PEDIATRIC CONCERNS
From the 30th Annual Spring/Fall Family Practice Review, sponsored by the Temple University School of Medicine,
Philadelphia, PA
| JAUNDICE IN INFANTS —Andrea C.S. McCoy, MD, Associate Professor of Pediatrics, Temple University School of
Medicine, Philadelphia, PA
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| Introductory remarks: clinicians can assess severity of jaundice in infants and decide whether there is need for treatment;
since introduction of RhoGAM, continue to see kernicterus and significant preventable morbidity from hyperbilirubinemia
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| Conjugated vs unconjugated hyperbilirubinemia in newborn: conjugated—always pathologic; causes include
sepsis, viral infections, hypothryroidism or hypopituitarism, anatomic abnormalities, Dubin-Johnson or Rotor’s
syndrome, and various inborn errors of metabolism; unconjugated—physiologic condition; common (occurs in ≤60%
of babies); causes include breast-feeding, inherited conditions (eg, Crigler-Najjar syndrome, Gilbert syndrome)
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| Epidemiology of hyperbilirubinemia: 50% to 60% of full-term babies develop some degree of jaundice; hyperbilirubinemia
typically peaks at 3 to 5 days; however, can last for several weeks; because so many babies develop jaundice,
question becomes at what level does disease require treatment (not clear there is safe level, and clinicians should not be
complacent about what appear to be “physiologic levels” of jaundice)
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| Pathophysiology of hyperbilirubinemia in infants: contributing factors—faster breakdown of red blood cells
(RBCs); babies born with levels of hemoglobin and hematocrit significantly higher than needed in outside world; decreased
caloric and fluid intake; immature uridine diphosphate (UDP)-glucuronyl transferase system; delayed meconium
passage; intestinal bacterial colonization; protein binding
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| Acute bilirubin encephalopathy: early stage—lethargy; hypotonia; weak suck; intermediate stage—babies become
stuporous, irritable, and often have high-pitched cry that can alternate with lethargy; hypertonia; at this point, emergent
exchange transfusion can reverse symptoms and prevent kernicterus from developing; advanced stage—
retrocollis; opisthotonus; refusal to feed; stupor/coma; apnea; seizures (once baby reaches this point, symptoms resolve,
but irreversible damage done to brain and basal ganglia); end result of chronic bilirubin encephalopathy is yellow staining
of brain; syndrome characterized by athetoid cerebral palsy (CP), paralysis of upward gaze, hearing loss, and dysplasia
of dental enamel; intellectual deficits variable
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| Risk factors: prematurity; hypoxemia; hemolytic disease; breast-feeding; bruising/cephalhematomas; East Asian race;
macrosomic infant of diabetic mother; previous sibling with jaundice; delayed cord clamping
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| Assessment: must be ongoing; clinical assessment should be done on every shift; transcutaneous measurements increasing
in popularity (meters fairly accurate up to level of 15 mg/dL); serum levels gold standard for measuring bilirubin in
babies (assessment based on age in hours)
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| Management: ensure adequate feedings and adequate wet diapers; ensure adequate support for breast-feeding babies as
well; phototherapy standard of care; baby undergoing phototherapy should have bilirubin levels assessed every 6 to 12
hr; phototherapy discontinued after bilirubin reaches 1.5 to 3.0 mg/dL below that at which therapy started; follow-up bilirubin
levels should be done 6 to 12 hr after discontinuing therapy; intravenous (IV) gamma globulin studied (proven effective
in trials, but not yet used in clinical practice); exchange transfusion still necessary in babies who fail to respond to
phototherapy; hemoxygenase inhibitors (investigational; promising treatment for babies at risk for significant jaundice)
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| Breast-feeding and jaundice: breast-feeding jaundice starts in first 2 days after birth; management for these children
includes ensuring adequate feeding and early follow-up; recent studies identified β-glucoronidase inhibitors (eg, L-aspartic
acid) as potential intervention
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| Follow-up: important; includes parent education and early office visits (babies should be seen within 2 days of discharge
if they go home at 48 hr, 3 days if they go home at 72 hr)
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| HIP PAIN IN CHILDREN —James J. McCarthy, MD, Assistant Chief of Staff, Shriners Hospital for Children, Philadelphia,
PA
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| Introductory remarks: hip disorders in children can be slightly more subtle than in adults; pain from hip disorders
tends to be in groin, sometimes in anterior thigh; acute or chronic; usually activity-related; can have locking or snapping
quality
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| Physical examination: patients often hold hip flexed or experience pain when hip flexed; internal or external rotation
of hip may elicit pain; “C-sign” indication of pain around groin; patient may walk with limp (any limp in child abnormal,
even if painless); if in doubt, check hip; if still in doubt, check spine; with hip disorders in children, if patient’s age
known, have good clue to underlying condition
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| Hip dysplasia: occurs in 1 in 1000 children; not painful as infant or child, but may be as adolescent or adult; includes variety
