Neonatal Jaundice: Aetiology, Diagnosis And Treatment -
Current Issues in Neonatal CareNeonatal jaundice: aetiology, diagnosisand treatmentA significant proportion of term and preterm infantsdevelop neonatal jaundice. Jaundice in an otherwisehealthy term infant is the most common reason forreadmission to hospital. Jaundice is caused by anincrease in serum bilirubin levels, largely as a result ofbreakdown of red blood cells. Bilirubin is conveyed inthe blood as ‘unconjugated’ bilirubin, largely bound toalbumin. The liver converts bilirubin into a conjugatedform which is excreted in the bile. Very high levels ofunconjugated bilirubin are neurotoxic. Phototherapyis a simple and effective way to reduce the bilirubinlevel. Most term babies have ‘physiological’ jaundicewhich responds to a short period of phototherapy,and requires no other treatment. A few babies haverapidly rising bilirubin levels which place them at riskof kernicterus. Current management of jaundice inthe UK is guided by the NICE guideline. Any infant withhigh serum bilirubin or a rapidly rising bilirubin levelneeds to be treated urgently to avoid neurotoxicity.High levels of conjugated bilirubin in a term baby canindicate biliary atresia, and babies with persistingjaundice must have their level of conjugated bilirubinmeasured. Preterm infants on long-term parenteralnutrition may develop conjugated jaundice whichgenerally improves with the introduction of enteralfeed and weaning of intravenous nutrition.Keywords: Neonatal jaundice, kernicterus, conjugatedjaundice, phototherapy, exchange transfusionDr Subhabrata MitraConsultant Neonatologist, Neonatal Unit, ElizabethGarrett Anderson Wing, University College LondonHospital, London NW1 2BUDr Janet RennieConsultant Neonatologist, Neonatal Unit, ElizabethGarrett Anderson Wing, University College LondonHospital, LondonCorrespondence to: Dr Subhabrata Mitrasubhabrata.mitra.13@ucl.ac.uk14 Neonatal jaundice is one of the most commonclinical signs in newborn infants. Jaundicepresent as yellow discolouration of the skinand sclera in infants, indicating a raised serumbilirubin level leading to accumulation of bilirubinin the tissues, including the skin and mucousmembranes. Jaundice is thought to be visible atbilirubin levels of around 90 mmol/litre in babieswith pale skin tones. The detection of jaundice ismore difficult in babies with dark skin tones, but thesclerae are always white and inspection of the eyesis a crucial part of visual assessment of jaundice.Around 60% of term and 80% of preterm infantsdevelop jaundice in the first week of life and 10% ofbreastfed infants remain jaundiced up to 1 monthof age. Jaundice was the most common reason foradmission from home to neonatal units in Englandfor term infants (Battersby et al, 2017).Most infants who become jaundiced developjaundice in the first week of life, and in the majorityof cases it is mild and harmless. Breast-fed infants aremore prone to develop physiological jaundice in thefirst week of life. The key challenge is to differentiatethe rare baby with significant jaundice which mightlead to bilirubin encephalopathy and kernicterusfrom the majority of babies in whom jaundice will beharmless. It is also essential to identify infants withconjugated hyperbilirubinaemia who have biliaryatresia as early as possible to improve outcome. Theoutcome for babies with biliary atresia whose surgeryis performed at less that 6 weeks of age is muchbetter than in those whose surgery is delayed by latediagnosis.The current national guideline in UK from theNational Institute for Health and Care Excellence(NICE) (2016) recommends a review of all infantswith risk factors for neonatal jaundice within the first48 hours of life and assessment of serum bilirubinlevel in any infant with clinical jaundice. The riskfactors are outlined in Table 1.Bilirubin metabolismIn newborn infants, bilirubin is mostly producedfrom the breakdown of red blood cells. Haemoglobin, 2017 MA Healthcare LtdAbstract
