Hypothermia is the cooling of the body’s core temperature to below 35°C (Campbell & Glasper 1999). Neonates are at risk of hypothermia primarily because of their size because, although small, they have a large surface area in proportion to body weight, a large head size (through which heat is lost) in relation to the rest of the body and an immature hypothalamus resulting in poor vasomotor control. Those neonates primarily at risk of cold stress are (Crawford & Morris 1994):

Temperature regulation is a complex process. The hypothalamus, which is located at the base of the brain, is responsible for temperature regulation. Receptors in the skin, abdomen, spinal cord and internal organs provide the hypothalamus with information to maintain temperature balance. The hypothalamus produces hormones in response to temperature imbalance and, together with the autonomic and sympathetic nervous systems, regulates temperature (Hackman 2001). For example, if the neonate is subject to reduction in body temperature, cold stress stimulates thermoreceptors to send impulses to the heat-promoting control centre in the hypothalamus, which in turn triggers responses to retain body heat. Vasoconstriction reduces heat loss through the skin. The adrenal medulla releases hormones that increase cellular metabolism and the thyroid gland releases thyroid hormone, which increases metabolic rate. Significantly, this requires an intact central nervous system. Furthermore, temperature regulation requires oxygen because it is an aerobic process. Glucose is also needed to carry out this aerobic process for heat production.

Non-shivering thermogenesis is a significant and unique form of heat production in the neonate (Klaus & Fanaroff 1993). Neonates generate most of their heat from the breakdown of brown fat. ‘Brown fat’ refers to the deeply red, highly vascularised areas surrounding an infant’s scapular, clavicular and sternal areas. It is rich in fats and glycogen. The full-term infant has sufficient storage of brown fat to maintain temperature for up to 4 days. Heat is generated by hydrolysis of triglycerides in brown fat utilising oxygen in the process. The responses to cold of neonates in a hypoxic state will be jeopardised. Non-shivering thermogenesis is inhibited by drugs, intracranial haemorrhage and hypoglycaemic states.

There are four main routes of heat loss: evaporation, convection, conduction and radiation (Avery 1987). Evaporative heat loss occurs when water is converted to water vapour during perspiration or respiration. Neonates, wet from amniotic fluid and delivered into a cool labour ward can lose heat at a rate 0.25°C/minute (Roberton 1992). It is therefore important to dry the neonate thoroughly with warmed towels and dress him or her promptly. Convective heat loss occurs when the infant’s heat is lost to surrounding cooler air, which is why it is important to dress infants and to keep them out of draughts.

Conductive heat loss occurs when the infant comes into direct contact with a cool surface. One way to prevent this would be to prewarm anything in contact with the neonates skin. Finally, radiative heat losses occur when the infant radiates heat to a cold exposed surface such as a window. In this case the neonate should be nursed away from windows and a constant environmental temperature maintained (Sheeran 1996).

The effect of cold stress is well documented. Constriction of skin blood vessels occurs in response to cold in neonates. The effect of peripheral vasoconstriction is to increase the core skin temperature gradient. Increased metabolic rate leads to increased oxygen consumption, lactic acid production, hypoglycaemia, and in very low birthweight infants decreased surfactant synthesis and secretion. Blood coagulopathies also occur leading to increased capillary permeability and haemorrhage.

The neutral thermal environment (NTE) is the provision of an environmental temperature that minimises oxygen consumption. The neutral thermal environment varies according to the maturity of the neonate and whether the infant is nursed in an incubator or a radiant heater and is dressed or not. Optimal weight gain and normal physical development occur when a neonate is cared for in a neutral thermal environment appropriate to his or her age and weight. Neonates should be nursed in a neutral thermal environment that maintains the neonate’s peripheral temperature at 36.5°C.

Initially, a thorough assessment of the neonate and history are required. Does the neonate look pale? How does the infant feel? Is the infant cool to touch? Is there a difference between central and peripheral temperatures? A hypothermic infant may appear pale and is cool to touch. This is primarily due to vasoconstriction. Is there associated acrocyanosis, a blueish discoloration around the mouth? Is the infant tachypneoic or in respiratory distress? A hypothermic infant may develop respiratory distress secondary to the bodies attempt to maintain a normal temperature consuming oxygen in the process. How does the infant handle? Is the infant irritable or lethargic? Behavioural changes may occur as cold stress continues.

Although rectal temperature recording has been described as the gold standard for core temperature assessment, there are potential problems with this method for example, bowel perforation and cross-infection (Roberton 1992). Intermittent axillary measurement is the most commonly and frequently used method in neonatal care. Accuracy depends on consistent and universal measurement for a duration of 3 minutes at the same site (Sheeran 1996). Continuous skin and core temperature measurements are recorded in critically ill neonates. A temperature gradient is significant determining tissue perfusion.

Hypoglycaemia is described as a low blood sugar. Neonatal values for low plasma blood sugars vary from below 1.7 mmol/L to below 2.6 mmol/L (Fleming et al 1991). Significant hypoglycaemia depends on the infant’s age, weight and clinical status. Neonates are at risk of hypoglycaemia because of a lack of glycogen and fat stores.

In response to adaptation to extrauterine life, the healthy neonate creates fuel from glycogen and fat. While postnatal hormones mediate this response certain conditions predispose the neonate to hypoglycaemia. There are two main reasons for hypoglycaemia in neonates, the increased utilisation of glucose and the decreased production of glucose stores.

