Vol. II No.8February 1990
AMERICAN ACADEMY OF PEI)IATRICS
Pediatrics Review andEducation Program
227#{149}Pediatrician’s Perspectives: OddThoughts On Well-Child Care -Nazarian
229#{149}Precocious Puberty - Pescovitz
239#{149}Insulin-dependent DiabetesMellitus - Feliner
249#{149}Congenital Dislocation of the Hip- MacEwen and Millet
CONTE NTS
COMMENTARY
227 Pediatrician’s Perspective: Odd Thoughts on Well-
Child CareLawrence F. Nazarian
ARTICLES
229 Precocious Puberty
Ora Hirsch PeScovitz
239 Insulin-Dependent Diabetes MellitusFredda Ginsberg-Fellner
249 Congenital Dislocation of the Hip
G. Dean MacEwen and Chad Millet
ABSTRACTS
228 Ocular Complications in Very Low Birth Weight Infants
237 Bicycle Safety
238 Phenobarbital Therapy for Refractory Status Epilepticus
238 Antibiotic Treatment of Secretory OtitiS Media
248 Lactation Failure SeCondary to Insufficient Mammary
Glandular Tissue
253 Short-Term Corticosteroids for the Treatment of Acute
Asthma
254 Acute Cocaine Intoxication
255 Neurologic Sequelae of Cardiac Surgery
Cover: Breton Girls, Dancing, Pont Aven, by Paul GAUGUIN (Copyright,
National Gallery of Art, Washington, DC; Collection of Mr and Mrs Paul
Mellon). Gauguin was a French Symbolist and lived from 1848 to 1903.
Gauguin traveled the world as a seaman and pursued a career in bankingin Paris and Copenhagen before concentrating on his skills as a painter and
sculptor. He was determined to develop a new approach to painting through
which to symbolically express a thought or mood, in contrast to the impres-
sionist approach which sought to reproduce a scene through the exact
recording of every nuance of color and light. Completed in 1888, Breton
Girls Dancing, Pont Aven is one of Gauguin’s earliest works in this new
style. The themes of friendship, community, exercise, and appreciation of
nature depicted here are important elements in the total health and devel-
opment of every child,
�‘ The printIng and production of
______ Z Pediatrics in Review is made possible,
�. ROSS L� in part, by an educatIonal grant fromRoss Laboratories.
Answer Key: iD; 2.E; 3.A; 4.B; 5.A; 6.C; 7.D; 8.A; 9.A; lOB; hA; 12.E; 13.A; 14.D;15.C.
Vol. 11, No.8, February 1990
Pediatricsin ReviewEDITORRobert J. HaggertyNew York Hospital-CornellMedical CenterNew York, NY
Editorial Office:The William T. Grant Foundation515 Madison Aye, 6th Floor,New York, NY 10022-5403
ASSOCIATE EDITORLawrence F. NazananPanorama Pediatric GroupRochester, NY
Mailing Address:29 Surrey PlacePenfield, NY 14526
EVALUATION EDITORWilliam H. Milbum, Lyons, CO
MANAGING EDITORJo A. Largent, Elk Grove Village, IL
EDITORIAL CONSULTANTVictor C. Vaughan III, Stanford, CA
EDITORIAL BOARDRalph Cash, Detroit, MlDaniel D. Chapman, Ann Arbor, MlEvan Chamey, Worcester, MARussell Chesney, Nashville, TNAlan L. Goldbloom, Toronto, ONJ. Stephen Latimer, Bethesda, MDMarie C. McCormick, Boston, MAKurt Metzl, Kansas City, MOPhilip A. Pizzo, Bethesda, MDRobert Rennebohm, Columbus, OHWilliam 0. Rob&tson, Seattle, WARon Rosenfeld, Stanford, CARobert Schwartz, Providence, RIRobert J. Touloukian, New Haven, CTW. Allan Walker, Boston, MA
PUBLISHERAmerican Academy of PediatricsNancy Wachter, Copy Editor
PEDIATRICS IN REVIEW(ISSN 0191-9601)is owned and
controlled by the American Academy of Pediatrics. It ispubbshed ten times a year (July through April) by the Arner-can Academy of Pediatrics, 141 Northwest Point Blvd. ElkGrove village, IL 60009-0927.
