Humans are homotherms; capable of maintaining body temperature at a relatively constant level despite changes in the external environment. The ability of infants to regulate temperature in response to thermal stress is limited. Infants are unable to sweat in order to give off excessive heat when they become overheated.
The infant is capable of heat production through three mechanisms 1) voluntary muscle activity, 2) involuntary muscle activity, and 3) metabolism. Voluntary and involuntary muscle activity is limited and requires a chemical reaction utilizing large stores of energy. Term infants are capable of assuming a flexed position when cool and an extended position when overheated. The ability is limited in the premature infant, though it may be present to some extent.
Non-shivering thermo genesis appears to be the most consistent method of heat production in the neonate regardless of gestational age or birth weight. The major source of heat energy in the newborn is fatty acids. Thermo genesis is directly dependent on tissue oxygenation to utilize heat energy. Oxidized fatty acids generally are believed to derive from brown fat stores in the neonate.
Brown fat has high vascularization and is virtually nonexistent in preterm infants. Term infants have approximately 16 percent of body tissue mass as adipose tissue, but the preterm infant may have as little as 3.5 percent adipose tissue per body weight. Brown fat is located around the mediastinal structures, kidneys, scapulas, axilla and nape of the neck. Primitive brown cells first appear at 26-30 weeks gestation and ordinarily disappear by three to five weeks after birth.
Upon exposure to cold, thermal receptors in the skin (many of which are located in the face) signal the neonate’s central hypothalamus resulting in sympathetic nervous system arousal and the release of norepinephrine. The release of norepinephrine then stimulates the hydrolysis or breakdown of the brown fat. The rapid metabolism of brown fat produces heat, which warms the blood perfusing surrounding tissue. This heat is then transferred via the circulation to the rest of the body. This process consumes a lot of oxygen and glucose.
Asphyxia and hypoxia further compromise the infant’s ability to generate heat. Utilizing energy to produce heat requires an increase in oxygen consumption. In the hypoxic state, two molecules of adenosine triphosphate (ATP) are generated from a molecule of glucose instead of 38 molecules of ATP generated in the normally oxygenated infant. In order to produce heat energy in the hypoxic state, greater glucose stores must be utilized. Without sufficient oxygenation, asphyxiated or hypoxic infants have a decreased ability to generate heat. When the infant with already limited resources for heat production encounters environmental changes that threaten his ability to maintain an adequate temperature, a serious condition exists.
The metabolic rate gradually increases during the first week of life. Heat production also improves during the first few days of life with the institution of feedings. It is not clear why heat is produced. It may be due to increased metabolism during digestion, or it may be that heat can be generated when sufficient energy is provided via ingestion. Ingestion of human milk has been found to increase metabolism in low birth weight infants, leading to production of heat. Thermoregulatory needs gradually change as the infant grows, matures and feeds.
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Purpose: In 2010, approximately 14.9 million babies (11.1%) were born preterm. Because preterm infants suffer from an immature thermoregulatory system they have difficulty maintaining their core body temperature at a constant level. Therefore, it is essential to maintain their temperature at, ideally, around 37°C. For this, mathematical models can provide detailed insight into heat transfer processes and body-environment interactions for clinical applications.
Methods: A new multi-node mathematical model of the thermoregulatory system of newborn infants is presented. It comprises seven compartments, one spherical and six cylindrical, which represent the head, thorax, abdomen, arms and legs, respectively. The model is customizable, i.e. it meets individual characteristics of the neonate (e.g. gestational age, postnatal age, weight and length) which play an important role in heat transfer mechanisms. The model was validated during thermal neutrality and in a transient thermal environment.
Results: During thermal neutrality the model accurately predicted skin and core temperatures. The difference in mean core temperature between measurements and simulations averaged 0.25±0.21°C and that of skin temperature averaged 0.36±0.36°C. During transient thermal conditions, our approach simulated the thermoregulatory dynamics/responses. Here, for all infants, the mean absolute error between core temperatures averaged 0.12±0.11°C and that of skin temperatures hovered around 0.30°C.
Conclusions: The mathematical model appears able to predict core and skin temperatures during thermal neutrality and in case of a transient thermal conditions.
Keywords: Bioheat model; Computer simulation; Physiological processes; Premature infants; Thermoregulation.