Acholuric jaundice in a newborn infant.

Mrs. C., the mother, of the affected infant, came under observation for the first time in 1940, with a history of chronic backache, puffiness of the eyes, and frequency of micturition. These symptoms were discovered to be due to pyelitis which was treated with sulphonamide, with marked improvement. At this time she was noticed to be slightly jaundiced and her spleen was enlarged to three fingers' breadth below the costal margin. A routine blood count showed haemoglobin 45%O, red blood cells 3,060,000, colour index 0 73. The red cells were said to be normal in size and shape in stained films. She was discharged home after four weeks in hospital with instructions to take iron at home. Her first child was born in 1941. The notes of this delivery were unfortunately lost owing to the war-time dislocation of the hospital's routine. The infant was apparently normal but the mother received several transfusions in the lying-in period. The second pregnancy in 1943 was complicated by toxaemia with oedema and albuminuria. She was admitted for treatment and was found to be grossly anaemic, her haemoglobin being 23%. She was again transfused and went into premature labour which resulted in the birth of a male infant weighing 4 lb. 15 oz. This infant progressed satisfactorily until the sixteenth day when he was noted to be very pale; the infant died suddenly on the following day. Post-mortem examination revealed the cause of death to have been bronchopneumonia complicating haemolytic anaemia which was attributed to erythroblastosis foetalis. After this confin nt the mother's blood was fullly investigated and she was found to have typical acholuric jaundice. Her red cells showed definite spherocytosis (mean corpuscular average thickness 3 74). Fragility tests in saline solutions showed haemolysis beginning at 0 65% and almost complete at 0-45%O. Early in 1944 her spleen was removed and microscopic examination was said to show a ' structU typical of acholuric jaundice '. The third pregnancy terminated in 1948 in the birth of a normal full-term male infant. Repeated blood investigations on this infant (including fragility tests) failed to reveal any evidence of a blood dyscrasia. The fourth pregnancy also went to term and resulted in the birth of a mature female infant. The mother's Wassermann reaction was negative in this as in the other pregnancies. This child was carefully watched and the following blood values were obtained: