Metabolic acidosis and fetal reserve.
Dr Bailey, Director of the National Institute of Neurological Diseases and Blindness, Bethesda, Maryland, introduced the 1956 symposium on 'Neurological and psychological deficits of asphyxia neonatorum' by saying. 'Medical research in regard to cerebral palsy and other neurological disabilities has been relatively neglected. For a truly comprehensive attack on this problem we must focus a sharper scientific search for greater knowledge of those adverse biological factors which operate in the perinatal period. The proper point of departure in such a search is through controlled animal observations, for which purpose monkeys are best suited' (Windle, 1958). Our understanding of the significance of asphyxia is built on the foundation of the laboratory research that has followed upon this initiative. Laboratory studies in fetal monkeys and fetal lambs have clearly demonstrated that the fetus can initially compensate for an asphyxial insult and protect the vital organs. However, if the hypoxaemia progresses to a severe metabolic acidosis and cardiovascular decompensation with hypotension, brain damage will occur. There is a growing body of clinical evidence that supports the contention that the human fetus responds in a similar manner. The varied nature of hypoxic and ischaemic insults has been well demonstrated in animal studies. Total anoxia and isolated cerebral ischaemia are uncommon events in the human fetus. The common insult, particularly during labour, is a degree of hypoxia present over a variable period of time. This is fortunate in that such insults are associated with a period of fetal compensation that may last several hours, during which time a diagnosis of a developing metabolic acidosis can be made. This is the clinician's window of opportunity, when a definitive diagnosis of an asphyxial insult can be made and if necessary intervention made before the threshold of decompensation has been reached. A consensus on the threshold of decompensation has yet to be achieved. However, there is a growing body of evidence that the threshold is in the range of an umbilical artery base deficit of 12-16 mmol/l. Since the aim of the obstetrician during labour is the prevention of asphyxial morbidity and mortality, the determination of this threshold is important to provide criteria for clinical action. A blood gas and acid-base assessment with the determination of a metabolic acidosis is the best measure of an asphyxial insult that may be of clinical significance. The definition of the threshold of metabolic acidosis requiring intervention will continue to be clarified with future clinical research. However, there are many factors that will influence the fetal response to an asphyxial insult, which may require that a range of threshold be acknowledged. The effect upon the fetus will be influenced by whether the asphyxial event is the first or the last of a series of asphyxial episodes, and the duration of the asphyxial episode. The characteristics of the fetus, i.e. maturity (pre-term versus term), and fetal growth small for gestational age (SGA) or appropriate for gestational age (AGA) may influence the fetal response to an asphyxial insult. Improved understanding of these issues will provide a better rationale for clinical management.
Low
J A
JA
Department of Obstetrics & Gynaecology & Paediatrics, Queen's University/Kingston General Hospital, Ontario, Canada.
D000138:Acidosis / Q000097:blood / Q000209:etiology*; D001784:Blood Gas Analysis; D004195:Disease Models, Animal; D005260:Female; D005313:Fetal Death / Q000209:etiology; D005311:Fetal Hypoxia / Q000150:complications* / Q000401:mortality / Q000503:physiopathology; D006801:Humans; D007226:Infant Mortality; D007231:Infant, Newborn; D009017:Morbidity; D011247:Pregnancy; D011256:Pregnancy Outcome