2017 MA Healthcare LtdCurrent Issues in Neonatal Carereleased from broken-down red blood cells, undergoesa two-stage catabolism within the reticuloendothelialsystem to produce bilirubin. This unconjugated (orindirect) bilirubin is transported in the circulationbound with serum albumin. Unconjugated bilirubincombines with glucuronic acid in the smoothendoplasmic reticulum inside the liver to producewater-soluble mono- or di-glucuronides of bilirubin,commonly referred as conjugated (or direct) bilirubin.Conjugated bilirubin is a component of bile andenters the gut via the biliary system. Although aproportion of conjugated bilirubin can be hydrolysedby beta-glucuronidase to unconjugated bilirubin inthe small gut, from where it is reabsorbed (theenterohepatic circulation), the majority is excretedwith the stool. Establishing gut motility and a normalpattern of stooling is an important component ofreducing the bilirubin load from the enterohepaticcirculation in the first few days, which is part of thereason why breastfeeding support is an essentialcomponent of the management of neonatal jaundice.An excellent new e-learning resource packageregarding physiology of bilirubin metabolism underNHS Health Education England will be availablefor health-care professionals rialManagement.aspx? materialId 15591&rl prj& prjid 15146).higher peak in serum bilirubin levels along with alonger duration of hyperbilirubinaemia compared toterm infants.Infants with bruising related to birth trauma,scalp haematoma (e.g. cephalhaematoma) and bornafter delayed cord clamping need to be carefullymonitored early on as they have an increased risk ofdeveloping jaundice.Glucose-6-phosphatase deficiency (G6PD) is animportant underlying cause of kernicterus, bothworldwide and in the UK. Male babies of Asianethnicity are particularly at risk but this condition isnot confined to this group.Normal pattern of neonatal jaundiceBilirubin encephalopathyMost newborn infants develop jaundice in the firstweek of life. In term infants, the serum bilirubin levelreaches a clinically detectable level by day 3 or 4. Thisgradually falls over the next few days before reachingthe normal childhood serum bilirubin level by the endof the second week of life. This is generally referredto as physiological jaundice. Although prolongedunconjugated jaundice was previously attributedmainly to ‘breast milk jaundice’, it is becoming clearthat many of these cases have an underlying geneticexplanation (Bhutani, 2012). Up to one-third ofexclusively breast-fed infants remain jaundiced at theend of 2 weeks and this group contributes to mostcommunity referrals to hospital for review at this age.A confident diagnosis of breast milk jaundice canonly be made after exclusion of other possible causesand parents need an explanation of the nature ofthe problem. Beta-glucuronidase is present in breastmilk and can cause increased levels of unconjugatedbilirubin that enters the enterohepatic circulationfrom the gut. Altered gut flora in breast-fed infantshas also been implicated in the reduction of theconversion of bilirubin glucuronides to urobilinoids.Jaundice in preterm infants is characterised by aSick and preterm infants are more vulnerable to theneurotoxic effect of raised bilirubin levels (Gartneret al, 1970). Pathophysiological mechanisms includecell membrane function disruption, loweringof action potential, disturbed energy metabolismand disturbance in neurotransmitter synthesis(Volpe, 2008; Brites et al, 2009). The depositionof bilirubin in the brain, noted during autopsy ofinfants who had died as a result of acute bilirubintoxicity, was described as ‘kernicterus’. Involvementof the brainstem, hippocampus, cerebellum, globuspallidus and subthalamic nuclei has been described.This anatomical predisposition might be related toincreased metabolic activity and regional cerebralblood flow.Hypoxia, acidosis, hypercarbia, sepsis, seizuresand disturbances to the blood–brain barrier areco-existing risk factors for acute bilirubintoxicity (Wennberg et al, 2006). Medications thatinterfere with bilirubin albumin binding or inhibitp-glycoprotein