The global population is increasing overall, with a notable rise in the number of people aged 65 years and over [1]. As the geriatric population grows, addressing the health challenges associated with aging has become increasingly important. When approaching geriatric patients, anesthesiologists must recognize the tremendous heterogeneity or variability in aging, both in the body as a whole and in individual organ systems. Among these challenges, perioperative unintentional hypothermia has become a growing concern for anesthesiologists because of its association with systemic responses to various complications [2,3]. Geriatric populations are especially vulnerable to disturbances in thermoregulation due to the physiological changes that accompany aging and senescence [4,5].

This review examined the factors and management strategies associated with unintentional hypothermia in the geriatric patients. First, we explored age-related changes in the thermoregulatory physiology and other contributing factors. Next, we reviewed the current methods for monitoring and managing hypothermia in this population. Finally, we discussed existing controversies and identified areas that require further investigation.

The normal thermoregulation system is mediated by various of mechanisms (Fig. 1). A normal thermoregulation system comprises afferent thermal sensing, central regulation, and efferent responses [6]. Afferent signals are primarily derived from various tissues, including the skin, deep tissues, and the spinal cord. Cold stimuli are transmitted via Aδ fibers, whereas warm stimuli are conveyed through unmyelinated C fibers [7]. These thermal signals ascend through the spinothalamic tract of the anterior spinal cord to reach the hypothalamus, which is the central integrator of thermoregulatory control [8,9]. Upon integration, effector responses are initiated once the afferent input surpasses specific threshold values, with the response magnitude increasing along a defined slope until the maximal intensity is achieved [10]. Threshold, gain, and maximal response intensities are independently determined for each thermoregulatory effector [11]. The effector systems are categorized into behavioral and autonomic components. Behavioral responses are predominantly regulated by thermal inputs from the skin surface, whereas approximately 80% of autonomic responses are governed by thermal inputs from core structures. Behavioral regulation is the most powerful thermoregulatory effector that allows humans to tolerate extreme environments. In the autonomic cold-defense system, vasoconstriction and thermogenesis play central roles [9]. Vasoconstriction significantly reduces blood flow through arteriovenous shunts on the skin surface, thereby minimizing convective and radiative heat loss and effectively conserving metabolic heat [10]. This response is primarily mediated by local α-adrenergic sympathetic nerve activity. Meanwhile, non-shivering thermogenesis, which occurs in skeletal muscle and brown adipose tissue, enhances metabolic heat production without muscular activity and is regulated by norepinephrine released from adrenergic nerve terminals [12,13]. Shivering thermogenesis, while capable of increasing heat production by 300-500%, contributes less significantly overall. Conversely, autonomic warmth defense mechanisms involve sweating and vasodilation. Sweating, mediated by the postganglionic cholinergic nerves, promotes efficient heat dissipation through evaporative cooling. Vasodilation, the physiological opposite of cold-induced vasoconstriction, is mediated by nitric oxide (NO), which facilitates heat loss by increasing blood flow to the skin. Under extreme heat conditions, blood flow through arteriovenous shunts can reach 6-8 L/min, approximating the entire resting cardiac output [8]. The interthreshold range, which is the temperature interval between the activation thresholds of cold (i.e., vasoconstriction) and warm (i.e., sweating) autonomic responses, defines the zone of normal thermoneutrality wherein autonomic thermoregulatory responses are not triggered. In humans, this range is maintained with high precision, typically within 0.2°C [7]. Moreover, it is reported to be approximately 0.3-0.5°C higher in women compared to men and approximately 0.4°C lower in older individuals [14,15].