Subscriptions will be accepted until December 31, 1989for the 1989-90 cycle. Subscription price per year: Candi-
date Fellow of the AAP $40; AAP Fellow $65; Nonmember
or Institution $85. Current single issues $8.Second-class postage paid at ELK GROVE ViLLAGE,
ILLINOIS 60009-0927 and at additional mailing offices.
C American Academy of Pediatrics. 1990All Rights Reserved. Printed in U.S.A. No part may be
duplicated or reproduced without permission of the Amen-can Academy of Pediatrics.
POSTMASTER: Send address changes to PEDIATRICS INREVIEW, American Academy of Pediatrics. 141 Northwest
Point Blvd. Elk Grove Village, IL 60009-0927
Pediatrician’s PerspectiveOdd Thoughts on Well-Child Care
It is good to take a hard look atlongstanding habits. Well-child careis at the heart of pediatrics; yet, eventhis most sacred of commitments hasbeen under scrutiny in recent years,and rightly so. But those of us whospend half of our time in well-childvisits are frustrated by studies thatfail to demonstrate any measurablebenefits from our efforts, with theexception of immunization programs.Are researchers really looking at theright parameters? Are there too manyvariables to allow a truly scientificevaluation of these practices?
At least it is comforting to hear thatparental satisfaction and confidenceare acknowledged by-products of ourwork, and intuitively we believe thatthis effect is good for growing chil-dren. But, as the song says, “Is thatall there is?” I believe there is a greatdeal more, and in this reflection Iwould like to focus on one particularbenefit of well-child care that is notoften discussed.
The pediatrician cannot properlyappreciate the infinite shadings of dis-ease without broad exposure to nor-mality, which includes all the varia-tions that are found in healthy, con-stantly changing children. A list ofanatomic idiosyncrasies alone wouldgo on for pages. How many differentshapes do we see in rib cages? Amodern phrenologist could make acareer cataloguing the different con-tours of normal infant heads. Let usnot even get started on toes, moles,and facial expressions. Then, there isphysiology. Vibratory murmurs, gaits,breathing patterns, sleep cycles-allhave their spectrum within the
boundaries of normality. Even morevaried is behavior, which can rangefrom withdrawn to near-maniacal,with everything in between, and stillbe considered normal. To all of thesepermutations and combinations, addthe constant metamorphosis of thegrowing and developing child andmultiply by countless environmentalscenarios. The result is a world ofchildren who possess such a dazzlingarray of characteristics that even de-fining normality becomes a struggle.
I contend that one cannot properlydiagnose illness and aberration with-out absorbing the features and de-tails of the normal landscape, and thebest way to digest this abundance isto spend considerable time with nor-mal children. Determining that a smallinfant is lethargic or breathing withlabor is possible, at least in the subtlesituation, only after observing largenumbers of infants going about theirusual business. Deciding at midnightwhether a toddler with a fever needsan involved and uncomfortable septicworkup is possible only after one haslogged many hours with tired buthealthy toddlers and anxious parents.Similarly, someone unfamiliar with themonosyllabic replies of 1 5-year-oldboys is at a disadvangage whentrying to evaluate a teenager’s mentalstatus. An inexperienced examinerwatching a 1-year-old baby’s early,awkward steps may find a disorderthat does not exist or miss one thatcauses a gait not quite like the usualwaddle.
Every child who comes in for aroutine health maintenance visit addsto the background against which the
pediatrician judges not only that childbut all the others as well. If there wereno other reasons to encourage well-child care-and I believe there aremany other justifications-this func-tion alone would make a strong ar-gument in favor of continuing the in-teraction between healthy childrenand their physicians.
Having presented the virtues, Imust also warn about a subtle butever-present danger accompanyingwell-child care.
The general pediatrician sees lotsof well children and many youngsterswith mild, self-limited disease. He orshe also encounters serious acuteillness and a modest share of chronicdisease although these account foronly a small portion of the encoun-ters. Consequently, the practitionergradually develops the bias that“there probably is no serious diseasehere,” and, most of the time, the real-ity is that serious disease is not pres-ent. But sometimes it is, when youleast expect it.
Residents and those just out oftraining have just the opposite bias.Every newborn who gags has a tra-cheoesophageal fistula. Every feverin a 2-month-old infant means sepsisor meningitis. A kid with a funny faceis sure to have an exotic syndrome,even though his father may look ex-actly the same. This way of lookingat things is also perfectly understand-able when one realizes that theseyoung pediatricians spend most oftheir time with children who do haveserious disorders.
The wellness bias that the practi-tioner develops may also be strength-
Self-Evaluation Quiz-CME Credit
As an organization accredited for continuing medical education,the American Academy of Pediatrics certifies that completion of theself-evaluation quiz in this issue of Pediatrics in Review meets thecriteria for two hours of credit in Category I of the Physician’sRecognition Award of the American Medical Association and twohours of PREP credit.
The questions for the self-evaluation quiz are located at the endof each article in this issue. Each question has a SINGLE BEST
ANSWER. To obtain credit, record your answers on your quiz replycards (which you received under separate cover), and return thecards to the Academy. On each card is space to answer thequestions in five issues of the journal: CARD 1 for the July throughNovember issues and CARD 2 for the December through Aprilissues. To receive credit you must currently be enrolled in PREP ora subscriber to Pediatrics in Review-and we must receive bothcards by June 30, 1990.
Send your cards to: Pediatrics in Review, American Academy ofPediatrics, 141 Northwest Point Blvd. P0 Box 927, Elk Grove Village,IL 60009-0927.
The correct answers to the questions in this issue appear on theinside front cover.
This One
I’ll Illu pediatrics in review #{149} vol. 11 no. 8 february 1990 PIR 227
EDUCATIONAL OBJECTIVE
52. The pediatrician should haveappropriate familiarity with the in-jury risk of bicycle riding and theimportance of protecting againsthead injuries by wearing protectivehead gear (Recent Advances, 89/90).
ENDOCRINOLOGY
pediatrics in review #{149} vol. 1 1 no. 8 february 1990 PIR 237
SUGGESTED READING
Kelch RP, Marshall JC, Sauder S, HopwoodNJ, Ream NE. Gonadotropin regulation dur-ing human puberty. In: Norman AL, ed. Neu-roendocrine Aspects of Reproduction. 5cc-ond Oregon Regional Primate ResearchCenter Symposium on Primate ReproductiveBiology; October 8-9, 1982; Beaverton, OR.New York, NY: Academic Press Inc;1983:229-257
Pescovitz OH, Comite F, Hench K, Barnes K,McNemar A, Foster C, et al. The NIH expe-nence with precocious puberty: diagnosticsubgroups and response to short-term lu-teinizing hormone releasing hormone ana-logue therapy. J Pediatr. 1986;108:47-54
Rosenfield A. Precocious puberty. In: KaplanSA, ed. Clinical Pediatric and AdolescentEndocrinology. Philadelphia, PA: WB Saun-ders Co; 1982:217-268
Wierman ME, Beardsworth DE, Badger TM,Crawford JD, Cngler JF Jr, Mansfield MJ, etal. Puberty without gonadotropins: a uniquemechanism of sexual development. N EngI JMed. 1 985;31 2:65-72
Self-Evaluation Quiz
1. Features of isolated premature adren-arche may include each of the followingexcept:
A. Pubic hair.B. Axillary hair.C. Acne.D. Accelerated closure of the epiphyses.E. Pubertal body odor.
2. Features of precocious puberty due to21-hydroxylase deficiency include each ofthe following except:
A. Virilization in girls.B. Acne.C. Accelerated linear growth.0. Accelerated epiphyseal closure.E. Testicular enlargement in boys.
