Pediatric secrets fifth edition

Adamson, MDProfessor of Pediatrics and Pharmacology, Department of Pediatrics, University of Pennsylvania School of Medicine; Director, Clinical and Translational Research, The Children’

PEDIATRIC

Director, Division of Neonatology

Morgan Stanley Children’s Hospital of New York, New York Mark F Ditmar, MD

Director, AtlantiCare/duPont Pediatric Hospitalist Program AtlantiCare Regional Medical Center

Atlantic City, New Jersey

Clinical Associate Professor of Pediatrics

Jefferson Medical College

Philadelphia, Pennsylvania

PEDIATRIC SECRETS, FIFTH EDITION ISBN: 978-0-323-06561-0Copyright© 2011, 2005, 2001, 1997, 1989 by Mosby, Inc., an affiliate of Elsevier Inc.All rights reserved No part of this publication may be reproduced or transmitted in any form or byany means, electronic or mechanical, including photocopying, recording, or any information storageand retrieval system, without permission in writing from the publisher Permissions may be soughtdirectly from Elsevier’s Rights Department: phone: (þ1) 215 239 3804 (US) or (þ44) 1865 843830(UK); fax: (þ44) 1865 853333; e-mail:healthpermissions@elsevier.com You may also completeyour request on-line via the Elsevier website athttp://www.elsevier.com/permissions.

NOTICEKnowledge and best practice in this field are constantly changing As new research andexperience broaden our knowledge, changes in practice, treatment and drug therapy maybecome necessary or appropriate Readers are advised to check the most current informationprovided (i) on procedures featured or (ii) by the manufacturer of each product to be

administered, to verify the recommended dose or formula, the method and duration ofadministration, and contraindications It is the responsibility of the practitioner, relying on theirown experience and knowledge of the patient, to make diagnoses, to determine dosages and thebest treatment for each individual patient, and to take all appropriate safety precautions To thefullest extent of the law, neither the Publisher nor the Editors/Authors assumes any liability forany injury and/or damage to persons or property arising out of or related to any use of thematerial contained in this book

Library of Congress Cataloging-in-Publication Data

Pediatric secrets / [edited by] Richard A Polin, Mark F Ditmar – 5th ed

p ; cm – (Secrets series)

Includes bibliographical references and index

ISBN 978-0-323-06561-0

1 Pediatrics–Examinations, questions, etc 2 Pediatrics I Polin, Richard A (Richard Alan),

1945-II Ditmar, Mark F I1945-II Series: Secrets series

[DNLM: 1 Pediatrics–Examination Questions WS 18.2 P3716 2011]

RJ48.2.P65 2011

618.9200076–dc22

2010010434

Acquisitions Editor: James Merritt

Developmental Editor: Andrea Vosburgh

Project Manager: Janaki Srinivasan Kumar

Printed in Canada

Last digit is the print number: 9 8 7 6 5 4 3 2 1

Peter C Adamson, MD

Professor of Pediatrics and Pharmacology, Department of Pediatrics, University of

Pennsylvania School of Medicine; Director, Clinical and Translational Research, The Children’sHospital of Philadelphia, Philadelphia, Pennsylvania

Kwame Anyane-Yeboa, MD

Professor of Clinical Pediatrics, Department of Pediatrics, Columbia University College ofPhysicians and Surgeons; Attending Pediatrician, Division of Genetics, Department of

Pediatrics, Columbia University Medical Center, New York, New York

Richard Aplenc, MD, MSCE

Assistant Professor, Department of Pediatrics, University of Pennsylvania; Assistant Physician,Department of Pediatrics, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania

Joan Bregstein, MD

Assistant Clinical Professor of Pediatrics, Director, Community Outreach, Department ofPediatrics, Division of Pediatric Emergency Medicine, Morgan Stanley Children’s Hospital ofNew York-Presbyterian, New York, New York

Elizabeth Candell Chalom, MD

Assistant Professor, Department of Pediatrics, University of Medicine and Dentistry of NewJersey, Newark, New Jersey; Chief, Pediatric Rheumatology, Department of Pediatrics, SaintBamabas Medical Center, Livingston, New Jersey

Mark F Ditmar, MD

Director, AtlantiCare/duPont Pediatric Hospitalist Program, AtlantiCare Regional MedicalCenter, Atlantic City, New Jersey; Clinical Associate Professor of Pediatrics, Jefferson MedicalCollege, Philadelphia, Pennsylvania

Andrew H Eichenfield, MD

Chief, Division of Pediatric Rheumatology, Mount Sinai Medical Center, New York, New York;Assistant Clinical Professor of Pediatrics, College of Physicians and Surgeons, ColumbiaUniversity, New York

vii

Anders Fasth, MD, PhD

Professor, Department of Pediatrics, Institution of Clinical Sciences, University of Gothenburg;Department of Pediatric Immunology, The Queen Silvia Children’s Hospital; Director, TheSwedish National Cord Blood Bank, Sahlgrenska University Hospital, Gothenburg, Sweden

Mary Pat Gallagher, MD

Assistant Professor of Clinical Pediatrics, Department of Pediatrics, Columbia UniversityCollege of Physicians and Surgeons; Assistant Attending Physician, Department of Pediatrics,Morgan Stanley Children’s Hospital of New York-Presbyterian, New York, New York

Maria C Garzon, MD

Professor of Clinical Dermatology and Clinical Pediatrics, Columbia University College ofPhysicians and Surgeons; Director, Department of Pediatric Dermatology, Morgan StanleyChildren’s Hospital of New York-Presbyterian, New York, New York

Andrew B Grossman, MD

Clinical Assistant Professor of Pediatrics, Department of Pediatrics, University of PennsylvaniaSchool of Medicine; Attending Physician, Division of Gastroenterology, Hepatology, andNutrition, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania

Daniel Esten Hale, MD

Professor of Pediatrics, Department of Pediatrics, University of Texas Health Science Center atSan Antonio; Senior Physician, Pediatric Endocrinology and Diabetes, Christus Santa RosaChildren’s Hospital; Attending Physician, Children Center at the Texas Diabetes Institute,University Health System, San Antonio, Texas

Constance J Hayes, MD

Professor of Clinical Pediatrics, Emeritus, Division of Pediatric Cardiology, Department ofPediatrics, Columbia University College of Physicians and Surgeons; Attending Physician,Division of Pediatric Cardiology, Department of Pediatrics, Morgan Stanley Children’s Hospital

of New York-Presbyterian, New York, New York

Georg A Holla¨nder, MD

Professor of Molecular Medicine in Paediatrics, Department of Biomedicine, University ofBasel; Professor of Molecular Medicine in Paediatrics and Head, Department of Research,The University Children’s Hospital of Basel, Basel, Switzerland

Allan J Hordof, MD

Professor of Clinical Pediatrics, Fellowship Program Director, Division of Pediatric Cardiology,Department of Pediatrics, Columbia University College of Physicians and Surgeons; SeniorAttending Physician, Division of Pediatric Cardiology, Department of Pediatrics, MorganStanley Children’s Hospital of New York-Presbyterian, New York, New York

Emily G Lipsitz, MD

Pediatric Hematology-Oncology Fellow, Departments of Hematology and Oncology,The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania

Carlos D Rose´, MD, CIP

Professor of Pediatrics, Department of Pediatrics, Thomas Jefferson University, Philadelphia,Pennsylvania; Director, Pediatric Rheumatology, Department of Pediatrics, Alfred I DuPontChildren’s Hospital, Wilmington, Delaware

Cindy Ganis Roskind, MD

Assistant Clinical Professor of Pediatrics, Division of Pediatric Emergency Medicine,

Department of Pediatrics, Columbia University College of Physicians and Surgeons; Division ofPediatric Emergency Medicine, Department of Pediatrics, Morgan Stanley Children’s Hospital

of New York-Presbyterian, New York, New York

Philip Roth, MD, PhD

Director of Neonatology, Chairman, Department of Pediatrics, Staten Island UniversityHospital, Staten Island, New York; Associate Professor of Pediatrics, Department of Pediatrics,State University of New York - Downstate Medical Center, Brooklyn, New York

Benjamin D Roye, MD, MPH

Assistant Professor, Department of Orthopaedic Surgery, Mount Sinai School of Medicine;Attending Physician, Department of Pediatric Orthopaedic Surgery, Morgan Stanley Children’sHospital of New York-Presbyterian, Columbia Medical Center; Attending Physician, Department

of Orthopaedic Surgery, Beth Israel Medical Center, New York, New York

Robert L Seigle, MD

Assistant Professor of Clinical Pediatrics, Division of Pediatric Nephrology, Department ofPediatrics, Columbia University College of Physicians and Surgeons; Assistant AttendingPediatrician, Department of Pediatrics, Morgan Stanley Children’s Hospital of New

York-Presbyterian, New York, New York

F Meridith Sonnett, MD

Associate Clinical Professor of Pediatrics, Department of Pediatrics, Columbia UniversityCollege of Physicians and Surgeons; Chief, Division of Pediatric Emergency Medicine, MorganStanley Children’s Hospital of New York-Presbyterian, New York, New York

It has been more than 20 years (and in the interim one Phillies and two Red Sox World Series championships) since the publication of the initial Pediatric Secrets With this new edition, we strove to continue the principles of past editions by incorporating topics and questions about common (and less common) pediatric issues that are discussed every day in inpatient and outpatient settings It is a constant dialogue involving pathophysiology, diagnosis, and therapy that leads to greater understanding We have again tried to highlight major areas in pediatrics that remain controversial and less clearly defined.

We thank the chapter authors for their diligence in revising and updating, particularly

in more novel aspects of pediatric medicine We are very grateful to Andrea Vosburgh of Elsevier for her thoughtful suggestions, attention to detail, and patience with deadlines.