are implicated in increasing the risk ofacute bilirubin encephalopathy (Watchko et al, 2002).More apoptosis was noted in less well-differentiatedastrocytes and neurons (Brites et al, 2009) indicating Table 1. Factors related to higher susceptibility ofnewborn infants for development of physiologicaljaundiceHigh haemoglobin concentration in newborn infantsImmaturity of hepatic uptake, transport and conjugationsystemShorter lifespan for neonatal red blood cells comparedto those of adultsIncreased level of beta-glucuronidase in the gut,releasing more unconjugated bilirubin to enter theenterohepatic circulation15
Current Issues in Neonatal CareSerum bilirubin level 340 mmol/litre in a term infant( 37 weeks)Rapid rise in the serum bilirubin level ( 8.5 mmol/litre/hour)Clinical signs suggestive of bilirubin encephalopathythe importance of the developmental stage of thebrain in relation to bilirubin toxicity. A UK surveillancestudy has reported an occurrence of kernicterus in 1in 100 000 live births (Manning et al, 2007).Risk factors for developing kernicterus arepresented in Table 2.Previously described different stages of bilirubinencephalopathy (Connolly and Volpe, 1990) are nowrare in current clinical practice. Opisthotonus (Figure1) generally indicates neuronal toxicity. Magneticresonance imaging of the brain is the investigationof choice in suspected cases and presents acharacteristic picture in cases of kernicterus (FigureFigure 1. Typical opisthotonic posture in a baby with neonataljaundice and acute bilirubin encephalopathy.Figure 2. Characteristic changes in kernicterus. a and b.Hyperintense signal and symmetrical scarring in globus palliduson T2-weighted imaging on brain magnetic resonance imagingin kernicterus in two different cases and (c) macroscopicappearance of brain in kernicterus with characteristic yellowbilirubin staining.a16 bc2). High intensity areas in the posteromedial borderof the globus pallidus on T2-weighted imaging isthe most sensitive finding (Yokochi, 1995; Govaertet al, 2003). It is important to remember that longterm neurological impairment can be associatedwith normal magnetic resonance imaging after acutebilirubin encephalopathy (Katar et al, 2008). Longterm features include extrapyramidal disturbances,sensorineural hearing loss, auditory impairment andupward gaze palsies. The resultant cerebral palsynormally includes a degree of athetosis.It is difficult to correlate a specific serum bilirubinlevel to the onset of bilirubin neurotoxicity. Thereport from the Pilot USA Kernicterus Registrysuggested that a bilirubin level 598 mmol/litre canhave a profoundly deleterious effect (Bhutani andJohnson, 2009).Analysis of the NHS Resolution data regardingsettled kernicterus claims in England also found thatterm babies had bilirubin levels above 600 mmol/litre at presentation (J Rennie et al on behalf of theNHS Improvement Patient Safety Programme, 2017,unpublished data).Aetiology of neonatal jaundiceIn view of the current era of early postnatal dischargeand community support in the NHS, risk factors(Khoury et al, 1988; Newman et al, 2002; Kerenet al, 2005; Maisels et al, 2009) associated withdevelopment of significant jaundice need to bereviewed before discharge (Table 3). The NICE(2016) guideline recommends that a second clinicalexamination is conducted before 48 hours of age.A detailed family history and clinical examinationis extremely important in all infants with jaundice forunderstanding of the possible aetiopathophysiology.Appropriate investigations can identify treatableconditions early (e.g. isoimmunisation, infection,biliary atresia) and improve outcome.Early jaundiceClinical jaundice within the first 24 hours of life islikely to be pathological and commonly a result ofisoimmunisation (most commonly ABO or rhesusincompatibility) or other causes of significanthaemolysis. Blood group and rhesus status for bothmother and infant need to be reviewed along with adirect agglutination test (DAT). Anti-D prophylaxis inrhesus-negative mothers can cause a weakly positiveDAT result as a result of passive transfer of antibody.A positive DAT test does not always correlate withthe severity of jaundice (Bakkeheim et al, 2009).Reticulocyte count and blood film also carry a low 2017 MA Healthcare LtdTable 2. Risk factors associated with the developmentof kernicterus
