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Shivering

Shivering is an involuntary physiological response involving rapid, rhythmic contractions of skeletal muscles that generate heat through inefficient ATP utilization, primarily to maintain core body temperature around 37°C when it drops below the hypothalamic set point.^[1] It is triggered mainly by cold exposure, where peripheral cold signals from skin thermoreceptors and spinal cord excite the shivering center in the dorsomedial hypothalamus while being inhibited by the warmer anterior hypothalamic-preoptic area.^[1] Beyond hypothermia, shivering—often manifesting as chills—can occur during febrile states due to pyrogenic signals like prostaglandin E2 elevating the body’s temperature set point, or in response to infections (viral, bacterial, or parasitic), post-anesthesia effects, emotional stress, or adrenaline surges.^[2]^[3] Physiologically, it increases metabolic heat production up to five times the basal rate,^[4] complementing mechanisms like vasoconstriction, but ceases in severe hypothermia below 29.4°C due to central nervous system depression.^[1] In clinical contexts, persistent shivering signals underlying issues like infections or trauma, warranting warming interventions for cold-induced cases or targeted treatments (e.g., antipyretics for fever) to address root causes.^[5]^[3]

Overview

Definition

Shivering is an involuntary physiological response characterized by rapid, rhythmic contractions and relaxations of skeletal muscles, primarily aimed at generating heat to maintain core body temperature. These contractions occur across multiple muscle groups, often involving the limbs, trunk, and jaw, and are triggered by the body's detection of cold stress or other thermoregulatory imbalances. Unlike deliberate actions, shivering involves alternating bursts of muscle activity without conscious control, distinguishing it as a reflexive mechanism rather than a coordinated voluntary movement.^[3]^[6]^[7] The oscillations during shivering typically occur at frequencies of 8-10 Hz, as measured through electromyographic (EMG) analysis. This rhythmic pattern contrasts sharply with sustained voluntary contractions, which lack the oscillatory nature and are initiated by higher cortical centers for purposeful tasks, or with pathological tremors such as those in Parkinson's disease, which are lower frequency (4-6 Hz) and irregular. Shivering is also distinct from epileptic seizures, which arise from abnormal hypersynchronous neuronal discharges in the brain, often leading to loss of consciousness, tonic-clonic convulsions, or postictal states, whereas shivering remains a coordinated, heat-producing response without neurological disruption.^[8]^[9]^[10] Descriptions of shivering as a thermoregulatory phenomenon first appeared in 19th-century medical literature, particularly in studies of hypothermia and cold exposure, where it was noted as a symptomatic response to environmental chilling. For instance, an 1859 case report detailed a patient exhibiting shivering alongside confusion and poor attention after snowstorm exposure, highlighting its role in early understandings of body temperature regulation. Shivering frequently accompanies chills, serving as the primary muscular component of this broader response; while chills encompass subjective sensations of cold, piloerection (goosebumps), and peripheral vasoconstriction to conserve heat, shivering specifically denotes the oscillatory muscle activity that elevates metabolic rate for warmth production.^[11]^[12]

Physiological Role

Shivering serves as a key mechanism in shivering thermogenesis, a process that generates heat through the rapid, involuntary contractions of skeletal muscles, primarily via the hydrolysis of ATP to ADP and inorganic phosphate, which dissipates energy as heat rather than mechanical work.^[13] This contrasts with non-shivering thermogenesis, which occurs predominantly in brown adipose tissue (BAT) through uncoupled mitochondrial respiration mediated by uncoupling protein 1 (UCP1), allowing for heat production without muscle activity.^[14] In mammals, shivering thermogenesis activates when environmental cold challenges core body temperature, elevating the whole-body metabolic rate by 2- to 5-fold above basal levels, depending on the intensity and duration of exposure.^[15]^[16] The physiological integration of shivering occurs via the hypothalamic thermoregulatory center, particularly the preoptic area and posterior hypothalamus, which coordinates responses to cold signals from peripheral thermoreceptors.^[17] Shivering emerges as a short-term, high-capacity heat-generating response when BAT-mediated non-shivering thermogenesis proves insufficient to maintain thermal homeostasis, such as during acute cold stress or in adults with limited BAT activity.^[18] This hierarchical activation ensures efficient energy allocation, with shivering providing rapid compensation until behavioral adaptations or longer-term physiological adjustments take effect. During intense shivering, energy expenditure can reach approximately 100-200 kcal per hour in humans, accounting for a substantial portion of total heat production and primarily fueled by glycogenolysis in skeletal muscles, which supplies glucose for anaerobic and aerobic metabolism.^[19] Muscle glycogen serves as the dominant carbohydrate source, supplemented by blood glucose and fatty acids, enabling sustained thermogenesis but potentially leading to fatigue if prolonged.^[13]^[20] Evolutionarily, shivering represents a conserved thermoregulatory mechanism across homeothermic animals, including mammals and birds, enabling survival in cold environments by preventing hypothermia and supporting metabolic processes at optimal temperatures.^[21] This ancient adaptation likely predates the divergence of endothermic lineages, providing a reliable, muscle-based strategy for heat generation that complements more specialized traits like insulation or BAT.^[22]

Mechanisms

Neural Control

The neural control of shivering begins in the preoptic area of the hypothalamus, which serves as the primary integrator of thermal signals for thermoregulation. Cold-sensitive neurons in this region detect decreases in core body temperature through inputs from peripheral thermoreceptors expressing transient receptor potential melastatin 8 (TRPM8) and ankyrin 1 (TRPA1) channels, which are activated by innocuous and noxious cold, respectively. These signals, relayed via the spinothalamic tract and lateral parabrachial nucleus, indicate that core temperature is below the hypothalamic set point of about 37°C, initiating shivering when core temperature falls approximately 0.5–1°C below this threshold, though this can vary by 1–2°C depending on individual variability and environmental factors. Warm-sensitive neurons in the medial preoptic area tonically inhibit shivering pathways under normothermic conditions, but cold exposure disinhibits these circuits, activating downstream effectors for heat production.^[23]^[24]^[25] Shivering is executed through brainstem and spinal cord circuits that generate rhythmic motor patterns. The dorsomedial hypothalamus activates premotor neurons in the rostral raphe pallidus nucleus of the medullary raphe nuclei, which project via reticulospinal tracts to alpha motor neurons in the spinal cord's ventral horn. These connections produce oscillatory bursts of activity, synchronizing skeletal muscle contractions at frequencies of approximately 8–12 Hz to maximize heat generation without excessive fatigue. Gamma motor neurons, co-activated by these pathways, maintain muscle spindle sensitivity during the tremors, ensuring coordinated recruitment of motor units across antagonist muscle groups. This central pattern generation in the brainstem allows shivering to persist as an automatic reflex even under partial spinal anesthesia.^[24]^[26] Autonomic modulation by the sympathetic nervous system enhances the intensity and efficiency of shivering. Activation of sympathetic preganglionic neurons in the intermediolateral cell column, driven by hypothalamic inputs, releases norepinephrine onto beta-adrenergic receptors in skeletal muscle, potentiating contractility. Sympathetic activation, through co-transmitters like ATP, can enhance shivering intensity and thermogenesis, increasing glycogenolysis and metabolic rate in muscles.^[27]^[28] Proprioceptive feedback mechanisms prevent overstimulation and fatigue during prolonged shivering. Muscle spindles, via Ia afferent fibers, detect length changes and provide excitatory input to alpha motor neurons through the stretch reflex arc, while Golgi tendon organs sense excessive tension and trigger inhibitory Ib afferents to suppress motor output via interneurons in the spinal cord. This negative feedback loop modulates shiver amplitude and frequency, protecting against muscle damage and allowing sustained thermogenesis for hours in cold exposure.^[24]^[29]

Muscular and Metabolic Processes

Shivering involves the recruitment of skeletal muscle fibers, primarily fast-twitch type II fibers, which undergo asynchronous contractions to generate heat without producing significant mechanical work. These contractions predominantly occur in large muscle groups around the torso and proximal limbs, such as the trunk and leg muscles, while sparing fine motor areas like the hands and face to maintain essential functions.^[13]^[30] The metabolic basis of shivering centers on the hydrolysis of adenosine triphosphate (ATP) through the myosin-ATPase cycle during cross-bridge cycling in muscle fibers. This process couples ATP breakdown to actin-myosin interactions, where only about 20-25% of the energy is converted to mechanical work in typical contractions, with the remainder dissipated as heat; in shivering, since no external work is performed, nearly all energy from ATP hydrolysis contributes to thermal output.^[30]^[31] Heat production during shivering can be quantified using the basic equation for thermal energy:

Q = m \cdot c \cdot \Delta T

where Q is the heat generated, m is the mass of the body or affected tissues, c is the specific heat capacity of the body (approximately 3.0 kJ/kg·°C for humans, based on recent estimates), and \Delta T is the change in temperature. Through sustained shivering, this mechanism can raise core body temperature by approximately 0.5–1 °C per hour under moderate cold exposure, helping to counteract hypothermia.^[1]^[13]^[32] Shivering is limited in duration by fatigue mechanisms, including the buildup of lactic acid in fast-glycolytic fibers due to anaerobic metabolism, which leads to acidosis and impaired contractility, as well as calcium dysregulation from prolonged sarcoplasmic reticulum activity. These factors typically restrict maximal intense shivering to 1–2 hours before exhaustion sets in, after which heat production declines.^[30]

Causes

Thermal Triggers

Shivering is primarily triggered by a drop in either core body temperature or mean skin temperature, with the latter contributing approximately 20% to the control of the response in unanesthetized humans.^[33] The core temperature threshold for shivering onset typically occurs around 35.5–36.5°C, while significant peripheral cooling can independently initiate the thermogenic response by activating cold-sensitive afferents in the skin.^[34] Environmental factors like wind chill exacerbate this by enhancing convective heat loss from the skin, thereby accelerating the rate of temperature decline and hastening shivering onset compared to still air conditions.^[35] In the context of hypothermia, shivering intensity varies with the stage of core temperature reduction. During mild hypothermia (core temperature 32–35°C), shivering is most vigorous, serving as the primary mechanism to generate metabolic heat and counteract further cooling.^[4] As core temperature falls below 30–32°C in moderate to severe stages, shivering ceases due to neuromuscular exhaustion and impaired muscle function, leaving the body reliant on residual non-shivering thermogenesis or external warming.^[4] High-altitude environments impair shivering efficiency through hypoxia, which suppresses the metabolic intensity of the response and reduces overall heat production.^[36] Reduced oxygen availability limits aerobic capacity in skeletal muscles, diminishing the effectiveness of shivering thermogenesis despite cold exposure. Similarly, immersion in cold water dramatically accelerates heat loss via conduction and convection, removing heat from the body up to 25 times faster than exposure to air at the same temperature, thereby triggering shivering more rapidly and intensely.^[37] Among mammals, shivering efficiency is influenced by body size and the surface area-to-volume (SA/V) ratio, with larger species like humans exhibiting lower relative heat loss but reduced shivering efficacy compared to smaller mammals. Smaller mammals, possessing a higher SA/V ratio, experience greater passive heat dissipation and thus rely on more intense, proportionally higher metabolic rates during shivering to maintain euthermy.^[38] In contrast, humans' larger body mass results in a lower SA/V ratio, which conserves heat but limits the scalability of shivering-generated warmth relative to total body volume.^[39]

Non-Thermal Triggers

Shivering can be triggered by emotional states such as fear or anxiety, where surges in adrenaline (epinephrine) activate the sympathetic nervous system, leading to physiological responses that mimic the thermoregulatory shivering pathway. This activation involves the hypothalamus and brainstem nuclei, resulting in involuntary muscle contractions often described as "chills" or shakiness. For example, intense excitement, such as from listening to music, can evoke similar frisson responses with shivers down the spine due to reward-related neural activity in brain regions like the nucleus accumbens.^[40]^[41] Shivering frequently occurs during fever, where endogenous or exogenous pyrogens such as interleukin-1 and prostaglandin E2 act on the hypothalamus to raise the body's temperature set point. This results in thermoregulatory shivering (chills) to generate heat and achieve the elevated set point, commonly associated with infections including viral, bacterial, or parasitic.^[2]^[3] Metabolic disturbances unrelated to ambient temperature can also induce shivering by altering the body's thermoregulatory set point. In hypoglycemia, blood glucose levels below 3.5 mmol/L trigger counter-regulatory hormone release, including epinephrine and glucagon, which stimulate shivering as part of the autonomic response to restore energy balance. Similarly, thyroid storm—a life-threatening hyperthyroid crisis—disrupts metabolic homeostasis, lowering the effective thermoregulatory set point and provoking tremors and shivering alongside symptoms like fever and tachycardia.^[42]^[43] Pharmacological factors, including drug withdrawal and certain medications, represent another category of non-thermal triggers for shivering. Withdrawal from opioids, such as during abrupt cessation after chronic use, elicits a noradrenergic surge in the locus coeruleus, manifesting as flu-like symptoms including chills and shivering, often peaking within 24-48 hours. Stimulant withdrawal, as seen with amphetamines or cocaine, can similarly involve autonomic instability leading to shakiness, though less prominently than in opioid cases. Additionally, amphotericin B, an antifungal agent, frequently causes infusion-related rigors (intense shivering) in up to 70% of patients, attributed to cytokine release and prostaglandin synthesis rather than pyrogenesis.^[44]^[45]