We have watched our own families grow, and in some cases begin families of their own, during the span of these editions To Helene, Allison, Mitchell, Jessica, and Gregory Polin and to Nina, Erin, Cara, and Grace Ditmar, thank you for providing a lifetime of support and for continuing to leave the light on for us.

Since the publication of our last edition, Dr Jean Cortner has passed away Dr Cortner was physician-in-chief at the Children’s Hospital of Philadelphia from 1974 until 1986.

He was a mentor, colleague, and friend, as well as a consummate physician with intellectual verve, genuine compassion, and remarkable insight He is very much missed We dedicate this 5th edition of Pediatric Secrets to his memory.

Richard A Polin, MD Mark F Ditmar, MD

xi

TOP 100 SECRETS

These secrets are 100 of the top board alerts They summarize the concepts,

principles, and most salient details of clinical practice

1 Always consider ovarian torsion in the differential diagnosis of abdominal pain in girls,particularly during the ages of 9 to 14 years, when ovarian cysts as potential lead pointsare more common because of the maturing reproductive hormonal axis

2.A pelvic examination is not required before prescribing oral contraceptives for teenagerswithout risk factors Appropriate screening for sexually transmitted infections andpossible cervical dysplasia can be scheduled, but delaying oral contraception

unnecessarily increases the risk for pregnancy

3 Emergency contraception should be discussed with all sexually active adolescents;90% of teenage pregnancies are unintended

4 Nutritional and hormonal interventions may be needed should an active girl or youngwoman develop the “female athletic triad,” which encompasses the distinct butinterrelated conditions of disordered eating, amenorrhea, and osteoporosis

5 Teenagers with attention-deficit/hyperactivity disorder and conduct disorders are at highrisk for substance abuse disorders Substance abuse is often associated with comorbidpsychiatric disorders

6 In preadolescents and younger adolescents, being overweight is more commonlyassociated with an advanced skeletal age and increased height compared with

nonobese peers Relative short stature in a younger obese patient may indicateendocrine disease

7 The most common chronic disease of childhood is early dental caries

8 Calluses over the metacarpophalangeal joints of the index and/or middle fingers (Russellsign) may indicate repetitive trauma from self-induced attempts at vomiting in patientswith eating disorders

9 The three essential features of autism are impaired social interaction, absent orabnormal speech and language development, a narrow range of interests, and

stereotyped or repetitive responses to objects

10 Bilingual children develop speech milestones normally; two-language households shouldnot be presumed as a cause of speech delay

11.Most amblyopia is unilateral; vision testing solely with both eyes open is inadequate

12.The “atopic march” is the phenomenon in which about half of infants with

atopic dermatitis eventually develop asthma, and two thirds develop allergic

rhinitis

1

13 Contact dermatitis should be suspected with rashes that are well-demarcated,geometric, and/or linear in nature, and may appear in uncommon or specific areas (e.g.,earlobes, weight-bearing surfaces of feet).

14 Patients with atypical Kawasaki disease are usually younger (<1 year old) and mostcommonly lack cervical adenopathy and extremity changes

15 Neonates with midline lumbosacral lesions (e.g., sacral pits, hypertrichosis, lipomas)above the gluteal crease should have screening imaging of the spine performed tosearch for occult spinal dysraphism

16 Infantile acne necessitates an endocrine workup to rule out precocious puberty

17 The most common finding on the examination of a child’s genitalia after suspectedsexual abuse is a normal examination

18 High-dose epinephrine is no longer recommended in pediatric resuscitation because ithas not been shown to be beneficial compared with standard dosing and may actually beharmful in cardiac arrest secondary to asphyxia

19 The single most important step for treating all chemical exposures (including acts ofterrorism) is an initial decontamination strategy of immediate removal of clothing, whichcan eliminate about 90% of contaminants

20 In the setting of bites, prophylactic antibiotics have been shown to significantly reduceinfections in only two settings: bites to the hands and human bites Some expertsrecommend treatment for other “high-risk” injuries, such as cat bites, foot wounds,puncture wounds, and wounds treated more than 12 hours after the injury

21 Consider the use of prostaglandin E1to maintain the patency of the ductus arteriosus in

a newborn younger than 1 month who presents in shock with evidence of congestiveheart failure and cyanosis because of the possibility of a ductal-dependent cardiaclesion, such as hypoplastic left heart syndrome

22 The most common cause of overdose deaths in children and adolescents in the UnitedStates is acetaminophen, owing to its widespread availability and frequency of use inaccidental and suicidal intoxications

23 Midline neck masses usually involve the thyroid gland or thyroid remnants, such as athyroglossal duct cyst

24 Because 20% to 40% of solitary thyroid nodules in adolescents are malignant,

an expedited evaluation is needed if a nodule is discovered

25 An initial bolus of insulin (typically, 0.1 units/kg), previously used as standard treatmentfor diabetic ketoacidosis, is no longer recommended because it is thought to beunnecessary and may increase the risk for cerebral edema

26 Unlike patients with type 1 diabetes, most youth with type 2 diabetes have little or noweight loss and absent or mild polyuria or nocturia Most have glycosuria withoutketonuria (although up to 33% can have ketonuria)

27 Acanthosis nigricans is found in 90% of youth diagnosed with type 2 diabetes

28.More than 40% of infants regurgitate effortlessly more than once a day.

29 Nasogastric lavage is a simple method for differentiating upper gastrointestinal bleedingfrom lower gastrointestinal bleeding

30.Potential long-term complications of pediatric inflammatory bowel disease includechronic growth failure, abscesses, fistulas, nephrolithiasis, and toxic megacolon

31.Bilious emesis in a newborn represents a sign of potential obstruction and is a truegastrointestinal emergency

32.The most common condition presenting as a food impaction in an adolescent iseosinophilic esophagitis

33.About 99% of full-term infants pass stool at less than 24 hours after birth Failure topass stool within the first 48 hours of life should be considered abnormal until provedotherwise

34.The most common cause of bloody diarrhea in infants younger than 1 year is allergic(or nonspecific) colitis, usually attributed to cow milk–based formula

35.About 80% of children will outgrow (that is, develop a tolerance to) certain food allergies,particularly eggs and milk, by age 10 years or earlier However, only about 20% outgrow apeanut allergy Food allergies that develop after age 3 years are less likely to be outgrown

36 In patients with Down syndrome and behavioral problems, do not overlook hearing loss(both sensorineural and conductive); it occurs in up to two thirds of patients with thiscondition, and it can be a possible contributor to those types of problems

37 Three or more minor malformations should raise concern about the presence of a majormalformation

38 An infant with nonsyndromic sensorineural hearing loss should be tested for mutations

in the connexin 26 gene Mutations in that gene contribute to at least 50% of autosomalrecessive hearing loss and about 10% to 20% of all prelingual hearing loss

39 Carbon monoxide poisoning is often misdiagnosed because the presenting symptomscan be flu-like

40 Hospitalization is indicated for significant burns involving the hands, feet, joints,

or perineum or if there are circumferential burns

41 Fecal soiling is almost always associated with severe functional constipation and notHirschsprung disease

42 Interpretation of stool tests for Clostridium difficile is more problematic in younginfants because up to 70% may be colonized with the organism By the second year

of life, this rate declines to about 6%, and above age 2 years to 3%, which is theapproximate rate in adults

43 The classic picture of appendicitis is anorexia followed by pain, then by nausea andvomiting, with subsequent localization of findings to the right lower quadrant However,there is a large degree of variability, particularly in younger patients

44 Absence of anemia does not exclude the possibility of iron deficiency because irondepletion is relatively advanced before anemia develops.

45 After iron supplementation for iron deficiency anemia, the reticulocyte count shoulddouble in 1 to 2 weeks, and hemoglobin should increase by 1 g/dL in 2 to 4 weeks.The most common reason for persistence of iron deficiency anemia is poor compliancewith supplementation

46 Because 30% of patients with hemophilia have no family history of the disorder andnew mutations are the cause, clinical suspicion is important in the presence of excessiveand frequent ecchymoses

47 Up to 20% of adolescents with menorrhagia will have a bleeding disorder, mostcommonly von Willebrand disease, and screening is recommended

48 In patients with sickle cell disease, use of transcranial Doppler ultrasound to measureintracranial blood flow and regular transfusions to reduce the hemoglobin S content forthose with abnormal values can significantly lower the likelihood of stroke

49 The determination of immunoglobulin G subclass concentrations is meaningless inchildren who are younger than 4 years

50 The most common specific etiology diagnosed in pediatric patients with a systemicfebrile illness after international travel is malaria More than half of the world’spopulation lives in areas where malaria is endemic

51 A male child with a liver abscess should be considered to have chronic granulomatousdisease until it is proved otherwise

52 Perinatal asphyxia accounts for less than 15% of cases of cerebral palsy

53 Leukocyte adhesion deficiency should be considered in a newborn with a significantlydelayed separation of the umbilical cord (>6 weeks)

54 The most common congenital infection is cytomegalovirus, which in some largescreening studies occurs in up to 1.3% of newborns About 90% to 95% of affectednewborns do not have symptoms, but some may later develop hearing loss

55 Hyperbilirubinemia generally is not an indication for the cessation of breastfeeding butrather for increasing its frequency

56 Vigorous correction of constipation has been shown to diminish both enuresis and thefrequency of urinary tract infections

57 The two most productive facets of patient evaluation to explain renal disease as apossible cause of symptoms are (1) the measurement of blood pressure and (2) theexamination of the first-morning void after the bladder is emptied of urine storedovernight (when a specimen is most likely to be concentrated)

58 The most common cause of persistent seizures is an inadequate serum antiepilepticlevel

59 Migraine headaches are usually bilateral in children but unilateral (75%) in adults

60.Seizures with fever in patients older than 6 years should not be considered febrileseizures.

