Obstructive jaundice in haemolytic disease of the newborn treated with magnesium sulphate.

Obstructive jaundice seldom follows haemolytic disease of the newborn. It may occur at the height of the haemolytic process or not until some weeks later. In the latter instance, an evanescent phase of haemolytic jaundice may occur after birth with a recurrence of icterus after a few weeks, and then biliary obstruction. The degree of biliary obstruction is usually only partial but it may be complete. Jaundice may continue for any period between 3 weeks and 6 months of age, with an average duration of seven to eight weeks (Hsia, Patterson, Allen, Diamond and Gellis, 1952). Still (1927) was the first to describe this type of obstructive jaundice and he thought that the bile arising from excessive haemolysis had become too viscid to pass freely along the ducts. Ladd (1935) also considered that some of these cases of obstructive jaundice were due to 'inspissated bile, with stenosis or narrowing of the common duct though without definite evidence of atresia. Skelton and Tovey (1945) accepted the inspissated bile theory but also suggested that, in some cases, the bile ducts might be converted into a fibrous cord following organization of a plug of inspissated bile. Lightwood and Bodian (1946) thought that the inspissated bile theory did not adequately explain the facts and pointed out that a markedly obstructive phase did not necessarily go with the greatest haemolysis nor with the deepest preceding jaundice. They suggested that biliary obstruction was due to swelling of damaged liver cells. Gilmour (1944) and Craig (1950) have described the post-mortem appearances in the liver consisting of erythropoiesis, distortion of hepatic cords, pigmentation and necrosis of liver cells and bile thrombi in the canaliculi. Craig also noted giant multinucleated cells and suggested that they might accompany regeneration of liver cells in young infants. Hsia et al. (1952), discussing both theories, thought that it was not clear whether inspissation occurred as the result of damage to the liver parenchyma or whether the excessive load of bilirubin presented to the liver caused blockage of the ducts during excretion. Assuming the latter to be true, it was probable that the biliary system was gradually cleared of inspissated bile as the haemolytic process ceased and as the bile ducts became larger. The fact that obstructive jaundice occurs in some patients and not in others might, they thought, be due to variation in functional maturity of the liver and size of the bile ducts in infants. Harris, Andersen and Day (1954) agreed with Bodian and Lightwood that the major abnormality was in the liver cells and that plugs of inspissated bile in the biliary canaliculi were present as a secondary phenomenon. This also occurs in infective hepatitis where stagnation of bile may be seen in canaliculi just outside the areas of maximal necrosis. Two cases of obstructive jaundice associated with haemolytic disease of the newborn will now be reported and their treatment described.