Current Issues in Neonatal CareTable 3. Risk factors in babies more likely todevelop significant jaundiceGestational age 38 weeksHistory of previous sibling needingphototherapyExclusive breast feedingClinical jaundice visible within first 24 hours oflifesensitivity and specificity for diagnosis of haemolysisin newborn infants (Newman and Easterling, 1994).Review of maternal antenatal notes oftengives vital information about other blood groupincompatibilities (e.g. Kell group) or the presence ofother antibodies. Infection should always be excludedin sick newborns with early jaundice. Although G6PDdeficiency-related jaundice presents after 48 hours,it needs to be part of the investigations in infantswith relevant ethnicity (parents with Mediterranean,Asian or African origin). If haemolysis is ruled out,Crigler–Najjar syndrome should be considered.Although rare, it can develop a rapidly deterioratingnon-haemolytic unconjugated jaundice early in life.Infants with G6PD deficiency can also present withnon-haemolytic jaundice in the neonatal period. 2017 MA Healthcare LtdProlonged jaundicePersistent clinical jaundice in term infants at 2 weeksand in preterm infants at 3 weeks of age is termedprolonged jaundice. This is a common referral fromthe community and mostly presents as unconjugatedjaundice noted in breastfed infants. Feeding history,colour of stool and urine and clinical examinationcan mostly rule out pathological causes. Theinvestigations should be done stepwise depending onthe results from first-line investigations.Initial investigations for infants with prolongedjaundice:ll Check the colour of stool (whether yellow or palechalky stool)ll Check the urine (whether it is dark and stains thenappy easily)ll Measure total and split bilirubinll Full blood count, blood group and DATll Liver function testll Urine culture and sensitivityll Ensure Guthrie card sent for routine metabolicscreeningll Thyroid function testll G6PD level. Conjugated jaundiceSerum conjugated bilirubin level of 25 mmol/litreis generally considered as conjugated jaundice.Although in clinical practice a 10% cut-off valuefor total serum bilirubin level is sometime used,this can give false reassurance in the case of hightotal bilirubin level. Pale chalky stool and darkurine can be important associated symptoms. Initialinvestigations should include a liver function test andcheck for any clotting abnormality. A liver ultrasoundcan provide further input in cases with suspectedobstructive jaundice. Further investigations can ruleout congenital infections, sepsis, glucosaemia andaminoacidaemias. Preterm infants on total parenteralnutrition often have a marked increase in conjugatedbilirubin fraction which improves gradually aftertotal parenteral nutrition is stopped.Assessment of neonatal jaundiceExamination of the newborn for visual assessmentof clinical jaundice should be performed in a well-litroom. Visual assessment is unreliable, particularlyunder artificial light and after phototherapy hasbegun. It can also be difficult in dark-skinned infants,in whom examination of sclera, gums and pinchedskin are also important. For any infant with clinicaljaundice, the serum bilirubin level must be measuredto allow planning of management. Clinical jaundiceusually becomes visually evident at a serum bilirubinlevel of 80–90 mmol/litre in babies with pale skin.In recent years, use of a transcutaneousbilirubinometer has transformed community careof jaundiced infants in UK. Bilirubin measurementsfrom these instruments correlate well with serumbilirubin level and can avoid unnecessary blood testsand/or referral to hospital. Although transcutaneousbilirubinometer measurement highly correlates withserum bilirubin measurement, the average