NEONATAL RESUSCITATION THERMOREGULATION
Category: Child Health
Abstract : neonatal resuscitation - Thermoregulation It is essential to prevent heat loss during the resuscitation. Intrauterine thermoregulation is passive, with no use of calories or oxygen by the fetus. This intrauterine thermoregulation allows for maximal intrauterine growth without fetal energy expenditure for thermal homeostasis. Brown fat storage begins during the third trimester. It is the brown f
neonatal resuscitation - Thermoregulation
It is essential to prevent heat loss during the resuscitation. Intrauterine thermoregulation is passive, with no use of calories or oxygen by the fetus. This intrauterine thermoregulation allows for maximal intrauterine growth without fetal energy expenditure for thermal homeostasis. Brown fat storage begins during the third trimester.
It is the brown fat that is used for heat production in the newborn period.
Several factors lead to increased heat losses in the newborn infant. The neonate has a large skin surface area - to - body weight ratio, which increases heat and fluid evaporative loss. The fluid loss from the skin (not due to sweating but caused by direct transdermal water loss) results in massive heat loss. The thin skin with blood vessels that are near the surface provides poor insulation, leading to further heat loss. Additionally, the newborn infant (especially if premature) has a limited capacity to change body position for heat conservation. Animals ordinarily attempt to decrease heat loss by decreasing exposed surface area. This reduction in exposed surface area is accomplished by assuming a flexed position; however, premature, critically ill, and depressed infants are unable to accomplish flexed positioning.
Neonates have a very limited capacity for metabolic heat production. The newborn infant has limited energy stores, largely because of decreased subcutaneous fat and brown fat stores. This paucity of fat stores is more pronounced in premature and growth-retarded infants. Additionally, infants do not shiver effectively, which is a major source of heat production in the adult. The main source of heat production in the newborn is nonshivering thermogenesis.
Thermoreceptors in the face have a marked sensitivity to heat and cold. Stimulation by cold leads to norepinephrine production and thyroid hormone release causing brown fat to be metabolized. Brown fat is highly vascularized and stored in pockets around the neonate's body. When brown fat is metabolized, triglycerides are hydrolyzed to fatty acids and glycerol. Additionally, glycolysis is initiated and glycogen stores are used; both processes resulting in glucose production. Heat is produced as a byproduct of the increased metabolic rate and oxygen consumption.
Infants who experience heat loss have an increased metabolic rate and use more oxygen. Increased oxygen consumption can be dangerous in infants who are experiencing respiratory compromise. The addition of cold stress in infants who are poorly oxygenated potentially can lead to a change from aerobic to anaerobic metabolism. This change in metabolism may lead to tissue hypoxia and acidosis because of the buildup of metabolic byproducts such as lactate. Because of the inefficiency of anaerobic metabolism, the infant uses up glucose and glycogen reserves rapidly and still produces only a limited amount of energy for heat production. Therefore, cold stress can lead to both metabolic acidosis and hypoglycemia.
Based on this information, it is essential to prevent excessive heat loss in the delivery room. Newborns should be dried with prewarmed blankets or towels and placed on a prewarmed heat source. Open bed warmers, which use radiant heat, are used in most delivery rooms. They provide warmth during resuscitation and for any subsequent invasive procedures. It is important for the practitioner to keep in mind that this source of heat does not protect the infant from evaporative heat loss but, instead, encourages evaporative heat losses.
It is also necessary to consider the environmental temperature in relationship to controlling heat loss in the newborn. As a fetus, the thermal environment is regulated precisely by the mother's core temperature, and heat losses are nonexistent. Following delivery, even when drying and a radiant heat source are used, infants continue to lose large amounts of heat. This occurs by convective and evaporative heat loss. When the environmental air is less than the neutral thermal environment for the infant being resuscitated, this cooler air causes further thermal losses.
Heat losses are related to the differences both in water concentrations between the skin and the air as well as the absolute temperature gradient. The primary goal in neonatal thermoregulation is to prevent heat loss, compared to later rewarming a cold infant. Ideally, an area (eg, a stabilization room) should be separate from the operating room (OR) or labor room that allows special attention to the unusual thermal and environmental needs of the newborn high-risk infant. This stabilization area should be kept as warm as possible, balancing the requirements of the high-risk infant with the comfort of the adult staff in that area. Centers with such stabilization areas generally quote temperature goals in the range of 80-88°F.
Another common source of heat loss in the newborn infant undergoing resuscitation is the use of unheated nonhumidified oxygen sources for the bag-valve-mask device. Inspired gasses that are sent to the lungs are subsequently heated and humidified by the infant, thus resulting in massive heat exchange and insensible water loss. Therefore, whenever possible, warmed and humidified gasses should be provided in the resuscitation area. Alternatively, the intubated and ventilated infant should be placed on a heated ventilator circuit as soon as is feasible.
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