A female infant is born at 38 weeks gestation to a G2P1 mother with known gestational diabetes via scheduled, repeat C-section. Initial Apgar scores are 8 and 9 at 1 and 5 minutes, respectively. About an hour later, the child begins to develop tachypnea (RR 70), nasal flaring, and grunting, which improves with supplemental oxygen via nasal cannula. A chest X-ray is obtained, which showed findings consistent with the diagnosis of Transient Tachypnea of the Newborn. What findings would be expected on chest X-ray for this patient?

A. Diffuse parenchymal infiltrates with fluid in the interlobar fissure

B. Diffuse parenchymal infiltrates with air bronchograms or lobar consolidation

C. Diffuse, bilateral ground-glass opacities with air bronchograms

D. Diffuse, patchy infiltrates with areas of hyperinflation

E. Left-sided intrathoracic stomach bubble with shift of the mediastinum and cardiac silhouette to the right

The correct answer is A, Diffuse parenchymal infiltrates with fluid in the interlobar fissure. There is a great Pediatrics in Review article from 2014 titled Respiratory Distress in the Newborn that discusses the majority of these disease processes, linked below in the references.


Answer Choice A: Diffuse parenchymal infiltrates with fluid in the interlobar fissure

This is the correct answer! Transient Tachypnea of the Newborn (TTN) is a common newborn cause of respiratory distress due to retained fetal lung fluid in term and late pre-term infants. During fetal development, the lung alveoli are fluid-filled, and towards the end of pregnancy, the fetus starts removing this alveolar fluid to allow for effective gas exchange. This process is enhanced by labor, so naturally, TTN tends to occur more often in neonates who do not undergo labor (i.e. precipitous labor and scheduled C-sections). Other risk factors include gestational age <39 weeks, fetal distress, maternal sedation, and maternal diabetes. This disease process is usually self-limited and normally does not require use of mechanical ventilation. However, use of antenatal corticosteroids (such as 2 doses of Betamethasone) given at least 48 hours prior to C-section can help decrease respiratory morbidity in these infants.


Answer Choice B: Diffuse parenchymal infiltrates with air bronchograms or lobar consolidation

Neonatal Pneumonia can be acquired at birth or during pregnancy (perinatal vs congenital pneumonia). Perinatal pneumonia is the most common cause of neonatal pneumonia, with the common causative organism being Group B Streptococcus (GBS). Congenital pneumonia, however, can be passed transplacentally from the mother and can be caused by a myriad of organisms, such as Rubella, Cytomegalovirus, Adenovirus, Enteroviruses, Mumps, Toxoplasma gondii, Treponema pallidum, Mycobacterium tuberculosis, Listeria monocytogenes, Varicella Zoster virus, and HIV. Risk factors for developing this infection include prolonged rupture of membranes (PROM), maternal infection, and prematurity.

This infectious process often presents as part of a generalized septic illness, requiring blood and CSF cultures and empiric antibiotics (see our previous episode on Management of the Febrile Neonate for further discussion). There is also a great neonatal early-onset sepsis calculator published by Kaiser Permanente if you need further guidance on obtaining a blood culture and starting empiric antibiotics in infants at least 34 weeks gestation. It calculates your patient’s septic risk based on gestational age, maternal temperature, ROM duration, maternal GBS status, and use of intrapartum antibiotics. The higher the maternal temperature and longer the ROM, the more likely it will recommend considering a blood culture and starting empiric antibiotics.


Answer Choice C: Diffuse, bilateral ground-glass opacities with air bronchograms

Respiratory Distress Syndrome (RDS) is incredibly common in premature infants due to alveolar surfactant deficiency. But before we can talk about how infants get surfactant, we should take a step back and talk globally about the 5 embryonal stages of lung development.