3. Most instances of central precocious pu-berty are due to:
A. Unknown causes.
B. Hypothalamic hamartoma.
C. Craniopharyngioma.0. Trauma.E. Acquired hypothyroidism.
4. During the initial evaluation of the childwith signs of precocious puberty, the mostcritical laboratory examination among thefollowing is:
A. Measurement of follicle-stimulating hor-mone and luteinizing hormone levels.
B. Assessment of bone age.
C. Measurement of 17-hydroxyprogester-one production.
D. Measurement of dehydroepiandrosteronesulfate levels.
E. Computed tomographic and magneticresonance imaging scans of the head.
5. Gonadotropin-releasing hormone ana-logues are used effectively in the manage-ment of precocious puberty of:
A. Central origin.B. Ovarian origin.C. Testicular origin.0. Adrenal origin.
Bicycle Safety
A Case-Control Study of the Effectiveness of Bicycle Safety Helmets. ThompsonRS et al.N Engl J Med. 1989;320:1 363.
In the United States each year, 1300 deaths result from bicycle injuries. Most ofthese deaths are the result of head injuries. In a careful statistical study, these authors
I provide compelling evidence that safety helmets for bicyclers “are highly effective inpreventing head injury. . . .[They] are particularly important for children since they
� suffer the majority of serious head injuries from bicycling accidents. . . .Riders who do� not wear helmets appear to be at a 6.6-fold greater risk of head injury and an 8.3-fold
greater risk of brain injury than riders who do. . . .Head injuries from bicycling are animportant problem that grows as cycling continues to increase in popularity. . . Safetyhelmets are effective, but they are not being used enough. The time has come for amajor campaign to increase their use.”
Comment: In an associated editorial in the New England Journal of Medicine, there isdiscussion about the possible need for safety helmet laws and the infringement onpersonal freedom that such laws produce. I believe that this argument deflects ourthinking from the basic issue. Seat belts save lives. We need to encourage their useby whatever means are available. Education? Certainly. Collective pressure? Why not.Seat belt laws? If necessary. The same holds true for bicycling helmets.
For me, these are easier ethical issues than the ones we face every day in ournursery or pediatric intensive care unit, where what seem to me to be the real ethicaldilemmas constantly unfold. Bicycles are fun; they are good exercise. Helmets areperceived to be bulky and uncomfortable (they need not be) and seem silly andunnecessary. Not so! Physicians need to begin the process of education. To do so,they need to educate themselves. (R.H.R.)
METABOLISM
pediatrics in review #{149} vol. 1 1 no. 8 february 1990 PIR 247
REFERENCES
1 . Rubinstein P, Suciu-Foca N, Nicholson JF.Genetics of juvenile diabetes mellitus: arecessive gene closely linked to HLA-Dand with a 50% penetrance. N EnglJ Med.1977;297:1 046-1050
2. Todd, JA, Bell JI, McDevitt HO. HLA-DQBgene contributes to susceptibility and re-sistance to insulin-dependent diabetesmellitus. Nature. 1987;329:599-604
3. Tattersall RB, Pike PA. Diabetes in identi-cal twins. Lancet. 1972;2:1120-1124
4. Rubinstein P, Ginsberg-Fellner F, Falk CT.Genetics of type I diabetes: a single, re-cessive, predisposition gene mapping be-tween HLA-B and GLO. Am J Hum Genet.198133:865-882
5. Rayfield E J, Seto V. Viruses and thepathogenesis of diabetes mellitus. Diabe-tes. 1978;27:1 126-1140