differencebetween these measurements was 12.7 32.9 mmol/litre (Campbell et al, 2011), and this discrepancyincreases further above levels of 250 mmol/litre. NICEguidance recommends checking a serum samplewhen transcutaneous bilirubinometer recordsindicates a bilirubin level higher than 250 mmol/litre.Most neonatal units in UK have the facility toestimate total serum bilirubin level from a benchbilirubinometer using direct spectrometry. Forany specific measurement of conjugated andunconjugated bilirubin, a sample should be sent tothe hospital biochemistry laboratory.The investigation pathway for neonatal jaundice(NICE, 2016) is presented in Figure 3.17
Current Issues in Neonatal CareFigure 3. Investigation pathway for neonatal jaundice. Adapted from NICE (2016) guideline.Care for all babiesAQ please confirmpermission fromNICE to reproducethis and figure 4and details of theacknowledgementrequired ?Ensure adequate supportis offered to all womenwho intend to breastfeedexclusively³Go to exchange transfusionpathway (see page 16)Urgent additional care for babieswith jaundice in the first 24 hoursMeasure and record serum bilirubin levelwithin 2 hoursNoDoes baby have any other factors? gestational age under 38 weeks a previous sibling with neonatal jaundice requiring phototherapy mother’s intention to breastfeed exclusivelyYesNoExamine for jaundice atevery opportunity,especially in first72 hoursCheck for signs of acutebilirubin encephalopathyYesDoes baby have suspected or obvious jaundice in the first 24 hours?Ensure babiesreceive an additionalvisual inspectionby a healthcareprofessional within48 hoursAdditional care forbabies who are morelikely to develophyperbilirubinaemiaExamine the baby for jaundice at every opportunity, especially in the first 72 hoursDoes baby have visible jaundice?The threshold table is onthe foldout page at thefront of this quick referenceguide. The treatmentthreshold graphs areavailable in a separatefile fromwww.nice.org.uk/guidance/CG98NoYesRoutine careMeasure and record serum bilirubin level within 6 hoursContinue to measure theserum bilirubin level every6 hours until the levelis both: below the treatmentthreshold stable and/or fallingArrange a referral toensure that an urgentmedical review isconducted (as soonas possible and within6 hours) to excludepathological causes ofjaundiceManage hyperbilirubinaemia Interpret results using threshold table and treatment threshold graphsMonitor bilirubin levelsTreat using phototherapyTreat using exchange transfusionGo to phototherapy pathway (see page 15)Go to exchange transfusion pathway (see page 16)Management of neonatal jaundiceThe management of neonatal jaundice is targetedat identifying the rare baby who has a rapidly risingbilirubin level and is at risk of kernicterus from themajority of term babies whose jaundice will remainharmless. Adequate early support (both pre-dischargeand in the community) for mothers and infants forestablishment of breast feeding reduces the risk ofdeveloping raised serum bilirubin level and can avoidthe need for hospital readmission.Unconjugated jaundicePhototherapyPhototherapy is the first step in the management ofraised unconjugated jaundice in newborn infants. Itis a safe and convenient method of lowering serumbilirubin levels and reduces the need for more invasivetreatment, exchange transfusion. Phototherapyis effective only after bilirubin enters the skin atserum bilirubin level 80 mmol/litre (Tan, 1982). Theefficacy of phototherapy depends on the dose andwavelength of light used as well as the surface areaof the infant’s body exposed to it. Increasing thedose can be achieved by placing phototherapy unitsat the minimum safe distance from the infant andincreasing the number of units used. The AmericanAcademy of Pediatrics has defined the characteristicsof a phototherapy device that contribute to theeffectiveness in reducing the serum bilirubin level– emission of light in the blue–green range thatoverlaps the in vivo plasma bilirubin absorption18 Care for babies withsigns of acute bilirubinencephalopathyIdentify