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A mosaic chromosome complement, 46,XY/47,XY,+r(15), was detected at prenatal diagnosis. Family studies showed the mother and one of her two children to have a bisatellited supernumerary marker chromosome (SMC) in all lymphocytes examined. The maternal grandfather also showed a bisatellited SMC, but in only 2 per cent of his lymphocytes. NOR, DA/DAPI, and chromosome 15 centromere and short arm-specific probes confirmed the identify of the bisatellited SMC and of ring SMC as derived from chromosome 15. An apparently normal male was born at full term. At age 1 year, the baby continues to have normal growth and development. The bisatellited 15 likely originated by somatic mutation in the grandfather (2 per cent cells), was transmitted unchanged to the daughter and grandson (germline transmission, no mosaicism), and then evolved by excising the satellites and forming a ring SMC in the index case. Progressive changes in the frequency and subsequent changes in the structure of this SMC illustrate the unusual characteristics of chromosome 15.

Fetal distress is a widely used but poorly defined term. This confusion of definition compounds the difficulty of making an accurate diagnosis and initiating appropriate treatment. The fetus reacts at the onset of asphyxia with a remarkable series of responses, primarily a complexly regulated redistribution of blood flow that serves to limit the deleterious effects of oxygen limitation in vital organs. This enables the fetus to survive asphyxia intact unless the insult is profound or prolonged. The most common asphyxial stresses imposed on the fetus during labor are insufficiency of uterine blood flow, or insufficiency of umbilical blood flow, and occasionally decrease in uterine arterial oxygenation. Each of these stresses produces characteristic fetal heart rate patterns: late decelerations, variable decelerations, or prolonged bradycardia. There is strong evidence that the presence of normal fetal heart rate variability represents normal central nervous system integrity, including adequate oxygenation. A decrease or loss of variability in the presence of these patterns is a sign that the physiologic compensations are overwhelmed as a result of the severity of asphyxia. Knowledge of the fetal responses to asphyxia, together with the known evolution of fetal heart rate patterns during asphyxia, should allow a more accurate definition of the onset of unacceptable asphyxia, and more rational management and timing of intervention.