Neonatal perspective

Thermoregulation is a critical physiological function in the neonate – closely linked to survival and health status. Birth precipitates the baby into a harsh and cold environment requiring major physiological adaptations and changes, including thermoregulatory independence. Newborn babies are less efficient than adults in the ability to thermoregulate.

The ability to generate heat depends on body mass and environmental heat loss, a large surface-area-to-mass ratio (about three times higher than in the adult) leading to difficulty in maintaining body temperature in a cold environment.

Babies with a low body mass are more at risk. Although full-term babies have control over peripheral vascular circulation equal to adults, the autonomic thermoregulatory responses are not fully developed. The healthy baby can increase basal heat production by 2.5 times in response to cold within 1–2 days of birth, though less so in the first 24 hours. Newborn babies are rarely able to shiver and the increased heat comes from the noradrenergic lipolysis of the brown fat deposits characteristic of the neonate and activation of specially adapted mitochondria in the brown fat to produce heat.

The most dangerous time for the newborn to lose heat is during the first 10–20 minutes of life. If measures are not taken to halt heat loss, the baby becomes hypothermic (temperature <36.5°C) soon after birth. A premature or sick baby who becomes hypothermic will be at risk of developing health problems and of dying (CESDI 2003) but the chances of survival are greatly increased if the temperature stays above 36°C. Birth should always take place in an environmental temperature above 25°C.

Hyperthermia (temperature >37.5°C) can occur and in extreme cases can cause death within the first 24 hours after birth. Hyperthermia increases the metabolic rate, leading to increased oxygen and glucose consumption plus water loss through evaporation. This causes hypoxia, metabolic acidosis and dehydration. A core temperature above 42°C may lead to neurological damage (WHO 1994).

Hyperthermia can be caused by infection; it is not possible to distinguish between infection and environmental factors by measuring the body temperature or by clinical signs. Therefore, a temperature above 37.7°C in the newborn is a deviation from normal and the baby must be urgently referred to the neonatologist for assessment, diagnosis and management.

Internal and external gradients

The external and internal gradients are interdependent. The internal gradient is the temperature differential between the core of the body and the skin and results in the transfer of heat from within the body to its surface. This process relies on an effective and extensive blood flow in capillaries and venous plexi influenced by tissue insulation provided by subcutaneous fat and the convective movement of heat through the blood. Heat conduction is under sympathetic control that results in changes in the skin blood flow by vasoconstriction and vasodilatation.

In the neonate, heat loss through this gradient is increased because of the thinner layer of subcutaneous fat and larger surface-to-volume ratio than in the adult (Blackburn 2007).

The external gradient results in heat loss from the body surface to the environment – the rate of heat loss is directly proportional to the difference between the temperature of the skin and that of the environment.

Heat transfer by the external gradient is increased in the neonate because of an increased surface area and thermal transfer coefficient. The neonate maintains temperature by means of the external gradient, that is, temperature skin changes, whereas the adult uses the internal gradient. This is especially significant for the preterm baby, for whom the control and effects of changes in the environment temperature are more profound.

Heat loss and gain

Babies at term are homeotherms; meaning having the ability to produce heat to maintain body temperature within a comparatively narrow range. The newborn cannot regulate body temperature as well as an adult can, and, when the environment becomes too cold or hot, is unable to respond and maintain temperature, therefore tolerating a limited range of environmental temperatures. Thermal stability improves gradually as the baby increases in weight and age.

There are four main routes of heat loss (Hammarlund & Sedin 1986):

1 Evaporation: heat loss through evaporation of water from the skin and respiratory tract; highest immediately following delivery and bathing, and reduced by:

drying baby’s head after birth and following a bath

using a hat

removing wet towels quickly following birth

delaying bathing until the baby’s temperature is stable and above 36.8°C.

2 Convection: heat loss to moving air or fluid around the neonate, and dependent on the difference between skin and air or fluid temperature; the amount of body surface exposed to the environment; and the speed of air or fluid movement. Heat loss can be prevented by:

increasing the birthing room temperature

keeping room temperature above 25°C when the baby is naked

covering the baby with a blanket.

3 Radiation: heat is radiated from the skin to surrounding colder solid objects, including windows or incubator walls. This is the predominant mode of heat loss after the first week of life in babies born before 28 weeks and in all other babies throughout the neonatal period. Heat loss can be prevented by:

keeping the baby away from windows and draughts.

4 Conduction: heat loss through contact with cold objects, including cold mattress, scales and radiograph plates (Avery et al 1994). Heat loss can be prevented by:

warming all surfaces that the baby is likely to come in contact with (resuscitaire, scales, bedding).

(See website for more information.)

Insensible water loss (that is, loss through the skin, urine, faeces and respiratory tract) may lead to significant heat loss – increased in preterm and low birthweight babies (Rutter 1985) because of the large ratio of surface area to body mass; limited subcutaneous fat; immature epidermal skin layer structure; and increased body water content. Risks rise in environments where insensible water loss is increased, as 0.58 kcal of heat is lost with each gram of water lost through evaporation (Hammarlund & Sedin 1986).

