Neonatal jaundice

Neonatal jaundice
Other namesNeonatal hyperbilirubinemia, neonatal icterus, jaundice in newborns
Jaundice in a newborn
SpecialtyPediatrics
SymptomsYellowish discoloration of the skin and white part of the eyes[1]
ComplicationsSeizures, cerebral palsy, kernicterus[1]
Usual onsetNewborns[1]
TypesPhysiologic, pathologic[1]
CausesRed blood cell breakdown, liver disease, infection, hypothyroidism, metabolic disorders[2][1]
Diagnostic methodBased on symptoms, confirmed by bilirubin[1]
TreatmentMore frequent feeding, phototherapy, exchange transfusions[1]
Frequency>50% of babies[1]

Neonatal jaundice is a yellowish discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin levels.[1] Other symptoms may include excess sleepiness or poor feeding.[1] Complications may include seizures, cerebral palsy, or kernicterus.[1]

In most of cases there is no specific underlying physiologic disorder.[2] In other cases it results from red blood cell breakdown, liver disease, infection, hypothyroidism, or metabolic disorders (pathologic).[2][1] A bilirubin level more than 34 μmol/L (2 mg/dL) may be visible.[1] Concerns, in otherwise healthy babies, occur when levels are greater than 308 μmol/L (18 mg/dL), jaundice is noticed in the first day of life, there is a rapid rise in levels, jaundice lasts more than two weeks, or the baby appears unwell.[1] In those with concerning findings further investigations to determine the underlying cause are recommended.[1]

The need for treatment depends on bilirubin levels, the age of the child, and the underlying cause.[1][3] Treatments may include more frequent feeding, phototherapy, or exchange transfusions.[1] In those who are born early more aggressive treatment tends to be required.[1] Physiologic jaundice generally lasts less than seven days.[1] The condition affects over half of babies in the first week of life.[1] Of babies that are born early about 80% are affected.[2] Globally over 100,000 late-preterm and term babies die each year as a result of jaundice.[4]

Sign and symptoms

Bronze baby syndrome (dark pigmentation of skin).

The primary symptom is yellowish discoloration of the white part of the eyes and skin in a newborn baby.[1] Other symptoms may include excess sleepiness or poor feeding.[1]

A bilirubin level more than 34 μmol/L (2 mg/dL) may be visible.[1] For the feet to be affected level generally must be over 255 μmol/L (15 mg/dL).[1]

Complications

Prolonged hyperbilirubinemia (severe jaundice) can result in chronic bilirubin encephalopathy (kernicterus).[5][6] Quick and accurate treatment of neonatal jaundice helps to reduce the risk of neonates developing kernicterus.[7]

Infants with kernicterus may have a fever[8] or seizures.[9] High pitched crying is an effect of kernicterus.[citation needed]

Exchange transfusions performed to lower high bilirubin levels are an aggressive treatment.[10]

Causes

In newborns, jaundice tends to develop because of two factors—the breakdown of fetal hemoglobin as it is replaced with adult hemoglobin and the relatively immature metabolic pathways of the liver, which are unable to conjugate and so excrete bilirubin as quickly as an adult. This causes an accumulation of bilirubin in the blood (hyperbilirubinemia), leading to the symptoms of jaundice.[citation needed]

If the neonatal jaundice is not resolved with simple phototherapy, other causes such as biliary atresia, Progressive familial intrahepatic cholestasis, bile duct paucity, Alagille syndrome, alpha 1-antitrypsin deficiency, and other pediatric liver diseases should be considered. The evaluation for these will include blood work and a variety of diagnostic tests. Prolonged neonatal jaundice is serious and should be followed up promptly.[11]

Severe neonatal jaundice may indicate the presence of other conditions contributing to the elevated bilirubin levels, of which there are a large variety of possibilities (see below). These should be detected or excluded as part of the differential diagnosis to prevent the development of complications. They can be grouped into the following categories:

Neonatal jaundice
Unconjugated bilirubinConjugated bilirubin
PathologicPhysiological jaundice of neonatesHepaticPost-hepatic
HemolyticNon-hemolytic
Intrinsic causesExtrinsic causes