babies as being more likely to develop significanthyperbilirubinaemia if they have any of the following factors: gestational age under 38 weeks a previous sibling with neonatal jaundice requiring phototherapy mother’s intention to breastfeed exclusively visible jaundice in the first 24 hoursspectrum ( 460–490 nm) and a spectral irradiance ofat least 30 microW/cm2/nm (Bhutani et al, 2011).Fibreoptic biliblankets are an effective wayto reduce bilirubin level. They help to continuephototherapy during cuddles with parents and can bean effective way to give ‘double’ phototherapy whenused together with an overhead unit. They can beplaced in direct contact with the infant as they emitan insignificant degree of heat.The predominant method of bilirubin eliminationis the irreversible photoalteration of bilirubin to astructural isomer called lumirubin, which is a watersoluble compound and is excreted with bile andurine. Two other important pathways of bilirubinphotoalteration are photo-oxidation of bilirubin tocolourless polar molecules that are excreted in theurine and configurational isomerization of bilirubinisomer to more water-soluble and less toxic isomers(Vreman et al, 2004).Although phototherapy is generally benign,side effects can include diarrhoea, erythematousrash, increased fluid loss, temperature instabilityand skin discolouration (tanning and bronze babysyndrome). Improvement of phototherapy systemshas dramatically reduced these side effects over thelast decade.The NICE (2016) guideline recommends the use ofgestational age-specific treatment threshold graphsfor babies with neonatal jaundice which is gestationalage specific and gives a clear visual idea about theneed for the modality of treatment at start as well as 2017 MA Healthcare LtdOffer parents/carersinformation about neonataljaundice (see page 9)
Current Issues in Neonatal CarePharmacological agentsHigh dose intravenous immunoglobulin is theonly pharmacological treatment used in clinicalpractice for infants presenting with high jaundicelevels secondary to rhesus or ABO isoimmunisation.Although it reduces the need for exchange transfusion,the duration of phototherapy and the length ofhospital stay (Gottstein and Cooke, 2003), it is mostlyused to buy time before starting exchange transfusionin severe cases of unconjugated jaundice.Exchange transfusionIn recent years the need for exchange transfusion hassignificantly reduced because of improved antenatalmanagement and the availability of improved highlyeffective phototherapy systems. It is an importantintervention for infants who do not respond well tomultiple phototherapy and appropriate hydration.It is also indicated in infants born with significantanaemia as a result of in utero haemolysis. In additionto the small risk of blood-borne infection, exchangetransfusion carries a risk of morbidity and mortalityfrom vascular injuries, cardiovascular complications,biochemical and haematological disturbance(Keenan et al, 1985). It is vital to monitor the infantclosely throughout the procedure and check thehaematological and biochemical parameters before,during and after exchange transfusion. 2017 MA Healthcare LtdConjugated jaundiceIdentification of the aetiology is key for themanagement of an infant with conjugated jaundice.If a congenital obstruction is suspected, the infantneeds to be reviewed in a surgical centre for furtherinvestigations and management. Biliary atresia is themost common surgically correctable liver condition inthis age group and constitutes one fifth of the infantsreferred to one hepatobiliary referral centre in the UK.In one third of infants with biliary atresia stools arepigmented initially as the intra- and extrahepatic bileducts may remain patent in the first few weeks of life.As they become atretic, the flow of bile stops and thecolour of stool changes to a white, chalky appearance.Success of surgery is highest in earlier infancy, aswith time, the intrahepatic biliary ducts obliterateand the chance of success of portoenterostomy dropssignificantly. Ursodeoxycholic