of hip disorders; risk factors—female sex; first born; breech birth; family history; increased flexibility; conditions
suspicious for hip dysplasia—metatarsus adductus; torticollis; signs suggesting hip dysplasia (Ortolani sign; Barlow
sign); always document hip range of motion at well baby checks, especially hip abduction; pitfalls in hip
examination—using too much force; child not relaxed; too little time; if unsure, repeat examination; if still unsure, order
ultrasonography or (in older child) hip x-ray; signs of hip dysplasia in child 3 to 6 mo of age—Galeazzi sign;
asymmetric thigh skin folds; decreased abduction
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 | Treatment: 0 to 6 mo of age—brace; the earlier child seen and treated, the better; 2 yr of age—requires casting; >3 yr
of age—more aggressive surgery needed; patients must be followed until skeleton matures, ie, until adulthood (residual
hip dysplasia in young adult can be problem)
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| Septic arthritis: difficult to diagnose in infant, but devastating if not diagnosed and treated within hours; in differential diagnosis,
toxic (transient) synovitis most common; characteristics of septic arthritis vs characteristics of toxic synovitis; classic
study found combination of fever, non-weight bearing (NWB), erythrocyte sedimentation rate (ESR) >40 mm/hr, and white
blood cell (WBC) count >12,000 cells/mm3 99% predictive of septic arthritis (having 3 of 4 93% predictive)
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| Management: if not detected and treated early, septic arthritis destroys hip; diagnosis made through hip joint aspiration;
risk factors for poor results—age <6 mo; diagnosis delayed >4 days; associated osteomylitis or Staphylococcus aureus
infection; prematurity
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| Neonatal septic arthritis: even harder to diagnose, as child cannot say whether he or she has hip pain, and often does not
have signs indicative of septic arthritis (fever, increased ESR, increased WBC), thus, must have high index of suspicion
in these children
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| Legg-Calvé-Perthes disease: presents in children 4 to 8 yr of age, often as painless limp; recurrent avascular necrosis
(AVN) of femoral head; etiology unclear; tends to occur more in boys than in girls; 10% of cases bilateral; patients almost
always skeletally immature and tend to be white; 33% of patients hyperactive; management—children <6 yr of age do
fairly well without treatment, while those >8 yr of age do poorly without treatment; thus, management tends to concentrate
on treating disease in children >8 yr of age; treatment varies
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| Slipped capital femoral epiphysis (SCFE): tends to occur in children 11 to 14 yr of age; can occur with very little
trauma (thus, hard to make diagnosis); fairly uncommon; often seen in children who are heavier; etiology believed partly
mechanical and partly related to weight; can also be associated with endocrine abnormalities (eg, hypothyroidism), especially
in child <10 yr of age; can be unstable or acute (occurs quickly, almost like fracture; patients tend to have poor outcome)
or chronic (tends to occur very slowly; patients do much better); can be classified by degree of slip (mild,
moderate, or severe)
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| Management: diagnosis—clinical examination most important; must have high index of suspicion; patients often have
groin pain; any teenager with groin pull needs x-ray of hip, both anteroposterior (AP) and lateral; also suspect in any
teenager walking with limp, especially if walking with external rotation; x-rays can be subtle or obvious; treatment is
surgery
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| Hip fractures in children: extremely uncommon (<1% of all pediatric fractures and <1% of all hip fractures); occur with
high-energy trauma, eg, motor vehicle accidents (MVAs); stress fractures occur in teenagers who do great deal of walking or
marching
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| Chondrolysis of hip: uncommon but worth considering in teenager who presents with progressive hip pain; defined as
decreased joint space; seen in young pregnant women and in teenagers; etiology typically unknown; can be associated
with SCFEs or with other disorders (eg, trauma, burns, immobilization); treatment early on includes range of motion
(ROM) exercises, nonsteroidal anti-inflammatory drugs (NSAIDs), traction, and bed rest; important to treat aggressively;
not clear surgical treatment helpful
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| Coxa saltans: also known as “snapping hip”; typically occurs in teenagers and young adults; most common type iliotibial
band (common in young women; almost never requires management other than conservative treatment); can also get iliopsoas
(“tendon popping”) or interarticular lesions such as labral tears or loose bodies (treatment hip arthroscopy; works very
well)
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| CHILDHOOD ASTHMA —Derek Johnson, MD, Assistant Professor of Pediatrics, and Director, Division of Allergy and
Immunology, Temple University School of Medicine, Philadelphia, PA
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| Introductory remarks: asthma most common chronic disorder in children and most common discharge diagnosis at pediatric
institutions; up to 5000 deaths annually from pediatric and adult asthma, most of which preventable with appropriate
treatment
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| Pediatric asthma: epidemiology—disproportionate racial and economic distribution (high prevalence among blacks
and in lower socioeconomic groups); during last 30 yr, 232% increase in incidence of asthma and other atopic diseases vs