The appropriate temperature of a baby depends upon the baby’s age, gestation and weight. If left wet and naked, the newborn infant cannot cope with environmental temperatures of less than 32°C. If a thermometer is not available in a room, the environment must be assessed through personal comfort – what appears very warm and uncomfortable for an adult dressed in thin clothes with short sleeves is likely to be appropriate for the newborn.

Neonatal heat production

The hypothalamus and the autonomic and sympathetic nervous systems are important aspects of maintaining the temperature within narrow set limits of 36.5–37.5°C in the newborn (see website). Constant body temperature is achieved by a functioning neurological system balancing heat gain with heat loss effector systems.

In the newborn, heat production results from metabolic processes that generate energy by oxidative metabolism of glucose, fats and proteins. The organs that generate the greatest energy are the brain, heart and liver. To maintain a constant body temperature, heat loss from the surface of the body must equal heat gain.

In the baby, though the hypothalamus will receive cold alert messages from the skin, abdomen, spinal cord and internal organs, to regulate temperature stimuli from other areas of the body, the most sensitive receptors are contained within the trigeminal area of the face (Hackman 2001).

The responses of the skin surface are determined by:

• the skin temperature

• the rate and direction of temperature change

• the size of area stimulated.

In the human newborn, cooling of the skin has been shown to increase metabolic heat production without any change in the core temperature (Polin et al 2004).

Physical mechanisms include involuntary reactions, including shivering, and voluntary reactions involving muscular activity, through crying, restlessness and hyperactivity. These responses can be affected by anaesthetics, damage to the brain, muscle relaxants or sedative drugs.

The baby may generate heat by crying and become hyperactive when cold stress is severe enough to cause jitteriness, although shivering does not appear. If cold stress is not eliminated at this point, the baby may become extremely hypothermic, hypoglycaemic, hypoxic, acidotic and lethargic, and eventually death will ensue, caused by cold injury. The full-term baby can flex the body into the ‘fetal’ position, which provides some protection against cold stress, but the lack of muscle tone and flaccid posture of an immature or ill baby results in a higher heat loss. Babies can also reduce shunting of internal heat to body surfaces by constricting peripheral vessels.

Chemical or non-shivering thermogenesis is the process by which the neonate generates heat through an increase in the metabolic rate and through brown adipose tissue (BAT) metabolism. This process can be utilized by adults and neonates – in the adult the metabolic rate can be increased by about 10–15%, whereas the neonate can increase the metabolic rate by up to 100% (Cannon & Nedergaard 2004).

Heat production and brown adipose tissue (BAT)

A cold-stressed baby depends primarily on mechanisms that cause chemical thermogenesis. Neonatal heat production is mainly through non-shivering thermogenesis. When the baby becomes hypothermic, noradrenaline and thyroid hormones are released, inducing lipolysis in brown fat. This process can be affected by pathological events, including hypoxia, acidosis and glycaemia.

Brown adipose tissue is believed to constitute 2–7% of the newborn’s weight, depending on gestation and weight. Brown fat starts to be deposited in the fetus from 28 weeks’ gestation (Blackburn 2007). The brown adipocyte is uniquely suited to its role in newborn thermogenesis and differs from white adipose tissue because it is capable of rapid metabolism, heat production and heat transfer to the peripheral circulation.

The total amount of heat produced in the neonate is unknown, but may be up to 100% of its requirements (Blackburn 2007). The sympathetic nervous system stimulates the adrenal gland to release adrenaline, increasing the metabolism of brown fat and catecholamines and releasing the required glucose. The thyroid gland is also stimulated by the pituitary to release thyroid-stimulating hormone, also producing thyroxine (T₄) – known to enhance heat production from BAT.

Heat production within BAT is not fully understood but it is known that BAT contains high concentrations of complex mitochondria, stored triglycerides, sympathetic nerve endings, and a rich capillary network to carry heat around the body. The presence of an uncoupling protein within the mitochondria of brown fat cells supports the combustion of fatty acids to produce heat.

BAT is especially prominent in the mammalian fetus, and anatomical distribution is important to its function. The largest mass of tissue envelops the kidneys and adrenal glands; smaller masses are present around the blood vessels and muscles in the neck and there are extensions of these deposits under the clavicles and into the axillae. Further extensions accompany the great vessels entering the thoracic inlet. The proximity of BAT to large blood vessels and vital vascular organs provides the ability for rapid transfer of heat to the circulation (Okken 1995, Polk 1988). The activation of BAT metabolism only occurs following birth. During intrauterine life, maternal prostaglandins and adenosine do not allow non-shivering thermogenesis to take place. With the clamping of the cord, this mechanism is blocked, enabling the hypothalamus to react to hypothermia (see website).