Various components of the thermoregulatory system are influenced by aging, as well as by associated comorbidities and polypharmacy (Table 1) [15,16]. One of the primary areas affected is the nervous system. The perception of changes in body temperature is significantly blunted in geriatric populations. This impairment is attributed to a decline in the function of thermoreceptors distributed across the skin, with attenuation of warm-signal detection preceding that of cold-signal detection, and with distal regions affected before proximal regions [4,15]. Furthermore, aging diminishes the sensitivity of the central thermoregulatory center, the hypothalamus, to temperature changes. The responses of the autonomic nervous system also become less robust with advancing age [16,17]. The resulting decline in subjective thermal perception, coupled with a reduced awareness of environmental risks, physical limitations such as arthritis, and impaired mobility, collectively contribute to a decreased behavioral thermoregulatory response. Consequently, older adults are more vulnerable to thermal injury [18].

In addition to impairing neural components, aging induces significant changes in the cardiovascular system that affect thermoregulation. In geriatric populations, baseline sympathetic norepinephrine levels are elevated, but responsiveness to stimuli is diminished [11,19]. This reduction is attributed to age-related increases in reactive oxygen species (ROS), which impair the synthesis and secretion of norepinephrine. Consequently, the vasoconstrictive response to cold signals is markedly blunted, reducing the ability to conserve heat in cold environments and thereby increasing the risk of hypothermia [17]. Similarly, the vasodilatory response to warm stimuli is attenuated with aging. This decline is primarily due to the increased oxidative degradation of NO resulting from ROS accumulation. As a result, geriatric adults are at greater risk of heat-related illnesses under high-temperature conditions. Age-associated cardiopulmonary senescence, characterized by a limited cardiac output reserve, further exacerbates thermoregulatory challenges during thermal stress.

Aging-associated changes in the skin and sweat glands further contribute to impaired thermoregulation in geriatric populations [20]. With advancing age, the dermis becomes thinner, cutaneous vascular density declines, and the vascular walls undergo hypertrophy, leading to increased stiffness [15,21]. As previously discussed, these vascular changes diminish the thermoregulatory vascular responses to thermal stimuli. Subcutaneous fat decreases with age, thereby reducing the ability of the body to preserve its thermal content in response to cold exposure. Sweating capacity declines, primarily because of the functional deterioration of sweat glands rather than a reduction in their number [15,16]. This decrease begins in the lower extremities and progresses sequentially to the back, anterior chest, upper extremities, and face.

Shivering thermogenesis is attenuated in the geriatric patients [22]. While sarcopenia, the age-related loss of skeletal muscle mass, contributes to this decline, reduced thermogenic capacity has been observed even in geriatric individuals with preserved muscle mass, suggesting that functional impairment plays a predominant role in this decline. Sarcopenia diminishes shivering thermogenesis and impairs passive heat distribution and insulation due to the reduced vascularity of skeletal muscle, ultimately leading to decreased basal and resting metabolic rates, which affect the overall heat production and distribution. Additionally, various hormones, including epinephrine, thyroxine, and cortisol, play key roles in thermogenic mechanisms; thus, aging of the endocrine system further compromises heat production [23]. Cardiopulmonary aging, by limiting oxygen delivery and consumption, exacerbates deficits in thermogenesis. Other factors associated with aging, such as reduced caloric intake, decreased basal metabolic rate, reduced body fat mass, comorbidities, and the effects of polypharmacy, collectively impair thermoregulatory capacity in the geriatric populations [16]. Finally, the diminished physiological reserve associated with aging increases the risk of complications arising from hypothermia.

The effect of anesthesia on thermoregulation has been well established. During anesthesia, robust behavioral thermoregulatory responses cannot be elicited, and autonomic responses are significantly impaired [2,3,7]. Most anesthetic agents currently in use exert direct vasodilatory effects, particularly by promoting the dilation of thermoregulatory arteriovenous shunts. Consequently, the threshold for the strong cold defense response, characterized by vasoconstriction, decreases proportionally to the anesthetic dose, while the threshold for shivering decreases, maintaining an approximate 1°C difference between the two. The thresholds for warm-defense responses are slightly increased, resulting in a substantial expansion of the inter-threshold range to 2-4°C, roughly 10-20 times wider than the normal range of approximately 0.2°C [7]. Within this expanded inter-threshold range, the core temperature becomes highly labile, resembling that of a poikilothermic state. Anesthesia lowers the thresholds for effector responses and reduces their gain and maximal intensity, resulting in a delayed onset of autonomic responses, with their rate of increase and maximum efficacy diminished [2].

