This editorial accompanies an article by Mullington et al., Anaesthesia 2018; 73: 1500-6.Winter invokes thoughts of cozy scarves, plump down comforters and roaring wood fires marshalled against frigid temperatures, treacherously icy roads and arctic snow squalls. Thermostats in homes, office suites and operating rooms are the site of quotidian conflicts on what is considered the 'optimal temperature'. These skirmishes also occur internally, as human thermoregulation, which is controlled by the pre-optic/anterior hypothalamus, responds to information relayed from internal (core) and surface (skin) sensors. Heat conservation, generation or dissipation is controlled through a series of feedback loops, with afferent temperature stimuli from the core being significantly more influential than that from the skin; in contrast, efferent thermal responses are mostly dependent on cutaneous vasodilation and constriction to effect change. During exercise or heat exposure, skin blood flow can increase from a resting baseline of 250 ml.min À1 up to 8 l.min À1 through increases in cardiac output, redistribution of blood flow from other areas such as the splanchnic region and sweating to dissipate heat effectively [1]. In cold environments, heat conservation is reliant on cutaneous vasoconstriction, which decreases skin blood flow and heat transfer from the core to the periphery.
Too cold?Despite a dynamic relationship between the hypothalamus, core and surface sensors and blood flow, the accompanying science appears 'frozen' by limitations in instrumentation or imagination. Our understanding of the thermal influences of pregnancy, labour, neuraxial analgesic and anaesthetic agents and mode of delivery remains nascent. Although a few centrally-located temperature monitoring sites (e.g. urinary bladder, oesophageal, uterine and rectal) have been studied in pregnancy, intra-arterial thermistors (particularly within the pulmonary artery, since 1972) represent the gold, but seldom used, standard [2]. Peripheral thermometers (e.g. tympanic membrane, temporal artery, axillary or oral), although more convenient for clinical use, suffer from poor diagnostic accuracy, especially in their sensitivity for detecting low-grade fever [2]. The thermal effects of pregnancy hormones and commonly used agents further confuse matters. Oestrogen, oxytocin and neuraxial morphine are associated with hypothermia, although the mechanisms for these effects remain speculative [3]. The use of neuraxial analgesia has been associated with an increase in temperature in approximately 20% of labouring women. The hyperthermia likely represents a non-infectious, systemic inflammatory process and is typically modest (simultaneously obtained mean temperature at baseline to labour maximum by site: oral, 36.6°C-37°C; tympanic, 36.8°C-37°C and intrauterine, 37.2°C-37.6°C) [4], but occasionally can progress to a clinical fever (38°C; labour epidural analgesia-associated fever (LEAF)) [5]. In contrast, most women undergoing neuraxial anaesthesia during caesarean section ...