  1. The first stage, Embryonic, is the first 6 weeks of development where the trachea and bronchi are formed. If this stage has defective growth, infants can develop tracheoesophageal fistulas (TEF) or pulmonary sequestration.
  2. The second stage, Pseudoglandular, lasts from weeks 7-16, and this is where the bronchioles, terminal bronchioles, and lung circulation develop. This is also where infants can develop defects such as bronchogenic cysts, congenital diaphragmatic hernias (talked about in detail in a minute), and congenital cystic adenomatoid malformations.
  3. The third stage, Canalicular, is from weeks 17-24, and now the respiratory bronchioles and primitive alveoli develop. If these grow incorrectly, infants can develop pulmonary hypoplasia, RDS, BPD, and alveolar capillary dysplasia.
  4. The fourth stage, Terminal Sac, lasts from weeks 25-36 weeks gestation. This is when the fetus develops alveolar ducts, thin-walled alveolar sacs, and throughout this stage, they increasingly gain function in Type 2 pneumocytes. These Type 2 pneumocytes are the surfactant-producing cells in the lungs. If children are born during this stage, they are at risk for developing RDS and Bronchopulmonary Dysplasia (BPD).
  5. The fifth and final stage is the Alveolar stage and goes from week 37 until the infant is born. This is when the lungs develop definitive alveoli and mature Type 2 pneumocytes. Infants born during this stage are at risk for developing TTN, MAS, neonatal pneumonia, and Persistent Pulmonary Hypertension (PPHN).

So back to RDS, these kids are typically born before 36 weeks and have not yet developed enough surfactant. Surfactant decreases the surface tension in the alveoli and prevents microatelectasis and low lung volumes and instead allows the alveoli to remain open and allow for gas exchange.

Risk factors for RDS include prematurity, gestational diabetes, multiple gestation, and male infants. Infants of a diabetic mother are at increased risk because hyperinsulinemia has been shown to delay fetal lung development. However, administration of corticosteroids 48 hours prior to delivery (2 doses of Betamethasone) has been shown to stimulate surfactant production and decrease the rate of RDS in premature infants.  


Answer Choice D: Diffuse, patchy infiltrates with areas of hyperinflation

Meconium Aspiration Syndrome (MAS) is due to neonates aspirating meconium, which causes a chemical pneumonitis and partial obstruction, leading to air trapping and hyperaeration. Additionally, meconium has many components, one of which is bile acids. These bile acids locally inactivate pulmonary surfactant, causing atelectasis.

Meconium is present in the fetal GI tract as early as 16 weeks, but it does not move into the descending colon until about 34 weeks gestation. Therefore, it is uncommon to see MAS prior to 37 weeks gestation.

Risk factors include meconium stained amniotic fluids, post-term gestation (>40 weeks gestation), fetal stress, and African American ethnicity.


Answer Choice E: Left-sided intrathoracic stomach bubble with shift of the mediastinum and cardiac silhouette to the right

These findings would be suggestive of Congenital Diaphragmatic Hernia (CDH). Due to a defect in the diaphragm, abdominal organs are able to migrate into the chest during embryonic development, leading to pulmonary hypoplasia on the affected side(s). Per a Pediatrics in Review article from 1999, about 85% of the diaphragmatic defects are left-sided, 13% right-sided, and 2% bilateral. CDH can be a solitary defect, combined with multiple other defects, or due to chromosomal abnormalities (i.e. Trisomies 18 and 21). This defect might be noted prenatally with low maternal serum alpha-fetoprotein (MS-AFP) and ultrasonographic findings of polyhydramnios and an intrathoracic gastric bubble. If you’re interested in reading more about management of CDH, there’s a great NeoReviews article from the AAP in 2016 listed in the references.



  1. Reuter S, Moser C, Baack M. Respiratory distress in the newborn. Pediatr Rev. 2014 Oct;35(10):417-28; quiz 429. doi: 10.1542/pir.35-10-417. PMID: 25274969; PMCID: PMC4533247.
  2. Hermansen CL, Mahajan A. Newborn Respiratory Distress. Am Fam Physician. 2015 Dec 1;92(11):994-1002. PMID: 26760414.
  3. Kuzniewicz MW, Puopolo KM, Fischer A, Walsh EM, Li S, Newman TB, Kipnis P, Escobar GJ. A Quantitative, Risk-Based Approach to the Management of Neonatal Early-Onset Sepsis. JAMA Pediatr. 2017 Apr 1;171(4):365-371. doi: 10.1001/jamapediatrics.2016.4678. PMID: 28241253 
  4. Escobar GJ, Puopolo KM, Wi S, Turk BJ, Kuzniewicz MW, Walsh EM, Newman TB, Zupancic J, Lieberman E, Draper D. Stratification of risk of early-onset sepsis in newborns > 34 weeks’ gestation. Pediatrics. 2014 Jan;133(1):30-6. doi: 10.1542/peds.2013-1689. Epub 2013 Dec 23. PMID: 24366992
  5. Kuzniewicz MW, Walsh EM, Li S, Fischer A, Escobar GJ. Development and Implementation of an Early-Onset Sepsis Calculator to Guide Antibiotic Management in Late Preterm and Term Neonates. Jt Comm J Qual Patient Saf. 2016 May;42(5):232-9. doi: 10.1016/s1553-7250(16)42030-1. PMID: 27066927.
  6. Van Meurs K, Lou Short B. Congenital diaphragmatic hernia: the neonatologist’s perspective. Pediatr Rev. 1999 Oct;20(10):e79-87. doi: 10.1542/pir.20-10-e79. PMID: 10512896.