6. Ginsberg-Fellner F, Witt ME, Fedun B, etal. Diabetes mellitus and autoimmunity inpatients with the congenital rubella syn-drome. Rev Infect Dis. 1985;70(suppl1):S170-Si 76
7. Menser MA, Forrest JM, Bransby JM. Ru-bella infection and diabetes mellitus. Lan-cet. i978;i:57-60
8. Bottazzo GF, Florin-Christensen A, Don-iach D. Islet cell antibodies in diabetesmellitus with autoimmune polyendocnnedysfunction. Lancet. 1974;2:i 279-i 283
9. Bottazzo GF, Gleichmann H. Immunologyand diabetes workshops: report of theFirst International Workshop on the Stand-ardization of Cytoplasmic Islet Cell Anti-bodies. Diabetologia. 1 986;29:i 25-i 26
io. Ginsberg-Fellner F, Witt ME, Franklin BH,et al. Triad of markers for identifying chil-dren at high risk for the development ofinsulin-dependent diabetes mellitus.JAMA. 1 985;254:i 469-i 472
1 1 . Nayak AC, Omar MAK, Rabizadeh A, etal. “Cytoplasmic” islet cell antibodies: cvi-dence that the target antigen is a slab-glyco-conjugate. Diabetes. i985;34:6i 7-6i 9
12. Baekkeskov S, Nielsen JH, Marner B, etal. Autoantibodies in newly diagnosed di-abetic children immunoprecipitate humanpancreatic islet proteins. Nature. 1982;298:i 67-169
13. Drell DW, Notkins AL. Multiple and tran-sient immunological abnormalities in pa-tients with insulin-dependent diabetesmellitus. Diabetologia. 1987;30:i32-i43
i4. Horita M, Suzuki H, Onodera T, et al.Abnormalities of immunoregulatory T cellsubsets in patients with insulin-dependentdiabetes mellitus. J Immunol. 1982;129:1426-i 429
1 5. Bottazzo GF, Path MAC, Dean BM, et al.In situ characterizations of autoimmunephenomena and expression of HLA mole-cules in the pancreas in diabetic insulitis.N EngI J Med. 1985;3i 3:353-360
16. Stiller CR, Dupre J, Gent M, et al. Effectsof cycbosporine immunosuppression inIDDM of recent onset. Science. 1984;223:1 362-i 365
17. Sibley AK, Sutherland DE, Goetz FC, etal. Recurrent IDDM in pancreatic iso- andallografts: a light and electron microscopicand immunohistochemical analysis of 4cases. Lab Invest. 1985;53:i 32-i 44
18. Srikanta 5, Aicker AT, Mcdulloch DK, etal. Autoimmunity to insulin, �1 cell dysfunc-tion and developmentof insulin-dependentdiabetes mellitus. Diabetes. 1 986;35:1 39-142
19. Ginsberg-Fellner F, Dobersen MJ, WittME, et al. HLA antigens, cytoplasmic isletcell antibodies and carbohydrate tolerancein families of children with insulin-depend-ent diabetes mellitus. Diabetes. i982;3i:292-298
20. Srikanta S, Ganda OP, Eisenbarth GS, etal. Islet cell antibodies and �1-cell functionin monozygotic triplets and twins initiallydiscordant for type I diabetes mellitus. NEngi J Med. 1983;308:322-329
21 . Koenig RJ, Peterson CM, Jones AL, et al.Correlation of glucose regulation and he-moglobin Al C in diabetes. N Engl J Med.1976;295:4i 7-420
SUGGESTED READING
Brink SJ. Pediatric and Adolescent DiabetesMellitus. Chicago, IL: Year Book MedicalPublishers, Inc; 1987
The Physician’s Guide to type I Diabetes(IDDM). American Diabetes Association nc,Clinical Education Program, 1988
Self-Evaluation Quiz
6. Each of the following is a true statementabout the genetic factors involved with in-
sulin-dependent diabetes mellitus (IDOM),except:
A. At least 90% of white patients who haveIDDM have HLA-DR3 and/or -DR4.
B. HLA-DR2 and -DR5 appear to protectagainst IDDM.
C. The mechanism of inheritance of IDDM isan autosomal dominant trait.
D. Genetic susceptibility alone is not suffi-cient to result in clinical diabetes.
E. Genetic factors appear to outweigh envi-ronmental factors in the development of
clinical diabetes.
