Emergency and critical care patients presenting to a veterinary hospital commonly exhibit significantly abnormal core temperatures. While variances are sometimes primary in nature, they are often secondary to disease processes or clinical syndromes and may be part of a series of life-sustaining compensatory mechanisms. Patients admitted into the hospital wards and intensive care units (ICUs) are also frequently at risk of temperature variations. While thermoregulatory control is widely discussed in veterinary nursing concerning patients undergoing anaesthesia, there is less emphasis on critical patients. In these cases, it is essential for the veterinary nurse (VN) to not only understand normal thermoregulatory homeostasis but also to consider how to appropriately correct these disturbances without causing further harm. This review aims to equip VNs with the foundational knowledge to pre-empt and recognise thermoregulatory abnormalities in critical canine and feline patients, understand the underlying physiology, and become confident in addressing these changes within the scope of their role in practice while also considering the associated risks.
Thermoregulation
In endothermic mammals, temperature is controlled by the thermoregulation centre in the anterior chamber of the hypothalamus. The hypothalamus in the brain acts as the body's ‘thermostat,’ setting the normal temperature range (Todd, 2023). This has inspired temperature control systems in building engineering, which can be beneficial when learning by considering their frameworks in a similar way (McCafferty et al, 2018). The predetermined temperature is the range within which the body can maintain normal metabolic function, and it varies significantly among different species based on their respective metabolic demands. Essentially, mammals require thermoregulatory homeostasis to maintain optimal function of body systems and essential chemical processes necessary for survival. The body communicates its temperature through a network of nerve cells from peripheral and central thermoreceptors. Peripheral thermoreceptors are located in the skin and muscles, where they sense surface and peripheral temperatures, allowing for a rapid response to environmental changes (McCafferty et al, 2018; Mota-Rojas et al, 2021; Todd, 2023). Central thermoreceptors are distributed throughout the central system in the viscera and skeletal muscle (McCafferty et al, 2018; Mota-Rojas et al, 2021). These receptors monitor temperature and transmit afferent signals to the hypothalamus via the spinal cord and midbrain to identify abnormalities (Mota-Rojas et al, 2021). In response, the hypothalamus triggers efferent drives to normalise the temperature through a variety of mechanisms within the central nervous system (CNS). While peripheral temperatures can fluctuate significantly, core temperatures should remain stable (Todd, 2023). Thermoregulatory adaptations are broadly categorised as behavioural or physiological (McCafferty et al, 2018).
Behavioural adaptive mechanisms
Behavioural thermoregulation wholly depends on voluntary decisions (Mota-Rojas et al, 2021). Afferent signals relay a change in temperature, and the patient must then decide to seek out warmer or cooler areas. This uses the methods of conduction (direct) and radiation (indirect) to transfer heat to or from another object.
Physiological adaptive mechanisms
Physiological thermoregulation is largely involuntary and encompasses autonomic responses to generate or dissipate heat. Subtle adaptations can occur, such as skin control of water loss and piloerection, or more significant adaptations can be induced, such as cutaneous vasomotor adjustments that bring blood vessels closer to the surface of the skin, where heat can dissipate through radiation more efficiently (Kleftouri et al, 2017; Mota-Rojas, 2021; Todd, 2023). Contrary to popular belief, canines and felines do possess sweat glands that can be activated, but they are not particularly effective in evaporative cooling because of their limitations (Verena et al, 1994). Instead, other methods, like evaporation, are used to manage rising temperatures, such as salivation. This is complemented by panting, which employs convection via air from the respiratory tract to dissipate heat (Mota-Rojas et al, 2021). Sympathetic changes may be triggered during thermoregulatory stress, resulting in adjustments to vasomotor tone that use blood vessels as conduits to transport warm blood where it is prioritised (Oncken et al, 2001; Kleftouri et al, 2017). In cases of hypothermia, vasoconstriction redirects warm blood to the central circulation, sustaining vital organ function, whereas, during hyperthermia, vasodilation redirects warm blood toward the periphery for active heat dissipation from the skin. In humans, exercise serves as a voluntary mechanism for heat production, whereas other mammals depend on involuntary mechanisms. Activation of the shivering reflex can generate heat through muscle contraction (Mota-Rojas et al, 2021). Metabolism produces heat as a byproduct, making hormone levels that directly influence the basal metabolic rate essential for thermoregulation. An increase in the release of thyroxine, adrenaline, noradrenaline, and corticosteroids will promote further heat production, while a decrease will limit it (Kleftouri et al, 2017). The hypothalamus may also signal the pancreas to reduce insulin secretion, allowing for greater availability of glucose to meet higher energy demands during compensatory thermoregulation (Mota-Rojas et al, 2021).