acid (Willot et al, Key pointsll Neonatal jaundice is common in both term andpreterm infantsll In most cases the jaundice is harmless and requiresno treatment or responds to phototherapyll High levels of unconjugated bilirubin can causepermanent brain damage, kernicterusll High levels of conjugated bilirubin can be a markerof biliary atresia, which requires urgent surgeryll The risk of kernicterus is low but means that allbabies with jaundice should have their bilirubinlevels monitored closely; babies with risk factorsneed an evaluation for jaundice at 48 hours.Figure 4. NICE treatment threshold graph for babies born at 38 weeks. Individual charts need to be adjusted according to thegestational age before use.Treatment threshold graph for babies with neonatal jaundiceBaby's nameDate of birthHospital numberTime of birthDirect Antiglobulin TestClick below and choose gestationBaby's blood groupShade for phototherapy 38Mother's blood groupweeks gestationMultipleSingle550500Total serum bilirubin (micromol/litre)the response to treatment. Two clear lines indicate thethreshold of phototherapy and exchange transfusionover the first few weeks and days of life. Figure 4gives an example of the treatment threshold chart forinfants 38 weeks gestation (NICE, 2016).Exchange 01234567891011121314Days from birth2008) and phenobarbital (Davenport et al, 1997) areused to improve the bile flow, and supplementationof fat-soluble vitamins is also required.Prolonged use of parenteral nutrition causescholestasis and hepatocellular damage in earlyinfancy and the incidence increases with the degreeof prematurity. Treatment focuses on increasingthe bile flow with either ursodeoxycholic acid orphenobarbital and early introduction of enteralfeeding.ConclusionsNeonatal jaundice is the most common conditionneeding medical attention in the neonatal period. Themajority of these cases present with unconjugatedhyperbilirubinaemia and most infants respond wellto phototherapy when the bilirubin level reachesthe treatment threshold. Infants with risk factors19
for developing significant hyperbilirubinaemia needto be monitored closely and treated early to preventbilirubin neurotoxicity. Current research may, infuture, facilitate the use of the camera facility onmobile phones as an objective measure of the colourof the sclerae (Leung et al, 2015).Bakkeheim E, Bergerud U, Schmidt-Melbye AC, AkkökCA, Liestøl K, Fugelseth D, Lindemann R (2009)Maternal IgG anti-A and anti-B titres predict outcome inABO-incompatibility in the neonate. Acta Paediatr 98(12):1896–1901. ttersby C, Michaelides S, Upton M, Rennie JM (2017)Term admissions to neonatal units in England: a role fortransitional care? A retrospective cohort study. BMJ Open7(5): e016050. https://doi.org/10.1136/bmjopen-2017-016050Bhutani VK; Committee on Fetus and Newborn; AmericanAcademy of Pediatrics (2011) Phototherapy to preventsevere neonatal hyperbilirubinemia in the newborn infant35 or more weeks of gestation. Pediatrics 128(4): e1046–e1052. https://doi.org/10.1542/peds.2011-1494Bhutani VK (2012) Jaundice Due to Glucose-6-PhosphateDehydrogenase Deficiency. Neoreviews 13: e166Bhutani VK, Johnson L (2009) Kernicterus in the 21st century:frequently asked questions. J Perinatol 29: s D, Fernandes A, Falcão AS, Gordo AC, Silva RF, BritoMA (2009) Biological risks for neurological abnormalitiesassociated with hyperbilirubinemia. J Perinatol 29 Suppl 1:S8–S13. https://doi.org/10.1038/jp.2008.214Campbell DM, Danayan KC, McGovern V, Cheema S, Stade B,Sgro M (2011) Transcutaneous bilirubin measurement atthe time of hospital discharge in a multiethnic newbornpopulation. Paediatr Child Health 16(3): 141–145.Connolly AM, Volpe JJ (1990) Clinical features of bilirubinencephalopathy. Clin Perinatol 7(2): 371–379.Davenport M, Kerkar N, Mieli-Vergani G, Mowat AP, HowardER (1997) Biliary atresia: the King’s College Hospitalexperience (1974-1995). J Pediatr Surg 32(3): 611-4Gartner LM, Snyder RN, Chabon RS, Bernstein J (1970)Kernicterus: high incidence in premature infants with