The typically low ambient temperature of operating rooms (ORs) combined with impaired thermoregulation due to anesthesia leads to significant intraoperative heat loss. Approximately 40% of heat loss occurs through radiation, 30% through convection due to air movement, 25% through evaporation, and a minor amount through conduction to the operating table [2,24,25]. However, the rapid initial decrease in core temperature at approximately 1.0-1.5°C within the first hour of anesthesia-cannot be explained by heat loss alone [26]. Instead, this phenomenon is primarily due to the redistribution of body heat from the core to the periphery, facilitated by anesthesia-induced vasodilation, which account for approximately 81% of the initial temperature drop. Subsequently, the core temperature decreases more gradually as a function of the imbalance between heat loss and metabolic heat production, eventually reaching a thermal steady-state after 3-4 h [26].

Neuraxial anesthesia, such as spinal or epidural anesthesia, also impairs thermoregulation by reducing both the vasoconstriction and shivering thresholds by approximately 0.6°C [27]. This impairment is thought to result from the central effects of neuraxial blockade, as well as altered central interpretation of afferent thermal inputs, where the blocked segments are perceived to have elevated temperatures [28]. Additionally, vasodilation in blocked dermatomes increases skin temperature, enhancing patients’ subjective thermal comfort and further blunting behavioral responses, which then creates a dangerous clinical paradox that exacerbates hypothermia [29]. These thermoregulatory impairments are proportional to the number of blocked segments and are characterized by the absence of gain and maximal intensity responses in the affected regions. Unlike general anesthesia, temperature decreases under neuraxial blockade occurs rapidly due to initial redistribution, followed by gradual cooling without a subsequent plateau phase, as ongoing heat loss exceeds metabolic heat production [28,29]. Temperature decreases are more pronounced during combined general and regional anesthesia [30]. In contrast, peripheral nerve blockades such as brachial plexus blocks do not result in clinically significant impairment of thermoregulation even in geriatric patients [2,31]. In a study conducted on geriatric patients undergoing hand surgery under brachial plexus block, the body temperature at the end of surgery remained close to 37°C regardless of prewarming. Moreover, body temperatures measured every 15 min from the start to the end of surgery did not differ from those measured before the brachial plexus block [31].

Thermoregulatory function during anesthesia is further compromised in geriatric patients due to age-associated alterations in the thermoregulatory system, as described earlier [16]. Previous studies have reported that isoflurane anesthesia reduces the vasoconstriction threshold by approximately 1°C, whereas sevoflurane anesthesia decreases it by approximately 0.8°C in geriatric patients [14,32]. Consistent with these findings, intraoperative hypothermia is more pronounced in geriatric patients, with greater decreases in core temperature and prolonged recovery times than in younger individuals. Similar trends have been observed under neuraxial anesthesia [33]. Although earlier studies have indicated an increased susceptibility to intraoperative hypothermia in geriatric patients, some researchers have suggested that the risk may be lower than previously thought or even comparable to that in younger patients [34-36]. This discrepancy remains a subject of active debate and is likely attributable to advances in minimally invasive surgical techniques and the implementation of active warming strategies during surgery. The use of processed electroencephalography, such as the bispectral index, effectively reduces the anesthetic requirements in geriatric patients, thereby mitigating the impact of anesthetics on the thermoregulatory system. Nonetheless, given the well-documented vulnerability of the thermoregulatory system in the geriatric patients, careful interpretation of these newer findings is warranted.

