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We identified children diagnosed with kernicterus in the California Department of Developmental Services and estimated an incidence of 0.42 per 100 000 births from 1988 to 2014, significantly decreasing to 0.04 per 100 000 births after 2009. We also examined national infant kernicterus mortality from 1979 to 2016 using CDC data. It did not decrease significantly.

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BACKGROUND: Neonatal acute liver failure (NALF) is a rare and life-threatening condition. It causes bilirubin to accumulate to a dangerous level in the body, causing permanent damage to vital organs such as the brain and lungs. In many cases, the etiology of NALF remains unknown. CASE PRESENTATION: We described a case of an 8-day-old baby girl who presented with poor oral intake, lethargy, and jaundice. Her clinical condition rapidly deteriorated with progression to multi-organ failure, and despite intensive resuscitation efforts, she expired. At autopsy, the most significant findings were liver necrosis, yellow hyaline membrane deposition in the lungs, and bilirubin deposition in the brain (kernicterus). CONCLUSIONS: NALF is a rare and potentially fatal condition necessitating prompt recognition and disease-specific treatment approaches. Toxic accumulation of bilirubin in the lungs can lead to hypoxia and precipitate further ischemic injury to the liver.

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Background Neonatal acute liver failure (NALF) is a rare and life-threatening condition. It causes bilirubin to accumulate to a dangerous level in the body, causing permanent damage to vital organs such as the brain and lungs. In many cases, the etiology of NALF remains unknown. Case presentation We described a case of an 8-day-old baby girl who presented with poor oral intake, lethargy, and jaundice. Her clinical condition rapidly deteriorated with progression to multi-organ failure, and despite intensive resuscitation efforts, she expired. At autopsy, the most significant findings were liver necrosis, yellow hyaline membrane deposition in the lungs, and bilirubin deposition in the brain (kernicterus). Conclusions NALF is a rare and potentially fatal condition necessitating prompt recognition and disease-specific treatment approaches. Toxic accumulation of bilirubin in the lungs can lead to hypoxia and precipitate further ischemic injury to the liver.

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OBJECTIVE: To evaluate whether teaching mothers about neonatal jaundice will decrease the incidence of acute bilirubin encephalopathy among infants admitted for jaundice. STUDY DESIGN: This was a multicenter, before-after and cross-sectional study. Baseline incidences of encephalopathy were obtained at 4 collaborating medical centers between January 2014 and May 2015 (Phase 1). Structured jaundice instruction was then offered (May to November 2015; Phase 2) in antenatal clinics and postpartum. Descriptive statistics and logistic regression models compared 3 groups: 843 Phase 1 controls, 338 Phase 2 infants whose mothers received both antenatal and postnatal instruction (group A), and 215 Phase 2 infants whose mothers received no instruction (group B) either because the program was not offered to them or by choice. RESULTS: Acute bilirubin encephalopathy occurred in 147 of 843 (17%) Phase 1 and 85 of 659 (13%) Phase 2 admissions, which included 63 of 215 (29%) group B and 5 of 338 (1.5%) group A infants. OR for having acute bilirubin encephalopathy, comparing group A and group B infants adjusted for confounding risk factors, was 0.12 (95% CI 0.03-0.60). Delayed care-seeking (defined as an admission total bilirubin ≥18 mg/dL at age ≥48 hours) was the strongest single predictor of acute bilirubin encephalopathy (OR 11.4; 6.6-19.5). Instruction decreased delay from 49% to 17%. Other major risk factors were home births (OR 2.67; 1.69-4.22) and hemolytic disease (hematocrit ≤35% plus bilirubin ≥20 mg/dL) (OR 3.03; 1.77-5.18). The greater rate of acute bilirubin encephalopathy with home vs hospital birth disappeared if mothers received jaundice instruction. CONCLUSIONS: Providing information about jaundice to mothers was associated with a reduction in the incidence of bilirubin encephalopathy per hospital admission.