Unconjugated

Hemolytic

Intrinsic causes of hemolysis
Extrinsic causes of hemolysis

Non-hemolytic causes

Conjugated (Direct)

Liver causes

Post-liver

Non-organic causes

Breastfeeding jaundice

"Breastfeeding jaundice" (or "lack of breastfeeding jaundice") is caused by insufficient breast milk intake,[13] resulting in inadequate quantities of bowel movements to remove bilirubin from the body. This leads to increased enterohepatic circulation, resulting in increased reabsorption of bilirubin from the intestines.[14] Usually occurring in the first week of life, most cases can be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production.[15]

Breast milk jaundice

Whereas breastfeeding jaundice is a mechanical problem, breast milk jaundice is a biochemical occurrence and the higher bilirubin possibly acts as an antioxidant. Breast milk jaundice occurs later in the newborn period, with the bilirubin level usually peaking in the sixth to 14th days of life. This late-onset jaundice may develop in up to one third of healthy breastfed infants.[16]

  1. The gut is sterile at birth and normal gut flora takes time to establish. The bacteria in the adult gut convert conjugated bilirubin to stercobilinogen which is then oxidized to stercobilin and excreted in the stool. In the absence of sufficient bacteria, the bilirubin is de-conjugated by brush border β-glucuronidase and reabsorbed. This process of re-absorption is called enterohepatic circulation. It has been suggested that bilirubin uptake in the gut (enterohepatic circulation) is increased in breast fed babies, possibly as the result of increased levels of epidermal growth factor (EGF) in breast milk.[17] Breast milk also contains glucoronidase which will increase deconjugation and enterohepatic recirculation of bilirubin.
  2. The breast-milk of some women contains a metabolite of progesterone called 3-alpha-20-beta pregnanediol. This substance inhibits the action of the enzyme uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase responsible for conjugation and subsequent excretion of bilirubin. In the newborn liver, activity of glucuronyl transferase is only at 0.1-1% of adult levels, so conjugation of bilirubin is already reduced. Further inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood.[18] However, these results have not been supported by subsequent studies.[19]
  3. An enzyme in breast milk called lipoprotein lipase produces increased concentration of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to decreased conjugation and subsequent excretion of bilirubin.[20]

Physiological jaundice

Most infants develop visible jaundice due to elevation of unconjugated bilirubin concentration during their first week. This is called physiological jaundice. This pattern of hyperbilirubinemia has been classified into two functionally distinct periods.[21]

  • Phase one
  1. Term infants - jaundice lasts for about 10 days with a rapid rise of serum bilirubin up to 204 μmol/L (12 mg/dL).
  2. Preterm infants - jaundice lasts for about two weeks, with a rapid rise of serum bilirubin up to 255 μmol/L (15 mg/dL).
  • Phase two - bilirubin levels decline to about 34 μmol/L (2 mg/dL) for two weeks, eventually mimicking adult values.
  1. Preterm infants - phase two can last more than one month.
  2. Exclusively breastfed infants - phase two can last more than one month.

Mechanisms involved in physiological jaundice include:

  • Relatively low activity of the enzyme glucuronosyltransferase which normally converts unconjugated bilirubin to conjugated bilirubin that can be excreted into the gastrointestinal tract.[22] Before birth, this enzyme is actively down-regulated, since bilirubin needs to remain unconjugated in order to cross the placenta to avoid being accumulated in the fetus.[23] After birth, it takes some time for this enzyme to gain function.
  • Shorter life span of fetal red blood cells,[22] being approximately 80 to 90 days in a full term infant,[24] compared to 100 to 120 days in adults.
  • Relatively low conversion of bilirubin to urobilinogen by the intestinal flora, resulting in relatively high absorption of bilirubin back into the circulation.[22]

Diagnosis

Diagnosis is often by measuring the serum bilirubin level in the blood.[3] In those who are born after 35 weeks and are more than a day old transcutaneous bilirubinometer may also be used.[3] The use of an icterometer, a piece of transparent plastic painted in five transverse strips of graded yellow lines, is not recommended.[3]

