Temperature Control
Kimberlee Chatson
I. HEAT PRODUCTION.
In adults, thermoregulation is achieved by both metabolic and muscular activity (e.g., shivering). During pregnancy, maternal mechanisms maintain intrauterine temperature. After birth, newborns must adapt to their relatively cold environment by the metabolic production of heat because they are not able to generate an adequate shivering response.
Term newborns have a source for thermogenesis in brown fat, which is highly vascularized and innervated by sympathetic neurons. When these infants face cold stress, norepinephrine levels increase and act in the brown fat tissue to stimulate lipolysis. Most of the free fatty acids (FFAs) are re-esterified or oxidized; both reactions produce heat. Hypoxia or β-adrenergic blockade decreases this response.
II. TEMPERATURE MAINTENANCE
Premature infants experience increased mechanisms of heat loss combined with decreased heat production capabilities. These special problems in temperature maintenance put them at a disadvantage compared with term infants; premature infants have the following:
A higher ratio of skin surface area to weight
Highly permeable skin, which leads to increased transepidermal water loss
Decreased subcutaneous fat, with less insulative capacity
Less-developed stores of brown fat
Decreased glycogen stores
The inability to take in enough calories to provide nutrients for thermogenesis and growth
Limited oxygen consumption when pulmonary problems exist
Cold stress. Premature infants subjected to acute hypothermia respond with peripheral vasoconstriction, causing anaerobic metabolism and metabolic acidosis. This can cause pulmonary vessel constriction, which leads to further hypoxemia, anaerobic metabolism, and acidosis. Hypoxemia further compromises the infant’s response to cold. Premature infants are therefore at great risk for hypothermia and its sequelae (i.e., hypoglycemia, metabolic acidosis, increased oxygen consumption). The more common problem facing premature infants is caloric loss from unrecognized chronic cold stress, resulting in excess oxygen consumption and inability to gain weight.
Neonatal cold injury occurs in low birth weight infants (LBWs) and term infants with central nervous system (CNS) disorders. It occurs more often in home deliveries, emergency deliveries, and settings where inadequate attention is paid to the thermal environment and heat loss. These infants may have a bright
red color because of the failure of oxyhemoglobin to dissociate at low temperature. There may be central pallor or cyanosis. The skin may show edema and sclerema. Core temperature is often <32.2°C (90°F). Signs may include the following: (i) hypotension; (ii) bradycardia; (iii) slow, shallow, irregular respiration; (iv) decreased activity; (v) poor sucking reflex; (vi) decreased response to stimulus; (vii) decreased reflexes; and (viii) abdominal distention or vomiting. Metabolic acidosis, hypoglycemia, hyperkalemia, azotemia, and oliguria are present. Sometimes, there is generalized bleeding, including pulmonary hemorrhage. It is uncertain whether warming should be rapid or slow. Setting the abdominal skin temperature to 1°C higher than the core temperature in a radiant warmer will produce slow rewarming, and setting it to 36.5°C will also result in slow rewarming. If the infant is hypotensive, normal saline (10—20 mL/kg) should be given; sodium bicarbonate is used to correct metabolic acidosis. Infection, bleeding, or injury should be evaluated and treated.
Hyperthermia, defined as an elevated core body temperature, may be caused by a relatively hot environment, infection, dehydration, CNS dysfunction, or medications. Placing newborns in sunlight to control bilirubin is hazardous and may be associated with significant hyperthermia.
If environmental temperature is the cause of hyperthermia, the trunk and extremities are the same temperature and the infant appears vasodilated. In contrast, infants with sepsis are often vasoconstricted, and the extremities are 2°C to 3°C colder than the trunk.
III. MECHANISMS OF HEAT LOSS
Radiation. Heat dissipates from the infant to a colder object in the environment.
Convection. Heat is lost from the skin to moving air. The amount lost depends on air speed and temperature.
Evaporation. The amount of loss depends primarily on air velocity and relative humidity. Wet infants in the delivery room are especially susceptible to evaporative heat loss.
Conduction. This is a minor mechanism of heat loss that occurs from the infant to the surface on which he or she lies.
IV. NEUTRAL THERMAL ENVIRONMENTS
minimize heat loss. Thermoneutral conditions exist when heat production (measured by oxygen consumption) is minimum and core temperature is within the normal range (Table 15.1).
V. MANAGEMENT TO PREVENT HEAT LOSS
Healthy term infant
Standard thermal care guidelines include (i) maintaining the delivery room temperature at 25°C (WHO), (ii) immediately drying the infant (especially the head), (iii) removing wet blankets, and (iv) wrapping the infant in prewarmed blankets. It is also important to prewarm contact surfaces and minimize drafts. A cap is useful in preventing significant heat loss through the scalp, although evidence suggests that only caps made of wool are effective.
Table 15.1 Neutral Thermal Environmental Temperatures
Age and weight
Temperature*
At start (°C)
Range (°C)
0-6 h
Under 1,200 g
35.0
34.0-35.4
1,200-1,500 g
34.1
33.9-34.4
1,501-2,500 g
33.4
32.8-33.8
Over 2,500 g (and >36 weeks’ gestation)
32.9
32.0-33.8
6-12 h
Under 1,200 g
35.0
34.0-35.4
1,200-1,500 g
34.0
33.5-34.4
1,501-2,500 g
33.1
32.2-33.8
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