Kernicterus with or without jaundice
			Asphyxia, as inflicted by Ranck and Windle (1959), prevented the lungs from functioning and cutoff circulation from the placenta.  This caused a catastrophic ischemia of the brain.  The immediate reaction would appear to be breach of the blood-brain barrier, especially in the brainstem nuclei of high metabolic rate, a desperate response to open any channel that might overcome the lack of oxygen.
		Lucey et al. (1964) determined that high levels of bilirubin did not damage the brains of monkeys not subjected to asphyxia.  Bilirubin stained the same brainstem nuclei injured by asphyxia, and only in monkeys subjected to asphyxia.
			Oxygen insufficiency, not bilirubin, is the root cause of kernicterus.  How to avoid even a brief lapse in respiration at birth should be the first priority.   Immediate clamping of the umbilical cord runs the risk of producing a lapse in respiration, especially if it is clamped before the first breath.  Ischemic damage of brainstem nuclei as found in the experiments of Ranck and Windle produces kernicterus, with or without bilirubin.  Infiltration of bilirubin into these brainstem nuclei simply highlights where the primary damage has occurred.