Transcutaneous bilirubinometer

This is hand held, portable and rechargeable but expensive. When pressure is applied to the photoprobe, a xenon tube generates a strobe light, and this light passes through the subcutaneous tissue. The reflected light returns through the second fiber optic bundle to the spectrophotometric module. The intensity of the yellow color in this light, after correcting for the hemoglobin, is measured and instantly displayed in arbitrary units.[citation needed]

Pathological jaundice

Any of the following features suggests pathological jaundice:[citation needed]

  1. Clinical jaundice appearing in the first 24 hours or greater than 14 days of life.
  2. Increases in the level of total bilirubin by more than 8.5 μmol/L (0.5 mg/dL) per hour or (85 μmol/L) 5 mg/dL per 24 hours.
  3. Total bilirubin more than 331.5 μmol/L (19.5 mg/dL) (hyperbilirubinemia).
  4. Direct bilirubin more than 34 μmol/L (2.0 mg/dL).

The signs which help detect pathological jaundice are the presence of intrauterine growth restriction, stigma of intrauterine infections (e.g. cataracts, small head, and enlargement of the liver and spleen), cephalohematoma, bruising, signs of bleeding in the brain's ventricles. History of illness is noteworthy. Family history of jaundice and anemia, family history of neonatal or early infant death due to liver disease, maternal illness suggestive of viral infection (fever, rash or lymphadenopathy), maternal drugs (e.g. sulphonamides, anti-malarials causing red blood cell destruction in G6PD deficiency) are suggestive of pathological jaundice in neonates.[citation needed]

Treatment

The bilirubin levels for initiative of phototherapy varies depends on the age and health status of the newborn. However, any newborn with a total serum bilirubin greater than 359 μmol/L ( 21 mg/dL) should receive phototherapy.[25]

Phototherapy

Phototherapy is the main treatment of neonatal jaundice

Babies with neonatal jaundice may be treated with colored light called phototherapy, which works by changing trans-bilirubin into the water-soluble cis-bilirubin isomer.[26][27][28]: 2533 

The phototherapy involved is not ultraviolet light therapy but rather a specific frequency of blue light. The light can be applied with overhead lamps, which means that the baby's eyes need to be covered, or with a device called a biliblanket, which sits under the baby's clothing close to its skin.[27]

The use of phototherapy was first discovered, accidentally, at Rochford Hospital in Essex, England, when a nurse, Sister Jean Ward, noticed that babies exposed to sunlight had reduced jaundice, and a pathologist, Dr. Perryman, who noticed that a vial of blood left in the sun had turned green. Drs Cremer, Richards and Dobbs put together these observations,[29] leading to a landmark randomized clinical trial which was published in Pediatrics in 1968; it took another ten years for the practice to become established.[27][30] Massage therapy could be useful in addition to phototherapy in order to reduce the phototherapy duration. However, it does not appear to reduce the requirement for phototherapy in the treatment of neonatal jaundice.[31]

Recent studies from several countries show that phototherapy can safely and effectively be performed in the family's home, and since 2022 home phototherapy is recommended as an alternative to readmission to hospital in the American national guidelines.[32][33][34] However, there have been several reports about the possible relationship between neonatal phototherapy and the increased risk of future cancer. A recent systematic review has found that there may be a statistically significant association between phototherapy and various hematopoietic cancers (especially myeloid leukemia).[35]

Exchange transfusions

Much like with phototherapy the level at which exchange transfusion should occur depends on the health status and age of the newborn. It should however be used for any newborn with a total serum bilirubin of greater than 428 μmol/L ( 25 mg/dL ).[25][28]: 2533 

Research

Penicillamine was studied in the 1970s in hyperbilirubinemia due to ABO hemolytic disease.[36] While tin mesoporphyrin IX may decrease bilirubin such use is not recommended in babies.[36] Preclinical studies have looked at minocycline to help prevent neurotoxicity.[36] Clofibrate may decrease the duration of phototherapy.[36] Evidence as of 2012 however is insufficient to recommend its use.[37]