Various complications can occur in geriatric patients due to hypothermia (Table 2). Intraoperative hypothermia is defined by previous guidelines and other clinical standards as a decrease in core temperature below 36.0°C during anesthesia [37,38]. Intraoperative hypothermia is associated with several complications. Hypothermia significantly increases the risk of surgical wound infection. Multiple studies have demonstrated that hypothermia impairs bacterial resistance and wound healing, likely through both direct suppression of immune function and indirect effects caused by thermoregulatory arteriovenous vasoconstriction, which reduces local tissue perfusion [39,40]. Moreover, hypothermia impairs platelet function and inhibits the enzymatic activity within the coagulation cascade, leading to coagulopathy, increased blood loss, and increased greater transfusion requirements [41-43]. Neuromuscular blockade is prolonged during hypothermia: the duration of action for agents such as vecuronium and atracurium is extended when core temperature decreases by 2-3°C [44,45]. Furthermore, the pharmacokinetics of anesthetics are altered: plasma concentrations of propofol may increase by approximately 30% with a 3°C drop in core temperature, and the minimum alveolar concentration for volatile anesthetics decreases [45,46]. Collectively, these effects contribute to prolonged anesthetic recovery times and extended hospital stays [47]. Mild hypothermia increases the risk of adverse cardiac complications [48,49]. This is thought to result from sympathetic activation and elevated levels of catecholamine and cortisol, leading to an increased heart rate and a mismatch between myocardial oxygen supply and demand [50]. In addition to these major complications, intraoperative hypothermia can exacerbate minor outcomes, such as thermal discomfort and postoperative shivering [9].

Various strategies are required to maintain perioperative normothermia in geriatric patients (Table 3). Accurate monitoring of core temperature is essential for maintaining intraoperative normothermia. To reliably reflect core body temperature, measurements should be obtained from well-perfused and thermally stable sites. Although pulmonary artery temperature monitoring provides the most accurate measurement, its invasiveness limits its routine use. Therefore, distal esophageal, tympanic membrane (with a contact thermistor or thermocouple), and nasopharyngeal temperature monitoring are considered appropriate and reliable alternatives [51]. Other sites, such as the sublingual area, rectum, skin, axilla, and urinary bladder, are used but are more susceptible to external factors. Thus, caution should be exercised if the temperature is outside the normal range [52]. Numerous recent trials have demonstrated relatively good agreement between zero-heat-flux (ZHF) thermometers and conventional devices for measuring the reference core temperature [53-57]. Although the ZHF thermometer is a skin-surface device, it reflects the temperature of the deep forehead and offers the advantages of being noninvasive, providing an acceptable estimation of the core temperature, and enabling continuous monitoring. Monitoring the distal esophageal temperature is particularly challenging during regional or neuraxial anesthesia, and there are limited options for continuous core temperature measurement in these settings. Therefore, the ZHF thermometer may serve as a valuable tool for reliably estimating the core temperature in geriatric patients undergoing regional or neuraxial anesthesia. Previous guidelines recommend temperature monitoring at least every 30 min during surgery and every 15 min in the recovery room [37,38]. However, the use of a ZHF thermometer enables non-invasive and continuous near-core temperature monitoring, allowing for the implementation of more proactive hypothermia prevention strategies in geriatric patients who are more vulnerable to perioperative hypothermia.

Effective intraoperative thermal management requires a multimodal approach. The previous guidelines recommended maintaining a patient temperature of at least 36.0°C. However, a recent study suggested that maintaining intraoperative core temperatures above 35.5°C may also be acceptable [58]. This study reported no significant differences in major outcomes such as myocardial injury after non-cardiac surgery, non-fatal cardiac arrest, 30-day mortality, surgical site infection, or transfusion requirements between patients actively warmed to 37.0°C and those maintained at 35.5°C. Subgroup analyses demonstrated no significant differences in outcomes among patients aged ≥ 65 years. Nevertheless, minor outcomes such as postoperative shivering remain a concern, and further attention to these aspects is warranted when determining intraoperative temperature management strategies.