61.After age and white blood cell count, early response to therapy is the most importantprognostic feature for children with acute lymphoblastic leukemia

62.Leukemias and lymphomas that have a high proliferation and cell turnover rate(e.g., Burkitt lymphoma, T-cell lymphoblastic leukemia) place patients at the highestrisk for complications from tumor lysis syndrome

63 Eighty percent or more of patients who present with acute lymphoblastic leukemia have

a normochromic, normocytic anemia with reticulocytopenia

64.Older children with unexplained unilateral deformities (e.g., pes cavus) of an

extremity should have screening magnetic resonance imaging to evaluate for intraspinaldisease

65.Asthma rarely causes clubbing in children Consider other diseases, particularly cysticfibrosis

66 Most children with recurrent pneumonia or persistent right middle lobe atelectasis haveasthma But all that wheezes is not asthma

67.A normal respiratory rate strongly argues against a bacterial pneumonia

68.Nasal polyps or rectal prolapse in children suggests cystic fibrosis

69.The three most common causes of anaphylaxis in pediatric hospitals and emergencydepartments are latex, food, and drugs Suspected allergies to shellfish, peanuts,and nuts warrant a prescription for an epinephrine pen because of the increased risk forfuture anaphylaxis

70.Up to 10% of normal, healthy children may have low-level (1:10) positive antinuclearantibody testing that will remain positive Without clinical or laboratory features ofdisease, it is of no significance

71.The daily spiking fevers of systemic juvenile rheumatoid arthritis can precede thedevelopment of arthritis by weeks to months

72 Abdominal pain (mimicking an acute abdomen) and arthritis can frequently precede therash in Henoch-Scho¨nlein purpura disease and thus confuse the diagnosis

73 Premature babies should be immunized in accordance with postnatal chronologic age

74 Without a booster after age 5 years, pertussis protection against infection is about80% during the first 3 years after immunization, dropping to 50% after 4 to 7 years,and to near 0% after 11 years

75 When administering an intramuscular vaccination, aspiration is not necessary because

no large blood vessels are located at the recommended sites for injection

76 About 6% of children are streptococcus carriers and will have positive throat culturesbetween episodes of pharyngitis

77 Apgar scores at 1 and 5 minutes do not predict long-term outcome.

78 Sodium bicarbonate should never be administered to newborns without first ensuringadequate ventilation

79 Coagulase-negative staphylococci are the most common bacterial pathogensresponsible for nosocomial infections in the neonatal intensive care unit

80 In more than 90% of cases, intraventricular hemorrhages in preterm infants occurduring the first 3 days of life

81 Recovery occurs in about 90% of patients with brachial plexus injuries

82 Isolated primary nocturnal enuresis rarely has identifiable organic pathology

83 Asymptomatic microscopic hematuria is found in 0.5% to 2% of schoolchildren and isbenign in most; evaluation yields no renal or urologic pathology

84 Significant proteinuria, in addition to hematuria, is much more likely to cause anunderlying pathology compared with hematuria alone

85 Clean-bagged specimens in infants and toddlers are unreliable for culture diagnosis ofurinary tract infections because of the high contamination rate

86 Uncircumcised male infants have a 10-fold greater risk for urinary tract infectioncompared with circumcised males

87 During the first year of life, hypotonia is more common than hypertonia in patients whoare ultimately diagnosed with cerebral palsy

88 Monitor patients with cerebral palsy (especially with spastic diparesis) regularly for hipsubluxation because earlier identification assists therapy

89 Headaches that awaken children from sleep, are associated with vomiting without nausea,are made worse by straining or coughing, and have intensity changes with changes inbody position are concerning for pathology that is causing increased intracranial pressure

90 Establishing the maturity level of the skeletal bones in a patient with scoliosis is importantbecause the risk for progression is increased with greater degrees of skeletal immaturity

91 In adolescents, progressive scoliotic curves are seven times more likely to occur in girlsthan boys

92 PaCO2measurements that are normal (40 mm Hg) or rising in asthmatic patients withtachypnea or significant respiratory distress are worrisome for evolving respiratory failure

93 In half of patients with chlamydial pneumonia, conjunctivitis precedes pneumonia

94 Hilar adenopathy suggests tuberculosis

95 In a febrile infant or toddler with a white blood cell count greater than 20,000/mm3,consider a chest radiograph to look for pneumonia, which can be present in up to 10%without respiratory symptoms

96 Although the incidence of rheumatic fever is low in the United States, worldwide it is theleading cause of cardiovascular death during the first five decades of life.

97 Because up to 10% of patients can have asymptomatic Borrelia burgdorferi infection andboth immunoglobulin M and immunoglobulin G antibodies to B burgdorferi can persistfor 10 to 20 years, the diagnosis of Lyme disease in older children and adolescents can

be tricky in patients with atypical clinical presentations

98.Compared with viral meningitis, Lyme meningitis is more likely to have a cranialneuropathy (usually facial nerve), papilledema, and a longer duration of symptomsbefore seeking medical care

99 About 10% to 20% of patients with Rocky Mountain spotted fever do not develop a rash,

so a high index of suspicion is needed for any patient in an endemic area who presentswith fever, myalgia, severe headaches, and vomiting

100 Most pediatric deaths in the United States associated with influenza tend to result fromeither (1) an exacerbation of an underlying medical condition or invasive procedure, or(2) coinfection from another pathogen, most commonly Staphylococcus aureus

ADOLESCENT MEDICINE

Mark F Ditmar, MD

CLINICAL ISSUES

1 What are the major health risks for adolescents?

nUnintentional injury: The leading cause of death, particularly alcohol-related automobileaccidents Adolescents account for 6% of total drivers but 14% of fatal crash victims

nViolence: Homicide is the second leading cause of death among 15- to 24-year-olds andthe leading cause for black males in this age range Suicide is the third leading cause ofdeath in adolescents aged 10 to 19 years

nSubstance abuse: In surveys, nearly 10% of 12- to 17-year-old adolescents admit to illicitdrug use during the previous 30 days

nSexually transmitted Infections (STIs): May involve 1 in 4 teenagers Up to 30% of allSTIs reported annually to the Centers for Disease Control and Prevention (CDC) involveadolescents Adolescents between 15 and 19 years of age have the highest age-specificrates of chlamydial and gonorrheal infections of any population group

nTeen pregnancy: 90% are unintended

nObesity: 15% of U.S teenagers are obese (body mass index [BMI]
95% for age), and15% are at risk for obesity (BMI between 85% and 95% for age)

2 Name the major risk factors that are associated with injuries to adolescents

nUse of alcohol while engaged in activities (e.g., driving, swimming, boating): 20% of alladolescent deaths are alcohol-related car crashes

nFailure to use safety devices (e.g., seat belts, motorcycle or bicycle helmets): Seat beltuse among adolescents is the lowest of any age group (10% admit to never or rarely usingone), and fewer than 10% use bicycle helmets

nAccess to firearms: 50% of deaths among black male teenagers and 20% of deathsamong white male teenagers are due to firearms, primarily handguns

nAthletic participation: Most injuries are reinjuries, which highlights the importance ofproper rehabilitation

3 Which sport causes the greatest number of catastrophic injuries in teenagers?Catastrophic injuries are those that result in death or permanent severe functional disability Forboys, football is the leading cause For girls, cheerleading is number one cause, owing to thegymnastic-type stunts that are performed, which can result in falls from significant heights.Mueller FO: Catastrophic head injuries and high school and collegiate sports, J Athl Train 36:312–315, 2001

4 What diagnoses require mandatory disclosure regardless of confidentiality?

In most states

nNotification of child welfare authorities under state child-abuse (physical and sexual)reporting laws

nNotification of law enforcement officials of gunshot and stab wounds

nWarning from a psychotherapist to a reasonably identifiable victim of a patient’s threat ofviolence

8

nNotification to parents or other authorities if a patient represents a reasonable threat tohimself or herself (i.e., suicidal ideation)

5 When can teenagers give their own consent for medical care or procedures?Teenagers who are married, who are parents themselves, who are members of the

armed forces, who are living apart from their parents, who are high school graduates,and/or who have evidence of independence (financial or otherwise) may fit the definition of an

“emancipated” or “mature” minor However, the definition varies from state to state.Bruce CR, Berg SL, McGuire AL: Please don’t call my mom: pediatric consent and confidentiality,Clin Pediatr 48:243–246, 2009

6 For which services do many states waive the legal requirement for parentalconsent for patients under age 18?

These include care for STIs, contraception services, pregnancy-related care, substance abusetreatment, mental health services, and treatment for rape or sexual assault

7 How does the “HEADS FIRST” system assist in adolescent interviewing?This mnemonic, which was originally devised at State University of New York Upstate MedicalUniversity, allows for a systematic approach to multiple health issues and risk factors thataffect teenagers:

Home: living arrangements, family relationships, support

Education: school issues, study habits, achievement, employment, expectations

Abuse: physical, sexual, emotional, verbal

Drugs: peer and personal use, alcohol, tobacco, marijuana, cocaine, others

Safety: injury prevention, safety equipment, seat belts, helmets, hazardous activitiesFriends: peer pressure, interaction, confidants

Image: self-esteem, body image, weight management

Recreation: exercise, relaxation, television and media time

Sexuality: changes, feelings, experiences, orientation, contraception

Threats: depressed or upset easily, suicidal ideation or attempts, harm to others

Cavanaugh RM Jr: Managing the transitions of early adolescence, Adolesc Health Update 20:1–8, 2008

EATING DISORDERS

8 What types of dieting raise concern for the development of an eating

disorder?

