both viral and bacterial pathogens in the middle ear effusion (MEE). Least often it is exclusively caused by viral pathogens in MEE. Acute otitis media should be classified as severe or non-severe to aid in treatment decisions (Box 1-1).
The criteria most recently accepted as diagnostic for AOM include a bulging TM with some increased opacity or intense erythema plus recent onset of symptoms, either otalgia or fever equal to or higher than 39°C (102.2°F).
Clinical symptoms associated with AOM may be relatively minor or even absent particularly early in the course of AOM. Because viral URTIs often precede or accompany AOM, their signs may be difficult to differentiate from those of AOM. These include fever, irritability, decreased activity, or decreased appetite. Viral-induced symptoms also often make it difficult to determine whether the AOM is improving early in the course of management.
Otalgia is a reasonably specific symptom of AOM that is caused by traction on the annulus of the TM by increased middle ear pressure. However, "ear pain" can also be caused by intense paratonsillar inflammation due to pharyngotonsillitis or recent tonsillectomy. Likewise, otitis externa (also called swimmer's ear) can produce similar pain; but, in otitis externa the pain is intensified by compression of the tragus (the tragus sign, which is not seen in uncomplicated AOM). Ear tugging is considered by some to be a possible surrogate for otalgia. However, ear tugging may simply be a sign of overall infant irritability and thus is not highly specific.
Physical examination is paramount in diagnosing AOM. Bulging of the TM and presence of an inflammatory effusion are the essential findings. Without both bulging and an inflammatory effusion, the diagnosis is not AOM, regardless of the color of the TM. The clinician must have sufficient visualization of the TM to make a confident decision on the diagnosis. Therefore, cleaning cerumen or foreign material from the external ear canal is the first step toward a correct diagnosis.
Given that the major criterion, and sine qua non, of AOM on examination is bulging of the TM, assessing for its presence should be the primary goal during otoscopy. The portion of the TM that first shows bulging is the pars flaccida in the upper pole of the TM. This portion is composed of only 2 opposing membranes. Therefore, it is less rigid than the pars tensa, which has the same 2 membranes but also an intervening relatively stiff middle fibrous layer, sandwiched between the membranes.
Initially the pars flaccida will bulge and partially obscure the usually visible ossicle (the long process of the malleolus) (Figure 1-1). As the pressure and volume of the purulent material in the middle ear increase, the pars tensa eventually bulges as well. At some point, the ossicle is completely obscured, resulting in no visible landmarks. Often the TM is then reminiscent of a donut or bagel (Figure 1-2).
Presence of an effusion is also considered essential. Effusions may be detected by reduced movement on insufflation of the external ear canal with a pneumatic otoscope. Opacity of the TM or a visible meniscus also adds credence to the presence of an MEE.
Tympanometry has been used to confirm the presence of an effusion but cannot distinguish the MEE of AOM from that of OME. Tympanometry involves applying constant low levels of sound to a sealed external ear canal and measuring reflected versus absorbed sound while varying the pressure in the canal from negative (< 1 atm) to positive (> 1 atm). This results in a linear readout for which the shape indicates whether an effusion is present.
A normal middle ear produces a tympanogram readout designated as an A curve, in which a peak occurs at zero pressure (the point at which most of the sound is absorbed). When sound is reflected and not absorbed (meaning the TM is less flexible than usual and is under positive or negative pressure), the linear readout runs closer to the baseline. The more sound that is reflected, the closer to baseline the curve drops. Three tympanogram results are consistent with an effusion.
The tympanogram of AOM is a relatively flat B curve (no true peak) close to the baseline. The flat curve indicates that nearly all the sound is being reflected back from the TM at all pressures, because the volume of MEE dampens any TM movement that would transmit sound through the ossicles (ie, prevents proper vibration of the TM).
At times, early AOM may have a C2 curve when the amount of effusion has yet to completely dampen TM mobility. The peak occurs, but it is generally of lower than normal amplitude and at a negative pressure. Less frequently, early AOM may have an App curve with a peak that is blunted because of decreased absorption of sound due to the evolving middle ear pus, but the peak is shifted to the positive pressure region. C2 curves are precursors to App curves that are in turn precursors to B curves as AOM evolves.
There is no role for radiologic evaluation in management of uncomplicated AOM. When potential mastoid, temporal bone, or intracranial extensions of AOM become a concern, computed tomographic scans or magnetic resonance images are warranted. Discussion with the radiologist is recommended to ensure that the modality is appropriate for the desired results.
Overall, neither topical nor systemic decongestants or antihistamines have been shown to be beneficial in increasing clinical cure for AOM.
