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Fetal and Neonatal Care
Congenital anomalies: initial recognition and workup in the newborn
Clinical Overview and When to Suspect
Congenital anomalies affect ~3% of all live births and are the leading cause of infant mortality in the United States. Recognition begins in the delivery room and continues through the nursery exam.
— Malformation: intrinsic abnormality of morphogenesis (e.g., VSD, cleft palate)
— Deformation: extrinsic mechanical force on normal tissue (e.g., clubfoot from oligohydramnios)
— Disruption: breakdown of previously normal tissue (e.g., amniotic band sequence)
— Dysplasia: abnormal cellular organization (e.g., skeletal dysplasias)
Anomalies may be identified prenatally (anatomy US at 18–22 weeks, fetal echo, MRI) or discovered on postnatal exam
Categories:
Board pearl: A single minor anomaly is common (~15% of newborns) and usually insignificant; ≥3 minor anomalies → ~20% chance of an underlying major anomaly → triggers comprehensive evaluation
The general pediatrician's role: recognize the anomaly, determine if it is isolated vs. part of a pattern (syndrome, sequence, association), initiate appropriate workup, and coordinate subspecialty referral
Key distinction: Sequence = single primary defect → cascade of secondary effects (e.g., Potter sequence); syndrome = multiple anomalies from a single cause (e.g., trisomy 21); association = statistically linked anomalies without a known unifying etiology (e.g., VACTERL)
History — Prenatal Clues and Maternal Factors
A careful prenatal and maternal history often provides the first clues to congenital anomalies:
— Alcohol → fetal alcohol spectrum disorders (smooth philtrum, thin vermilion border, short palpebral fissures, microcephaly, cardiac defects)
— Poorly controlled diabetes → caudal regression, cardiac defects (TGA, VSD), macrosomia, sacral agenesis
— Valproate → neural tube defects, facial dysmorphism
— Isotretinoin → craniofacial, cardiac, thymic, CNS malformations
— TORCH infections → IUGR, microcephaly, hepatosplenomegaly, calcifications
Prenatal ultrasound findings: polyhydramnios (esophageal atresia, duodenal atresia, anencephaly), oligohydramnios (renal agenesis, posterior urethral valves, prolonged ROM → pulmonary hypoplasia), echogenic bowel (CF, CMV, trisomy 21), single umbilical artery (↑ risk renal & cardiac anomalies)
Maternal exposures:
Family history: consanguinity (↑ autosomal recessive conditions), prior affected children, known genetic conditions
Board pearl: Maternal pregestational diabetes (not gestational) carries the highest teratogenic risk, particularly in the first 8 weeks when organogenesis occurs — HbA1c >8% in the first trimester correlates with ↑ anomaly risk
Physical Exam — Systematic Approach to the Dysmorphic Newborn
The newborn dysmorphology exam should be systematic, head-to-toe, documenting both major and minor anomalies:
Head: fontanelle size, craniosynostosis (ridged suture, abnormal head shape), microcephaly (<3rd %ile), macrocephaly
Face: palpebral fissure length/slant, intercanthal distance (hyper/hypotelorism), nasal bridge, philtrum, ear position/morphology (low-set = upper helix below line from lateral canthus)
Eyes: red reflex (absent → cataracts, retinoblastoma), coloboma, microphthalmia
Mouth: cleft lip/palate (palpate hard and soft palate), micrognathia (Pierre Robin sequence → airway obstruction)
Chest/Heart: precordial activity, murmurs, femoral pulse strength (absent/weak → coarctation)
Abdomen: omphalocele (midline, covered by membrane — associated with trisomies), gastroschisis (right of midline, no membrane — usually isolated)
Extremities: polydactyly, syndactyly, single palmar crease, clinodactyly, limb reduction defects, radial ray abnormalities (Fanconi anemia, VACTERL, Holt-Oram)
Spine: sacral dimple (simple vs. deep/deviated → US if concerned), tufts of hair, hemangioma over spine