An infant was born weighing 1,250g at 30 weeks gestation due to premature rupture of membranes.  Pregnancy complications included maternal cocaine use and intrauterine growth restriction.  As feeds were introduced with donor breast milk, the infant appeared to have increased discomfort with feeds.  The baby went on to develop necrotizing enterocolitis, also known as NEC, at 20 days of life.  Which of the following is NOT a risk factor for the development of NEC?

A. Pre-term birth

B. Very low birth weight (defined as < 1,500g)

C. Intrauterine growth restriction

D. Maternal cocaine use

E. Feeding with donor breast milk


The correct answer is E, Feeding with donor breast milk is NOT a risk factor for the development of Necrotizing Enterocolitis (NEC).


Before we get into the risk factors, let’s learn a little more about NEC.  Infants present with poor feeding tolerance, increasing gastric residuals, increasing abdominal distension, and blood bowel movements.  The pathognomonic finding on abdominal X-ray is pneumatosis intestinalis which has been described as a “bubbly appearance” throughout the bowel.  Pneumatosis intestinalis results from intramural gas generated from anaerobic bacteria becoming trapped in the submucosal layer of the bowel wall.  Serial abdominal x-rays are the current gold standard to evaluate for disease progression.  Treatment includes making the infant NPO, placing a gastric tube for decompression, empiric antibiotics, and providing nutrition via TPN.  A surgical consult is also appropriate as approximately 30% of infants will progress to surgical disease. 

Now you may be wondering what antibiotics you should start… unfortunately there is no consensus recommendation on empiric antibiotics.  What the experts do agree on is that coverage should be broad and should target gram negative and anaerobic bacteria.  Typically, empiric coverage should last somewhere between 7-14 days.  A Cochrane systematic review completed in 2012 looked at various antibiotic regimens and concluded that there was insufficient evidence to recommend a particular antibiotic regimen for the treatment of NEC.  A randomized control trial would be needed to address this issue.  Most NICU’s will have standard empiric antibiotics based on provider preference and the local antibiogram.  Complications include intestinal perforation, intestinal stricture formation, intestinal malabsorption and short bowel syndrome, cholestatic liver disease, and neurodevelopmental delay.


So now that we have heard about a quick overview, let’s get back to our question. Feeding with breast milk, including donor breast milk, has been identified as the only consistent intervention for the prevention of NEC.  It is currently recommended that infants at risk for NEC, specifically those born with very low birth weight and born premature, receive feeds with breast milk or with donor breast milk if their own mother’s milk is not available.  Additionally, if fortification is needed, human milk derived fortifiers decrease the rate of NEC, specifically NEC which requires surgical treatment.  Formula feeding is a known risk factor for the development of NEC in both preterm and term infants.


The biggest risk factors for the development of NEC are prematurity and low birthweight.  Most NEC occurs in infants born at less than 32 weeks gestational age, and NEC affects 5-9% of all very low birth weight infants. About 90% of all NEC cases occur in pre-term infants.


Some additional risk factors to keep in mind are the need for packed red blood cell transfusion, a patent ductus arteriosus or other congenital heart disease, birth asphyxia or hypoxia, intrauterine growth restriction, polycythemia, chorioamnionitis, premature rupture of membranes, maternal cocaine use, chromosomal abnormalities, sepsis, gastroschisis, hypothyroidism, maternal pre- eclampsia, and maternal gestational diabetes.


The onset of NEC is inversely related to gestational age, the earlier the baby is born, the later the onset of NEC.  This is believed to be due to the fact that the timing of the onset of NEC often correlates with the initiation or advancement of feeds.  Typically, infants born near or at term are introduced to feeds sooner than their preterm counterparts therefore the onset of NEC is typically seen at an earlier post gestational age.