The first step in management of AOM is to control pain as much as is safely feasible (Evidence Quality Grade B, Recommendation Strength: Strong per the AAP Guideline). Pain relief can take several forms with varying degrees of efficacy.
No data support homeopathic remedies, nor are there convincing data that application of heat, cold, or unmedicated oils provides benefit (Evidence Level II-1).
Topical agents containing anesthetics (eg, benzocaine, procaine, or lignocaine) seem to provide brief relief of pain in children older than 5 years. They may be of benefit for younger children, but data are inconclusive (Evidence Level I).
Orally administered acetaminophen, ibuprofen, naproxen, or codeine/ codeine analogs have been shown to be modestly effective (Evidence Level I). Nonnarcotic agents are recommended for routine use. Potential narcotic use must take into account added cost and risks inherent with narcotics.
Spontaneous perforation relieves much of the pain, but the ragged edges may heal poorly. If pressure relief is desired, controlled release via tympanocentesis or myringotomy is preferred (Evidence Level II-2). This is quite effective but requires special training to prevent procedural complications. Thus, tympanocentesis is not routine in most practices.
Antimicrobial Treatment Decisions
The choice of initial antibiotics versus observation is outlined in Table 1-2. Various antibiotic recommendation options are outlined in Box 1-2.
Observation is reasonable because many children spontaneously improve (up to 50%, particularly if non-typeable H influenzae or M catarrhalis is the pathogen) within 48 to 72 hours and do not require antibiotics. Among the usual oto-pathogens, only pneumococcus is invasive. Invasive disease is more likely in younger children with high fevers and if they have not been fully immunized with pneumococcal 13-valent conjugate vaccine (PCV13). This is one rationale for the universal recommendation to prescribe antibiotics with high fever (severe AOM) in young children.
Some experts recommend giving families a "rescue" prescription for antibiotics when initially choosing observation (Evidence Level I). Data indicate that less than half the families need to use the rescue prescription. Parents are instructed to call the clinician to report worsening or failure to improve within 72 hours. In this case the prescription can be filled without a return office/clinic visit. The return call can be important so that the clinician can feel assured that a serious invasive complication, one that might require parenteral antibiotics or even hospitalization, has not occurred.
Specific Antibiotic Choices
When a decision has been made to prescribe antibiotics, the choice of antibiotic depends on the clinical presentation or frequency of AOM episodes and recent antibiotic use.
First-line antibiotics can be used for intermittent AOM in patients with no antibiotic use in the past month (Table 1-3).
Amoxicillin at 90 mg/kg/day divided into 2 doses administered every
o Expectation: Better than 85% clinical resolution, with failures shared near evenly between highly penicillin-resistant pneumococci (minimal inhibitory concentration ≥ 2.0 mcg/mL) and β-lactamase-producing non-typeable H influenzae.
If the AOM patient is penicillin allergic but not exhibiting type I allergy, use a β-lactamase-stable cephalosporin, either cefdinir or cefuroxime axetil at 30 mg/kg/day divided in 2 doses administered every 12 hours or cefpodoxime proxetil at 10 mg/kg/day divided in 2 doses every 12 hours (Evidence Level I). Cefdinir tastes better but has less clinical efficacy than amoxicillin (against pneumococcus) or its two cephalosporin alternatives (against nontypeable H influenzae), even at the "high dose" recommended here. This 30 mg/kg daily dose of cefdinir is not in the package insert but is based on pharmacokinetic data and expected susceptibility of likely oto-pathogens. Cefixime is the best oral cephalosporin for non-typeable H influenzae but is active against only highly penicillin-susceptible pneumococci, so it is currently not recommended as monotherapy in the AAP guidelines.