Controlling the ambient temperature of an OR is critical because it is one of the most influential factors for preventing heat loss. An ambient temperature of at least 21°C is recommended, with temperatures above 24°C advised for pediatric surgeries [37,59]. Previous study has demonstrated that maintaining an OR temperature of 26°C significantly reduces the incidence of intraoperative hypothermia and complications [39].

Active warming devices such as heating mattresses and forced air warming systems directly transfer heat to patients [60,61]. Heating mattresses placed beneath the patient are less effective because of the insulation properties of the operating table and carry an increased risk of pressure-related injuries and burns [62,63]. In contrast, forced-air warming blankets combine passive insulation with convective heat transfer at the body surface, offering a more effective method of maintaining body temperature [61,64,65]. Recent meta-analyses support the use of forced-air warming as a highly effective modality [66-68]. Previous guidelines recommend the application of forced-air warming in patients who have anesthesia for more than 30 min or less than 30 min if they are at a higher risk of inadvertent perioperative hypothermia [37,38]. The guideline defined the high risk of hypothermia as American Society of Anesthesiologist grade II to V, preoperative temperature < 36.0°C, combined general and regional anesthesia, major surgery, and risk of cardiac complications. However, geriatric patients are at high risk of developing hypothermia because they are vulnerable to perioperative hypothermia. Passive insulation using blankets or surgical drapes can reduce the exposed surface area and create an insulating air layer between the patient and the covering material [37,69,70]. The type or material of covering did not significantly affect the insulation efficiency, and simply increasing the number of layers did not proportionally enhance the warming effect. Thus, reducing the exposed surface area is key factor. Recently, self-heating blankets have gained popularity as warming devices. According to a recent meta-analysis, self-heating blankets were reported to be as effective as forced-air warmers in preventing hypothermia [71]. Given that they do not require complex equipment for warming, they offer the advantage easy application, particularly for geriatric patients

Other supportive measures include airway gas heating and humidification, as well as warming of intravenous fluids [72,73]. Although warmed fluids cannot actively transfer heat, fluid warming is essential to prevent hypothermia when administering large volumes or during transfusion [2,72,74]. One unit of refrigerated blood or 1 L of unwarmed fluid decreases mean body temperature by approximately 0.25°C and finally increases the risk of hypothermia [75]. Therefore, the guidelines recommend warming intravenous fluids or blood products to 37°C when administering volumes greater than 500 ml/h, and suggest that irrigation fluids should be warmed to 38-40°C [37].

Active warming strategies are effective intraoperatively and during the preoperative and postoperative periods. Preoperative warming (prewarming) aims to increase peripheral heat content and temperature, thereby reducing the core-to periphey temperature gradient and minimizing redistribution hypothermia during the first hour after anesthesia induction [76-78], and even 10-20 min of prewarming was effective in preventing hypothermia [79,80]. Although studies have confirmed the benefits of prewarming in geriatric patients, a previous study suggested that its effectiveness may be relatively limited compared to that in younger patients [81]. This finding indicates that meticulous thermal management is particularly important in geriatric patients. Postoperative warming is less effective than intraoperative warming because vasoconstriction associated with emergence and postoperative pain inhibits peripheral-to-core heat transfer. Nevertheless, postoperative warming remains important for improving the thermal comfort of patients and reducing the incidence of postoperative shivering [37,82].

This review has certain limitations. Research focusing exclusively on temperature management in geriatric patients remains limited and no specific guidelines are currently available. Therefore, further studies targeting this population are warranted. With the ongoing development of various temperature monitoring tools, continued evidence of their clinical utility is essential. Given the importance of continuity in temperature management, the relative lack of emphasis on post-warming strategies compared with prewarming and intraoperative measures highlights the need for further investigation in this area. Despite recent advancements in temperature management, geriatric patients remain at increased risk of intraoperative hypothermia owing to their intrinsic physiological vulnerabilities. Comprehensive, multimodal temperature management strategies tailored to this population are essential for improving surgical outcomes and minimizing perioperative hypothermia-related complications.