Studies in the research laboratory have demonstrated the complex relationship between fetal and newborn asphyxia and brain damage, a balance between the degree, duration and nature of the asphyxia and the quality of the cardiovascular compensatory response. Clinical studies would support the contention that the human fetus and newborn behave in a similar manner. An accurate diagnosis of asphyxia requires a blood gas and acid base assessment. The clinical classification of fetal asphyxia is based on a measure of metabolic acidosis to confirm that fetal asphyxia has occurred and the expression of neonatal encephalopathy and other organ system complications to express the severity of the asphyxia. The prevalence of fetal asphyxia at delivery is at term, 25 per 1000 live births of whom 15% are moderate or severe; and in the preterm, 73 per 1000 live births of whom 50% are moderate or severe. It remains to be determined how often the asphyxia recognized at delivery may have been present before the onset of labor. There is a growing body of indirect and direct evidence to support the contention that antepartum fetal asphyxia is important in the occurrence of brain damage. Although much of the brain damage observed in the newborn reflects events that occurred before delivery, newborn asphyxia and hypotension, particularly in the preterm newborn, may contribute to the brain damage accounting for deficits in surviving children.

Determining the contribution of asphyxia to brain damage in the neonate

Animal models for the study of perinatal hypoxic-ischemic encephalopathy: a critical analysis☆

Fetal response to carbon dioxide pneumoperitoneum in the pregnant ewe

Basic science: Chronic fetal hypoxia increases activin A concentrations in the late‐pregnant sheep

Regional blood flow and metabolism in ovine fetuses during severe cord occlusion

To test the hypothesis that fetal lambs are able to maintain oxygen delivery to myocardial, brain and adrenal tissues during reduction in uterine blood flow to 25% of control, we performed experiments on five ewes and their fetuses. A snare occluder was placed around the maternal common hypogastric artery and catheters were placed for measurement of blood pressures, flows, blood gas tensions, pH and oxygen content. After a five day recovery period, control measurements were made. The snare occluder was then closed until the artery was fully occluded. The arterial occlusion caused uteroplacental blood flow to fall to 32 +/- 4% and maternal placental blood flow to fall to 25 +/- 3% of control values. This level of asphyxia was maintained for 19 +/- 3 minutes, when maternal and fetal blood flows were measured again. In response to occlusion, fetal ascending aortic PO2 fell from 21 +/- 2 (SEM) to 13 +/- 2 mmHg (P less than or equal to 0.01), oxygen content from 4.3 +/- 0.3 to 1.4 +/- 0.2 mM (P less than or equal to 0.01) and pH from 7.37 +/- 0.01 to 7.21 +/- 0.05 (P less than or equal to 0.01). PCO2 rose from 48 +/- 1 to 62 +/- 3 mmHg (P less than or equal to 0.01). Fetal arterial blood pressure increased from 51 +/- 3 to 61 +/- 3 mmHg (P less than or equal to 0.001) and heart rate decreased from 172 +/- 10 to 104 +/- 4 beats.min-1 (P less than or equal to 0.01). The heart, brain and adrenals showed vasodilation in response to the asphyxic stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

D Darr

Papers

Effects of severe reduction in maternal placental blood flow on blood flow distribution in the sheep fetus.