Dieting that is associated with

nDecreasing weight goals

nIncreasing criticism of body image

nIncreasing social isolation

nAmenorrhea or oligomenorrhea

9 How is the diagnosis of anorexia made?

Anorexia nervosa consists of a spectrum of psychological, behavioral, and medical

abnormalities The 1996 Diagnostic and Statistical Manual for Primary Care: Child andAdolescent Version criteria list five components:

nRefusal to maintain body weight or BMI at or above minimal norms for age and height(<85% of expected weight for height or a BMI of <17.5 in an older adolescent)

nIntense fear of gaining weight or becoming fat despite being underweight

nDisturbances of perception of body shape and size

nDenial of seriousness of weight loss or low body weight

nIn postmenarchal girls, amenorrhea (i.e., the absence of at least three consecutivemenstrual cycles)

National Eating Disorders Association:http://www.nationaleatingdisorders.org

National Association of Anorexia Nervosa and Associated Disorders:http://www.anad.org

10 What are good and bad prognosticators for recovery from anorexia?Good: Early age at onset (<14 years), high educational achievement, improvement in bodyimage after weight gain, emotionally well-adjusted, supportive family, shorter duration

of illness

Bad: Late age at onset, continued overestimation of body size, self-induced vomiting orbulimia, laxative abuse, family dysfunction, male, comorbid mental illness, substanceabuse, longer duration of illness

11 What hormonal abnormalities may be seen in anorexia nervosa?

Amenorrhea is seen in most cases due to hypothalamic and pituitary dysfunction with verylow levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) Twenty-fivepercent of affected girls experience amenorrhea before significant weight loss occurs,which suggests that there is a psychological effect on physiology Symptoms thatare suggestive of hypothyroidism—constipation, cold intolerance, dry skin, bradycardia, andhair or nail changes—are common Thyroid studies, however, have relatively normalresults, except for a low triiodothyronine (T3) and an increased reverse T3(rT3), which is

a less active isomer

The T3/rT3reversal is also seen in conditions that are associated with weight loss,possibly indicating that it is a physiologic means of adapting to a lower energy state.Other abnormalities include a loss of diurnal variation in cortisol, diminished plasmacatecholamine levels, normal or increased growth hormone levels, and flattened glucosetolerance curve

12 In addition to underweight and amenorrhea, what other clinical features may

be found in patients with anorexia nervosa?

Symptoms: Cold intolerance, constipation, fatigue, postural dizziness, early satiety, bloatingSigns: Pubertal delay, growth retardation, development of lanugo hair, abnormal skin (dry,hyperkeratotic; sometimes orange due to increased carotene), hypothermia, bradycardia,postural hypotension, acrocyanosis, dependent edema

Morris J, Twaddle S: Anorexia nervosa, BMJ 334:894–898, 2007

13 What are some indications that a pediatric patient with anorexia nervosashould be admitted to a hospital?

n>75% of ideal body weight or ongoing weight loss despite intensive management

nDehydration

nElectrolyte abnormalities (e.g., hypokalemia, hyponatremia, hypophosphatemia)

nHeart rate less than 50 beats per minute daytime, less than 45 beats per minute nighttime

nSystolic blood pressure less than 80 mm Hg

nOrthostatic changes in pulse (>20 beats per minute) or blood pressure (>10 mm Hg)

nTemperature less than 96F

nCardiac dysrhythmia

nAcute medical complication of malnutrition (syncope, seizure, congestive heart failure,pancreatitis)

nSevere coexisting psychiatric disease

American Academy of Pediatrics: Committee on Adolescence: Identifying and tolerating eating

14 What causes sudden cardiac death in patients with anorexia nervosa?

Chronic emaciation affects the myocardium Anorectic patients develop depressed cardiovascularfunction and an altered conduction system Electrocardiogram (ECG) changes are common.Patients with anorexia have significantly lower heart rates (averaging 20 beats per minute less thanpeers), lower R values in V6, and longer QRS intervals These ECG changes often occur withoutunderlying electrolyte abnormalities The arrhythmogenic potential is heightened if electrolytes(specifically potassium) are distorted by excessive vomiting or laxative abuse Sudden death islikely as a result of the culmination of chronic myocardial injury in emaciated patients (>35% to40% below ideal weight) with resultant heart failure and dysrhythmia

Panagiotopoulos C, McCrindle BW, Hick K, Katzman DK: Electrocardiographic findings in adolescentswith eating disorders, Pediatrics 105:1100–1105, 2000

15 Do males and females with anorexia nervosa have a similar clinical profile?

It is estimated that less than 5% of anorexia nervosa involves boys Males are more likely to

nHave been obese before the onset of symptoms

nBe ambivalent regarding the desire to gain or lose weight

nHave more issues about gender and sexual identity

nInvolve dieting with sports participation

nEngage in “defensive dieting” (avoiding weight gain after an athletic injury)

Domine F, Berchtold A, Akre C, et al: Disordered eating behaviors: what about boys? J Adolesc Health44:111–117, 2009

Rosen DS: Eating disorders in adolescent males, Adolesc Med 14:677–689, 2003

KEY PO INTS: ANOR EXIA NERVOSA

1 Hallmark: Intense fear of gaining weight despite being underweight

2 BMI< 17.5 in older adolescents strongly suggests anorexia

3 95% female, but evidence suggests increasing prevalence among males

4 Inquire about the possibility of an eating disorder with a direct question: “How do you feelabout your weight?”

5 Sedimentation rates: Usually normal in eating disorders; elevation suggests other diagnoses,such as inflammatory bowel disease

6 Most common causes of death: cardiac dysfunction and suicide

16 How is the diagnosis of bulimia nervosa made?

Bulimia nervosa is a syndrome of voracious, high-caloric overeating and subsequent forcedvomiting (by gagging or ipecac) and/or other purging methods (e.g., laxatives, diuretics).This often occurs during periods of frustration or psychological stress Its incidence isthought to be higher than that of anorexia nervosa, and males are rarely involved Thediagnosis is made using a patient’s history

17 List the medical complications of bulimia nervosa

Electrolyte abnormalities: Hypokalemia, hypochloremia, and metabolic alkalosis may occur.The hypokalemia can cause a prolonged QT interval and T-wave abnormalities

Esophageal: Acid reflux with esophagitis and (rarely) Mallory-Weiss tear may be found.Cardiac: Ipecac use can result in cardiomyopathy due to a toxic effect of one of its principalcomponents, the alkaloid emetine

Central nervous system: Neurotransmitters can be affected, thereby causing changes in thepatient’s perceptions of satiety.

Miscellaneous: Enamel erosion, salivary gland enlargement, cheilosis, and knuckle callusesare signs of recurrent vomiting

Mehler PS: Bulimia nervosa, N Engl J Med 349:875–881, 2003

18 How do anorexia nervosa and bulimia nervosa differ?

SeeTable 1-1

19 What modalities are used to treat eating disorders?

Nutritional rehabilitation: Patients are often begun on 1200 to 1500 kcal per day, increasing

by 500 kcal every 1 to 4 days up to 3500 kcal (for females) and to 4000 kcal (for males).Overnight nasogastric feedings are routinely recommended Total parenteral nutrition israrely required

Medication: Prokinetic agents (e.g., domperidone) are used to minimize postprandial bloating.Antidepressants, including serotonin-specific reuptake inhibitors (e.g., fluoxetine), andatypical neuroleptic mediations (e.g., risperidone) have been used with some limited success.Psychotherapy: Individual and family therapy may both be useful

Attia E, Walsh BT: Behavioral management for anorexia nervosa, N Engl J Med 360:500–5006, 2009.Yager J, Andersen AE: Anorexia nervosa, N Engl J Med 353:1481–1488, 2005

20 Name the three features that constitute the “female athletic triad.”

Disordered eating, amenorrhea, and osteoporosis These three distinct yet interrelateddisorders are often seen in active girls and young women All female athletes are at riskfor developing this triad, with 15% to 60% of female athletes demonstrating abnormalweight-control behaviors Diagnosis is based on history, physical examination, and laboratoryevaluation The basic laboratory workup should include urine human chorionic gonadotropin,thyroid-stimulating hormone, prolactin, FSH, LH, testosterone, dehydroepiandrosteronesulfate (DHEA-S), and progesterone challenge test Ongoing counseling is often indicated,

TABLE 1-1 C O M P A R I S O N O F A N O R E X I A N E R V O S A A N D B U L I M I A N E R V O S A

Vomiting or diuretic/laxative abuse

uncommon

Vomiting or diuretic/laxative abuseSevere weight loss Less weight loss; avoidance of obesity

Eating behavior may be considered

normal

Eating behavior is egodystonic and asource of self-esteem

Obsessional fears with paranoid features Histrionic features

Death from starvation/suicide Death from hypokalemia/suicide

From Shenker IR, Bunnell DW: Bulimia nervosa In McAnarmey ER, Kreipe RE, Orr DP, Comerci GD(eds): Textbook of Adolescent Medicine Philadelphia, W.B Saunders, 1992, p 545

as are nutritional and hormonal interventions Treatment commonly includes calciumsupplements and oral contraceptives.

