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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Jun 19, 2016 | Posted by in PEDIATRICS | Comments Off on Primary Care and Adolescent Medicine

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