Fetal-to-neonatal maladaptation

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Summary

Although the majority of newly born babies will establish normal respiratory and circulatory function without help, 1–2% might run into difficulties because of a disturbance in the normal adaptive processes required for a smooth transition from intrauterine to extrauterine life. An understanding of the normal and abnormal perinatal physiology is important to appreciate the practical differences in the approach to caring for such babies, and also for avoiding actions that might be detrimental in the longer term.

Introduction

Adaptation to extrauterine life, also referred to as transition, involves functional modifications in virtually every organ and system of the body. The most crucial events are: (1) the conversion of the fluid-filled lungs into a hollow organ distended with air and capable of gaseous exchange sufficient to support life, and the establishment of ‘adult’-type circulation; (2) the separation of the fetus from the stable thermal environment of the uterus; and (3) metabolic adaptation to extrauterine life. In fact, the event of birth tests the integrity of cardiorespiratory, thermal and metabolic homeostasis, and failure to adequately make these conversions (maladaptation) can lead, directly or indirectly, to death or severe disability. Therefore, any supportive care provided in the immediate newborn period must be based on an understanding of the pathophysiology of these homeostatic mechanisms.

Section snippets

Respiratory adaptation

Human lung development goes through pseudoglandular (5–17 weeks), canalicular (16–26 weeks), saccular (24–38 weeks) and finally alveolar (36 weeks–2 years) stages. During intrauterine development, the fetal lungs are filled with liquid secreted by the pulmonary epithelium. The volume and rate at which the liquid is secreted into the fetal lungs are calibrated to maintain lung volume at about functional residual capacity, and are the major determinants of normal lung growth.1 In the hours preceding

Circulatory adaptation

The placenta is the organ of gas exchange in fetal life. The circulation is modified to accommodate placental perfusion and is designed so that fetal arterial blood with the greatest oxygen content supplies the heart and brain and less saturated blood passes to the lower part of the body and placenta. This is accomplished in utero by creating shunts, which favour the flow of blood in the direction of the placenta. Placental vascular resistance is very low, primarily as a result of the

Metabolism

Glycogen stores in the fetal liver increase with gestation but there is a rapid rise from 36 weeks onwards; during this time, glycogen is also deposited in muscle and heart. Under normal circumstances, the fetus in utero is entirely dependent on its mother for glucose delivery. During delivery, plasma concentrations of adrenaline, noradrenaline and glucagon increase rapidly, whereas insulin concentration declines. The effect of this is to mobilise stored glycogen and fatty acids. After birth,

Thermoregulation

At birth, babies have a high surface area:mass ratio and lose heat quickly. They are born wet into a relatively cool environment, having been kept warm by their mother until the time of birth. Fetal thermogenesis is normally inactive; however, fetal basal heat production is approximately twice that of an adult. After birth, the temperature falls and the newborn responds by increasing oxygen consumption, utilisation of energy sources (especially brown fat) and thus heat production.

In response to

Respiratory maladaptation in the newborn

In the newborn, the oxygen tension needed to maintain the arterial haemoglobin saturation above 90% varies between 40 and 60 torr (approximately 5–8 kPa), depending on the proportion of haemoglobin that is fetal, and the arterial pH (a drop in pH of 0.2 eliminates the left shift produced by 70% of the haemoglobin being fetal). Thus, in the newborn period, respiratory failure can also be defined in terms of oxygen saturation, but there are no widely accepted criteria.

Hypoxaemia in the neonatal

Persistent pulmonary hypertension of the newborn

Persistent pulmonary hypertension of the newborn (PPHN) also known as persistent fetal or transitional circulation (PFC), is an acute neonatal emergency resulting from the failure of the normal post-birth decrease in pulmonary vascular resistance (PVR), which leads to a variable degree of right-to-left shunting of deoxygenated blood through persistent fetal channels (the foramen ovale and patent ductus arteriosus). This, in turn, leads to severe hypoxemia, acidosis, and further pulmonary

Conclusion

Adaptation, or transition, is a highly complex biological event that enables the fetus to become an independent being and able to exist separate and apart from the uteroplacental unit. In the overwhelming majority of cases, this process occurs normally and without consequence. However, in some situations, prior or ongoing pathology might hinder successful adaptation and place the newborn at jeopardy for death or long-term disability.

Recognition of conditions that can lead to maladaptation and

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