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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 AAP Red Book, or Report of the Committee on Infectious Diseases of the American Academy of Pediatrics, is a hardcover, softcover, and electronic reference to the "manifestations, etiology, epidemiology, diagnosis, and treatment of some 200 childhood infectious diseases". The Red Book first appeared as an eight-page booklet in 1938. The most ...
The conjugated hyperbilirubinemia is a result of defective endogenous and exogenous transfer of anionic conjugates from hepatocytes into bile. [5] Impaired biliary excretion of bilirubin glucuronides is due to a mutation in the canalicular multiple drug-resistance protein 2 (MRP2). A darkly pigmented liver is due to polymerized epinephrine ...
The AAP recommends "In isoimmune hemolytic disease, administration of intravenous γ-globulin (0.5-1 g/kg over 2 hours) is recommended if the TSB is rising despite intensive phototherapy or the TSB level is within 2 to 3 mg/dL (34-51 μmol/L) of the exchange level .
Crigler–Najjar syndrome is a rare inherited disorder affecting the metabolism of bilirubin, a chemical formed from the breakdown of the heme in red blood cells. The disorder results in a form of nonhemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants.
Hereditary hyperbilirubinemia refers to a group of conditions where levels of bilirubin, a byproduct of red blood cell metabolism, are elevated in the blood due to a genetic cause. [1] Various mutations of enzymes in the liver cells, which breakdown bilirubin, cause varying elevated levels of bilirubin in the blood. [ 2 ]
The syndrome cannot cause severe indirect hyperbilirubinemia in neonates by itself, but it may have a summative effect on rising bilirubin when combined with other factors, [10] for example in the presence of increased red blood cell destruction due to diseases such as G6PD deficiency.
Hyperbilirubinemia may be observed when hemolysis produces too much bilirubin through the excessive breakdown of red blood cells, and the bilirubin builds up in the patient's blood and tissue fluids without proper excretion. [43] Untreated or inadequately treated hyperbilirubinemia will lead to other complications such as kernicterus. [12]