Physiological effects of hypothermia
Hypothermia in canines and felines can be defined as a temperature below 37°C that is primary or secondary in nature (Todd, 2023). Primary hypothermia occurs with exposure to a cold environment. Secondary hypothermia is triggered because of disease, clinical syndromes, toxicity, drug administration, or ongoing recumbency. Small, underweight, paediatric and senior patients are at a higher risk because of the lack of thermoregulatory mechanisms, increased surface area to mass ratios, lack of insulation fat or inadaptability. Clinical signs linked to hypothermia levels vary depending on whether it is a primary cause or a secondary cause. Primary causes allow temperatures to drop much lower (below 32°C) before life-threatening changes impact the cardiovascular, respiratory and neurological body systems. This is considered to be because of the patient being able to compensate well until this point (Oncken et al, 2001; Todd, 2023). Many emergency and critical care patients will present with secondary hypothermia because of their primary problem list. During periods of mild secondary hypothermia (36.7°C-37.7°C), clinical signs are relatively normal or there may be evidence of an early compensatory increased heart rate (Oncken et al, 2001). In moderate cases (35.5°C–36.7°C), patients may display neurologically dull mentation and late compensatory cardiovascular changes such as severely increased heart rate in canines and bradycardia in felines as well as peripheral vasoconstriction (Oncken et al, 2001). In severe cases (33°C–35.5°C), patients may no longer be able to compensate which leads to bradycardia, hypotension and respiratory depression (Oncken et al, 2001). In profound cases (<33°C), patients become moribund (Oncken et al, 2001) and when temperature drops below 31°C, thermoregulation may cease completely. As hypothermia progresses, arrhythmias may occur from a decrease in myocardial conduction and respiratory drive may become compromised from lack of carbon dioxide production in lower states of cellular metabolism (Todd, 2023). Acid base changes can occur from respiratory and metabolic changes and decreased buffer and hydrogen ion regulation. Platelet production and coagulation factor function may be disrupted (Todd, 2023), but interestingly, in-house coagulation testing such as prothrombin time and activated partial thromboplastin time may return normal results because of the machines rewarming the blood. While impairment of immune responses may also be seen, it has not been evidenced in mild cases (Todd, 2023).
Physiological effects of hyperthermia
When discussing hyperthermia, it is crucial to distinguish whether the patient is truly hyperthermic or pyrexic, as the underlying causes and recommended treatments differ significantly.
Non-pyrogenic hyperthermia
Hyperthermia is classified as a temperature exceeding the normal range (>39.2°C) (Newfield, 2019). It can occur in a manner similar to hypothermia, either as a primary or secondary cause. Primary causes of hyperthermia typically occur as a result of patients being exposed to high temperatures. Secondary causes are equally common, making it essential to consider hyperthermia in patients who have risk factors for increased heat production (for example, seizures or tremors), high metabolic energy demand (for instance, excessive exercise), or ineffective heat loss mechanisms (such as respiratory compromise). Hyperthermia has significant effects on organ function and cellular health. Cytokines are produced in response to hyperthermia as a form of cytoprotection; however, if this response becomes excessive, it can lead to systemic inflammatory response syndrome (SIRS), progress to disseminated intravascular coagulation (DIC) and ultimately result in multiple organ dysfunction syndrome (MODS) (Newfield, 2019; Miller, 2023). As temperature rises, so does cell metabolism and oxygen consumption. Temperatures above 41.6°C can result in these increases surpassing the normal delivery of oxygen, leading to inadequate cellular function and integrity. Hypoxic ischemic damage can onset gastrointestinal mucosal sloughing, ventricular arrhythmias, and impairment of renal and hepatic system function (Newfield, 2019). Exertional heat stroke and malignant hyperthermia may trigger rhabdomyolysis and consequent renal damage (Miller, 2023). Temperatures exceeding 43°C could result in brain cell death (Newfield, 2019). All organs are susceptible to thermal damage, poor perfusion, metabolic abnormalities and haemorrhage.
Pyrogenic hyperthermia
Pyrexia is commonly known as a fever A true fever can be induced by exogenous causes such as bacterial toxins, drug administration, or neoplasia. This leads to the release of endogenous pyrogens, such as cytokine activation and immune responses (Miller, 2023), or in primary immune-mediated diseases, the cause can be endogenous alone. When the patient is exposed to one of the above, cytokines travel to the hypothalamus and bind to endothelial cells, leading to the production of prostaglandin E2 (PGE2) (Miller, 2023). PGE2 causes the thermoregulatory cells to increase their set point through various mediators, tricking the body's thermostat into thinking that a higher temperature is normal. Normally, fevers will not reach temperatures high enough to risk the same life-threatening complications as hyperthermia (Miller, 2023).
Temperature monitoring can be conducted using rectal probes, axillary or inguinal thermometers, or infrared ear thermometers. Rectal probes are considered the most accurate and reliable in critical patients. In contrast, axillary, inguinal or ear thermometer measurements may underestimate core temperature, particularly in shock or hypoperfused states.
Interventions
Passive vs active
When critical patients are unable to maintain their own body temperatures, intervention may be necessary to prevent the physiological consequences described earlier. While discussing active warming and cooling techniques with clinicians is important as part of a patient's individualised treatment plan, implementation is typically carried out by the VN. Warming and cooling techniques can generally be divided into two groups: passive or active. Passive techniques focus on maintaining body temperature by preventing further heat loss or gain. Passive warming may include using blankets, bubble wrap, baby booties, clothing and foil blankets. Passive cooling is limited and primarily involves avoiding inadvertent warming and regulating normothermic environmental conditions. Active techniques use an external source for heating or cooling. Active warming may involve forced warm air, heated blankets, hot water bottles, or heat mats. Active cooling may include the application of tepid water, fans, cold surfaces or internal cooling (Todd, 2023; RECOVER Initiative, 2024). In critical and emergency situations, especially with patients who have comorbidities, the issue of active warming and cooling becomes more complex, as professionals must consider primary causes and subsequent compensatory mechanisms that influence thermoregulation. As always, weighing risks versus benefits should be paramount in veterinary professionals' considerations regarding approach and should be tailored to each individual patient's needs.
Addressing hypothermia in the emergency presentation phase
As described earlier, patients may present as hypothermic for a variety of reasons. If the primary cause is hypothermia, the obvious treatment is warming. In cases of secondary hypothermia, further precautions may be necessary to prevent harm. Passive warming techniques can be used to reduce heat loss and insulate any heat generated by the patient. In moderate to severe cases, active warming techniques should be implemented. The use of forced-air machines (such as the 3M Bair Hugger) is effective and minimises the risk of thermal injury compared to heat pads or hot water bottles (Todd, 2023).
Surface warming causes peripheral vasodilation, which can lead to relative hypovolaemia and subsequent hypotension, referred to as rewarming shock. Severe cases may occur in patients that are already hypotensive. If patients present in the compensatory phase of hypovolaemic shock, rewarming shock can reverse protective vasoconstriction, where blood is prioritised to the vital organs. Redistribution of perfusion peripherally can lead to ischaemic injury in hypoperfused organs, potentially causing irreversible damage. To reduce the likelihood of rewarming shock, hypovolaemic resuscitation should be prioritised before active warming is initiated.
The long-term impact of the rewarming shock is an under-researched aspect of critical care, but studies have found evidence of diminished contractile behaviour of cardiac myocytes, as well as clinical observations of ventricular dysfunction and impaired sympathetic cardiovascular control in rats (Schaible et al, 2016; Dietrich et al, 2018). Blood rapidly circulated from the hypoperfused periphery also carries the risk of transporting lactic acid, leading to rewarming acidosis (Quandt, 2018; Todd, 2023). This highlights the importance of assessing the primary cause of hypothermia, particularly in patients with evidence of vasoconstriction. If hypovolaemia is the cause, addressing the deficit should, in turn, reverse vasoconstriction with associated clinical improvements, including temperature regulation.
As cold peripheral blood re-enters the central circulation, core body temperature can drop even after an initial increase. This phenomenon, known as ‘after drop’, explains why some patients appear to ‘relapse’ into hypothermia once warming techniques are ceased. ‘After drop’ is defined as the continued decrease in core body temperature following warming (Mazzaferro, 2007). For this reason, close monitoring is recommended after discontinuation of warming.
Another important consideration is metabolic disease. Mild to moderate hypothermia can occur in cases of severe metabolic disease as a protective mechanism, reducing energy expenditure and oxygen demand to conserve energy for vital systems (Oncken et al, 2001). In patients with compromised metabolic ability or increased metabolic demand, warming can exacerbate perfusion deficits. When active warming is required to achieve normothermia, it should be concentrated over the central trunk—abdomen and thorax—to reduce risks associated with the phenomena. Peripheral warming is not recommended in these cases.