References

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  2. ^ a b c d "Jaundice in newborn babies under 28 days | Guidance and guidelines". NICE. October 2016. Retrieved 11 December 2017.
  3. ^ a b c d "Jaundice in newborn babies under 28 days". NICE. October 2016. Retrieved 11 December 2017.
  4. ^ Olusanya, BO; Teeple, S; Kassebaum, NJ (February 2018). "The Contribution of Neonatal Jaundice to Global Child Mortality: Findings From the GBD 2016 Study". Pediatrics. 141 (2): e20171471. doi:10.1542/peds.2017-1471. PMID 29305393.
  5. ^ Juetschke, L.J. (2005, Mar/Apr). Kernicterus: still a concern. Neonatal Network, 24(2), 7-19, 59-62
  6. ^ Colletti, JE; Kothari, S; Kothori, S; Jackson, DM; Kilgore, KP; Barringer, K (November 2007). "An emergency medicine approach to neonatal hyperbilirubinemia". Emerg. Med. Clin. North Am. 25 (4): 1117–35, vii. doi:10.1016/j.emc.2007.07.007. PMID 17950138.
  7. ^ Watchko, JF (December 2006). "Hyperbilirubinemia and bilirubin toxicity in the late preterm infant" (PDF). Clin Perinatol. 33 (4): 839–52, abstract ix. doi:10.1016/j.clp.2006.09.002. PMID 17148008. Archived from the original (PDF) on 8 August 2017. Retrieved 26 September 2019.
  8. ^ Shah, Z; Chawla, A; Patkar, D; Pungaonkar, S (March 2003). "MRI in kernicterus". Australasian Radiology. 47 (1): 55–7. doi:10.1046/j.1440-1673.2003.00973.x. PMID 12581055.
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  13. ^ Lynn C. Garfunkel; Jeffrey; Cynthia Christy (2002). Mosby's pediatric clinical advisor: instant diagnosis and treatment. Elsevier Health Sciences. pp. 200–. ISBN 978-0-323-01049-8. Retrieved 14 June 2010.
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  15. ^ CDC (13 November 2020). "Jaundice". Centers for Disease Control and Prevention. Retrieved 12 July 2021.
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  17. ^ Kumral, A; Ozkan H; Duman N; et al. (2009). "Breast milk jaundice correlates with high levels of epidermal growth factor". Pediatr Res. 66 (2): 218–21. doi:10.1203/pdr.0b013e3181ac4a30. PMID 19617811.
  18. ^ Arias, IM; Gartner LM; Seifter S; Furman M (1964). "Prolonged neonatal unconjugated hyperbilirubinemia associated with breast feeding and a steroid, pregnane-3(alpha), 20(beta)-diol in maternal milk that inhibits glucuronide formation in vitro". J Clin Invest. 43 (11): 2037–47. doi:10.1172/jci105078. PMC 441992. PMID 14228539.
  19. ^ Murphy, J F; Hughes I; Verrier Jones ER; Gaskell S; Pike AW (1981). "Pregnanediols and breast-milk jaundice". Arch Dis Child. 56 (6): 474–76. doi:10.1136/adc.56.6.474. PMC 1627473. PMID 7259280.
  20. ^ Poland, R L; Schultz GE; Gayatri G (1980). "High milk lipase activity associated with breastmilk jaundice". Pediatr Res. 14 (12): 1328–31. doi:10.1203/00006450-198012000-00011. PMID 6782543.
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  22. ^ a b c Page 45 in: Obstetrics & Gynaecology, by B. Jain, 2002. ISBN 8180562107, 9788180562105
  23. ^ McDonagh, A. F. (2007). "Movement of Bilirubin and Bilirubin Conjugates Across the Placenta". Pediatrics. 119 (5): 1032–1033, author 1033 1033. doi:10.1542/peds.2006-3669. PMID 17473108. S2CID 21269991.
  24. ^ Harrison, K. L. (1979). "Fetal Erythrocyte Lifespan". Journal of Paediatrics and Child Health. 15 (2): 96–97. doi:10.1111/j.1440-1754.1979.tb01197.x. PMID 485998. S2CID 5370064.
