Hypothermia (low body temperature) is defined as a core temperature of 35°C or below (Sequeira et al. [184]), which causes the metabolic rate to decrease (Cobas and Vera‐Arroyo [46]). Hypothermia may be classified as mild (32–35°C), moderate (30–32°C) and severe (below 30°C) (Malhotra et al. [108]). Hypothermia occurs when the body loses heat and is subsequently unable to maintain homeostasis (Grainger [75], Marieb and Keller [111]). In contrast to a raised temperature, during hypothermia cellular metabolism slows, and the need for oxygen is reduced as more oxygen remains bound to haemoglobin, leading to a reduction in respiratory rate (Tortora and Derrickson [199]).

If a patient's temperature falls below 35°C, they can start to shiver severely (O'Donnell and Waskett [146]). However, hypothermia can cause non‐specific symptoms, and ascertaining the exact temperature is challenging; for example, when using an oral thermometer, hypothermia frequently escapes detection (Bodkin et al. [23], Marini and Dries [112]). It can occur in all ages, although the elderly are at particular risk, and it is often multifactorial in origin with other risk factors, including a low body mass index or an ambient temperature lower than 20°C (Breathett et al. [27], Chambers and Burlingame [37], Torossian et al. [197]).

Hypothermia can arise as a result of:

Acute hypothermia occurs when the body is accidentally exposed to cold environmental temperatures, for example following cold water immersion or cold weather exposure, while chronic hypothermia can arise due to endogenous factors including ageing and diseases such as diabetes (Peiris et al. [158]). Induced hypothermia is based on the theorized protective effects on apoptosis and post‐traumatic immune response (RCUK [173]). Therapeutic hypothermia was previously common practice following cardiac arrest (Cobas and Vera‐Arroyo [46]). However, clinicians are now electing to use 36°C as the preferred target temperature following the recent large Target Temperature Management trial, which found no difference in mortality between target temperatures of 36°C and lower ones (Nielsen et al. [143], RCUK [173]). The use of therapeutic hypothermia in traumatic brain injury also remains controversial (Andrews et al. [4], Cobas and Vera‐Arroyo [46]), mainly due to a lack of robust evidence (Carney et al. [34], Cobas and Vera‐Arroyo [46]); hence, it has not been incorporated into the Brain Trauma Foundation guidelines (Carney et al. [34]).

Endogenous hypothermia results from a metabolic dysfunction with decreased heat production (e.g. hypothyroidism, hypoglycaemia and hypoadrenalism) or disturbed thermoregulation (e.g. intracranial tumour or degenerative neurological disorders) (Marieb and Keller [111]). Finally, accidental hypothermia is characterized by an unintentional decrease of the core temperature due to exposure to a cold environment without a thermoregulative dysfunction (Waugh and Grant [207]).

Surgical patients having procedures longer than 1 hour have increased disruption to normal homeostatic mechanisms, and this results in a drop in temperature (Marini and Dries [112]). Complications can include cardiovascular ischaemia, delayed wound healing, increased risk of wound infections and increase in post‐operative recovery time (Bashaw [15]). To prevent unplanned perioperative hypothermia, aggressive use of convective and conductive warming measures and an increased ambient temperature are recommended (Bashaw [15]), especially for the following patients:

Sudden temperature elevations usually indicate inflammation or infection, making it prudent to perform a physical examination and, if indicated, obtain appropriate cultures and institute antibiotics. However, although infection is the most common explanation, several life‐threatening, non‐infectious causes of fever are frequently overlooked (Marini and Dries [112]) (Table 14.9).

Fever caused by pyrexia (elevated body temperature) is the result of the internal thermostat resetting to a higher level (Tait et al. [194]). This is the result of the action of pyrogens, which are chemical substances now known to be cytokines (Tortora and Derrickson [199]). Cytokines are chemical mediators that are involved in cellular immunity; they enhance the immune response by being released from white blood cells, injured tissues and macrophages (Marieb and Hoehn [110]). This causes the hypothalamus to release prostaglandins, which in turn reset the hypothalamic thermostat (Zampronio et al. [221]). The body then promotes heat‐producing mechanisms such as vasoconstriction and, as a result, heat loss from the body surface declines, the skin cools and shivering begins to generate heat (Marieb and Keller [111]). These ‘chills’ are a sign that body temperature is rising and are often referred to as ‘rigors’ (Marieb and Hoehn [110]). A full list of the physiological changes that occur following a quick temperature rise is as follows:

All of these changes contribute to a rise in metabolism and a faster rate of diffusion, with increases in carbon dioxide excretion and the need for oxygen, leading to an increased respiratory rate (Tortora and Derrickson [199]). When the body temperature reaches its new ‘set point’, the patient no longer complains of feeling cold, shivering ceases and sweating commences (Marieb and Keller [111]).

There are several grades of pyrexia, and these are described in Table 14.10. However, the intensity of a pyrexia is not an indicator of the severity of infection (DeFronzo et al. [52], NICE [140]), as this varies from person to person (Wilkinson et al. [215]).