Again, the biggest risk factors to keep in mind are prematurity and low birth weight.  NEC onset is usually associated with the initiation or advancement of feeds.  While formula feeding is a known risk factor for the development of NEC, breast milk is protective.



  1. Samuels N, van de Graaf RA, de Jonge RCJ, Reiss IKM, Vermeulen MJ. Risk factors for necrotizing enterocolitis in neonates: a systematic review of prognostic studies. BMC Pediatr. 2017 Apr 14;17(1):105. doi: 10.1186/s12887-017-0847-3. PMID: 28410573; PMCID: PMC5391569.
  2. Chu A, Hageman JR, Caplan MS. Necrotizing Enterocolitis. NeoReviews Mar 2013, 14 (3) e113-e120; DOI: 10.1542/neo.14-3-e113.
  3. Rich BS, Dolgin SE. Necrotizing Enterocolitis. Pediatrics in Review Dec 2017, 38 (12) 552-559; DOI: 10.1542/pir.2017-0002.
  4. Wertheimer F, Arcinue R, Niklas V. Necrotizing Enterocolitis: Enhancing Awareness for the General Practitioner. Pediatr Rev. 2019 Oct;40(10):517-527. doi: 10.1542/pir.2017-0338. PMID: 31575803.
  5. Ross A, LeLeiko NS. Pediatrics in Review Apr 2010, 31 (4) 135-144; DOI: 10.1542/pir.31-4-135.
  6. Neu J, Walker WA. Necrotizing enterocolitis. N Engl J Med. 2011;364(3):255-264. doi:10.1056/NEJMra1005408.
  7. Kim SS, Albanese CT. Necrotizing Enterocolitis. Pediatric Surgery. 2006;1427-1452. doi:10.1016/B978-0-323-02842-4.50095-4.
  8. Gregory KE, Deforge CE, Natale KM, Phillips M, Van Marter LJ. Necrotizing enterocolitis in the premature infant: neonatal nursing assessment, disease pathogenesis, and clinical presentation. Adv Neonatal Care. 2011;11(3):155-166. doi:10.1097/ANC.0b013e31821baaf.
  9. Shah D, Sinn JK. Antibiotic regimens for the empirical treatment of newborn infants with necrotising enterocolitis. Cochrane Database Syst Rev. 2012 Aug 15;(8):CD007448. doi: 10.1002/14651858.CD007448.pub2. PMID: 22895960.

A child presents to your primary care clinic, who is a three-day old exclusively breast-fed female of European descent born at 36 weeks gestation.  Pregnancy, labor, delivery, and post-natal course were uncomplicated.  Mom’s blood type was A+, and this is her first child.  The infant was discharged at 24 hours of life, and her bilirubin level at that time was 6mg/dL, all indirect, which corresponded to a low intermediate risk level for developing severe hyperbilirubinemia.  She appears jaundiced on exam, and you note that she has lost approximately 8% of her birth weight.  Her current total serum bilirubin is 12mg/dL, all indirect.  You continue to trend bilirubin levels in your office throughout the week.  Her total bilirubin level peaks on day of life four and is down-trending by day of life six. What is the most likely etiology of her jaundice?

A. Breast milk jaundice

B. Breastfeeding jaundice

C. ABO incompatibility

D. Biliary atresia

E. G6PD deficiency


The correct answer is B, Breastfeeding jaundice.


Answer Choice B: Breastfeeding Jaundice

Over 60% of healthy newborns will develop jaundice.  The first step in any question about jaundice is to determine if the bilirubin is direct or indirect.  Breastfeeding jaundice is a form of indirect hyperbilirubinemia which develops between day of life two to four, peaks between day of life four to five, and typically resolves by two weeks of life.  Breastfeeding jaundice is mainly caused by inadequate milk intake.


Answer Choice A: Breast Milk Jaundice

This answer is easy to mix up with breast milk jaundice, which was answer A.  Breast milk jaundice develops later in life.  Breast milk jaundice is also a cause of indirect hyperbilirubinemia and peaks on day of life five to fifteen and can take up to 12 weeks to resolve.  In contrast to breast feeding jaundice, these infants are usually feeding well with good weight gain.


Answer Choice C: ABO Incompatibility

While ABO incompatibility is another cause of indirect hyperbilirubinemia, it is essentially ruled out in this situation as mom’s blood type is A+.  ABO incompatibility should primarily be considered in infants born to mothers whose blood is type O.


