Fetal-to-neonatal maladaptation
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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Medico-legal implications of the fetal inflammatory response syndrome
2020, Seminars in Fetal and Neonatal MedicineCitation Excerpt :Placental dysfunction may alter fetal heart rate patterns and give the appearance of an acutely hypoxemic fetus. An injured fetus may, in turn, have a poor tolerance of labor and display maltransition [12], presenting identically to the fetus/newborn who has undergone a significant intrapartum hypoxic-ischemic insult. A more recent confounder has been the introduction of neuroprotective hypothermia because it forces a clinician to make a qualifying diagnosis within 6 h of birth, a time when not all of the diagnostic information is available [13].
Rodent models of respiratory control and respiratory system development—Clinical significance
2019, Respiratory Physiology and NeurobiologyCitation Excerpt :While most infants transition without incident, up to 10% of newborns will need some respiratory assistance following birth (Wyckoff et al., 2015). Sustaining adequate ventilation and oxygenation requires a central respiratory drive, adequate muscle strength and chest wall recoil, clearance and opening of the airways, with functional gas-exchange and blood flow now occurring in the lung (Sinha and Donn, 2006). Disruptions of any aspects of the neonatal respiratory transition can result in insufficiency and needs for interventions such as positive airway pressure, mandatory ventilation, and supplemental oxygen (O2).
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