Greydanus DE, Omar H, Pratt HD: The adolescent female athelete: current concepts and conundrums,Pediatr Clin North Am 57:697-718, 2010

American Academy of Pediatrics Committee on Sports Medicine and Fitness: Medical concerns in thefemale athlete, Pediatrics 106:610–613, 2000

MENSTRUAL DISORDERS

21 What is the difference between primary and secondary amenorrhea?

Primary amenorrhea: No onset of menses by age 16 or within 3 years of onset of secondarysex characteristics or within 1 year of Tanner V breast and pubic hair developmentSecondary amenorrhea: No menses for 3 months after previous establishment of regularmenstrual periods or for 6 months if regular cycles have not been established

22 What causes primary amenorrhea?

The key feature in the differential diagnosis is whether the amenorrhea is associated with thedevelopment of secondary sex characteristics

Amenorrhea without secondary sex characteristics:

nChromosomal or enzymatic defects (e.g., Turner syndrome, chromosomal mosaics,17a-hydroxylase deficiency)

nCongenital absence of uterus

nGonadal dysgenesis (with elevated gonadotropins)

nHypothalamic-pituitary abnormalities (with diminished gonadotropins)

Amenorrhea with secondary sex characteristics:

nDysfunction of hypothalamic release of gonadotropin-releasing hormone (GnRH)

(e.g., stress, excessive exercise, weight loss, chronic illness, polycystic ovary disease,medications, hypothyroidism)

nAbnormalities of pituitary gland (e.g., tumor, empty sella syndrome)

nOvarian dysfunction (e.g., irradiation, chemotherapy, trauma, viral infection, autoimmuneinflammation)

nAbnormalities of genital tract (e.g., cervical agenesis, imperforate hymen, androgeninsensitivity with absent uterus)

nPregnancy

23 How can estrogen influence be evaluated on vaginal or cervical smears?Vaginal smear: In patients with normal estrogen, 15% to 30% of cells are superficial (smallpyknotic nuclei with large cytoplasm), and the remainder are intermediate (larger nuclei withvisible nucleolus but still with cytoplasm predominant) If parabasal cells are noted(nuclear-to-cytoplasmic ratio of
50:50), relative estrogen deficiency should be suspected.Cervical smear: Cervical mucus is smeared onto a glass slide and allowed to dry If a fernpattern appears, estrogen is normal (i.e., because salts crystallize only if estrogen isunopposed by progesterone) No fern pattern occurs during the second half of menses,after ovulation, because of the presence of progesterone Absence of ferning duringpregnancy is also a result of higher progesterone levels

24 What is the value of a progesterone challenge test in a patient with amenorrhea?

If bleeding ensues within 2 weeks after the administration of oral medroxyprogesterone

(5-10 mg daily for 5-10 days) or intramuscular progesterone in oil (5-10 mg daily for 5-10 days),the test is positive This indicates that the endometrium has been primed by estrogen and thatthe outflow tract is functioning No response indicates hypothalamic-pituitary dysfunction orovarian failure

25 A 14-year-old girl has Tanner III features and monthly abdominal pain but noonset of menstrual flow What is the likely diagnosis?

An anatomic abnormality of the vagina (e.g., imperforate hymen or transverse vaginalseptum) or cervix (e.g., agenesis)

26 An obese 16-year-old girl has oligomenorrhea, hirsutism, acne, and anelevated LH/FSH ratio What condition is likely?

Polycystic ovary syndrome This disorder is characterized by the triad of menstrual irregularities(amenorrhea or oligomenorrhea), hirsutism, and acne that begins during puberty Obesity iscommon In these individuals, there is an apparent gonadotropin-dependent, functionalovarian hyperandrogenism with elevated LH (or LH/FSH ratio of>3:1) and insulin resistance

A dysregulation of ovarian and adrenal synthesis of androgens and estrogen is likely Polycysticovaries, although commonly found on ultrasound, are not essential for the diagnosis.Baldwin CY, Witchel SF: Polycystic ovary syndrome, Pediatr Ann 35:888–897, 2006

27 What is the range of complications of polycystic ovary syndrome?

Pfeifer SM, Kives S: Polycystic ovary syndrome in the adolescent, Ob Gyn Clin North Am 36:129–152, 2009

28 What constitutes excessive menstrual bleeding in an adolescent?

As a rule, most menstrual periods do not last more than 7 days, do not occur more frequentlythan every 21 to 40 days, and are not associated with more than 80 mL of blood loss.The quantitation can be difficult because pad or tampon numbers correlate poorly with total bloodloss Blood clots or a change in pad numbers appears to have more reliability Suspicion ofexcessive loss should prompt an evaluation of hematocrit and/or reticulocyte count

29 Differentiate the “rhagia” types of menstrual problems

Menorrhagia: Hypermenorrhea or heavy menstrual bleeding with regular cyclic intervalsMetrorrhagia: Irregular bleeding due to varying cycles

Menometrorrhagia: Heavy bleeding that occurs at varying intervals

30 How common are anovulatory menstrual periods in adolescents?

Anovulatory cycles (and with them, an increased likelihood of irregular periods) occur in 50%

of adolescents for up to 2 years after menarche and in up to 20% after 5 years (the rate inadults) Anovulatory cycles result in unopposed estradiol production, which can cause thefollowing: (1) breakthrough bleeding at varying intervals due to insufficient hormone tosupport a thickened endothelium, and (2) heavy and prolonged menstrual flow due to lack ofprogesterone However, most anovulatory menstrual cycles are normal because the intactnegative feedback loop (i.e., rising estradiol lowers FH and LSH, which, in turn, lowerestradiol) does not allow for prolonged elevated estrogen with endometrial proliferation

31 Describe the evaluation for a patient with dysfunctional uterine bleeding (DUB).Dysfunctional uterine bleeding is irregular and/or prolonged vaginal bleeding in the absence

of structural pelvic pathology It remains a diagnosis of exclusion Depending on the age ofthe patient and her history of sexual activity, the following studies should be considered:

nSpeculum examination for evidence of trauma or vaginal foreign body

nBimanual examination for ovarian mass, uterine fibroid, and signs of pregnancy or pelvicinflammatory disease

nPapanicolaou (Pap) smear for cervical dysplasia

nPregnancy test

nSerum prolactin

nThyroid function tests

nCoagulation studies (especially for von Willebrand disease)

Albers JR, Hull SK, Wesley RM: Abnormal uterine bleeding, Am Fam Physician 69:1915–1932, 2004

32 How can the timing of abnormal uterine bleeding help identify the most likelycause?

Abnormal bleeding at the normal time of cyclic shedding:

nBlood dyscrasia (especially von Willebrand disease)

nEndometrial pathology (e.g., submucous myoma, intrauterine device)

Abnormal bleeding at any time during the cycle, but normal cycles:

nVaginal foreign body

nTrauma

nEndometriosis

nInfection

nUterine polyps

nCervical abnormality (e.g., hemangioma)

Noncyclic bleeding or abnormal cyclic bleeding (<21 days or >45 days, usually associatedwith anovulatory cycles):

nPhysiologic (especially during early adolescence)

nPolycystic ovary disease

34 How should a very anemic teenager with DUB and positive orthostatic signs

be managed?

If there are orthostatic changes and the hemoglobin is low (<7 mg/dL)

nHospitalize for oral combination medications (e.g., 30 mcg ethinyl estradiol/0.3 mg

norgestrel every 6 hours until bleeding slows with a medication taper up to 3 weeks);

if bleeding persists after two doses, begin high-dose intravenous conjugated estrogen therapy(e.g., 25 mg IV May repeat every 4 to 6 hours for up to 4 doses)

nBegin intravenous fluids and consider transfusion (usually not required)

nUnresponsive bleeding may require dilation and curettage (also rarely required in adolescents)

nCoagulation studies (owing to a higher likelihood of underlying coagulopathy; tests for vonWillebrand disease should be drawn before therapy because estrogen increases vonWillebrand factor concentrations)

nBegin iron supplementation

Braverman PK, Breech LL: Menstrual disorders In Slap GB, editor: Adolescent Medicine:

KEY PO INTS: MENSTRUAL DISO RDERS

1 Abnormally heavy bleeding at menarche or unusually long menstrual periods: Consider vonWillebrand disease

2 Irregular menstrual bleeding patterns: Common in early adolescence because regular ovulatorymenstrual cycles typically do not develop for 1 to 1½ years after the onset of menarche

3 Always consider pregnancy in a patient with secondary amenorrhea

4 Signs of androgen excess (hirsutism and/or acne) in the setting of menstrual irregularitiessuggest polycystic ovary syndrome

5 Progressively worsening dysmenorrhea suggests endometriosis as a cause of chronicpelvic pain in adolescents

6 Ask about dysmenorrhea: It affects>50% of teenage girls and causes considerableschool absence

35 How common is dysmenorrhea in adolescent females?

Up to 90% of adolescents are affected by primary dysmenorrhea The condition remains thesingle greatest cause of lost school hours in females However, fewer than 15% of teenagefemales with dysmenorrhea will seek medical care, so it is important to screen for theproblem Most cases are primary, but about 10% of patients with severe dysmenorrheasymptoms will have uterine or pelvic abnormalities, such as endometriosis

Harel Z: Dysmenorrhea in adolescents and young adults: etiology and management, J Pediatr AdolescGynecol 19:363–371, 2006

36 Why is dysmenorrhea more common in late rather than early adolescence?Dysmenorrhea occurs almost entirely with ovulatory cycles Menses shortly after the onset ofmenarche is usually anovulatory With the establishment of more regular ovulatory cyclesafter 2 to 4 years, primary dysmenorrhea becomes more likely

37 In a teenager with dysmenorrhea, what factors suggest an underlyingidentifiable pathologic problem rather than primary dysmenorrhea?

Primary dysmenorrhea is painful menses without identifiable pelvic pathology and accountsfor most cases in teenagers However, underlying pathology is more likely if any of thefollowing conditions are present: menorrhagia; intermenstrual bleeding; pain at times otherthan menses (suggesting outflow obstruction); or abnormal uterine shape on examination(suggesting uterine malformation)

38 What two classes of medications are most commonly used for dysmenorrhea?Nonsteroidal anti-inflammatory drugs (NSAIDs): Evidence strongly suggests a key role forprostaglandins (especially prostaglandin F2aand prostaglandin E2a) in pain because ofuterine hyperactivity NSAIDs can limit local prostaglandin production Naproxen,ibuprofen, and mefenamic acid may be effective in up to 80% of patients

Hormonal therapies: Oral contraceptives act by reducing endometrial growth, which limitsthe total production of endometrial prostaglandin Ovulation is suppressed, which alsominimizes pain A combined estrogen-progestin pill is preferred Improvement may not beseen for up to 3 months

Braverman PK: Dysmenorrhea and premenstrual syndrome In Neinstein LS, editor: Adolescent Health

39 What is the most common cause of chronic pelvic pain in adolescents without

a history of pelvic inflammatory disease?