  25. ^ a b American Academy of Pediatrics Subcommittee on Hyperbilirubinemia (July 2004). "Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation". Pediatrics. 114 (1): 297–316. doi:10.1542/peds.114.1.297. PMID 15231951.
  26. ^ Stokowski LA (December 2006). "Fundamentals of phototherapy for neonatal jaundice". Adv Neonatal Care. 6 (6): 303–12. doi:10.1016/j.adnc.2006.08.004. PMID 17208161. S2CID 31233601.
  27. ^ a b c Jones, Clay (9 May 2014). "Separating Fact from Fiction in the Not-So-Normal Newborn Nursery: Newborn Jaundice". Science-Based Medicine.
  28. ^ a b Wolkoff, Allan W. (2012). "Chapter 303: The Hyperbilirubinemias". In Longo, Dan L.; Kasper, Dennis L. (eds.). Harrison's principles of internal medicine (18th ed.). New York: McGraw-Hill. ISBN 978-0071748896.
  29. ^ CREMER, RJ; PERRYMAN, PW; RICHARDS, DH (24 May 1958). "Influence of light on the hyperbilirubinaemia of infants". Lancet. 1 (7030): 1094–7. doi:10.1016/s0140-6736(58)91849-x. PMID 13550936.
  30. ^ Lucey, J; Ferriero, M; Hewitt, J (June 1968). "Prevention of hyperbilirubinemia of prematurity by phototherapy". Pediatrics. 41 (6): 1047–54. doi:10.1542/peds.41.6.1047. PMID 5652916. S2CID 41816888.
  31. ^ Abdellatif, Mohammed (February 2020). "Massage therapy for the treatment of neonatal jaundice: A systematic review and network meta-analysis". Journal of Neonatal Nursing. 26 (1): 17–24. doi:10.1016/j.jnn.2019.09.002.
  32. ^ Anderson, Candice Megan; Kandasamy, Yogavijayan; Kilcullen, Meegan (August 2021). "The efficacy of home phototherapy for physiological and non-physiological neonatal jaundice: A systematic review". Journal of Neonatal Nursing. 28 (5): 312–326. doi:10.1016/j.jnn.2021.08.010. S2CID 238646014.
  33. ^ Pettersson, M.; Eriksson, M.; Albinsson, E.; Ohlin, A. (1 May 2021). "Home phototherapy for hyperbilirubinemia in term neonates—an unblinded multicentre randomized controlled trial". European Journal of Pediatrics. 180 (5): 1603–1610. doi:10.1007/s00431-021-03932-4. ISSN 1432-1076. PMC 8032579. PMID 33469713.
  34. ^ Kemper, A. R.; Newman, T. B.; Slaughter, J. L.; Maisels, M. J.; Watchko, J. F.; Downs, S. M.; Grout, R. W.; Bundy, D. G.; Stark, A. R.; Bogen, D. L.; Holmes, A. V.; Feldman-Winter, L. B.; Bhutani, V. K.; Brown, S. R.; Maradiaga Panayotti, G. M.; Okechukwu, K.; Rappo, P. D.; Russell, T. L. (2022). "Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation". Pediatrics. 150 (3). doi:10.1542/peds.2022-058859. PMID 35927462. Retrieved 20 September 2022.
  35. ^ Abdellatif, Mohammed, et al. "Association between neonatal phototherapy and future cancer: an updated systematic review and meta-analysis." European Journal of Pediatrics (2022): 1-13
  36. ^ a b c d Mancuso, Cesare (15 May 2017). "Bilirubin and brain: A pharmacological approach". Neuropharmacology. 118: 113–123. doi:10.1016/j.neuropharm.2017.03.013. PMID 28315352. S2CID 21001248.
  37. ^ Gholitabar, M; McGuire, H; Rennie, J; Manning, D; Lai, R (12 December 2012). "Clofibrate in combination with phototherapy for unconjugated neonatal hyperbilirubinaemia". The Cochrane Database of Systematic Reviews. 12 (3): CD009017. doi:10.1002/14651858.CD009017.pub2. PMC 6426433. PMID 23235669.