Excerpted from Succinct Pediatrics Book 2 by Leonard G. Feld, John D. Mahan. Copyright © 2017 American Academy of Pediatrics. Excerpted by permission of American Academy of Pediatrics.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Table of Contents
Contents Preface Introduction Core Knowledge for Medical Decision-MakingJeffrey R. Avner, MD Part 1Infectious Diseases Section 1Common Infectious Conditions
- Acute Otitis Media and Acute Bacterial RhinosinusitisChristopher Harrison **
- Central Venous Catheter–Associated Bloodstream InfectionsGina Weddle, DNP, RN, CPNP-AC
- GastroenteritisJames Christopher Day, MD
- MeningitisRoss E. Newman, DO, and Keith J. Mann, MD, Med
- Osteomyelitis and Septic ArthritisAngela L. Myers, MD, MPH
- Pneumonia an EmpyemaKrow Ampofo, MB, ChB
- Skin and Soft-Tissue InfectionsJoan E. Giovanni, MD, and Jason G. Newland, MD, Med
- Anaerobic InfectionsJason G. Newland, MD, MEd, and Mary R. Tanner, **
- BrucellaKimberly C. Martin, DO, and José R. Romero, MD
- Cat-Scratch DiseaseKevin B. Spicer, MD, PhD, MPH, and Dwight A. Powell, MD
- CholeraJason Harris, **
- DiphtheriaClaudia Espinosa, MD, MSc, and Kristina Bryant, MD
- Group A Streptococcal InfectionsAngela L. Myers, MD, MPH
- Group B Streptococcal InfectionsPia S. Pannaraj, MD, MPH
- Helicobacter pylori InfectionsKari Neemann, MD; Catherine O’Keefe, DNP, APRN-NP; and Archana Chatterjee, MD, PhD
- Listeria monocytogenes InfectionsJodi Jackson, MD, and Julie Weiner, DO
- Lyme DiseaseEugene D. Shapiro, MD
- Meningococcal DiseaseJoshua Wolf, MBBS, BA, and B. Keith English, MD
- PertussisJennifer Vodzak, MD, and Sarah S. Long, MD
- Rat-Bite FeverLaura M. Plencner, MD, and Mary Anne Jackson, MD
- Staphylococcus aureus InfectionsJ. Chase McNeil, MD, and Sheldon L. Kaplan, MD
- TetanusRenuka Verma, MD, Krithiha Raghunathan, MD, and Katrina Tinio, MD
- Tick-Borne Rickettsial DiseasesVictoria A. Statler, MD, and Gary S. Marshall, MD
- Tuberculosis and Nontuberculous Mycobacterial InfectionsAndrea T. Cruz, MD, MPH, and Jeffrey R. Starke, MD
- TularemiaKari A. Simonsen, MD, and Jessica Snowden, MD
- CytomegalovirusAmina Ahmed, **
- EncephalitisJo-Ann S. Harris, MD, and Robert R. Wittler, MD
- Enteroviruses and ParechovirusesJosé R. Romero, MD
- Epstein-Barr VirusAmina Ahmed, **
- HIVDiana L. Yu, PharmD, BCPS; Marc Foca, MD; and Gordon E. Schutze, MD
- InfluenzaRoya Samuels, MD; Michelle Sewnarine, MD, and Henry Bernstein, DO, MHCM
- Measles, Mumps, RubellaMichael Klatte, MD, and Barbara Pahud, MD, MPH
- ParvovirusJames Christopher Day, MD
- RabiesSergio E. Recuenco, MD, MPH, DrPH
- Respiratory VirusesChristelle M. Ilboudo, MD, and Janet A. Englund, MD
- RotavirusPenelope H. Dennehy, MD
- Varicella-Zoster VirusAnne A. Gershon, MD
- AspergillosisAndreas H. Groll, MD; Charalampos Antachopoulos, MD; Emmanuel Roilides, MD; and Thomas J. Walsh, MD
- CandidiasisEmmanuel Roilides, MD; Charalampos Antachopoulos, MD; Andreas H. Groll, MD; and Thomas J. Walsh, MD
- Endemic MycosesMartin B. Kleiman, MD
- MucormycosisCharalampos Antachopoulos, MD; Emmanuel Roilides, MD; Andreas H. Groll, MD; and Thomas J. Walsh, MD
- Intestinal Helminthic InfectionsBenjamin R. Hanisch, MD, and Chandy C. John, MD, MS
- MalariaKeren Z. Landman, MD, and Paul M. Arguin, MD
- Pneumocystis jiroveci InfectionJyoti Vidwan, ***
- SchistosomiasisShirley Molitor-Kirsch, MD
- ToxoplasmosisJohn A. Vanchiere, MD, PhD, and Joseph A. Bocchini Jr, MD
- AcneSadaf Hussain, MD, and Albert C. Yan, MD
- AlopeciaKristi Canty, MD
- Atopic Dermatitis and Eczematous DisordersRobert Sidbury, MD, MPH
- Diaper DermatitisKristi Williams, MD
- Erythema NodosumCynthia Marie Carver DeKlotz, MD, and Sheila Fallon Friedlander, MD
- Pigmented LesionsKimberly A. Horii, MD
- PruritusJeana Bush, MD
- Psoriasis and Papulosquamous DisordersRobert Sidbury, MD, MPH, and Morgan Maier, PA-C
- RashesCharles F. Willson, MD
- ScabiesMichelle Steinhardt, MD, MS, and Rachel Dawkins, MD
- Stevens-Johnson Syndrome and Toxic Epidermal NecrolysisDean Morrell, MD; Shelley Cathcart, MD; and Craig Burkhart, MD
- Warts and MolluscumBrandon D. Newell, MD