Endometriosis This condition results from the implantation of endometrial tissue to areas ofthe peritoneum outside the uterine cavity The pain is both noncyclic (may occur with

intercourse or defecation) and cyclic (often most severe just before menses, and dysmenorrhea

is common) When suspected, initial treatment is with NSAIDs and/or oral contraceptives.Intermenstrual bleeding is common Definitive diagnosis is by laparoscopy and biopsy Therapycan be surgical (e.g., excision, coagulation, laser vaporization) and/or medical (e.g., GnRHanalogues, combination oral contraceptives, medroxyprogesterone acetate)

Bulun SE: Endometriosis N Engl J Med 360:268–279, 2009

Mounsey AL, Wilgus A, Slawson DC: Diagnosis and management of endometriosis, Am Fam Physician74:594–602, 2006

40 What is the peak age for ovarian torsion?

In a study of 80 patients, nearly two thirds of cases occurred between the ages of 9 and

14 years, with a mean age of 11 years This early pubertal peak is thought to be due to theincreasing likelihood of the development of ovarian cysts by the maturing reproductivehormonal axis These cysts then act as lead points for torsion

Oltmann S, Fischer R, Barber R, et al: Cannot exclude torsion—a 15-year review, J Pediatr Surg44:1212–1217, 2009

41 Why do more ovarian torsions occur on the right than the left?

Multiple studies have noted this asymmetry in location, with nearly two thirds of ovariantorsions occurring on the right A leading theory is that the relative mobility of the cecumallows for more ovarian motion on the right compared with the relatively fixed sigmoid colon

on the left Because torsion manifests almost 100% of the time with pain, this right-sidedpreference causes ovarian torsion to be commonly confused with appendicitis Delays indiagnosis are common, which lessens ovarian salvage rates

Oltmann S, Fischer R, Barber R, et al: Cannot exclude torsion—a 15-year review, J Pediatr Surg44:1212–1217, 2009

42 Is ultrasonography typically diagnostic in the setting of ovarian torsion?The definitive diagnostic feature of torsion that could be detected by ultrasound—visualization

of the twisted pedicle—is seen in fewer than 10% of cases Certain ultrasonographic

features can suggest torsion, such as a pelvic mass of 5 cm or larger or diminished or absentarterial or venous (particularly venous) Doppler flow, but they are not diagnostic In somestudies with documented operative torsion, Doppler studies were normal in up to 60%.Anders J: Ovarian torsion in the pediatric emergency department: making the diagnosis and theimportance of advocacy, Clin Pediatr Emerg Med 10:31–37, 2009

OBESITY

43 What is the body mass index (BMI)?

BMI¼ (weight [kg]/height [m2]) As an indicator of body fat, it is recommended by theCDC as the main screening tool for obesity When plotted on standard charts for ageand gender, a BMI from 85% to 95% indicates “at risk for overweight,” and a BMI above the95th percentile indicates “overweight.” It is estimated that about 30% to 40% of U.S.adolescents are overweight or at risk for being overweight BMI growth charts for age andgender are available athttp://www.cdc.gov/growthcharts/

American Association of Pediatrics:http://www.aap.org/obesity

44 Why is an obese 10-year-old who is short potentially of more clinical concernthan one who is tall?

Being overweight is more commonly associated with an advanced skeletal age in preadolescentsand younger adolescents and thus increased height compared with nonobese peers Thus, relativeshort stature in an obese 10-year-old could be a sign of possible endocrine disease

Schneider MB Obesity In Neinstein LS, editor: Adolescent Health Care, ed 5, Philadelphia, 2008,Wolters Kluwer, pp 468

45 What percentage of obese teenage patients have an identifiable underlyingpathologic cause for their obesity?

5% 3% have endocrine problems (hypothyroidism, Cushing syndrome, hypogonadism),and 2% have uncommon syndromes (such as Prader-Willi, Laurence-Moon-Biedl).Schneider MB: Obesity In Neinstein LS, editor: Adolescent Health Care, ed 5, Philadelphia, 2008,Wolters Kluwer, pp 468

46 What are the risk factors for obesity in teenagers?

nPositive family history: With one obese parent, probability of obesity is 30%; with twoobese parents, this increases to 70% to 80%

nDegree of obesity as a child: More severe obesity is likely to persist

nSocioeconomic status: 10- to 17-year-olds living below the poverty line are 2½ timesmore likely to be overweight or obese

nTelevision viewing: Increased television viewing appears to correlate with a higherlikelihood of obesity

nRace: Rates for Mexican-Americans are higher than for rates for blacks, which are higherthan rates for whites

nFamily size: Obesity decreases as family size increases; it has the greatest prevalenceamong single children

Dietz WH, Robinson TN: Overweight children and adolescents, N Engl J Med 350:2100–2109, 2005

47 Are boys or girls more likely to remain obese teenagers throughout puberty?Girls During puberty, body fat decreases by 40% in boys and increases by 40% in girls.Puberty leads to the normalization of body weight in 70% of obese males but in only 20% ofobese females Girls who have early menarche (age,11 years) are twice as likely to becomeobese adults as are late maturers (age,
14 years) Girls also have significant declines inphysical activity during adolescence

48 What morbidities can be associated with adolescent obesity?

nAccelerated pubertal and skeletal development

nDiabetes mellitus, type 2

nPolycystic ovary syndrome

Fennoy I: Metabolic and respiratory comorbidities of childhood obesity, Pediatr Ann 39:140-146, 2010

49 What features constitute the metabolic syndrome?

nCentral obesity (excessive fat around the abdomen)

nLipid abnormalities

nInsulin resistance and/or glucose intolerance

nProthrombotic state

nProinflammatory state (elevated C-reactive protein)

Well-described in adults with obesity, this constellation of biomarkers and risk

factors for adverse cardiovascular outcomes has been increasingly recognized in

adolescents Its presence in adolescence increases the likelihood of cardiovascular disease

in adulthood

Morrison JA, Friedman LA, Gray-McGuire C: Metabolic syndrome in childhood predicts adult

cardiovascular disease 25 years later, Pediatrics 120:340–345, 2007

Weiss R, Dziura J, Burgert TS, et al: Obesity and the metabolic syndrome in children and adolescents,

N Engl J Med 350:2362–2374, 2004

50 What features on physical examination are particularly important in theevaluation of the obese patient?

nBlood pressure (hypertension)

nFacial dysmorphic features (evidence of genetic syndrome)

nTonsils (hypertrophy; potential for obstructive apnea)

nThyroid (goiter, possible hypothyroidism)

nAcanthosis nigricans (type 2 diabetes)

nHirsutism (polycystic ovary syndrome)

nStriae (Cushing syndrome)

nRight upper quadrant (RUQ) tenderness (gallbladder disease)

nSmall hands and feet, cryptorchidism (Prader-Willi syndrome)

nLimited hip range of motion (slipped capital femoral epiphysis)

nLower-leg bowing (Blount disease)

Eissa MAH: Overview of pediatric obesity: key points in the evaluation and therapy, Consultant Pediatr2:293–296, 2003

51 Do obese children and adolescents become obese adults?

In most tracking studies, only 25% to 50% become obese adults However, in somestudies, this rate has ranged as high as 85% The most important risk factors for persistence

of obesity are later age of onset and increased severity of obesity at any age

Dietz WH, Bellizzi MC: Overweight children and adolescents, N Engl J Med 352:2100, 2005

KEY PO INTS: OBESITY

1 Obesity: Most common chronic condition in children

2 Obesity and short stature—think thyroid abnormalities and evaluate thyroid-stimulatinghormone and T4levels

3 Only 5% of obese children have an identifiable underlying pathologic cause

4 If a child is at risk as a result of family history, the earlier the modifications (e.g., limitingtelevision time), the better

5 Keep weight reduction or stabilization goals reasonable; if too unrealistic, discouragement andweight cycling are more likely

52 What is the long-term outlook for the obese teenager?

Obesity in adolescence is associated with medical, economic, and social consequences.Obese teenagers, especially females, have lower rates of school completion, lower rates ofmarriage, lower household incomes, and higher rates of poverty Even if weight corrections occurlater, the early obesity is associated with increased atherosclerotic heart disease in men andwomen, with colorectal cancer and gout in men, and with arthritis in women

Schwimmer JB, Burwinkle TM, Varni JW: Health-related quality of life of severely obese children andadolescents, JAMA 289:1813–1819, 2003

53 How effective are intervention and treatment for obesity in adolescents?Weight-reduction regimens involving behavior modification and dietary therapy are modestlyeffective with regard to short-term results, but they are notoriously ineffective for theachievement of long-term weight loss

Appetite suppressants are uncommonly used in adolescents owing to problems of sideeffects and limited data on efficacy Gastric bypass and banding (bariatric surgery) can beconsidered for those with a BMI higher than 40, particularly if associated with complicatingproblems such as diabetes mellitus or sleep apnea

Wilfley DE, Stein RI, Saelens BE, et al: Efficacy of maintenance treatment approaches for childhoodoverweight: a randomized controlled trial JAMA 298:1661–1673, 2007

Dietz WH: What constitutes successful weight management in adolescents? Ann Intern Med145:81–90, 2006

SEXUAL DEVELOPMENT

54 What is Tanner staging for boys?

In 1969 and 1970, Dr James Tanner categorized the progression of stages of puberty,dividing pubertal development in boys into pubic and genital development (Table 1-2)

TABLE 1-2 T A N N E R S T A G I N G F O R B O Y S

Pubic Hair

II Countable; straight; increased pigmentation

and length; primarily at base of penisIII Darker; begins to curl; increased quantity

IV Increased quantity; coarser texture; covers most of pubic area

V Adult distribution; spread to medial thighs and lower abdomenGenital Development

II Testicular enlargement (>4 mL volume); slight rugation of

scrotumIII Further testicular enlargement; penile lengthening begins

IV Testicular enlargement continues; increased rugation

of scrotum; increased penile breadth

55 What is the normal progression of sexual development and growth for boysduring puberty?

Nearly all boys begin puberty with testicular enlargement This is followed in about 6 months

by pubic hair and then about 6 to 12 months later by phallic enlargement For boys, puberty lasts

an average of 3.5 years and begins an average of 2 years later than it does in girls (Fig 1-1)

56 What are the ranges of normal in the stages of pubertal development in girls?Tanner divided pubertal development in girls according to pubic hair and breast development(Table 1-3)

57 What is the normal progression of sexual development and growth for girlsduring puberty?

About 85% of girls begin puberty with the initiation of breast enlargement, whereas 15%have axillary hair as the first sign Menarche usually occurs about 18 to 24 months after theonset of breast development For girls, the duration of puberty is about 4.5 years, which islonger than that of boys (Fig 1-2)

Figure 1-1 Summary of pubertaldevelopment in boys (FromRosen DS: Physiologic growth anddevelopment during adolescence

II Countable; straight; increased pigmentation and

length; primarily on medial border of labiaIII Darker; begins to curl; increased quantity on mons pubis

IV Increased quantity; coarser texture; labia and mons well

covered

V Adult distribution with feminine triangle and spread to

medial thighsBreast Development

II Breast bud present; increased areolar size

III Further enlargement of breast; no secondary contour

IV Areolar area forms secondary mound on breast contour

V Mature; areolar area is part of breast contour; nipple projects

58 Has the age of menarche declined in the United States during the past

80 years?