Glucose is obtained from two sources: glycogenolysis and gluconeogenesis. Initially, hepatic and muscle glycogen stores are broken down to form glucose and are rapidly utilised in the first 24 hours. The process of converting glycogen back into glucose is known as glycogenolysis (Tortora & Gabrowski 1993).

In gluconeogenesis, glucose is formed from the breakdown of fats and proteins. Glucocorticoid hormones of the adrenal cortex mobilise proteins and thyroid hormones mobilise proteins and fats thus making glycerol available (Tortora & Gabrowski 1993). Gluconeogenesis is regulated by changes in insulin and glucose ratios, catecholamine release, fatty acid oxidation and activation of liver enzyme production (Stables 1999). Prior to stabilisation at an average blood glucose level of 3.6 mmol/L, neonatal blood glucose levels fall to their lowest level between 2 and 6 hours old (Stables 1999).

Infants primarily at risk of hypoglycaemia are small for gestational age (SGA) neonates. Reduced glycogen stores combined with increased glucose utilisation account for hypoglycaemic states. Preterm infants are also at risk of hypoglycaemia. In the low birthweight infant, reduced enteral or parenteral intake may explain low plasma glucose levels. Immature hepatocytes, impaired gluconeogenesis and glucogenolytic enzyme activity suggest that preterm neonates are dependent on continuous exogenous nutrition. Hypoxic neonates utilise glucose at an increased rate and are therefore at risk of hypoglycaemia. The main problem is the reduced rate at which glucose is formed during anaerobic glycolysis. The problem is compounded by the fact that the neonate is unable to feed in the regular way due to hypoxic state (Brooks 1997).

Hypothermic infants are also at risk of hypoglycaemia. In an attempt to maintain temperature with normal levels the neonate utilises glycogen and plasma glucose levels fall. Therefore early recognition of the effects of cold stress should involve consideration for administration of glucose intravenous infusion. Infants of diabetic mothers are one of the most common groups of neonates to experience hypoglycaemia. This is due to impaired glucose production and excessive insulin levels from prolonged intrauterine exposure to elevated blood sugar levels.

Infected infants frequently present with hypoglycaemia. Although this could be associated with inadequate calorie intake it is mainly as a result of sepsis-induced increased metabolic rate. Inborn errors of metabolism may give rise to a defective gluconeogenesis.

Nursing management is dependent on a thorough assessment of the potentially hypoglycaemic neonate. Knowledge of the causes of hypoglycaemia (hypothermia, poor feeding history), a thorough history to include maternal risk factors (infant of a diabetic) and difficulties during or after delivery (prolonged labour, birth asphyxia), signs (intrauterine growth retarded infant) and symptoms, and a plasma glucose level are important. Care centres on prevention of hypoglycaemia. Avoidance of risk factors is essential. The greatest risk factors are cold stress and poor feeding. Therefore it is important to nurse an infant in a neutral thermal environment. Unless contraindicated due to respiratory illness or birth asphyxia, early feeding is advocated.

Infants at risk of hypoglycaemia should have blood glucose levels monitored 4–6-hourly. If a Haemacue reading is less than 3.0 mmol/L, or YSI of below 2.6, a plasma glucose sample is obtained for analysis. If this result is lower than 2.6 mmol/L, the neonate is fed smaller amounts of milk more frequently by bolus intermittently or continuously via a nasogastric or orogastric tube. Fluid volumes are increased accordingly, usually calculated a day ahead of requirements. A hypoglycaemic neonate should be nursed in a warmed incubator or on a radiant warmer. Hypoglycaemic neonates with an apparently normal temperature may be working excessively to maintain their temperature within normal limits, thereby utilising glucose stores. Therefore it is important to monitor the infant’s temperature closely. The neonate is monitored for symptomatic hypoglycaemia and for signs of respiratory distress. A repeat blood sugar level within an hour will indicate the need for further treatment. If the readings are consistently low, intravenous therapy is commenced.

Physically growth of the intestine and maturation of intestinal absorption continue to develop. At birth, the intestine is approximately 250 cm long and the stomach has a capacity of 90 mL (Kanneh & Davies 2000). Neonates tolerate small amounts of milk and feed frequently. There is a well coordinated suck and swallow reflex. This suck and swallow reflex develops from 34 weeks’ gestation onwards. This has implications for feeding preterm infants, although some preterm infants can develop this reflex earlier. In terms of intestinal absorption, pancreatic function is immature hence there are limited enzymes for fat and carbohydrate breakdown. Therefore neonates are at risk of malabsorption characterised by intolerance to feeds. Inadequate liver enzymes can lead to physiological jaundice a common treatable illness of infanthood. Intestinal mucosal immunoglobulin levels are low and neonates are at increased risk of infection, therefore care of feeding equipment is essential. Glycogen stores are depleted in periods of extreme stress of hypoglycaemia and hypothermia. In neonates gluconeogenesis is impaired thereby limiting compensatory responses to adverse conditions of illness. This highlights the importance of adequate nutritional support. In addition to intestinal growth and maturation, the motility function of the gut continues to develop. A measure of gastrointestinal motility is the passage of stools in the first 24 hours of life, however, the more premature the infant the greater the delay in defaecation. Enteral feeding promotes gastric emptying and the release of hormones that can stimulate peristalsis in term and preterm infants (Mertenstein 2002). In neonates, however, the rate of gastric emptying is prolonged.