(2011). "Surgery and anesthesia: healing the body but harming the brain?". Anesthesia & Analgesia. 112 (5): 999–1001. doi:10.1213/ANE.0b013e3182160431. PMC 3092153. PMID 21515644. Rasmussen, L. S. (November 1998). "Defining postoperative cognitive dysfunction". European Journal of Anaesthesiology. 15 (6): 761–764. doi:10.1097/00003643-199811000-00026. PMID 9884870. Deiner, S.; Silverstein, J.H. (2009). "Postoperative delirium and cognitive dysfunction". British Journal of Anaesthesia. 103: i41–i46. doi:10.1093/bja/aep291. PMC 2791855. PMID 20007989. External links
International Study of Post-Operative Cognitive Dysfunction (ISPOCD)
The gut is sterile at birth and normal gut flora takes time to establish. The bacteria in the adult gut convert conjugated bilirubin to stercobilinogen which is then oxidized to stercobilin and excreted in the stool. In the absence of sufficient bacteria, the bilirubin is de-conjugated by brush border β-glucuronidase and reabsorbed. This process of re-absorption is called enterohepatic circulation. It has been suggested that bilirubin uptake in the gut (enterohepatic circulation) is increased in breast fed babies, possibly as the result of increased levels of epidermal growth factor (EGF) in breast milk. Breast milk also contains glucoronidase which will increase deconjugation and enterohepatic recirculation of bilirubin. The breast-milk of some women contains a metabolite of progesterone called 3-alpha-20-beta pregnanediol. This substance inhibits the action of the enzyme uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase responsible for conjugation and subsequent excretion of bilirubin. In the newborn liver, activity of glucuronyl transferase is only at 0.1-1% of adult levels, so conjugation of bilirubin is already reduced. Further inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood. However, these results have not been supported by subsequent studies. An enzyme in breast milk called lipoprotein lipase produces increased concentration of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to decreased conjugation and subsequent excretion of bilirubin. Physiological jaundice
Most infants develop visible jaundice due to elevation of unconjugated bilirubin concentration during their first week. This is called physiological jaundice. This pattern of hyperbilirubinemia has been classified into two functionally distinct periods.