Primary Care and Adolescent Medicine



Primary Care and Adolescent Medicine


Michele S. Duke

Anna Wheeler Rosenquist

Bradley Monash

Paritosh Prasad

Shannon E. Scott-Vernaglia



Breast-feeding


Breast-feeding Rates United States, 2001

(Pediatrics 2005;115:496)



  • 70% initiate, 33% at 6 mo, 18% at 1 yr of age


  • Goal for Healthy People 2010: 75% initiate, 50% at 6 mo, 25% at 1 yr of age


Infant Benefits



  • ↑ immunity: ↓ meningitis, bacteremia, UTI, AOM, diarrheal illness, URI, NEC


  • ↓ postneonatal infant mortality; decreased SIDS, incidence of Type I IDDM, lymphoma, leukemia, Hodgkin disease, obesity, hyperlipidemia, asthma


  • Enhanced performance on tests of cognitive development


Maternal Benefits



  • Decreases postpartum bleeding, risk of breast CA, and ovarian CA


  • May decrease incidence of osteoporosis and hip fractures after menopause


  • Earlier return to prepregnancy weight


Contraindications



  • Mother on contraindicated medications; tables available (Pediatrics 2001;108:776)


  • Infant with classic galactosemia (galactose 1-phosphate uridyltransferase deficiency)


  • Mother with HTLV


  • Mother receiving radioactive isotopes until cleared, antimetabolites or chemotherapeutic agents, or those using drugs of abuse


  • Herpes simplex virus lesions of the breast (may use other breast if unaffected)


  • HIV infection (must do risk-benefit analysis in developing countries because of lack of clean water supply, availability of formula, and frequency of dehydrating illnesses)


NOT Contraindicated



  • Maternal Hep B surface antigen positive, Hep C infection (Ab or RNA positive)


  • Maternal carriage of CMV (not recent converters), isolated maternal fever


Selected AAP Breast-feeding Recommendations



  • Vitamin D supplementation



    • Begin w/i 2 mo; 200 IU daily


    • D/c when daily consumption of Vitamin D fortified formula or milk >500 mL


  • Frequency of feeding



    • 8–12 times daily during initiation; 6–8 times daily when well established


  • Complementary foods and liquids



    • No water or juice needed under 6 mo; no cow’s milk until age 1 yr


    • Introduce complementary iron rich foods at 4–8 mo


  • Follow up visits



    • Check weight and breast-feeding at 3–5 d and 10–14 d


    • Special considerations for low-birth-weight, prematurity, or if risk for hemolysis


Breast-feeding Support



  • Lactation consultant www.ilca.org, La Leche League www.llli.org


Cow’s Milk Protein Allergy

See Allergy section


Reflux

See GI section


Sudden Infant Death Syndrome (SIDS)


Definition

(Pediatr Rev 2007;28:209)



  • Sudden unexplained death of an infant younger than 1 yr of age.


  • Usually previously healthy infant; cause of death unexplained despite investigation


Epidemiology



  • 2500 infants yearly in the U.S.; Male to female ratio 3:2


  • Rate ↓ from 1.2 to 0.57 deaths per 1000 live births from 1994 to 2002


  • Third leading cause of death in infancy, top cause of death in 1–12 mo olds



Risk Factors



  • Prone and side sleeping positions, soft bedding, overheating


  • Maternal smoking during pregnancy and environmental tobacco smoke


  • Inadequate prenatal care, young maternal age, prematurity or low-birth-weight


  • African American or Native American heritage (2–3× general population risk)


  • Family with one SIDS death has 2%–6% risk of a second SIDS death (see below)


Pathophysiology: Proposed Mechanisms



  • Rebreathing theory: prone infants trap exhaled CO2 around face, ↓ arousal: Some SIDS infants w/brainstem w/5HT-R abn at ventral medulla; ↓ arousal resp to hypercarbia and hypoxia


  • Some SIDS infants w/polymorphisms in 5HT transporter gene w/ ↓[5HT] at synapse


  • Other genes related to QT prolongation and autonomic nervous system development


Differential Diagnosis



  • Sepsis, PNA, cardiomyopathy, congenital heart dz, arrhythmia, prolonged QT, accidental or nonaccidental trauma, suffocation, and inherited metabolic disorders


Risk Reduction



  • Supine sleep position at all times (remind 2° caregivers). Side unacceptable.