Answer Choice D: Biliary Atresia

This is incorrect as it is a cause of direct hyperbilirubinemia as compared to indirect hyperbilirubinemia.  To learn more about this, feel free to look at our episode on direct hyperbilirubinemia.


Answer Choice E: Glucose-6-Phosphate Dehydrogenase Deficiency

Finally, G6PD, or glucose-6-phosphate dehydrogenase, deficiency, is another cause of indirect hyperbilirubinemia which is unlikely in this infant.  G6PD deficiency is an X-linked recessive genetic condition that is most common in males of African, Asian, Middle Eastern, and Mediterranean descent.  In the United States, African American males are the most commonly affected.  G6PD deficiency increases the vulnerability of erythrocytes to oxidative stress.  Fava beans and oxidative medications, including many sulfa medications and nitrofurantoin, should be avoided in G6PD deficiency as these may trigger an acute hemolytic reaction.  Fava beans and oxidative medications must also be avoided in breastfeeding mothers as they may be transmitted through breast milk and lead to a hemolytic reaction in the infant.


Here are some additional points about hyperbilirubinemia:

  1. The AAP recommends that any infant discharged at 24 hours of life or younger should be seen by their PCP by 72 hours of life.  
  2. Major risk factors for the development of severe hyperbilirubinemia include:
  • Jaundice in the first 24 hours of life
  • Blood group incompatibility with a positive direct Coomb’s test
  • Prematurity
  • Previous siblings requiring phototherapy
  • Cephalohematomas or other bruising
  • Exclusive breastfeeding
  • Infants of East Asian descent



  1. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004 Jul;114(1):297-316. doi: 10.1542/peds.114.1.297. Erratum in: Pediatrics. 2004 Oct;114(4):1138. PMID: 15231951.
  2. Maisels, MJ. Neonatal Jaundice. Pediatrics in Review Dec 2006, 27 (12) 443-454; DOI: 10.1542/pir.27-12-443.
  3. Anderson, NB, Calkins, KL. Neonatal Indirect Hyperbilirubinemia. NeoReviews Nov 2020, 21 (11) e749-e760; DOI: 10.1542/neo.21-11-e749.
  4. Drugs and Lactation Database (LactMed) [Internet]. Bethesda (MD): National Library of Medicine (US); 2006-. Fava Beans. [Updated 2018 Dec 3]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532498/.
  5. Frank JE. Diagnosis and management of G6PD deficiency. Am Fam Physician. 2005 Oct 1;72(7):1277-82. PMID: 16225031.
  6. Kaplan M, Hammerman C. Glucose-6-Phosphate Dehydrogenase Deficiency: A Worldwide Potential Cause of Severe Neonatal Hyperbilirubinemia. NeoReviews Feb 2000, 1 (2) e32-e39; DOI: 10.1542/neo.1-2-e32.
  7. Koosha A, Rafizadeh B. Evaluation of neonatal indirect hyperbilirubinaemia at Zanjan Province of Iran in 2001-2003: prevalence of glucose-6-phosphate dehydrogenase deficiency. Singapore Med J. 2007 May;48(5):424-8. PMID: 17453100.

A four week old infant is brought into your primary care office.  She was born at 39w6d via uncomplicated home delivery and missed her newborn appointment.  Mom received appropriate prenatal care, and the pregnancy was uncomplicated.  The child’s birth weight was appropriate for age.  She has been breast feeding well and has continued to gain weight along the 30th percentile.  She has had no fevers or other signs of illness. On exam the child is markedly jaundiced with prominent icteric sclera.  You note that she has a firm, palpable liver edge.  She has no dysmorphic features or murmurs on exam.  She has a stool in the office which is a pasty white color.  You check a total serum bilirubin which is notable for direct hyperbilirubinemia.  You also obtain an abdominal ultrasound, which is notable for a triangular fibrous mass at the porta hepatis.  What is the most likely diagnosis?  

A. Choledochal cyst 

B. Physiologic jaundice

C. Alagille syndrome

D. Biliary atresia

E. Galactosemia


The correct answer is D, Biliary atresia.


