The accessory organs: Pancreas, liver and gallbladder
Paul Ong, Rachel Skittrall in Gastrointestinal Nursing, 2017
Hyperbilirubinaemia is the excessive accumulation of bilirubin in the body. Although the neonate liver is immature it can perform the same functions as an adult liver albeit less effectively. This means the neonate liver is at risk of hyperbilirubinaemia. Bilirubin is generated from the breakdown of haemoglobin (Figure 6.14). The process begins with macrophages breaking down heme (blood pigment) to biliverdin. This is then broken down to bilirubin. Unconjugated or indirect bilirubin is insoluble and cannot therefore be excreted so it binds to plasma albumin and is transported to the liver hepatocytes where it is metabolised into conjugated or direct bilirubin which is soluble. Conjugated bilirubin is soluble so when it is in this form it can be excreted into bile and transported to the duodenum. Once in the small intestine the conjugated bilirubin is then metabolised by the bacterial flora to produce urobilin and stercobilin. It is stercobilin that gives stool its distinctive colour.
Immune Hemolytic Anemias
Harold R. Schumacher, William A. Rock, Sanford A. Stass in Handbook of Hematologic Pathology, 2019
Hyperbilirubinemia is usually related to the unconjugated indirect bilirubin. Values at birth may be only slightly higher than the upper limit of normal (50 μmol/L at birth), because excess bilirubin is handled by the placenta before birth. Cord bilirubin values higher than 90 μmol/L are unusual; when present, they are suggestive of severe disease. In severely affected infants, peak bilirubin levels are reached by the third neonatal day and may reach 550-850 μmol/L. Levels >350 μmol/L greatly increase the risk of kernicterus. Only unbound bilirubin is toxic to the central nervous system, and binding capacity of albumin for bilirubin is therefore of critical importance. Low albumin levels, drugs that displace bilirubin from its albumin-binding sites, and acidosis all decrease the effective binding capacity of albumin. Measurements of the plasma level of free (unbound) bilirubin are considered to provide a reliable index of bilirubin toxicity. Methods that determine the concentration of vacant bilirubin-binding sites on albumin (reserve albumin) also appear to be useful.
Preoperative assessment
Prem Puri in Newborn Surgery, 2017
Hyperbilirubinemia in the newborn may have a pathological basis such as severe sepsis, Rh and ABO incompatibilities, and congenital hemolytic anemias. Neonatal hemolytic jaundice usually appears during the first 24 hours of life, whereas physiological jaundice, as mentioned before, reaches a peak between 2 and 5 days of life. Other causes for prolonged hyperbilirubinemia, including those often associated with surgical conditions, are as follows: biliary obstruction, hepatocellular dysfunction, and upper intestinal tract obstruction. The diagnosis of extrahepatic biliary obstruction should be done as early as possible, because early operations for biliary atresia are essential to obtain good short-term as well as long-term results.45 The major concern in neonatal hyperbilirubinemia (high levels of unconjugated bilirubin) is the risk of kernicterus (bilirubin deposition in the brain), which can result in brain damage.
Neonatal hyperbilirubinaemia and type 1 diabetes: an unsolved enigma
Published in Paediatrics and International Child Health, 2020
Pei-Fen Liao, Hui-Hsien Pan, Jeng-Dau Tsai, Tung-Wei Hung, Ji-Nan Sheu
In this article, the neonates with hyperbilirubinaemia received inpatient phototherapy on the basis of the Taiwan National Health programme guidelines for the management of neonatal hyperbilirubinaemia. The fact that some neonates were presumed not to have received phototherapy implies that their serum bilirubin concentrations did not meet the criteria for phototherapy, but it did not mean that they had low bilirubin concentrations. Jogender and Jaivinder comment that bilirubin at higher concentrations may change from anti- to pro-oxidant; therefore, the link between pathological hyperbilirubinaemia and increased T1DM may be plausible. However, what is the real value or cut-off point ‘at higher concentration’ in neonates that could lead to T1D? The so-called ‘physiological’ or ‘pathological’ hyperbilirubinaemia is an arbitrary definition of bilirubin concentration in neonates in clinical practice. We believe that some are vulnerable neonates who have been exposed to bilirubin to a lesser degree than generally described in previous reports and that this can predispose them to develop childhood-onset T1D [3]. We therefore disagree with Jogender and Jaivinder that physiological hyperbilirubinaemia could be protective in neonates.
Comparative outcome of overhead and total body phototherapy for treatment of severe neonatal jaundice in Nigeria
Published in Paediatrics and International Child Health, 2020
Hippolite O. Amadi, Ruqayya A. Abdullahi, Olugbenga A. Mokuolu, Obumneme B. Ezeanosike, Christiana T. Adesina, Isyaku L. Mohammed, Eyinade K. Olateju, Amina L. Abubakar, Mustapha A. Bello, Augusta U. Eneh, Emeka Onwe Ogah, Bessie C. Eziechila, Assumpta U. Chapp-Jumbo, Abdulrasheed Jimoh, Jacob J. Udo
Hyperbilirubinaemia is the accumulation of abnormally high levels (17.1 μmol/L or >1 mg/dl) of unconjugated, non-polar, lipid-soluble bilirubin [1]. The most important causes of neonatal jaundice (NNJ) in Nigeria are associated with outborn infants, especially with late presentation, glucose-6-phosphate dehydrogenase deficiency, prematurity, infection and blood groups ABO incompatibility [2]. The condition is usually benign (physiological jaundice) [1], except in severe cases which are usually associated with delay in diagnosis and lack of effective therapy. Associated risks include acute and chronic bilirubin encephalopathy [3] and other long-term morbidities such as hearing impairment, cerebral palsy, especially the choreoathetoid type [4], epilepsy, speech and language disorders, mental retardation and the wider complications of kernicterus spectrum disorders [5,6].
Recognizing skin conditions in patients with cirrhosis: a narrative review
Published in Annals of Medicine, 2022
Ying Liu, Yunyu Zhao, Xu Gao, Jiashu Liu, Fanpu Ji, Yao-Chun Hsu, Zhengxiao Li, Mindie H. Nguyen
Jaundice (Figure 3(c)) describes discolouration of the skin, sclera and mucous membranes that is attributable to the accumulation of bilirubin and its metabolites in the tissues. Jaundice generally begins to become visible when the concentration of serum bilirubin surpasses about 2 mg/dL (34 mmol/L). The colour of the skin varies from lemon yellow to apple green, gradually evolving as the serum bilirubin level becomes elevated. According to the presence of conjugated or unconjugated components of bilirubin, we can classify the three major groups of underlying causes of jaundice: prehepatic, intrahepatic or post-hepatic. Prehepatic jaundice involves haemolytic anemias, which can also be seen in neonatal physiological jaundice and breast milk jaundice. Intrahepatic jaundice involves both conjugated and unconjugated hyperbilirubinemia resulting from liver failure-associated severe acute hepatitis or cirrhosis. Other intrahepatic causes of hyperbilirubinemia include intrahepatic cholestatic diseases, such as PBC and the various congenital genetic disorders involving bilirubin metabolism or transport such as Gilbert, Crigler–Najjar syndrome, or Dubin-Johnson syndrome. Post-hepatic jaundice involves conjugated hyperbilirubinemia arising from extrahepatic issues, such as biliary tract obstruction [1].