  • Firm crib mattress covered w/single sheet, blanket tucked in on 3 sides, below waist


  • Decrease tobacco exposure


  • Pacifier use confers protection (90% ↓ risk). Begin after breastfeeding established.


  • Avoid bed sharing


Skull Deformities

(Clin Pediatr (Phila) 2007;46:292; Pediatrics 2003;112:199)


Deformational Plagiocephaly

(J Craniofac Surg 2007;18:85)



  • Definition: Plagiocephaly: Greek. “Oblique head.”



    • Deformational (positional) plagiocephaly: benign positional molding, flattening of occiput 2/2 gravitational forces on nml malleable skull


  • Epidemiology: 1 in 68 have cranial asymmetry 2/2 deformational plagiocephaly (DP)



    • DP has ↑’ed 6-fold since institution of AAP’s “Back to Sleep” campaign


  • Etiology assoc w/supine pos, ↓ time on abd, ↑ use car seats/carriers, unvaried feed position



    • Can also result from or be exacerbated by congenital torticollis or visual deficits


  • Clinical presentation: Hx of symmetric head at birth



    • Flattening of occiput, anter displacement of ipsilateral ear, forehead, and cheek


    • Head takes on a parallelogram shape


    • Differential: Lambdoid craniosynostosis presents similarly; Rare: incidence 1 in 300,000



      • In contrast to DP, ear posteriorly displaced; head takes on a trapezoidal shape


      • Palpable bony ridge at lambdoid suture, between occipital and parietal bones


  • Diagnosis, Prevention, and Treatment



    • Imaging not needed; must rule out visual deficits, congen torticollis as cause


    • Positional: ↑ “Tummy time,” Δ sleep position (promote alt side of head against bed; pt will fall asleep facing area of activity), alter feeding position


    • Physical therapy: neck stretching and strengthening exercises


    • Helmet therapy: if no improvement after 2–3 mo of above interventions


    • Formal criteria for helmet involve transcranial diagonal diameter



      • Decision to refer: Assessment tool available at www.cranialtech.com


Craniosynostosis

Premature closure of sutures causing skull deformity



  • Epidemiology: Craniosynostosis is uncommon, seen in 1 in 2000


  • Etiology: Poorly described genetic and environmental factors


  • Clinical presentation: Frequently has history of abnormal head shape since birth



    • Head shape depends upon which sutures fuse prematurely


    • Head growth proceeds in direction perpendicular to prematurely fused sutures


    • Resulting head shape can lead to ↑ ICP, cognitive and neurologic deficits


    • Can be syndromic: Alagille, Apert, Cornelia de Lange, Crouzon, Treacher-Collins


  • Diagnosis and treatment



    • Immediate referral to neurosurgeon before imaging is appropriate if suspected


    • Treatment is with helmet and/or surgery



Neonatal Hyperbilirubinemia


Introduction

(Pediatr Rev 2006;27:443; Pediatrics 2004;114:297)



  • Jaundice = yellowing of skin, conjunctiva, and mucous membranes 2/2 deposition of bilirubin, which is produced from the breakdown of hemoglobin (Hgb)



    • Occurs in 60% of healthy FT infants; 10% develop severe jaundice (>17 mg/dL)


    • Appears w/cephalocaudal progression (face to trunk to palms and soles): Face = 5 mg/dL, chest = 10 mg/dL, abdomen = 12 mg/dL, and palms/soles >15 mg/dL. Not visible if <4 mg/dL. If above nipple line, level likely <12 mg/dL.