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The bronze baby syndrome is an infrequent dyschromia resulting from phototherapy in newborn babies with neonatal jaundice. Even though the common phenotype has been described in patients with direct neonatal hyperbilirubinemia secondary to cholestasis, several cases of patients with indirect neonatal hyperbilirubinemia who have managed to reverse it have been reported, as well as patients with isolated hyperbilirubinemia.Currently, the physiopathology of this condition is still a subject of controversy and, therefore, there is a lack of clear conducts for its correct diagnosis and treatment.Generally, this syndrome has been considered as a mild condition that is resolved with the suspension of phototherapy. Its duration is usually not greater than the neonatal period, and it has no long-term sequelae. However, its occurrence is considered an absolute contraindication for the continuation of phototherapy. In case of persistence, the recommendation is to decrease bilirrubin levels and proceed with exchange transfusion; this procedure, however, represents risks for the newborn, so our recommendation is to suspend phototherapy and reinitiate it if the direct bilirrubin value decreases, andcholestasis compromise has been discarded. Serial evaluations of acute encephalopathy caused by bilirrubin are absolutely recommended.The objective of this paper was to describe the case of a newborn with ABO incompatibility who developed the bronze baby syndrome. This patient responded satisfactorily to the suspension and resumption of phototherapy without exchange transfusion.

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Resumen El síndrome del bebe bronceado es una rara discromía que se presenta como una complicación de la fototerapia en recién nacidos con ictericia neonatal. Aunque el fenotipo común se ha descrito en pacientes con hiperbilirrubinemia directa secundaria a colestasis, también se conocen casos con hiperbilirrubinemia indirecta en quienes se invierte el patrón de hiperbilirrubinemia e, incluso, otros con hiperbilirrubinemia indirecta aislada. La fisiopatología de la enfermedad sigue siendo motivo de controversia, por lo que no se ha establecido claramente cuál es la mejor aproximación diagnóstica y terapéutica. En general, el síndrome se considera leve y se resuelve con la suspensión de la fototerapia; no suele prolongarse más allá del periodo neonatal y no tiene secuelas a largo plazo. Sin embargo, su aparición constituye una contraindicación absoluta para continuar la fototerapia. En caso de persistir, se recomienda disminuir los niveles de bilirrubina y recurrir a la exanguinotransfusión, pero dado que esta implica riesgos para el neonato, una conducta adecuada sería suspender la fototerapia y reiniciarla si la bilirrubina directa disminuye y se ha descartado el compromiso colestásico, aunque siempre evaluando en forma seriada posibles manifestaciones de encefalopatía aguda por bilirrubina. El objetivo de este estudio fue presentar el caso de un recién nacido con incompatibilidad de grupo sanguíneo ABO que presentó el síndrome del bebé bronceado. El bebé respondió satisfactoriamente a la suspensión de la fototerapia y a su posterior reanudación, sin necesidad de recurrir a la exanguinotransfusión.

Abstract The bronze baby syndrome is an infrequent dyschromia resulting from phototherapy in newborn babies with neonatal jaundice. Even though the common phenotype has been described in patients with direct neonatal hyperbilirubinemia secondary to cholestasis, several cases of patients with indirect neonatal hyperbilirubinemia who have managed to reverse it have been reported, as well as patients with isolated hyperbilirubinemia. Currently, the physiopathology of this condition is still a subject of controversy and, therefore, there is a lack of clear conducts for its correct diagnosis and treatment. Generally, this syndrome has been considered as a mild condition that is resolved with the suspension of phototherapy. Its duration is usually not greater than the neonatal period, and it has no long-term sequelae. However, its occurrence is considered an absolute contraindication for the continuation of phototherapy. In case of persistence, the recommendation is to decrease bilirrubin levels and proceed with exchange transfusion; this procedure, however, represents risks for the newborn, so our recommendation is to suspend phototherapy and reinitiate it if the direct bilirrubin value decreases, and cholestasis compromise has been discarded. Serial evaluations of acute encephalopathy caused by bilirrubin are absolutely recommended. The objective of this paper was to describe the case of a newborn with ABO incompatibility who developed the bronze baby syndrome. This patient responded satisfactorily to the suspension and resumption of phototherapy without exchange transfusion.

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