Genitalia: ambiguous genitalia → endocrine emergency (rule out CAH)
Board pearl: Always photograph (with consent) for genetics consultation — subtle dysmorphic features evolve and may be better appreciated over time
Diagnostic Workup — First-Line Approach
When a congenital anomaly is identified, the workup is guided by the specific finding and the suspicion for an underlying pattern:
— Multiple congenital anomalies
— Dysmorphic features suggestive of a syndrome
— Major structural defect (especially cardiac, renal, CNS) without a clear etiology
Chromosomal microarray (CMA) is the first-line genetic test for a newborn with:
CMA detects microdeletions/microduplications (e.g., 22q11.2 deletion) that standard karyotype misses
Karyotype is still indicated when aneuploidy is clinically suspected (trisomy 21, 18, 13) or for ambiguous genitalia (need to determine XX vs. XY)
FISH: rapid targeted test for specific loci — useful when clinical suspicion is high (e.g., FISH for 22q11.2 in truncus arteriosus + hypocalcemia)
Echocardiogram: obtain in ANY infant with ≥2 minor anomalies, any major anomaly, or clinical findings suggestive of CHD (murmur, cyanosis, weak pulses)
Renal ultrasound: indicated for many syndromes and associations (VACTERL, single umbilical artery, ear anomalies with pre-auricular pits)
Board pearl: CMA has largely replaced karyotype as the first-line test for unexplained multiple anomalies — but karyotype is still needed when balanced translocations or mosaicism are suspected
Advanced Genetic Testing and Imaging
Beyond CMA and karyotype, targeted testing may be required:
— Head US or MRI → CNS malformations (holoprosencephaly, agenesis of corpus callosum, Dandy-Walker)
— Spinal US (reliable <3 months of age) → tethered cord, spinal dysraphism in infants with sacral anomalies
— Skeletal survey → skeletal dysplasias or suspected non-accidental trauma
— Abdominal/pelvic US → renal anomalies, ambiguous genitalia (Müllerian structures)
Gene panels or whole exome sequencing (WES) → when CMA/karyotype are normal but strong clinical suspicion for a genetic condition persists (e.g., Noonan syndrome panel for RASopathies, skeletal dysplasia panel)
Methylation studies → for imprinting disorders (Beckwith-Wiedemann: macrosomia, omphalocele, macroglossia, hemihypertrophy, ear pits; Prader-Willi: neonatal hypotonia, poor feeding)
Specific single-gene testing → e.g., FGFR3 for achondroplasia, FBN1 for Marfan
Imaging studies guided by anomaly:
Board pearl: Spinal US is the preferred initial imaging modality in neonates <3 months because the posterior elements are not yet ossified; after 3 months → MRI is needed
Newborn metabolic screen may also reveal associated metabolic conditions (e.g., galactosemia, PKU) that compound the presentation
Management — Initial Stabilization of Major Anomalies
Some congenital anomalies require immediate delivery room or nursery interventions:
Congenital diaphragmatic hernia (CDH): NO bag-mask ventilation (inflates stomach in thorax) → immediate intubation, OG tube to continuous suction, lateral decubitus positioning
Gastroschisis/omphalocele: sterile saline-soaked dressing, plastic wrap (Silastic silo for gastroschisis), thermoregulation, NG decompression, IV fluids → surgical consultation
Esophageal atresia/TEF: inability to pass OG tube → Replogle suction catheter in proximal pouch on continuous suction, NPO, upright positioning → surgical repair
Myelomeningocele: prone positioning, sterile moist saline dressing over defect, latex precautions, neurosurgery consultation for closure within 24–72 hours
Duct-dependent cardiac lesions (critical CHD): prostaglandin E₁ (PGE₁) infusion at 0.05–0.1 mcg/kg/min to maintain ductal patency → monitor for apnea (common side effect)
Airway obstruction (Pierre Robin, bilateral choanal atresia): prone positioning, nasopharyngeal airway, possible intubation
Board pearl: PGE₁ side effects — apnea (have ventilatory support ready), fever, hypotension, flushing — apnea is the most tested