    • Need confirmation via transcutaneous or serum bilirubin measurement


  • Acute bilirubin encephalopathy (ABE) is the acute manifestation of bilirubin toxicity



    • Early ABE: Lethargy, poor feeding, high-pitched cry, hypotonia


    • Late ABE: Hypertonia; backward arching of neck (retrocollis) and trunk (opisthotonos); seizures, apnea, fever


  • Kernicterus: permanent sequelae of bili deposition in basal ganglia & brainstem.



    • MR, athetoid CP, upward gaze paralysis, hi-freq hearing loss/deafness, enamel dysp


Bilirubin Metabolism

(Pediatr Rev 2006;27:443)



  • Plasma: Hgb degraded by heme oxygenase and biliverdin reductase to unconj bilirubin, bound to albumin. Unconj bili fat soluble; able to cross the blood–brain barrier


  • Liver: unconj bili converted via glucuronosyltransferase (UGT-1) to conj bilirubin, excreted into bile via MRP2 transporter. Conj bili water soluble, can be excreted in urine, cannot cross blood–brain barrier to produce neurotoxicity.


  • Intestine: conj bili degraded by bacteria to urobilinogen and excreted in feces. Newborn gut sterile precludes breakdown; conj bili hydrolyzed back to unconj form and absorbed into enterohepatic circulation (EH circulation).


Pathophysiology

(Pediatr Rev 2006;27:443)



  • Hyperbilirubinemia 2/2 ↑ production, ↓ conjugation, or impaired excretion bilirubin.


  • ↑ Bili production (unconjugated)



    • Hemolytic (>6% reticulocyte count, hemoglobin <13, hepatosplenomegaly)



      • Coombs (+): ABO, Rh, and minor antigen incompatibility


      • Coombs (-): RBC memb defects (spherocytosis), enzyme def (pyruvate kinase, G6PD), Hgb defects (SCD, thal), drugs (streptomycin, Vit K)


    • Nonhemolytic (normal reticulocyte count and hemoglobin)



      • Extravascular blood: Cephalohematoma, bruising, CNS bleed


      • Intravascular blood = Polycythemia (High Hb/HCT): 2/2 delayed cord clamping, fetal-maternal xfusion, twin-twin xfusion, maternal DM or smoking, high altitude


      • Intestinal = ↑ EH circ; ↓ stooling, CF, Hirschsprung, pyloric stenosis, obstruct


  • ↓ Bili conj (unconj): Breast milk Jaundice, Hypothyroid, Gilbert and Crigler-Najjar


  • Impaired bilirubin excretion (conjugated)



    • Biliary obstruction: Biliary atresia, choledochal cyst, 1° sclerosing cholangitis, gallstones, Dubin-Johnson, and Rotor syndromes


    • Metabolic Disease: α-1 antitrypsin def, CF, galactosemia, glycogen storage dz, Gaucher, Wilson, Niemann-Pick, Genetic dz, Trisomy 21 and 18, Turner


    • Infection: UTI, sepsis, idiopathic neonatal hepatitis, Hep B, TORCH


  • ↓ Albumin binding (unconj): low albumin, meds (CTX, sulfa, steroids), acidosis


Physiologic Jaundice

(Pediatr Rev 2006;27:443)



  • Includes (1) Breast-feeding jaundice and (2) breast milk jaundice. 2/2 multi factors:



    • Newborn relatively polycythemic, which is resolved by hemolysis


    • Neonatal erythrocytes have shorter lifespan (80 vs 120 d) w/inc turnover


    • Immature liver: (1) ↓ glucuronyl transferase and (2) ↓ uptake of unconj bilirubin


    • ↑ EH circ: Sterile neonatal gut doesn’t degrade conj bili, reverts and is reabsorbed


    • Colostrum: Small vol leads to weight loss and slow passage of bili-rich meconium


  • Breast-feeding jaundice



    • Early onset; peaks DOL 3–4: 2/2 relative caloric depriv, mild dehyd, and delayed passage of mec; Rx: inc freq feeds (10×/d w/formula suppl as needed).