113% increase of other disabling childhood diseases (eg, diabetes, hypertension); hygiene hypothesis (suggests that elimination
of underlying risk factors and changes in host resistance resulted in increased rates of atopic diseases [eg, asthma,
eczema, atopic dermatitis] in industrialized societies); pathophysiology—genetic predisposition to disease and environmental
exposure combine to produce asthma and allergic rhinitis; persistence of childhood asthma
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| Myths about pediatric asthma: most pediatric patients have intermittent asthma—while some patients truly have
intermittent asthma, majority have persistent asthma (as defined by asthma control); small number of patients with persistent
disease have refractory asthma (very difficult to control); appropriate to treat asthma symptomatically—another
myth; most asthmatic children do not require maintenance therapy—study showed that relative risk for asthma-related
hospitalization increases dramatically in patients who require many prescriptions for rescue medications; “rules of
two” can be used to quickly determine if patient candidate for controller therapy; albuterol metered-dose inhaler (MDI)
usage effective marker for asthma control; mild asthma is not serious disease—Australian study from late 1980s reviewed
all pediatric asthma-related deaths over 3-yr period; classified 33% of patients as severe, 33% moderate, and 33%
mild; mild asthmatics may waver in lower limits of symptoms, then suddenly have severe exacerbation with bad outcome
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| Comments: results from Asthma in America survey clearly showed that patients in United States overestimate amount of
control they have over their disease; thus, cannot rely on patient’s perception
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| Stepwise approach to therapy (National Institutes of Health [NIH] guidelines): asthma divided into persistent
or intermittent disease; persistent disease further subdivided as mild, moderate, or severe; classification (severity)
of patient’s asthma based on symptoms before treatment; management based on treatment recommendations for
that classification; patients followed, and at 3 mo, if not doing well, may want to step up to next level of treatment (or
step down level, if patient doing well), until control of asthma achieved; patients classified based on most severe symptom
or feature
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| Recommended treatment: multiple studies shown that inhaled corticosteroids (ICS) best way to manage chronic inflammation
in lungs; mild persistent asthma—newer alternative therapies include mast cell stabilizers (eg, cromolyn,
nedocromil) and leukotriene receptor antagonists (LTRAs; eg, montelukast, zileuton); however, if control of disease
not established in first 2 wk, reconsider therapeutic approach and remember that ICS considered treatment of choice
for mild persistent asthma; moderate persistent asthma—low-dose ICS plus long-acting β-agonist; severe persistent
asthma—high-dose ICS plus long-acting β-agonist; although not included in NIH guidelines, omalizumab (Xolair)
monoclonal anti-IgE medication indicated for severe and moderate persistent asthma and shows promise in managing
previously difficult-to-control disease
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| Preventable causes of unnecessary systemic side effects of ICS: failure to back titrate dose; prescribing newer
drugs at old-drug doses; failure to take unusually good compliance into account; overreliance on single-drug therapy;
failure to minimize swallowed (nontherapeutic) portion of drug
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| Studies: Childhood Asthma Management Program (CAMP) study; effects of inhaled budesonide on adult height (Agertoft
& Pedersen 2000) study
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| Concluding comments: in asthma, some progressive airway remodeling present, and eventually becomes irreversible
airway disease; sooner treatment started, greater improvement in lung function; while prednisone good medication for
patient with persistent asthma, patient who requires prednisone burst for exacerbation that is out of control has not received
appropriate long-term therapy (typical dose of prednisone prescribed for patient having exacerbation of asthma 2
mg/kg per day for 5 days); keep in mind that repeated courses of oral systemic corticosteroids warning sign patient’s
asthma not well controlled; any amount of ICS better than repeated doses of systemic drug; exercise asthma (exercise
trigger for asthma; need to approach these patients as persistent asthmatics and address their underlying disease)
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Educational Objectives
| The goal of this activity is to provide an update on the management of pediatric conditions, specifically jaundice in infants,
hip pain in children, and childhood asthma. After hearing and assimilating this program, the clinician will be better able to:
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| 1. Describe the epidemiology and pathophysiology of neonatal hyperbilirubinemia.
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| 2. Assess patients for the presence of neonatal jaundice, measure its severity, and prescribe effective treatment.
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| 3. Diagnose common painful hip disorders in children, including hip dysplasia and septic arthritis.
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| 4. Effectively manage the underlying disorders responsible for hip pain in children.
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| 5. Dispel some of the common misperceptions about pediatric asthma.
