Hyperbilirubinemia Current Guidelines and Emerging Therapies

Division of Emergency Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Pediatric emergency care (Impact Factor: 0.92). 09/2011; 27(9):884-9. DOI: 10.1097/PEC.0b013e31822c9b4c
Source: PubMed

ABSTRACT It is estimated that about two thirds of newborns will appear clinically jaundiced during their first weeks of life. As newborns and their mothers spend fewer days in the hospital after birth, the number of infants readmitted yearly in the United States for neonatal jaundice over the last 10 years has increased by 160%. A portion of these infants present to the emergency department, requiring a careful history and physical examination assessing them for the risk factors associated with pathologic bilirubin levels. Although the spectrum of illness may be great, the overwhelming etiology of neonatal jaundice presenting to an emergency department is physiologic and not due to infection or isoimmunization. Therefore, a little more than a good history, physical examination, and indirect/direct bilirubin levels are needed to evaluate an otherwise well-appearing jaundiced newborn. The American Academy of Pediatrics' 2004 clinical practice guidelines for "Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation" are a helpful and easily accessible resource when evaluating jaundiced newborns (available at;114/1/297). There are several exciting developments on the horizon for the diagnosis and management of hyperbilirubinemia including increasing use of transcutaneous bilirubin measuring devices and medications such as tin mesoporphyrin and intravenous immunoglobulin that may decrease the need for exchange transfusions.

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    • "A significant increase in serum bilirubin, i.e. hyperbilirubinemia , can result in multiple neurologic impairment and deficits [1] [2] [3] [4]. In neonates, hyperbilirubinemia is a most common condition requiring evaluation and treatment [5] [6] [7] [8] [9] [10]. An increased understanding of the effect of hyperbilirubinemia on the brain and, in particular, promptly detection of neural impairment due to hyperbilirubinemia are crucial for timing treatment as to reduce the risk of kernicterus occurring, improving the outcome of infants with hyperbilirubinemia [11] [12]. "
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    ABSTRACT: Objective: We studied maximum length sequence brainstem auditory evoked response in term neonates with hyperbilirubinemia to further our understanding of hyperbilirubinemia on the neonatal auditory brainstem and to determine if maximum length sequence technique improves detection of brainstem auditory impairment due to bilirubin neurotoxicity. Methods: Maximum length sequence brainstem auditory evoked response was recorded and analysed shortly after confirming total serum bilirubin levels greater than 15mg/dL in fifty-seven term neonates with hyperbilirubinemia. Results: Most wave latencies and interpeak intervals in maximum length sequence brainstem auditory evoked response in the neonates with hyperbilirubinemia were correlated with the level of total serum bilirubin at some or most click rates used. Compared with age-matched normal term controls, wave V latency in these neonates was increased significantly at all 91-910/s click rates (p<0.05-0.001). The I-V and I-III interpeak intervals were also increased significantly at all these rates, and the III-V interval increased at 227-910/s clicks (p<0.05-0.001). The differences between the neonates with hyperbilirubinemia and the controls were more significant at higher than at lower click rates. The slopes of wave V latency-rate function and I-V and III-V interval-rate functions were all significantly increased. By comparison, the abnormalities in conventional BAER were less significant, with only I-III and I-V intervals were increased (both p<0.05). Conclusions: Functional status of the auditory brainstem is impaired in neonatal hyperbilirubinemia. Maximum length sequence technique at high click rates improves detection of bilirubin neurotoxicity to the neonatal auditory brainstem, particularly for the more rostral regions.
    Brain & development 04/2013; DOI:10.1016/j.braindev.2013.03.003 · 1.54 Impact Factor
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    ABSTRACT: "Common" neonatal jaundice can lead to dangerous levels of hyperbilirubinemia, causing neurological damage and even death. This article outlines evidence-based assessment techniques, management guidelines, and treatments for neonatal hyperbilirubinemia, addressing complexities that have arisen with new technologies and research results. We also explicate the role of the nurse in both prevention and care of patients and families who are affected by hyperbilirubinemia and jaundice.
    MCN. The American journal of maternal child nursing 11/2013; 38(6):377-82. DOI:10.1097/NMC.0b013e3182a1fb7a · 0.84 Impact Factor
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    ABSTRACT: Glucose 6-phosphate dehydrogenase (G6PD) catalyzes the rate-determining step in the pentose phosphate pathway, and produces NADPH to fuel glutathione recycling. G6PD deficiency is the most common enzyme deficiency in humans, and affects over 400 million people worldwide; however its impact on cardiovascular disease is poorly understood. The glutathione pathway is paramount to antioxidant defense, and G6PD deficient cells do not cope well with oxidative damage. Limited clinical evidence indicates that G6PD deficiency may be associated with hypertension. However, there is also data to support a protective role of G6PD deficiency in decreasing the risk of heart disease and cardiovascular-associated deaths, perhaps through a decrease in cholesterol synthesis. Studies in G6PD deficient (G6PDX) mice are mixed, and provide evidence for both protective and deleterious effects. G6PD deficiency may provide a protective effect through decreasing cholesterol synthesis, superoxide production, and reductive stress. However, recent studies indicate that G6PDX mice are moderately more susceptible to ventricular dilation in response to myocardial infarction or pressure overload-induced heart failure. Further, G6PDX hearts do not recover as well as non-deficient mice when faced with ischemia-reperfusion injury, and G6PDX mice are susceptible to the development of age-associated cardiac hypertrophy. Overall, the limited available data indicate a complex interplay in which adverse effects of G6PD deficiency may outweigh potential protective effects in the face of cardiac stress. Definitive clinical studies in large populations are needed to determine the effects of G6PD deficiency on the development of cardiovascular disease and subsequent outcomes.
    AJP Heart and Circulatory Physiology 12/2012; 304(4). DOI:10.1152/ajpheart.00721.2012 · 4.01 Impact Factor
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