Survey data of women from aged 20 to 80 years do indicate a decline over this time period

of about 15 months for black girls, 12 months for Mexican-American girls, and 10 monthsfor white girls A variety of factors may be contributing, including environmental (dietarychanges and increasing obesity), socioeconomic, and genetic

McDowell MA, Brody DJ, Hughes JP: Has age at menarche changed? Results from the National Healthand Nutrition Examination Survey (NHANES), J Adolesc Health 40:227–231, 2007

59 When do boys develop the ability to reproduce?

The average age of spermarche (as demonstrated by the presence of spermatozoa in thefirst morning urine) is 13.3 years Unlike what occurs in girls (in whom menarche follows thepeak height velocity), in boys, spermarche occurs before the growth spurt

60 When is delayed sexual development a concern?

Boys who are 14 years of age without testicular enlargement (>4 mL) or pubic hair andgirls who are 13 years without signs of breast development are considered to have delayedpuberty By definition, this is about 2.5% of healthy teens in the United States (2.5 standarddeviations below the mean) In girls with immature breast development, lack of menarche byage 15 years or within 5 years of onset of puberty is also considered abnormal A girl withnormal breast and pubic hair development but no menarche by age 16 years more properlyhas primary amenorrhea

61 Why should the sense of smell be tested in a teenager with delayed puberty?Kallmann syndrome is characterized by a defect in GnRH with resultant gonadotropindeficiency and hypogonadism Maldevelopment of the olfactory lobes occurs, with resultantanosmia or hyposmia Less commonly, cleft palate, congenital deafness, and color blindnesscan occur These patients require hormonal therapy to achieve puberty and fertility

62 What is the most common cause of delayed puberty?

Constitutional delay of growth and maturity, the cause in 70% to 90% of cases, is a form

of hypogonadotropic hypogonadism, in which there is delayed secretion of GnRH andactivation of the gonadal axis There is often a family history of late-onset puberty indicating astrong genetic component Children often are small for their age (5%) but have grownsteadily Bone age is delayed

63 What features suggest constitutional delay of puberty?

nFamily history of delayed puberty

nOften short (3rd to 25th percentile) compared with peers

Figure 1-2 Summary of pubertal

development in girls (From

Rosen DS: Physiologic growth and

development during adolescence

Pediatr Rev 25:198, 2004.)

nGrowth velocity slowed (4 to 7 cm/year) compared with same-age, same-sex peers(8 to 11 cm/year)

nBone age delayed (from 1.5 to 4 years) compared with chronologic age

nNormal prepubertal anatomy, sense of smell, prepubertal LH, FSH levels

64 Which laboratory tests should you consider in a boy or girl with delayedpuberty?

If history or physical examination does not suggest an underlying cause (e.g., anorexia nervosa,chronic disease), tests should includeLH, FSH, testosterone (male), and bone age These testshelp categorize the condition as hypergonadotropic with increased GnRH, LSH, and LH (implyingpossible gonadal defects, androgen insensitivity, or enzyme defects) or hypogonadotropic withdecreased GnRH and low to normal FSH and LH (implying constitutional delay or primaryhypothalamic-pituitary problems) Most cases involve decreased GnRH

Further testing is predicated on the results of these initial tests For example, a 14.5-year-oldmale with a bone age of 11.5 years and a total testosterone of 23 ng/dL (normal prepubertallevel is<10 ng/dL) will probably begin to show outward evidence of puberty within thesubsequent few months Therefore, no further studies are warranted On the other hand, ifthis boy has a bone age of 12.5 years, a testosterone level of less than 10 ng/dL, and noelevation of FH and LSH, specific testing of the hypothalamic-pituitary axis is indicated

65 What is the most common cause of primary gonadal failure in boys?

Klinefelter syndrome The frequency of this condition is 1 in every 500 to 1000 males

It is characterized in adolescence by gynecomastia and small, firm testes with seminiferoustubule dysgenesis, and it is found in more than 80% of XXY males (i.e., males with

47 chromosomes) Levels of FSH and LH are elevated in these patients

66 Can puberty be safely accelerated?

In some teenagers—more commonly boys—the constitutional delay in puberty has

significant psychological effects Studies have shown that, in boys, puberty can be

accelerated without any compromise in expected adult height In boys older than 14 yearswith plasma testosterone levels of less than 10 ng/dL, 50 to 200 mg of intramusculartestosterone enanthate can be given every 2 to 4 weeks for 4 to 6 months Treatment forgirls who are constitutionally delayed is less well studied Conjugated estrogen (0.3 mg[e.g., Premarin]) or micronized estradiol (0.5 mg) orally daily or transdermal estradiol,12.5-25 mcg daily for 4 to 6 months has been used in girls older than 13 years withoutbreast buds

Kaplowitz PB: Delayed puberty, Pediatr Rev 31:189-195, 2010

KEY PO INTS: SEXUAL D EVELOPMENT

1 If no signs of puberty by age 13 in girls and age 14 in boys, evaluate for an underlyingpathologic medical cause

2 Most cases of late puberty are constitutional (genetic) delay

3 Nearly all boys begin puberty with testicular enlargement; 85% of girls begin puberty withbreast enlargement

4 Gynecomastia occurs in up to 50% to 75% of boys during Tanner genital stages II and III

5 Mean time between the onset of breast development and menarche is slightly more than

2 years

67 How do you evaluate a breast lump noted by a teenage girl on

self-examination?

Although the incidence of cancerous lesions is extremely low in adolescents, it is not zero,and breast lumps do require careful evaluation Fibrocystic changes (i.e., the proliferation ofstromal and epithelial elements, ductal dilation, cyst formation) are common in lateradolescence and are characterized by variations in size and tenderness with menstrualperiods The most common tumor (70% to 95%) is a fibroadenoma, which is a firm, discrete,rubbery, smooth mass that is usually found laterally Other causes of masses includelipomas, hematomas, abscesses, simple cysts, and rarely, adenocarcinoma (especially if abloody nipple discharge is present)

The size, location, and other characteristics of a mass should be documented andreevaluated over the next one to three menstrual periods A persistent or slowly growingmass should be evaluated with fine-needle aspiration Ultrasound can be helpful fordistinguishing cystic from solid masses Mammography is a very poor tool for identifyingdistinct pathologic lesions in teenagers because the breast density of adolescents makesinterpretation difficult

Huppert JS, Zidenberg N: Breast disorders in females In Slap GB, editor: Adolescent Medicine:The Requisites in Pediatrics, Philadelphia, 2008, Mosby Elsevier, pp 146–151

68 Should breast self-examination be taught and emphasized for all teenagegirls?

Because the incidence of malignancy is very low in this age group, no data support benefitsfor breast self-examination, and indeed it may cause unnecessary anxiety and testing.Exceptions would be all adolescents with a history of malignancy, those who have hadradiation therapy to the chest more than 10 years ago, and adolescents 18 to 21 years oldwhose mothers carry the BRCA1 or BRCA2 gene

Huppert JS, Zidenberg N: Breast disorders in females In Slap GB, editor: Adolescent Medicine:The Requisites in Pediatrics, Philadelphia, 2008, Mosby Elsevier, p 150

SEXUALLY TRANSMITTED INFECTIONS

69 How does the prevalence of sexually transmitted infections (STIs) inadolescents compare with that of adults?

Among sexually active people, adolescents have a higher likelihood than adults ofbeing infected with an STI About 25% of adolescents contract at least one STI by thetime of high school graduation Reasons for the increased susceptibility include thefollowing:

nCervical ectropion: Neisseria gonorrhoeae and Chlamydia trachomatis more readily infectcolumnar epithelium, and the adolescent ectocervix has more of this type of epitheliumthan does that of an adult

nCervical metaplasia in the transformation zone (from columnar to squamous epithelium) ismore susceptible to human papillomavirus (HPV) infection

nThere is less frequent use of barrier methods of contraception among this population

70 What is the best way to screen for STIs?

The gold standard for STIs, particularly in any case of possible sexual abuse, is culture.However, nonculture techniques, particularly involving nucleic acid amplification tests(NAATs), such as polymerase chain reaction or transcription-mediated amplification, arewidely used and widely studied, primarily for chlamydial and gonococcal infections

Advantages of NAATs include more rapid results and less invasiveness Disadvantagesinclude higher costs and lack of antibiotic sensitivity testing.

