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Prevention of Neurodevelopmental Sequelae of Jaundice in the Newborn

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Prevention of Neurodevelopmental Sequelae of Jaundice in the Newborn DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY REVIEW Prevention of neurodevelopmental sequelae of jaundice in the newborn THOR W R HANSEN Department of Neonatology, Women's and Children's Division, Oslo University Hospital – Rikshospitalet; and Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Norway. Correspondence to Professor Thor Willy Ruud Hansen at Nyfødtavdelingen, Kvinne- og Barneklinikken, Oslo Universitetssykehus – Rikshospitalet, N-0027 Oslo, Norway. E-mail: [email protected] PUBLICATION DATA Although its cause, jaundice in the newborn, is extremely common, the disabling neurological dis- Accepted for publication 28th February 2011. order kernicterus is very rare. Kernicterus may be prevented by selecting those infants who are at risk of extreme jaundice or who may be particularly vulnerable to bilirubin neurotoxicity. Because ABBREVIATION the tools for achieving that goal are inadequate, a secondary strategy is needed. This involves a TSB Total serum bilirubin plan for emergency treatment of severely jaundiced infants, in particular those who present with neurological symptoms. In this paper I review the strategies for preventing extreme jaundice, and for reversing neurotoxicity in those infants for whom the principal strategies fail. Briefly, the tools for prevention include measurement of bilirubin while the infant is staying in the maternity unit, plotting the value on an hour-specific chart, assessing other risk factors for jaundice, and educat- ing the parents. Emergency treatment should include immediate, high-irradiance phototherapy, consideration of intravenous immune globulin, and preparation for an exchange transfusion. Kernicterus is a disabling neurological condition, the symp- treatment. In the intermediate phase, moderate stupor, irrita- toms of which include choreoathetosis, paresis of upward gaze, bility, and hypertonia are seen. Fever, high-pitched cry, sensorineural deafness, and occasionally developmental delays. drowsiness, and hypotonia may be present. Hypertonia is An apparent resurgence of kernicterus in recent years has manifested by backward arching of the neck (retrocollis) and prompted renewed interest in this disorder.1–6 Kernicterus is trunk (opisthotonos). Many believe that acute bilirubin caused by deposition of bilirubin in the basal ganglia, an event encephalopathy that has advanced to this stage is irreversible, that with rare exceptions only occurs in the newborn period but recent evidence suggests that reversibility may be possi- and is associated with neonatal jaundice. Neonatal jaundice is ble.2,3,9 In the advanced phase, pronounced retrocollis ⁄ opis- very common and in most infants a normal transitional phe- thotonos, shrill cry, anorexia, apnea, fever, deep stupor to nomenon. However, when jaundice becomes pronounced, or coma, and seizures may be seen, and the infants may die. The if infants are especially vulnerable to bilirubin toxicity, kern- damage to the central nervous system in this stage is probably icterus may occur. Kernicterus should largely be preventable. irreversible in most cases, although an apparently normal out- This review focuses on strategies for prevention of kernicte- come has been described.4 A scoring system (bilirubin-induced rus. neurological dysfunction: BIND) has been developed to fol- low the onset, severity, and progression of acute bilirubin KERNICTERUS ⁄ BILIRUBIN ENCEPHALOPATHY encephalopathy.10 In this scoring system, characteristics of Kernicterus (‘jaundice of the basal ganglia’) was described by mental state, muscle tone, and cry are grouped into three lev- German pathologists more than 100 years ago.7 The term has els of increasing abnormality: stage IA, minimal signs; stage also been used as a diagnosis in surviving infants with the clini- IB, progressive but reversible with treatment; stage II, cal picture described above. Recently, the term ‘bilirubin advanced and largely irreversible, but may be significantly encephalopathy’ has been preferred by several authors. A dis- decreased by treatment. Characteristics for each category are tinction is then made between ‘acute bilirubin encephalopathy’ given a weight of 1, 2, or 3 according to their severity and then and ‘chronic bilirubin encephalopathy’. The latter term corre- summed for an overall score. Greater risk is associated with sponds to kernicterus. higher numbers (0–9).10 In the 2004 American Academy of Pediatrics guidelines for Most infants who develop kernicterus have manifested some management of hyperbilirubinemia in newborn infants,8 the or all of the signs of acute bilirubin encephalopathy. However, three phases of acute bilirubin encephalopathy were