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Discussed on This Program
Albuterol (salbutamol sulphate in United Kingdom) [several trade names]
Beclomethasone dipropionate [several trade names]
Budesonide [Entocort EC, Pulmicort Respules, Pulmicort Turbuhaler, Rhinocort, Rhinocort Aqua]
Cromolyn sodium (disodium cromoglycate) [Crolom, Gastrocrom, Intal, NasalCrom, Opticrom]
Fluticasone propionate [Cutivate, Flovent, Flovent HFA, Flovent Diskus, Flovent Rotadisk, Flonase]
Immune globulin intravenous (IGIV) [several trade names]
Montelukast sodium [Singulair]
Nedocromil sodium [Alocril, Tilade]
Omalizumab [Xolair]
RhO (D) immune globulin (RhO [D] IGIM) [BayRho-D Full Dose, RhoGAM]
Zileuton [Zyflo]
Suggested Reading
Agertoft L, Pedersen S: Effect of long-term treatment with inhaled budesonide on adult height in children with
asthma. N Engl J Med 343:1064, 2000; Akobeng A: Neonatal jaundice. Clin Evid 12:501, 2004; Bhutani VK et al:
Risk management of severe neonatal hyperbilirubinemia to prevent kernicterus. Clin Perinatol 32:125, 2005; Caird MS
et al: Factors distinguishing septic arthritis from transient synovitis of the hip in children. A prospective study. J Bone
Joint Surg Am 88:1251, 2006; Carlsen KH: Pharmaceutical treatment of asthma in children. Curr Drug Targets Inflamm
Allergy 4:543, 2005; Forlin E et al: Treatment of developmental dysplasia of the hip after walking age with open
reduction, femoral shortening, and acetabular osteotomy. Orthop Clin North Am 37:149, 2006; Frick SL: Evaluation of
the child who has hip pain. Orthop Clin North Am 37:133, 2006; Gent E et al: Perthes' disease in the very young child.
J Pediatr Orthop B 15:16, 2006; Juretschke LJ: Kernicterus: still a concern. Neonatal Netw 24:7, 2005; Kocher MS
et al: A clinical practice guideline for treatment of septic arthritis in children: efficacy in improving process of care and effect
on outcome of septic arthritis of the hip. J Bone Joint Surg Am 85-A:994, 2003; Kocher MS et al: Differentiating
between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J
Bone Joint Surg Am 81:1662, 1999; Long-term effects of budesonide or nedocromil in children with asthma. The Childhood
Asthma Management Program Research Group. N Engl J Med 343:1054, 2000; Ninan TK, Russell G: The
changing picture of childhood asthma.Paediatr Respir Rev 1:71, 2000; Paton RW: Management of neonatal hip instability
and dysplasia. Early Hum Dev 81:807, 2005; Paton RW et al: The significance of at-risk factors in ultrasound
surveillance of developmental dysplasia of the hip. A ten-year prospective study. J Bone Joint Surg Br 87:1264, 2005; Paton
RW, Paniker J: The efficacy of the Pavlik harness, the Craig splint and the von Rosen splint in the management of
neonatal dysplasia of the hip. J Bone Joint Surg Br 85:1086, 2003; Schuh S, Johnson D et al: Hospitalization patterns
in severe acute asthma in children. Pediatr Pulmonol 23:184, 1997; Schuh S, Johnson DW et al: Comparison of albuterol
delivered by a metered dose inhaler with spacer versus a nebulizer in children with mild acute asthma. J Pediatr
135:22, 1999; Simmons AL: Primary care management of childhood asthma. J Ark Med Soc 102:85, 2005; Smitherman
H et al: Early recognition of neonatal hyperbilirubinemia and its emergent management. Semin Fetal Neonatal
Med 11:214, 2006; Spahn JD, Szefler SJ: Childhood asthma: new insights into management. J Allergy Clin Immunol
109:3, 2002; Tiker F et al: Extreme hyperbilirubinemia in newborn infants. Clin Pediatr (Phila) 45:257, 2006; Vreman
HJ et al: Phototherapy: current methods and future directions. Semin Perinatol 28:326, 2004; Wennberg RP et
al: Toward understanding kernicterus: a challenge to improve the management of jaundiced newborns. Pediatrics
117:474, 2006; Yang KD: Asthma management issues in infancy and childhood. Treat Respir Med 4:9, 2005.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. The following has been disclosed:
Dr. McCoy received research sponsorship from InfaCare Pharmaceutical Corp. Dr. Johnson is on the Speakers’ Bureau
of AstraZeneca Pharmaceuticals LP, Genetech, Inc., GlaxoSmithKline Inc., and Novartis Pharmaceuticals Corp.
Drs. McCoy, McCarthy, and Johnson spoke at the 30th Annual Spring/Fall Family Practice Review, held March 26-30,
2006, in Philadelphia, PA, and sponsored by the Temple University School of Medicine. The Audio-Digest Foundation
thanks Drs. McCoy, McCarthy, and Johnson and the Temple University School of Medicine for their cooperation in the production
of this program.
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