7. Which of the following is a likely findinglong before the development of clinicalIDDM?
A. Abnormal glucose tolerance.B. Sluggish insulin response to glucose chal-
lenge.C. Abnormal fasting blood glucose levels.D. Presence of antiislet cell antibodies.E. Glucosuria.
8. Which of the following is a practicaltechnique for maintaining near normogly-cemia with IDDM?
A. Individualized diet planning.B. No more than one insulin injection per
day.C. Use of short-acting insulin alone.D. Use of intermediate-acting insulin alone.
9. Capillary blood measurements in a childwho has IDDM need to be taken at each ofthe following times only once per week,except:
A. Before breakfast.B. Before lunch.
C. Before bedtime.D. At2or3AM.
10. Each of the following needs to be eval-uated annually in a child or adolescent whohas IDDM, except:
A. Growth percentile.B. Oral glucose tolerance.C. Renal function.D. Deep tendon reflexes.E. Thyroid status.
Congenital Dislocation of the Hip
PIR 252 pediatrics in review #{149} vol. 1 1 no. 8 february 1990
of choice by the majority of physi-cians is the use of a Pavlik harness.Described in 1 95714 this device en-courages both flexion and free ab-duction. It allows the femoral head tobe directed toward the acetabulumwhile preserving the capacity for mo-tion in a safe range, or “safe zone,”16facilitating reduction and minimizingthe risk of avascular necrosis.
Most (80% to 93%) childrenyounger than 6 months of age withcongenital dislocation of the hip maybe successfully treated with a Pavlikharness. The Pavlik method17 doesnot require hospitalization or surgerywhen it is successful in this agegroup. Stability of the hip in the new-born with the Pavlik harness can usu-ally be achieved in approximately 4weeks. After the newborn period, thetotal duration of treatment is approx-imately one to two times the age atwhich initial treatment was started. Ifthe femoral head does not becomecentered after 2 to 3 weeks, themethod should be abandoned andtraction and closed reduction may beperformed. A home traction programsupervised by a clinical nurse spe-cialist can minimize or even eliminatehospitalization, thereby reducing costand parental anxiety.
Other methods and devices havealso been successfully used to treatcongenital dislocation of the hip in-dude the Frejka pillow, the Craigsplint, and the von Rosen splint. Mul-tiple diapers are ineffective to stabi-lize a grossly unstable hip and arementioned here to be condemned.
SUMMARY
Early diagnosis and treatment arethe keys to a successful result ininfants with congenital dislocation ofthe hip. In the neonatal period, a ma-jority of infants with hips that wouldlater be found to be dislocated canbe detected and effectively treated.With the use of ultrasonography tosupplement clinical suspicion, thenumber of children with congenitaldislocation of the hip diagnosed in thenewborn period should be expectedto increase. Repeated examination,especially during the first 6 months oflife, can be expected to detect thoseadditional children with congenitaldislocation of the hip who were notdetected in the nursery.
The Pavlik harness has beenshown to obtain a successful resultin most children younger than 6months of age while holding the mci-dence of avascular necrosis to nearlyzero. Even though these results areencouraging, the problem must bediscovered early for the child withcongenital dislocation of the hip to betreated optimally. Thus, it is of theutmost importance that the physicianhave an awareness of this problem.The primary physician must also con-tinue to conscientiously examine thehips of patients on a regular basiseven after the initial examination and,when necessary, use the added mo-dalities available to him or her to ad-curately diagnose questionable hipconditions of patients.