Answer Choice D: Biliary Atresia

Biliary atresia is a form of direct hyperbilirubinemia.  The definition of direct hyperbilirubinemia can vary depending on laboratory systems.  In some systems, a direct bilirubin of more than 20% the total serum bilirubin is considered abnormal.  In other systems, any direct bilirubin greater than 1mg/dL is considered abnormal.  Due to variability in lab systems, the North American and Europeans Societies for Pediatric Gastroenterology, Hepatology and Nutrition recommend that any infant with a direct bilirubin > 1mg/dL are referred for further evaluation.   

Extrahepatic biliary atresia is the most common cause of neonatal cholestasis.  It typically presents with jaundice between 3-6 weeks of age.  These patients frequently have pasty white or acholic stools. Early referral to a pediatric gastroenterologist is key.  The ultrasound finding described in the question is suggestive of biliary atresia, but not diagnostic. The primary purpose of the ultrasound is to rule out a choledochal cyst, which was answer choice A.  A normal ultrasound does not rule out biliary atresia. Liver biopsy is diagnostic in 90-95% of cases and will demonstrate large duct obstruction, portal tract edema, bile ductular proliferation and the presence of bile plugs in bile ductules.  Patient’s then undergo intraoperative cholangiogram followed by a hepato-porto-enterostomy Kasai procedure which allows bile to drain into the intestine.  The younger the patient is at the time of the procedure the higher the success rate.  If these patients are not treated, they will most likely die from liver failure by 2 years of age. 


Answer Choice A: Choledochal Cyst

Choledochal cysts are cystic dilations of the bile duct which lead to obstruction and bile retention, which in turn leads to jaundice and liver enlargement.  There are five different types based on the site of the cyst or dilation.  They can be identified on ultrasound, and treatment is surgical.


Answer Choice B: Physiologic Jaundice

Physiologic jaundice is incorrect for several reasons.  First, all jaundice that persists past two weeks of life requires further investigation. Second, physiologic jaundice results in indirect hyperbilirubinemia.  In this case, the patient had direct hyperbilirubinemia which ALWAYS requires further investigation.  This is why it is essential to always obtain a fractionated serum total bilirubin; you cannot rely solely on transcutaneous bilirubin monitoring.  


Answer Choice C: Alagille Syndrome

Alagille syndrome is less likely in this patient.  While these patients do present with jaundice and acholic stools there are several other features to look for including

  1. Dysmorphic facies: prominent broad forehead, deep set eyes and a triangular chin
  2. Congenital heart disease, most commonly pulmonary stenosis
  3. Short stature and hypogonadism 
  4. Abnormalities of the eyes, kidneys, and butterfly vertebra 

This syndrome is inherited in an autosomal dominant fashion with variable penetrance and expressivity.  In contrast to biliary atresia, their liver size is normally normal in the neonatal period.  Histology demonstrates a paucity of normal intralobular bile ducts which are progressively lost with age.


We discuss more about galactosemia in our episode related to inborn errors of metabolism (Episode 15), but this is an unlikely etiology in this patient given the fact that they are overall clinically well appearing.  Children with biliary atresia are initially well appearing and are growing well, while infants with metabolic disorders or infections as the cause of their cholestatic jaundice are typically ill appearing and slow to gain weight.



1. Zallen GS, Bliss DW, Curran TJ, Marvin WH, silen, ML.  Biliary Atresia.  Pediatrics in Review Jul 2006, 27 (7) 243-248; DOI: 10.1542/pir.27-7-243.

2. Wang KS; Section on Surgery; Committee on Fetus and Newborn; Childhood Liver Disease Research Network. Newborn Screening for Biliary Atresia. Pediatrics. 2015 Dec;136(6):e1663-9. doi: 10.1542/peds.2015-3570. PMID: 26620065; PMCID: PMC4920543.

3. Suchy FJ. Neonatal Cholestasis.  Pediatrics in Review Nov 2004, 25 (11) 388-396; DOI: 10.1542/pir.25-11-388.

4. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004 Jul;114(1):297-316. doi: 10.1542/peds.114.1.297. Erratum in: Pediatrics. 2004 Oct;114(4):1138. PMID: 15231951.

5. Fawaz R, Baumann U, Ekong U, Fischler B, Hadzic N, Mack CL, McLin VA, Molleston JP, Neimark E, Ng VL, Karpen SJ. Guideline for the Evaluation of Cholestatic Jaundice in Infants: Joint Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. 2017 Jan;64(1):154-168. doi: 10.1097/MPG.0000000000001334. PMID: 27429428.