71 What should be the screening practice for STIs in male adolescents?

National recommendations for heterosexual males who are sexually active are less

explicit because of uncertainties related to cost-effectiveness and public health benefits.Screening for N gonorrhoeae and C trachomatis should be considered for high-risk males(multiple partners, inconsistent condom use) Universal screening for human immunodeficiencyvirus (HIV) is recommended For males who have had sex with males, CDC recommendationsinclude annual HIV and syphilis serology Annual or more frequent screening should be based

on specific sexual practices

Holland-Hall C: Sexually transmitted infections in teens, Contemp Pediatr 25:56–65, 2008

Centers for Disease Control and Prevention: Revised recommendations for HIV testing of adults,adolescents and pregnant women in health-care settings, Mortal Morb Wkly Rep 5:1, 2008

72 What is the most common STI in sexually active teenage males?

Urethritis, both gonococcal and nongonococcal Nongonococcal urethritis, particularly due to

C trachomatis, is more common and is often asymptomatic Other less common causes ofnongonococcal urethritis include Ureaplasma urealyticum, Trichomonas vaginalis, herpessimplex, HPV, and yeast

73 What should be the screening practice for STIs in female adolescents?For all sexually active females younger than 25 years, the U.S Preventive Services TaskForce recommends screening annually for C trachomatis and N gonorrhoeae Otherexperts recommend screening annually for T vaginalis infections as well Females at higherrisk, such as those with previous infections, irregular condom use, or multiple partners,may require screening more frequently Universal screening for HIV is recommended.Screening for syphilis and hepatitis B is on a case-by-case basis Screening for herpes isnot recommended

Holland-Hall C: Sexually transmitted infections in teens, Contemp Pediatr 25:56–65, 2008

Centers for Disease Control and Prevention: Revised recommendations for HIV testing of adults,adolescents and pregnant women in health-care settings, Mortal Morb Wkly Rep 55:1, 2008

74 Are pelvic examinations with specula always required to obtain specimens forpossible STIs in teenagers?

Trends in screening for STIs in teenage girls are shifting from endocervical sampling tourine-based and vaginal swab collection because:

nUrine testing for chlamydia and gonorrhea using nucleic acid amplification techniquesapproaches the sensitivity and specificity of specimens obtained using a speculum

nVaginal specimens obtained without the use of a speculum have a high screening validityfor trichomonas, bacterial vaginosis, and yeast infections

nSelf-collection by teenagers of vaginal specimens have yielded comparable resultscompared with physician-obtained cervical specimens when nucleic acid amplificationtesting was used

Fang J, Husman C, DeSilva L, et al: Evaluation of self-collected vaginal swab, first void urine,and endocervical swab specimens for the detection of Chlamydia trachomatis and Neisseria gonorrhoeae

in adolescent females, J Pediatr Adolesc Gynecol 21:355–360, 2008

75 Which STI is most closely linked to cervical cancer?

Human papillomavirus HPV affects 20% to 40% of sexually active adolescent females.More than 100 HPV types have been identified, of which about 40% are known to infect thegenital tract They differ in their likelihood of leading to cancer High-risk HPV includes types

16 and 18 Because of this association, the quadrivalent vaccine Gardasil and the bivalentvaccine Cervarix have been recommended by the Advisory Committee on ImmunizationPractices for adolescent females beginning at the 11 to 12-year visit.

76 What are the presentations of HPV infections?

Presentations of HPV are typically subclinical but can include anogenital condylomaacuminatum and cervical infection, which may lead to cervical dysplasia HPV is also

a cause of nonsexually transmitted disease, including deep plantar warts, palmarwarts, and common warts When compared with older adults, studies have demonstratedthat the natural history of cervical HPV infection in teenage girls is for spontaneousclearing of both the low-risk types (90%) and the high-risk types (75%) over a 6- to8-month period

77 When are Pap smears indicated in teenagers?

The American Cancer Society recommends a Pap screen within 3 years after the initiation ofsexual activity or by age 21 years, whichever comes first, with follow-up frequency dependent

on cytology and HPV DNA testing This reflects the high rates of regression of both HPVinfection and abnormal cytology (particularly low-grade squamous intraepithelial lesions) inadolescents

Greydanus DE, Omar H, Patel DR: Cervical cancer screening in adolescents, Pediatr Rev 30:23–25, 2009

78 Is the presence of an ectropion noted

on pelvic examination a concern?

An ectropion is the outward rolling of a

margin A cervical ectropion is the extension

of the erythematous columnar epithelium

from the os onto the duller, pink cervix It is

a relatively common finding in adolescents

However, large ectropions extending to

the vaginal wall or an abnormal cervical

shape can be associated with diethylstilbestrol

exposure in utero or chronic cervicitis

79 Describe the appearance of

condylomata acuminata

Condyloma acuminata (anogenital warts) are

soft, fleshy, wet, polypoid or pedunculated

papules that appear in the genital and

perianal area (Fig 1-3) They may coalesce

and take on a cauliflower-like appearance

Visualization of anogenital warts can be

enhanced by wetting the area with 3% to 5%

acetic acid (vinegar), which whitens

or surgical removal Recurrence rates can be as high as one third

Figure 1-3 Perianal condylomataacuminata (From Gates RH: InfectiousDisease Secrets, 2nd ed Philadelphia, Hanley

& Belfus, 2003, p 221.)

81 What are pearly penile papules?

This is a common condition in teenage males and is often misdiagnosed as condylomas.Multiple smooth, round, skin-colored papules develop most commonly at the corona of theglans penis and histologically are angiofibromas These are benign and have no associationwith papillomavirus

Kluger N, Dereure O: Penile papules N Engl J Med 360:1336, 2009

82 What is the typical presentation of chlamydial genital infections in both femaleand male teenagers?

Most are asymptomatic, which can persist for several months In females with symptoms,the disease should be suspected if vaginal discharge and bleeding are noted, especially afterintercourse; this may be due to endocervical friability In males, the most typical symptomsare dysuria and a penile discharge

Peipert JF: Genital chlamydial infections, N Engl J Med 349:2424–2430, 2003

83 A sexually active 17-year-old girl with adnexal and RUQ tenderness probablyhas what condition?

Fitz-Hugh-Curtis syndrome This is an infectious perihepatitis that is caused by gonococci or,less commonly, by chlamydiae It should be suspected in any patient with pelvic inflammatorydisease (PID) who has RUQ tenderness It may be mistaken for acute hepatitis or cholecystitis Thepathophysiology is thought to be the direct spread from a pelvic infection along the paracolicgutters to the liver, where inflammation develops and capsular adhesions form (the so-calledviolin-string adhesions seen on surgical exploration) If RUQ pain persists despite treatment forPID, ultrasonography should be done to rule out a perihepatic abscess

84 A teenage girl develops migratory polyarthritis, fever, and scattered petechiallesions several days before menses What condition should be suspected?Gonococcal-arthritis-dermatitis syndrome (GADS) After a migratory polyarthritis orpolyarthralgia, the arthritis settles in one or two large joints The patient then develops painfultenosynovitis over the tendon sheaths in addition to a characteristic crop of embolic skinlesions over the trunk and extremities Diagnosis is confirmed by culturing gonococci fromblood, synovial fluid, and/or rectal or genitourinary sites

85 What is the typical appearance of N gonorrhoeae on Gram stain?

Intracellular gram-negative diplococci (Fig 1-4)

Figure 1-4 Gram stain of Neisseriagonorrhoeae (From Gates RH:Infectious Disease Secrets, 2nd ed.Philadelphia, Hanley & Belfus,

2003, p 207.)

KEY POINTS: SEXUAL LY TRANSMITTED INFECT IONS

1 Regardless of the pathogen, most STIs in adolescents are asymptomatic

2 Nucleic acid amplification tests for chlamydia and gonorrhea are particularly useful whenscreening for urethritis in males and cervicitis in females

3 STI screening in girls is shifting from endocervical sampling to urine-based and vaginal swabcollection

4 The most common STI in adolescent males is urethritis due to Chlamydia trachomatis

5 Despite higher rates of STIs being found among adolescents than any other age group, cliniciansfrequently do not inquire about sexual activity, risk factors, or means of reducing risks

86 What is the minimal criteria for the diagnosis of Pelvic inflammatory disease (PID)?Any one of the following must be present:

nUterine tenderness

nCervical motion tenderness

nAdnexal tenderness

87 What additional criteria support the diagnosis of PID?

nOral temperature higher than 38.3C (101F)

nAbnormal cervical or vaginal discharge (with leukocytes> epithelial cells)

nElevated erythrocyte sedimentation rate (usually>15 mm/hour)

nElevated C-reactive protein

nCervical infection with N gonorrhoeae or C trachomatis

Because no single clinical aspect or laboratory test is definitive for PID, a constellation offindings is used to support the diagnosis

Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines, MortalMorb Wkly Rep 55:48, 2002

88 How is the diagnosis of PID definitively made?

nEndometrial biopsy with histopathologic evidence of endometritis (rarely done inteenagers due to low likelihood of endometrial cancer)

nTransvaginal or abdominal ultrasonography revealing tubo-ovarian abscess or fallopian tubeabnormalities (e.g., thickened, fluid-filled fallopian tubes with or without free pelvic fluid)

nLaparoscopy revealing abnormalities consistent with PID

American Academy of Pediatrics: Pelvic inflammatory disease In Pickering LK, editor: 2009 Red Book,

ed 28, Elk Grove Village, IL, 2009, American Academy of Pediatrics, pp 501–502

89 What are the sequelae of PID?

Twenty-five percent of patients with a history of PID will have one or more major sequelae ofthe disease, including the following:

nTubo-ovarian abscess

nRecurrent infection

nChronic abdominal pain: May include exacerbated dysmenorrhea and dyspareunia related

to pelvic adhesions in about 20% of patients with PID

nEctopic pregnancy: Risk is increased threefold to sevenfold

nInfertility: Up to 11% after one episode of PID, 30% after two episodes, and 55% afterthree or more episodes