REFERENCES
i . MacEwen GD, Ramsey PL. The Hip. In:Lovell WW, Winter AB, eds. Pediatric Or-thopaedics. Philadelphia, PA: JB Lippin-cott; 1985:703-736
2. Dunn PM. Perinatal observations on theetiology of congenital dislocation of thehip. Clin Orthop. 1976;i i9:11-22
3. Morrison DL, MacEwen GD. Congenitalmuscular torticollis: observations regard-ing clinical findings, associated conditionsand results of treatment. J Pediatr Orthop.i982;2:505
4. Wynne-Davies A. A family study of neo-natal and late diagnosis congenital dislo-cation of the hip. J Med Genet.i970;7:31 5-324
5. Kumar SJ, MacEwen GD. The incidenceof hip dysplasia with metatarsus adduc-tus. dIm Orthop. i982;i64:234-235
6. Wynne-Davies A. Family studies and thecause of congenital clubfoot: talipes equi-novarus, talipes calcaneovalgus, metatar-sus varus. J Bone Joint Surg Br.1964;46B:445-464
7. Hannson G, Nachemson A, Palmen K.Screening of children with congenital dis-location of the hip joint on the maternitywords in Sweden. J Pediatr Orthop.i 983;3:27i
8. Ogden JA. Changing patterns of proximalfemoral vascularity. J Bone Joint Surg AMi974;56A:94i
9. Wilkinson JS. Prime factors in the etiologyof congenital dislocation of the hip. J BoneJoint Surg Br. 1963;45B:268
io. Thieme WT, Wynne-Davies R, Blair HAF,Loraine JA. Clinical examination and un-nary estrogen assays in the newborn chil-dren with congenital dislocation of the hip.J Bone Joint Surg. Br. 1968;50B:546
1 1 . Chapple C, Davidson D. A study of therelationship between fetal positions andcertain congenital deformities. J Pediatr.i94i 18:483
12. Barlow TG. Early diagnosis and treatmentof congenital dislocation of the hip. J BoneJoint Surg Br. i962;44B:292
13. Pavlik A. De funktionelle Behand lungsmethode mittels Riemonbugel als Pninzipderkonservativen therapie bei angebone-nen (Huft gelenk suerren kungen) den San-glinge. Z Orthop 1972;89:34i
14. Coleman 55. Diagnosis of congenital dys-plasia of the hip in the newborn infant.JAMA. i956;i62:548-554
15. Clarke NMP, Hancke HT, McHugh P, LeeMS, Bonns PF, MacEwen GD. Real-timeultrasound in the diagnosis of congenitaldislocation and dysplasia of the hip. JBone Joint Surg Br. i 985;67B:406
16. Ramsey PL, Lasser 5, MacEwen GD.Congenital dislocation of the hip: use ofthe Pavlik harness in the child during thefirst 6 months of life. J Bone Joint SurgAm. i976;58A:i000
17. Filipe G, Carlioz H. Use of the Pavlik han-ness in treating congenital dislocation ofthe hip. J Pediatr Orthop. 1982;2:257-36i
Self-Evaluation Quiz
1 1. Dislocated hip is best defined as:A. Complete displacement of the femoral
head from the acetabulum.B. Complete displacement of the femoral
head from the acetabulum with slight
force.
C. Partial displacement of the femoral headfrom the acetabulum.
D. Partial displacement of the femoral headfrom the acetabulum with slight force.
12. Each of the following factors is likely tobe associated with an increased risk forcongenital dislocation of the hip (CDH) cx-cept:
A. Breech presentation.B. White race.C. Positive family history.D. Facial abnormalities.E. Male.
13. The most useful method for detectingCDH is:
A. Physical examination.B. Plain roentgenography.C. Real-time ultrasonography.D. Anthrography.E. Magnetic-resonance imaging.
14. The Ortolani method is best defined as:A. Dislocation of the hip by downward pres-
sure on the adducted flexed thigh.B. Reduction of the dislocated hip by down-
ward pressure on the adducted flexedthigh.
C. Dislocation of the hip by abduction of theflexed thigh.
D. Reduction of the dislocated hip by abduc-tion of the flexed thigh.
15. Effective treatments for CDH include theuse of each of the following except:
A. Pavlik harness.B. Frejka pillow.C. Triple diapers.D. Craig splint.E. von Rosen splint.