Management — Coordinated Subspecialty Care
Once stabilized, the workup and care of a newborn with congenital anomalies requires a team approach:
Genetics: central role in pattern recognition, diagnostic testing, recurrence risk counseling
Cardiology: echocardiogram for any major anomaly or syndrome associated with CHD (trisomy 21 → AVSD in 40%; 22q11.2 deletion → conotruncal defects; Turner syndrome → coarctation, bicuspid aortic valve)
Nephrology/Urology: renal anomalies are common across many syndromes; early renal US guides management
Surgery: pediatric surgery for GI anomalies (TEF, intestinal atresias, abdominal wall defects); neurosurgery for neural tube defects, hydrocephalus
Ophthalmology: exam for cataracts, coloboma, retinal anomalies (TORCH, trisomy 13, CHARGE)
Audiology: hearing screen + formal ABR if syndrome associated with hearing loss
Endocrinology: ambiguous genitalia → karyotype + 17-OHP (rule out CAH → salt-wasting crisis can be fatal in first 2 weeks)
Board pearl: Do NOT assign sex/gender in a newborn with truly ambiguous genitalia until genetic, hormonal, and anatomic evaluation is complete — this is a medical AND psychosocial emergency
Management — Feeding, Monitoring, and Hospital Course
Newborns with congenital anomalies often require modified feeding and monitoring plans:
Cleft lip alone → modified nipple (squeeze bottle), breastfeeding may be possible with positioning
Cleft palate → inability to generate suction → specialty bottles (e.g., Pigeon, Haberman/SpecialNeeds feeder); breastfeeding is typically unsuccessful until repair
Trisomy 21 → hypotonia impairs feeding; may need NG or supplemental feeding initially; screen for duodenal atresia (double-bubble on X-ray), evaluate for Hirschsprung disease if delayed meconium passage
TEF/esophageal atresia → NPO until surgical repair; TPN
Monitor weight closely — infants with anomalies often have ↑ metabolic demands and feeding difficulties
Anticipate prolonged NICU stays for major anomalies; involve social work, palliative care when appropriate
Board pearl: Infants with trisomy 21 should have: echocardiogram (even if prenatal echo was normal — postnatal anatomy may differ), CBC (risk of transient myeloproliferative disorder/TMD), TSH at birth and 6 months, ophthalmology by 6 months, audiology evaluation, and celiac screening later
Feeding OT/SLP consultation is underutilized but critical in infants with craniofacial, neurologic, or chromosomal anomalies
Age-Specific Considerations — Neonatal Period
The neonatal period (0–28 days) is when most major congenital anomalies first declare themselves:
Cardiac: duct-dependent lesions present as ductal closure progresses (typically days 2–7) with cyanosis (right-sided obstructive lesions: critical PS, pulmonary atresia, TGA) or shock (left-sided obstructive lesions: critical coarctation, HLHS, interrupted aortic arch)
GI: bilious emesis in first 24–48 hours → malrotation with volvulus until proven otherwise (upper GI series is the diagnostic study) — surgical emergency
Renal: posterior urethral valves → distended bladder, poor stream in males; bilateral hydronephrosis on prenatal US → postnatal renal US after 48 hours + VCUG
Skeletal: congenital hip dysplasia screening via Ortolani (already dislocated → reducible) and Barlow (dislocatable) maneuvers; if equivocal → hip US at 4–6 weeks
CNS: seizures in first 72 hours may indicate structural brain malformation, hypoxic-ischemic encephalopathy, or metabolic disorder
Board pearl: Bilious emesis in ANY neonate is malrotation with midgut volvulus until proven otherwise → upper GI series STAT, NPO, surgical consultation — delay = ischemic bowel
Late preterm infants (34–36 weeks) may have anomalies unmasked by immature compensatory mechanisms (e.g., critical CHD presenting earlier due to less physiologic reserve)
Age-Specific Considerations — Infancy and Beyond
Some congenital anomalies are not apparent at birth and present later:
Coarctation of the aorta: may not be detected until ductal closure → weak/absent femoral pulses, upper > lower extremity BP differential ≥20 mmHg; can present as heart failure at 2–6 weeks
Developmental hip dysplasia: Ortolani/Barlow may normalize → screening hip US recommended at 6 weeks for breech presentation, family history, or equivocal exam
Cryptorchidism: if testes not palpable at birth → re-examine at 4 months; if not descended by 6 months → referral for orchiopexy (ideally by 12 months) to preserve fertility and allow tumor surveillance
Craniosynostosis: may not be obvious at birth; progressive abnormal head shape (scaphocephaly → sagittal; plagiocephaly → assess for lambdoid vs. positional)
Pyloric stenosis: presents at 3–6 weeks with nonbilious projectile emesis, hypochloremic hypokalemic metabolic alkalosis → US diagnosis (pyloric muscle thickness ≥3 mm, length ≥15 mm)
Board pearl: Pyloric stenosis is NOT a congenital structural malformation — it develops postnatally; however, it is often grouped with congenital GI anomalies in board review. It is the classic cause of nonbilious projectile emesis in a 3–6 week old male firstborn
Hearing loss (congenital): if newborn screen passed but risk factors exist (family history, NICU >5 days, CMV) → repeat audiology by 6–9 months
Complications and When to Escalate Care
Failure to recognize or appropriately manage congenital anomalies can lead to life-threatening complications:
Missed critical CHD → ductal closure → cardiogenic shock or profound cyanosis → death if PGE₁ not initiated
Missed intestinal malrotation → midgut volvulus → bowel necrosis within hours → short gut syndrome or death
Unrecognized TEF → aspiration pneumonia, respiratory failure; H-type TEF (no atresia) is easily missed — presents with recurrent pneumonia, coughing/choking with feeds
Undiagnosed CAH with ambiguous genitalia → salt-wasting crisis at 1–3 weeks (hyponatremia, hyperkalemia, shock) → fatal if untreated
Missed posterior urethral valves → progressive renal damage, renal failure
Omphalocele rupture or gastroschisis complications → infection, bowel ischemia, necrotizing enterocolitis
Unrecognized choanal atresia (bilateral) → obligate nasal breathing in newborn → respiratory distress at rest, improved with crying (opens mouth)
Board pearl: Bilateral choanal atresia → cyclic cyanosis (worsens at rest/feeding, improves with crying); inability to pass catheter through nares; associated with CHARGE syndrome (Coloboma, Heart defects, Atresia choanae, Retardation of growth, Genital anomalies, Ear anomalies)
Emergencies Requiring Immediate Intervention
Several congenital anomalies represent true neonatal emergencies:
Tension pneumothorax from pulmonary hypoplasia (CDH, bilateral renal agenesis/severe oligohydramnios): needle decompression → chest tube
Obstructed total anomalous pulmonary venous return (TAPVR): profound cyanosis unresponsive to PGE₁; CXR shows small heart with pulmonary edema ("snowman" sign seen only in supracardiac type, often not visible in neonates) → emergent surgical repair
Ductal-dependent systemic circulation (HLHS, critical coarctation, interrupted aortic arch): PGE₁ + volume resuscitation + inotropes; do NOT give supplemental O₂ liberally (lowers PVR → ↑ pulmonary blood flow → steals from systemic circulation)
Congenital lobar emphysema: progressive hyperinflation of affected lobe → mediastinal shift → emergent lobectomy
Airway emergencies: large cervical teratoma, cystic hygroma → EXIT procedure planned prenatally if identified; if unrecognized → difficult airway management
Board pearl: In a cyanotic neonate unresponsive to PGE₁, think obstructed TAPVR — echocardiogram is diagnostic, and emergent surgery is required; this is one of the few cardiac emergencies where PGE₁ does NOT help
Key Differentials — Isolated vs. Syndromic Anomalies
The critical reasoning step: is the anomaly isolated or part of a broader pattern?