Preventing and addressing hypothermia in the hospitalised critical care patient
Patients in the ICU are often immobile because of physical or medical restrictions, which can result in hypothermia ranging from mild to severe. Examples include cases of snake envenomation, trauma and oxygen supplementation. While some patients may be taken out for regular walks, all ICU patients experience some level of restriction, requiring kennel confinement, which reduces movement and, therefore, heat production. Passive warming techniques should be considered to minimise heat loss, alongside the use of an appropriate room thermostat system for environmental control. This is particularly important for patients more susceptible to hypothermia, such as paediatric, senior, small or underweight animals (Figure 1), those with metabolic disease or those that have been significantly shaved (eg for tick paralysis treatment, surgery or ultrasound).
Ava, a 2.6 kg toy breed canine ICU patient who has passive warming implemented to avoid heat loss.
High-level critical patients may require sedation or anaesthesia as part of their treatment plan, such as those with status epilepticus, brachycephalic obstructive airway syndrome, laryngeal paralysis, tick paralysis or those requiring mechanical ventilation. In some cases, sedation or anaesthesia may be necessary for multiple days. It is essential to consider thermoregulation before hypothermia develops. When anaesthetic drugs are administered, body temperature has been reported to decrease rapidly by more than 1°C in the first hour, followed by a slower linear decrease over the next 2 hours before stabilising (Mazzaferro, 2007; Quandt, 2018). This occurs because of the vasodilatory effects of drugs, suppression of the hypothalamic thermoregulatory mechanisms and heat loss via intubation and breathing circuits (Mazzaferro, 2007; Todd, 2023).
Passive warming should be initiated early in normothermic or very mildly hypothermic (37.0–37.7°C) patients because of the expected temperature drop. Comfortable, warm bedding that wicks fluid away from the patient should also be considered for recumbent patients. Preventing hypothermia in these cases is significantly easier than correcting it.
For intubated patients, a heat and moisture exchange (HME) filter at the end of the endotracheal tube can be beneficial. These devices are designed to capture heat and moisture on exhalation, returning it to the respiratory tract on inhalation, thereby reducing heat loss.
If passive techniques are ineffective and more significant hypothermia occurs (<37°C), active warming measures should be considered unless contraindicated. Forced-air warming should be prioritised if available, as it reduces the risk of thermal burns, which can occur when patients are unable to move away from heat sources such as heat pads or hot water bottles. The HotDog warming blanket system includes built-in temperature sensors for monitoring and control, evenly distributing heat to minimise the risk of burns. These blankets can be positioned under, around or over patients. While they incur a purchase cost for the clinic, they provide a safer option for recumbent patients compared to standard heat pads or hot water bottles. Patients undergoing active warming should be closely monitored to avoid iatrogenic hyperthermia.
In some critical care patients experiencing prolonged hypotension, the potential metabolic benefits of hypothermia have been considered. In a normothermic state, the brain can sustain 5 to 6 minutes of ischaemia, with this time doubling for every 5°C reduction in temperature (Kleftouri et al, 2017). Therapeutic hypothermia, where hypothermia is induced as a protective measure for organs, is widely used in human medicine (Otto, 2015). While it is not practical to induce therapeutic hypothermia in veterinary patients, short periods of naturally occurring hypothermia may provide cardiac and neuroprotection against ischaemia until perfusion can be restored (Oncken, 2001). This may be relevant in cases of reduced blood flow to the heart and brain, such as post-cardiac arrest or severe hypotension caused by haemorrhage.
Evidence regarding the optimal rewarming rate in these cases is limited. However, slower rewarming rates appear to be preferable, with recommendations suggesting an increase of <1°C per hour (Smarick et al, 2012; RECOVER Initiative, 2024).
Preventing hyperthermia in the emergency and critical care patient
Because of the nature of emergency medicine, patients are at a heightened risk of increased stress, which can elevate energy requirements and myocardial oxygen demand (Waddel and King, 2018). Patients may exhibit physical movement, body language changes, panting or sympathetic nervous system responses such as fight, flight or freeze reactions. This increases heat generation, and if thermoregulatory responses are impaired, hyperthermia can rapidly develop. Hyperthermia is often observed in patients with upper airway obstruction, as insufficient airflow over the tongue during panting reduces the capacity for heat loss via evaporation (Waddel and King, 2018). Brachycephalic patients are at particularly high risk because of their conformation.
For these patients, early identification and appropriate prescription of anxiolytics or sedatives by the veterinarian is essential. In dyspnoeic patients, sedation is often the second priority after oxygen provision, not only for hyperthermia prevention but also to reduce myocardial oxygen demand.
A key consideration in hyperthermia management is the use of oxygen cages. Ideally, specialised ICU units should be used, as these allow for precise control of both temperature and humidity, reducing the risk of iatrogenic hyperthermia, which can develop rapidly. If specialised units are not available, other techniques, such as ice packs and adequate ventilation, should be implemented. Oxygen cages must have a method for measuring temperature and humidity to allow for continuous monitoring. Tight-fitting masks and makeshift oxygen tents using an Elizabethan collar can have similar hyperthermic effects, so alternative oxygen supplementation techniques should be considered for hyperthermic patients.
