Clinical view of disturbances in equine foetal maturation.

Summary This review summarises comparative aspects of equine pregnancy and birth. The allantochorion covers the entire endometrial surface of the mare's uterus and the placenta is microcotyledonary and epitheliochorial in structure. The foetus has, therefore, to pass through the allantochorion at birth. The umbilical cord has amniotic and allantoic portions and remains intact after delivery, enabling an arterial venous circulation to be maintained for several minutes. Maternal IgG does not cross the placental barrier and passive transfer post-natally is essential for immune status. Gestation in Thoroughbreds is 340 days with a wide range (320–360 days). Birth may be induced by oxytocin but dose rate is related inversely to gestational age. Normal foals rise, suck from the mare and gallop within 4 h after birth. Categorisation of newborn foal diseases into infective (Group 1) and non-infective (Groups 2, 3 and 4) conditions is presented. The neonatal maladjustment syndrome (NMS) affects full-term individuals, causing cerebral oedema, haemorrhage and/or ischaemic necrosis. NMS is related to the birth process and myocardial ‘injury’. Prematurity and dysmaturity have origins in pre-natal disturbances of foetal maturation and physiology. Prematurity is a term ascribed to foals delivered at less than 320 days gestation whereas dysmaturity, for clinical convenience, describes foals born in the full-term period showing premature-like signs. Dysmature foals are generally associated with placental pathology. However, the distinction between the two groups is tenuous. Recent evidence suggests that 1) placental pathology is often present in premature foals; 2) differences exist in the degree of adrenocortical function. These affect clinical signs, prognosis and course of the condition. Placental pathology results in precocious adrenocortical maturation but the effect on maturation of other organ systems requires further study. Premature/dysmature foals fall into two groups; those with a favourable clinical outcome and those which make progress during the first 24 h post partum but deteriorate with development of neurological, metabolic and respiratory deficits (second day syndrome). Two models have been established to study premature/dysmature foals. The first, developed in the early 1980s, was based on induction of mares from 280 days gestation to full term, using oxytocin. A premature, intermediary (twilight) and full-term status of adrenocortical function were identified; these categories correlating with changes in mammary secretion electrolytes. The same groupings have been related to other organ systems and metabolic functions of maturation. The second model establishes placental pathology from 220 to 260 days of gestation. A small area of placenta is separated from its uterine attachment, using a videoendoscope introduced through the cervix. Precocious adrenocortical function has been induced although further work is required to confirm the model as a means of investigating the pathogenesis of dysmaturity. Foetal injections of ACTH, CRH or betamethasone cause precocious increases in maternal plasma pregnane concentrations.