lowserum bilirubin concentrations. Pediatrics 45(6): 906–917.Gottstein R, Cooke RW (2003) Systematic review ofintravenous immunoglobulin in haemolytic disease of thenewborn. Arch Dis Child Fetal Neonatal Ed 88(1): F6–F10.https://doi.org/10.1136/fn.88.1.F6Govaert P, Lequin M, Swarte R et al (2003) Changes in globuspallidus with (pre)term kernicterus. Pediatrics 112(6 Pt 1):1256–1263.Katar S, Akay HO, Taskesen M, Devecioglu C (2008) Clinicaland cranial magnetic resonance imaging (MRI) findings of21 patients with serious hyperbilirubinemia. J Child Neurol23(4): 415–417. https://doi.org/10.1177/0883073807309780Keenan WJ, Novak KK, Sutherland JM, Bryla DA, Fetterly KL(1985) Morbidity and mortality associated with exchangetransfusion. Pediatrics 75(2 Pt 2): 417–421.Keren R, Bhutani VK, Luan X, Nihtianova S, Cnaan A,20 Schwartz JS (2005) Identifying newborns at risk ofsignificant hyperbilirubinaemia: a comparison of tworecommended approaches. Arch Dis Child 90(4): houry MJ, Calle EE, Joesoef RM (1988) Recurrence risk ofneonatal hyperbilirubinemia in siblings. Am J Dis Child142(10): 1065–1069.Leung TS, Kapur K, Guilliam A, Okell J, Lim B, MacDonaldLW, Meek J (2015) Screening neonatal jaundice basedon the sclera color of the eye using digital photography.Biom
jaundice must have their level of conjugated bilirubin measured. Preterm infants on long-term parenteral nutrition may develop conjugated jaundice which generally improves with the introduction of enteral feed and weaning of intravenous nutrition. Keywords: Neonatal jaundice, kernicterus, conjugated jaundice, phototherapy, exchange transfusion
The National Institute of Health and Clinical Excellence (NICE) has published a clinical guideline on neonatal jaundice which provides guidance on the recognition, assessment and treatment of neonatal jaundice in babies from birth to 28 days. Neonatal Jaundice Clinical Guideline guidance.nice.org.uk cg98 For more information go to nice.org.uk/cg98
the neonatal jaundice treatment to build a nursing protocol. Method: Comprehensive literature review, during period 2011-2016, conducted through literature searches in PubMed with the keywords "neonatal jaundice guidelines", "neonatal jaundice phototherapy"; in Cuiden, with the keywords "neonatal
NICE clinical guideline 98 – Neonatal jaundice 3 Introduction Jaundice is one of the most common conditions needing medical attention in newborn babies. Jaundice refers to the yellow colouration of the skin and the sclerae (whites of the eyes) caused by the accumulation of bilirubin in the skin and mucous membranes.
NICE clinical guideline 98 – Neonatal jaundice 3 Introduction Jaundice is one of the most common conditions needing medical attention in newborn babies. Jaundice refers to the yellow colouration of the skin and the sclerae (whites of the eyes) caused by the accumulation of bilirubin in the skin and mucous membranes.File Size: 1MBPage Count: 54
What is Jaundice Neonatal jaundice Definition Neonatal jaundice is the term used when a newborn has an excessive amount of bilirubin in the blood. Bilirubin is a yellowish-red pigment that is formed and released into the bloodstream when red blood cells are broken down. Jaundice comes from the French word jaune, which means
JAUNDICE Hepatocellular Jaundice: Due to Damage to liver cells Obstructive Jaundice: results from obstruction of the common bile duct. Obstruction can be a tumor or bile stones may block the duct preventing passage bilirubininto the intestine. Neonatal jaundice:Majority of newborn infants show a rise in bilirubin in the
Neonatal SHO should be contacted if baby develops jaundice . Direct Coombs test (negative test does not rule out haemolytic jaundice) FBC and blood film CRP, blood culture, IV antibiotics if unwell . (Inform Blood Bank that it is for an exchange transfusion) Ideally
3 PRACTICE TEST 01 May 2004 Question 1-10 All mammals feed their young. Beluga whale mothers, for example, nurse their calves for some twenty months, until they are about to give birth again and their young are able to