Addressing hyperthermia in the emergency patient
In patients that are hyperthermic on arrival, unless the cause is pyrogenic, the treatment approach remains the same. Pharmacological interventions have not been evaluated as effective, so active cooling—utilising the same mechanisms as the body's natural defences—should be implemented and has been widely assessed as effective (Drobatz, 2023). Whole-body cooling is recommended for patients with a rectal temperature over 40°C, as permanent organ damage and death can occur at temperatures exceeding 41.6°C (Miller, 2023). The aim should be gradual cooling to prevent damage to the hypothalamus due to cerebral swelling (Newfield, 2019). Stress levels should also be considered, and sedatives prescribed if indicated.
Tepid water should be used to wet the patient's whole body to facilitate evaporative cooling. Cold water is not recommended due to vasoconstrictive responses. While cold-water immersion is used in human medicine, it requires simultaneous muscle massage to maintain peripheral circulation and prevent paradoxical vasoconstrictive cooling inhibition (Drobatz, 2023). Towels can be used to wet the patient but should not be left in place, as this traps heat and worsens hyperthermia. Fans can be used to enhance convection and assist with evaporation via tepid or room temperature water’ as room temperature will be lower than the patient's temperature, but not cold (Todd, 2023; RECOVER Initiative, 2024).
Conduction techniques, such as contact with cold metal surfaces like examination tables, can also be used, but care should be taken to prevent water pooling beneath the patient, where it can quickly warm. The use of wet tables with metal grates is effective in preventing this and allows airflow beneath the patient. Alcohol is not recommended due to toxicity risks and fire hazards if defibrillation is required (Newfield, 2019; Drobatz, 2023). Shaving is also not recommended, as the associated stress often outweighs the potential benefits.
Internal cooling techniques, including cold gastric lavage, perineal lavage or enemas, have not demonstrated a clear advantage and carry risks such as aspiration, septic peritonitis and perforation (Newfield, 2019; Drobatz, 2023). The veterinarian may prescribe fluid therapy to support perfusion, correct dehydration, and address acid-base derangements and hypovolaemia. However, there is no evidence to support its effectiveness as a cooling method. Because of the high metabolic and oxygen demands associated with hyperthermia, oxygen supplementation may be beneficial for some patients.
Temperature should be closely monitored throughout active cooling, and measures should be discontinued before normothermia is reached, with a recommended cessation point of 39.4°C (Miller, 2023). This helps prevent rebound hypothermia, as temperature can continue to decrease after cooling has stopped. If rebound hypothermia occurs, there is a risk of irreversible hypothalamic damage and subsequent loss of thermoregulatory function, which is associated with a poor prognosis and increased risk of death (Newfield, 2019).
Addressing pyrexia in the emergency and critical care patient
Identifying pyrexia as the cause of hyperthermia is essential for appropriate treatment. This may be determined through history, diagnostic testing or a combination of both. As the hypothalamus perceives an elevated temperature as the new normal, active cooling in these patients triggers a compensatory response, increasing metabolic demand in an attempt to restore the higher set point. Patients with a fever often feel cold even when their body temperature is elevated, and active cooling can cause significant discomfort. In a human study, pyrogenic hyperthermia was induced, and active cooling resulted in increased oxygen consumption and reported physical discomfort (Cannon, 2013).
For this reason, active cooling is only recommended in pyrexic patients when the temperature exceeds 41°C and there is a risk of neurological or organ dysfunction (Newfield, 2018). Instead, treatment should be directed at addressing the primary cause of the pyrogenic response.
Conclusion
This review highlights the variable nature of emergency presentations and critical cases in veterinary medicine, emphasising the need for a thorough understanding of thermoregulatory pathophysiology. This knowledge enables veterinary professionals to recognise abnormalities, assess risk factors and respond appropriately without causing further harm to already compromised patients. While time is critical in emergency situations, taking a moment to consider the underlying causes of temperature variations allows for more informed decision-making, incorporating a risk-benefit analysis.
A lack of veterinary-specific research was identified regarding the benefits of therapeutic hypothermia, despite extensive literature on the subject in human medicine. Additionally, a research gap exists in relation to rewarming shock avoidance techniques, including evidence-based recommendations for rewarming temperatures, timeframes and the long-term physiological effects in veterinary patients that have experienced rewarming shock. Further research in these areas would be valuable in guiding future therapies within veterinary emergency and critical care.