  • Breast milk jaundice



    • Late onset; peaks DOL 6–14; jaundice begin ↓ at 2 wk, can be ↑ up to 3 mo


    • 2/2 breast milk substances (B-glucuronidases and nonesterified fatty acids), which inhibit normal bilirubin metabolism; actual causal substance unknown


    • Rx: interrupt breast-feeding ∼2 d (to ↓ bili level, pump in btw), then resume.



Pathologic Jaundice

(Am Fam Physician 2002;65:599)



  • Any jaundice w/i 1st 24 hr of life or after 14 d, any rapid rise Tbili (>5mg/dL/d), any Tbili >17 mg/dL in FT newborns, or any evidence of underlying illness.


Risk Factors for Development of Severe Hyperbilirubinemia

(Pediatrics 2004;114:297)



  • Predischarge bili level in the high-risk zone, jaundice in 1st 24 hr, ABO incomp or known hemolytic dz, GA <37 wk, prev sibling Rx’d w/phototherapy, cephalohematoma/bruising, exclusive breast-feeding, East Asian race. Minor factors: macrosomic infant of diabetic mother, maternal age >25 yr, males, albumin <3.0


  • Normogram for designation of risk (Pediatrics 1999;103:6)




image


Evaluation

(Am Fam Physician 2002;65:599)



  • Physical Exam



    • Cephalocaudal progression (face = 5, chest = 10, abd = 12, palms & soles >15)


    • Bruises, pallor, petechiae, hepatosplenomegaly, weight loss, and dehydration


  • Labs: Tbili/Dbili, blood type, direct Ab test (Coomb), CBC/diff/Retic/smear



    • Consider G6PD, thyroid fxn tests, galactosemia screen, CF screen, albumin, U/A and cx, and or full sepsis evaluation (blood cx and LP as well)


    • Can use online calculators using Bhutani nomogram; www.bilitool.org


Rx of Unconjugated Hyperbili

(Pediatrics 1999;103:6; Pediatrics 2004;114:297; J Peds 1998;133:705)



  • Phototherapy (PTX): light in blue–green spectrum (wavelength 425–490 nm) convert unconj bili to water-soluble form excreted in bile and urine w/o conjugation



    • Family history of porphyria is an absolute contraindication to phototherapy


    • If bili does not fall or continues to rise despite phototherapy, hemolysis is likely


    • Serum albumin <3.0 lowers threshold to start phototherapy


    • Stop phototherapy when bilirubin is <13–14 mg/dL


    • No need to delay discharge to check rebound bilirubin level. If hemolytic dz, or if PTX is d/c’d before infant is 4 d old, check rebound bili level 24 hr after d/c.


Guidelines for Phototherapy in Hospitalized Infants ≥35 Weeks (AAP Guidelines 2004)




image



  • Exchange transfusion: removes bilirubin and damaged erythrocytes from circulation



    • Reaching exchange transfusion levels (bili ≥25 mg/dL) is a medical emergency!


    • In isoimmune hemolytic dz, Rx w/IVIG (0.5–1g/kg over 2 hr) if bili is rising despite intensive PTX or if bili level is w/i 2 mg/dL of the exchange level.


    • Calculate “bilirubin/albumin” ratio to determine need for exchange transfusion:



      • Infants ≥ 38 weeks: 8.0; if higher then concerning


      • Infants 35–37.9 weeks and well, or if hemolytic disease: 7.2


      • Infants 35–37.9 weeks and high risk, or if hemolytic disease: 6.8

Guidelines for Exchange Transfusion in Infants ≥35 Weeks (AAP Guidelines 2004)




image



  • Pharmacology



    • Phenobarbital and ursodeoxycholic acid lower bili levels by facilitating bile flow


    • Tin-mesoporphyrin—inhibits production of heme oxygenase (not FDA approved)


Colic

See GI section



Normal Growth


(Nelson Textbook of Peds, 18th Ed. Saunders 2007. 70–74, 677, 2434)

(Pediatr Rev 2006 Jan;27(1):e1)



  • Term infants lose up to 10% of BW, then regain BW by 2 weeks.