— Trisomy 21: hypotonia, upslanting palpebral fissures, Brushfield spots, AV canal defect, duodenal atresia, single palmar crease
— Trisomy 18: IUGR, clenched fists (overlapping 2nd/5th digits), rocker-bottom feet, cardiac (VSD, PDA), omphalocele
— Trisomy 13: holoprosencephaly, midline cleft, polydactyly, cutis aplasia, cardiac
— Turner (45,X): lymphedema of hands/feet, webbed neck, coarctation, cystic hygroma prenatally
— 22q11.2 deletion: conotruncal cardiac defects (tetralogy of Fallot, truncus arteriosus, interrupted aortic arch), palatal anomalies, hypocalcemia, thymic hypoplasia, characteristic facies
Isolated anomaly: single defect, usually multifactorial inheritance, lower recurrence risk (e.g., isolated cleft lip ≈ 3–5% recurrence in sibling)
Syndromic anomaly: recognized pattern of multiple anomalies from a single etiology
Board pearl: An infant with truncus arteriosus or interrupted aortic arch type B + hypocalcemia → think 22q11.2 deletion → order FISH or CMA → check calcium, T-cell subsets (thymic function), and palate
Distinguishing Key Associations and Sequences
Beyond syndromes, recognizing associations and sequences is high-yield:
— Vertebral anomalies, Anal atresia, Cardiac defects, Tracheo-Esophageal fistula, Renal anomalies, Limb (radial ray) anomalies
— Need ≥3 features; no unifying genetic test; each system requires individual evaluation
— Coloboma, Heart defects, Atresia choanae, Retardation of growth/development, Genital hypoplasia, Ear anomalies (hearing loss)
VACTERL association (non-random co-occurrence; diagnosis of exclusion — must rule out genetic syndromes):
CHARGE syndrome (CHD7 gene mutation — autosomal dominant, usually de novo):
Potter sequence: bilateral renal agenesis → oligohydramnios → pulmonary hypoplasia + limb deformities + characteristic facies (flattened nose, recessed chin, low-set ears)
Pierre Robin sequence: micrognathia → glossoptosis → airway obstruction ± cleft palate; can be isolated or part of Stickler syndrome (most common syndromic cause)
Amniotic band sequence: asymmetric limb/digit constrictions, amputations — does NOT follow dermatomal/embryologic lines (distinguishes from true malformations)
Board pearl: VACTERL is a diagnosis of exclusion — always check chromosomes/CMA first, because trisomy 18 and 22q11.2 deletion can mimic VACTERL features
Preventive Care and Prenatal Strategies
Primary prevention and prenatal detection reduce the burden of congenital anomalies:
Folic acid supplementation (400 mcg daily for all women of childbearing age; 4 mg daily if prior NTD-affected pregnancy) → ↓ neural tube defects by 50–70%
Preconception glycemic control in diabetic women (target HbA1c <6.5% before conception) → ↓ cardiac, neural tube, and caudal regression anomalies
Avoidance of teratogens: alcohol (no safe amount in pregnancy), isotretinoin (must have two negative pregnancy tests and two forms of contraception), valproate (switch to safer anticonvulsant before conception if possible), warfarin (nasal hypoplasia, stippled epiphyses — switch to heparin)
Rubella vaccination prior to pregnancy (MMR is a live vaccine — contraindicated in pregnancy; check immunity and vaccinate if non-immune before conception)
Carrier screening: CF, SMA, hemoglobinopathies, fragile X — offered to all women preconceptionally or early in pregnancy
Board pearl: Folic acid prevents NTDs only if started BEFORE conception and continued through the first trimester — most NTDs occur by day 28 of gestation, often before pregnancy is recognized
Screening Schedules and Follow-Up After Diagnosis
Condition-specific screening after diagnosis ensures early detection of associated complications:
— Echocardiogram (newborn), TSH (newborn, 6 months, then annually), CBC (newborn — TMD), ophthalmology (6 months), audiology (birth + annually), cervical spine X-ray (3–5 years for atlantoaxial instability), celiac screening (2 years)
Trisomy 21 — AAP guidelines:
Turner syndrome: cardiology (echo + aortic imaging), renal US, audiology, thyroid, growth monitoring (GH therapy eligibility)
22q11.2 deletion: calcium levels (hypoparathyroidism), T-cell subsets (immune function), renal US, speech evaluation, developmental assessment, cardiac follow-up
VACTERL: each affected system requires individual longitudinal surveillance
Beckwith-Wiedemann: abdominal US every 3 months until age 8 (hepatoblastoma, Wilms tumor screening), AFP levels
Board pearl: Infants with trisomy 21 and a normal fetal echocardiogram STILL need a postnatal echocardiogram — postnatal anatomy may differ, and small VSDs or AVSDs may not be detected prenatally
General rule: any infant discharged with a diagnosed anomaly needs a clear follow-up plan including genetics, relevant subspecialties, early intervention referral, and primary care within 48–72 hours
Family Counseling and Psychosocial Considerations
The diagnosis of a congenital anomaly is a profound moment for families:
Deliver the news in person, in a private setting, with both parents present if possible; use the infant's name
Provide accurate, balanced information — avoid only listing negatives; describe the child first, then the condition
For chromosomal anomalies: explain recurrence risk (trisomy 21 from nondisjunction: ~1% or age-related risk, whichever is higher; translocation carriers may have significantly higher risk → parental karyotypes indicated)
For lethal conditions (trisomy 13, trisomy 18): involve palliative care early; discuss goals of care including comfort-focused management; respect family's wishes
Early intervention referral: federally mandated for all infants with developmental risk → PT, OT, speech, developmental services
Connect families with support organizations (Down syndrome parent groups, local genetics support networks)
Address guilt — many parents wonder if they caused the anomaly; reassure that most congenital anomalies are not caused by anything the parents did or did not do
Board pearl: Palliative care is not synonymous with withdrawal of care — it is a support framework that can be integrated alongside curative treatments, especially for complex anomalies with uncertain prognosis
High-Yield Associations and Rapid-Fire Board Facts
Single umbilical artery → ↑ risk renal and cardiac anomalies → renal US, consider echo if additional findings
Preauricular pit + hearing loss + renal anomaly → branchio-oto-renal syndrome
Macrosomia + macroglossia + omphalocele + ear creases → Beckwith-Wiedemann → screen for Wilms tumor/hepatoblastoma
Absent radius + thrombocytopenia → thrombocytopenia-absent radius (TAR) syndrome (thumbs PRESENT) vs. Fanconi anemia (thumbs absent/hypoplastic)
Rocker-bottom feet + clenched fists + IUGR → trisomy 18
Polydactyly + midline cleft + holoprosencephaly → trisomy 13
Coarctation + webbed neck + lymphedema → Turner syndrome (45,X)
Anorectal malformation → evaluate for VACTERL — obtain renal US, spinal US, echo, vertebral X-rays
Duodenal atresia (double-bubble sign) → associated with trisomy 21 in ~30% of cases
Esophageal atresia → most common type is proximal atresia with distal TEF (~85%)
Cleft lip ± palate → multifactorial; if midline cleft → think holoprosencephaly or trisomy 13
Board pearl: Absent thumbs = Fanconi anemia (check CBC, chromosomal breakage study); present thumbs + absent radii = TAR syndrome
One-Line Recap
Congenital anomalies (~3% of live births) require systematic recognition through prenatal history review and a thorough head-to-toe dysmorphology exam — the key clinical reasoning step is determining whether an anomaly is isolated (usually lower risk, multifactorial) or part of a syndrome (trisomy 21/18/13, 22q11.2 deletion, Turner), sequence (Potter, Pierre Robin), or association (VACTERL, CHARGE) — first-line genetic testing is chromosomal microarray (CMA) for unexplained multiple anomalies (karyotype still needed for suspected aneuploidy or ambiguous genitalia), with targeted FISH, gene panels, or WES as indicated — immediate stabilization priorities include PGE₁ for duct-dependent CHD, intubation for CDH (no bag-mask), sterile moist dressing for myelomeningocele, and NPO with Replogle suction for esophageal atresia — bilious emesis in any neonate is malrotation until proven otherwise — and every diagnosed anomaly mandates a coordinated follow-up plan encompassing genetics, condition-specific subspecialty screening (echo for trisomy 21 even if prenatal echo was normal), early intervention referral, and compassionate family-centered counseling.
Board Question Stem Patterns
Newborn with flat facies, hypotonia, single palmar crease, upslanting palpebral fissures → trisomy 21 → next step: echocardiogram + karyotype/CMA + TSH + CBC
Infant with clenched fists (overlapping fingers), IUGR, rocker-bottom feet → trisomy 18 → confirm with karyotype → discuss goals of care (median survival ~14 days)
Newborn with bilious emesis on day 1 of life → suspect malrotation with volvulus → next step: upper GI series → surgical emergency
Infant unable to pass NG tube + polyhydramnios history → esophageal atresia → next step: CXR showing coiled tube in proximal pouch
Term newborn, cyanosis at rest relieved by crying → bilateral choanal atresia → evaluate for CHARGE syndrome
Newborn with truncus arteriosus + hypocalcemia → 22q11.2 deletion → order FISH/CMA, calcium, T-cell subsets
Prenatal US showing echogenic bowel + polyhydramnios → differential includes CF, trisomy 21, CMV → postnatal workup: sweat test/IRT, CMA, CMV urine PCR
Male newborn with no palpable testes bilaterally + hypospadias → consider disorder of sexual development → karyotype, 17-OHP, pelvic US → do NOT assign sex until evaluation complete
Newborn with omphalocele + macroglossia + macrosomia → Beckwith-Wiedemann → methylation studies + tumor screening protocol
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