defined. infants may develop kernicterus without having exhibited signs The early phase presents with lethargy, hypotonia, and poor of acute bilirubin encephalopathy. The estimates of the inci- suck. These changes are usually reversible with appropriate dence of kernicterus vary from 1:30 000 to 1:100 000 births in 24 DOI: 10.1111/j.1469-8749.2011.04059.x ª The Author. Developmental Medicine & Child Neurology ª 2011 Mac Keith Press the industrialized world.9 However, in some developing coun- While developing a strategy for assessing risk for biliru- tries kernicterus is a major cause of cerebral palsy.11 bin encephalopathy, we must therefore keep more than one thought in our minds. First, we must attempt to iden- CAN KERNICTERUS BE PREVENTED? tify infants at risk for becoming excessively jaundiced. Sec- Because neonatal jaundice is extremely common whereas kern- ond, before discharge from the maternity unit, we need to icterus is very rare, strategies are needed on two levels. First, assess each infant carefully for factors suggesting low toler- we need to identify infants at risk of developing very high total ance for bilirubin neurotoxicity. Such infants need to be serum bilirubin (TSB) levels or who are especially vulnerable followed closely and treated at lower TSB values. Table I to bilirubin neurotoxicity. Second, if this strategy fails and an lists factors that may constitute risk for developing high infant develops extreme jaundice with or without signs of TSB levels, or for being more vulnerable to bilirubin tox- acute bilirubin encephalopathy, how can we reduce the risk icity. that this infant develop kernicterus? For infants with risk factors, careful evaluation and planning is necessary. Written and oral education of the parents is IDENTIFYING INFANTS AT RISK FOR EXTREME essential, as is assessment of their ability to understand instruc- JAUNDICE AND BILIRUBIN ENCEPHALOPATHY tions and to cope. Ease of access to medical care should be Historical data suggested that the risk for kernicterus was ascertained. Uncertainty on any point could be an argument associated with TSB levels, as cases of kernicterus increased in favour of delaying discharge. This may be particularly true sharply with levels >340 lmol ⁄ L(20mg⁄ dL).12 However, for infants who have risk factors both for developing high newer data showed that many healthy babies tolerated much TSB values and with increased vulnerability to bilirubin neu- higher TSB levels without damage, and a ‘kinder, gentler rotoxicity. Timing of follow-up should also take these factors approach’ was advocated.13 Higher TSB levels ought to be into consideration. The recommendations for evaluation sug- accepted in healthy, term infants.13 Therefore, 1994 American gested by the American Academy of Pediatrics are listed in Academy of Pediatrics guidelines recommended exchange Table II.8 transfusion at >430 lmol ⁄ L(25mg⁄ dL) in healthy infants older than 2 days if phototherapy failed to reduce TSB levels.14 From the mid-1990s, reports of kernicterus appeared to increase,5 as also reflected in data from the Kernicterus Table I: Risk factors for development of excessive neonatal jaundice and Registry.6 Although it was argued that this may reflect factors leading to increased vulnerability to bilirubin toxicity focus and reporting rather than a true increase in incidence, kernicterus continues to occur, whereas it ought to be May develop high TSB levels Infants of mothers who are Rhesus negative, blood group O, or avoidable. infants with other blood group antibodies It seems reasonable to ask whether there is a ‘safe’ TSB Family history or ethnicity suggesting haemolytic disease level below which we do not need to worry. In data from East Asian ethnicity 2 Infants with fractures, significant bruising or other haematomas the Kernicterus Registry, none of the infants with chronic Infants who are breast fed sequelae had peak recorded TSB levels below 20 mg ⁄ dL Jaundice in older siblings (340lmol ⁄ L). Further, among the infants with peak TSB Particularly if they needed therapy Remember Gilbert disease levels between 20 and 30 mg ⁄ dL (340–510lmol ⁄ L) and Visibly jaundiced within 24 h of birth chronic sequelae, most had complicating conditions which High age-specific bilirubin values while in maternity unit may have increased vulnerability to neurotoxicity. These May have increased sensitivity to bilirubin toxicity Prematurity conditions included sepsis, haemolysis, and dehydration Lower serum albumin values and low albumin affinity for bilirubin with hyperosmolality. However, assuming that the peak More exposed to bilirubin binding competitors in therapy TSB values were correct, kernicterus may occur in infants Both translating into higher unbound bilirubin levels Immaturity of blood–brain barrier? with peak TSB levels down to 20 mg ⁄ dL (340lmol ⁄ L) and Compatible
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