  • BW doubles by 4–5 mo, and triples by 1 yr; height doubles by age 3–4.


  • Exclusively breast-fed infants smaller than formula-fed from 6–12 mo; resolves by 1 yr


  • From 3–10 yrs old, children grow ∼2.5 inches/yr.


  • Anterior fontanelle: normal size 20 ± 10 mm; closes at 9–18 mo


  • Posterior fontanelle: closes by 2 mo


  • Excessively large fontanelle: IUGR, hypothyroid, prematurity, Trisomy 13/18/21, hydrocephalus, achondroplasia, Apert syndrome, Cleidocranial dysostosis, cong. rubella, Hallermann-Streiff syndrome, hypophos, Kenny syndrome, osteogenesis imperfecta, pyknodysostosis, Russell-Silver syndrome, Vit D def rickets


  • Excessively small fontanelles: microcephaly, craniosynostosis, hyperthyroidism


  • Average Growth and Caloric Requirements












































Age Average Weight Gain (g/d) Length (cm/mo) Head Circumference (cm/mo) Daily Caloric Allowance (Kcal/kg/d)
Birth – 3 mo 25 – 30 3.5 2.0 115
3 mo – 6 mo 20 2.0 1.0 110
6 mo – 9 mo 15 1.5 0.5 100
9 mo –12 mo 12 1.2 0.5 100
1 yr – 3 yr 8 1.0 0.25 100
4 yr – 6 yr 6 3 cm/yr 1 cm/yr 90–100


Midparental Height 1

3 cm (instead of ± 5 inches) if using metric units



  • Boys: (paternal height in inches + maternal height in inches + 5)/2


  • Girls: (parental height in inches + maternal height in inches – 5)/2


Growth Charts

(Am Fam Physician 2003;68:879) (growth charts at www.cdc.gov/growthcharts)



  • Length should be measured via length-board; height measured via stadiometer


  • Head circ measured just above eyebrow and ears, across most prominent part occiput


  • Special growth curves available for: Trisomy 21, Prader-Willi, Williams syndrome, Cornelia de Lange syndrome, Turner syndrome, Rubinstein-Taybi syndrome, Marfan syndrome, achondroplasia, and very low BW infants <1500 g (use Infant Health and Developmental Program (IHDP) growth curves)


Failure to Thrive

(Pediatr Rev 2006 Jan;27(1):e1; Clin Fam Pr 2003;5:293; Pediatr Rev 2000;21:257)


Introduction

(Am F Phys 2003;68:879)



  • No standard dx criteria exist; Failure to thrive (FTT) most commonly defined as decel growth across 2 major percentile lines, or weight for age less than fifth percentile


  • 1° etiology is malnut, 2/2 multi medical, behavioral, psychosocial, and environ causes


  • Malnutrition 1st decreases weight, then height then head circumference


Definition

(Am Fam Physician 2003;68:879)



  • Organic FTT: poor growth because of a known medical disorder


  • Nonorganic FTT: poor growth because of psychosocial factors, diagnosed by exclusion


  • Multifactorial FTT: poor growth 2/2 of both med & nonmed factors, most common


  • Gomez criteria for FTT severity: Compare current weight-for-age against expected weight for age (50th percentile)



    • <60% expected = severe FTT; 61%–75% expected = mod; 76%–90% = mild


Etiology

(Am Fam Physician 2003;68:879; Clin Fam Pr 2003;5:293; Pediatr Rev 2000;21:257)

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Aug 18, 2016 | Posted by in PEDIATRICS | Comments Off on Primary Care and Adolescent Medicine

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