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Si ce bandeau n'est plus pertinent, retirez-le. Cliquez ici pour en savoir plus. Cet article ne cite pas suffisamment ses sources (janvier 2022). Si vous disposez d'ouvrages ou d'articles de référence ou si vous connaissez des sites web de qualité traitant du thème abordé ici, merci de compléter l'article en donnant les références utiles à sa vérifiabilité et en les liant à la section « Notes et références » En pratique : Quelles sources sont attendues ? Co...

 

Italian actress This article does not cite any sources. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed.Find sources: Germana Paolieri – news · newspapers · books · scholar · JSTOR (December 2012) (Learn how and when to remove this template message) Germana PaolieriBorn(1906-08-29)29 August 1906Florence, Tuscany ItalyDied8 August 1998(1998-08-08) (aged 91)Montecatini, Tusca...

 

English actor and dramatist For other people with the same name, see Thomas Hull. Thomas Hull (1728–1808) was an English actor and dramatist. Thomas Hull, portrait from the 1760s Early life Born in 1728 in Strand, London, where his father practised as an apothecary, he was educated at Charterhouse School, with a view to a career in the church. He made an unsuccessful attempt to follow his father's profession.[1] Stage career According to Biographia Dramatica, Hull first appeared at ...

Public square in Damascus Marjeh Squareساحة المرجةMartyrs' Squareساحة الشهداءThe square and the Yalbugha MosqueCoordinates33°30′46″N 36°17′53″E / 33.5128°N 36.2980°E / 33.5128; 36.2980ConstructionCompletionlate nineteenth century Marjeh Square (Arabic: ساحة المرجة / ALA-LC: sāḥat al-Marjah), also known as Martyrs' Square (ساحة الشهداء sāḥat ash-Shuhadā’), is a square in central Damascus, Syria, just outside...

 

Anand in his breakthrough film Baazi (1951) Dev Anand (born Dharamdev Pishorimal Anand; 26 September 1923 – 3 December 2011), was an Indian actor, writer, director and producer known for his work in Hindi cinema. Anand is considered one of the greatest and most successful actors in the history of Indian cinema.[1] Through a career that spanned over six decades, he worked in more than 100 films. Anand is a recipient of four Filmfare Awards, including two for Best Actor. The Governmen...

 

Article principal : Élection générale québécoise de 2008. Cette liste des candidats à l'élection générale québécoise de 2008 indique l'ensemble des personnes étant officiellement candidates à l'élection générale québécoise de 2008 pour chacune des circonscriptions électorales du Québec. Les circonscriptions sont classées par région administrative. Jusqu'à ce que le Directeur général des élections publie la liste officielle des candidats, les informations contenu...

2012 video gameWonderbookDeveloper(s)London StudioPublisher(s)SCEEPlatform(s)PlayStation 3ReleaseNA: 13 November 2012AU: 15 November 2012EU: 16 November 2012JP: 7 November 2013Genre(s)Gaming Wonderbook is an augmented reality peripheral for the PlayStation 3 console. The user holds a physical book-like object and the software displays content on the television's screen. Development Wonderbook is an augmented reality book which is designed to be used in conjunction with the PlayStation Move an...

 

Motivasi adalah proses yang menjelaskan intensitas, arah, dan ketekunan seorang individu dalam mencapai tujuannya.[1] Tiga elemen utama dalam definisi ini diantaranya adalah intensitas, arah, dan ketekunan.[2] Berdasarkan teori hierarki kebutuhan Abraham Maslow, teori X dan teori Y Douglas McGregor maupun teori motivasi kontemporer, arti motivasi adalah 'alasan' yang mendasari sebuah perbuatan yang dilakukan oleh seorang individu. Seseorang dikatakan memiliki motivasi tinggi b...

 

Strategi Solo vs Squad di Free Fire: Cara Menang Mudah!