Clinical Significance

In Hypothermia and Cold Exposure

Shivering serves as the body's primary thermogenic response during mild hypothermia, typically induced by prolonged cold exposure, where core body temperature drops to 32–35°C (89.6–95°F). This involuntary muscle activity generates heat through rapid contractions, helping to maintain vital organ function, but it demands significant metabolic energy, often leading to glycogen depletion and fatigue if the cold stress persists. As hypothermia advances, the initial vigorous shivering may intensify before exhausting the body's reserves, marking a critical transition to more severe stages where protective mechanisms fail. In severe hypothermia, below approximately 30°C (86°F), shivering typically ceases due to neuromuscular impairment, ushering in a phase of paradoxical undressing. This phenomenon, observed in about 25% of hypothermia fatalities, involves confusion and a paradoxical sensation of warmth, prompting victims to remove clothing and accelerate heat loss through behaviors like stripping or burrowing into snow.^[46] Such actions exacerbate core cooling, often resulting from hypothalamic dysfunction and impaired judgment, and have been documented in forensic analyses of cold-related deaths.^[47] During rewarming efforts, the afterdrop phenomenon can occur, characterized by a continued decline in core temperature despite external heating. This results from peripheral vasodilation, which mobilizes cold blood from the extremities to the central circulation, potentially dropping core temperature by 0.5–1°C and risking arrhythmias if not monitored.^[48] Experimental studies in mild hypothermia confirm this convective cooling effect, emphasizing the need for controlled rewarming to mitigate cardiac strain.^[48] Shivering exhaustion in untreated mild hypothermia contributes to metabolic acidosis and muscle fatigue, accelerating progression to moderate or severe stages with potentially fatal outcomes. While mild cases are generally survivable with intervention, untreated progression elevates mortality risks, with overall accidental hypothermia fatality rates reported around 10–50% depending on comorbidities and exposure duration.^[4] In vulnerable populations, this exhaustion phase heightens the likelihood of cardiac arrest or respiratory failure. Occupational cold exposure significantly amplifies hypothermia risks among outdoor workers, particularly in Arctic regions during the 2020s. A 2023–2024 survey of Arctic workers found that 33% often or always felt cold at work, with median daily exposure below 10°C exceeding two hours for many roles like power grid maintenance, correlating to elevated shivering episodes and hypothermia potential.^[49] Such statistics underscore a 75% prevalence of intermittent cold discomfort across sectors, heightening annual incident rates in extreme environments compared to temperate zones.

In Fever and Infections

Shivering plays a central role in the febrile response during infections and inflammatory conditions, where it serves as a mechanism to elevate body temperature to a newly reset hypothalamic thermoregulatory set point. Exogenous pyrogens, such as bacterial endotoxins, trigger the release of endogenous pyrogens including interleukin-1 (IL-1), which act on the hypothalamus to increase the set point, creating a sensation of cold despite normal or elevated core temperature. This mismatch prompts the activation of heat-generating responses, including shivering, to rapidly raise body temperature until equilibrium is reached at the higher set point.^[50]^[51]^[52] Cytokines such as tumor necrosis factor-alpha (TNF-α) and prostaglandin E2 (PGE2) further mediate and amplify the neural signals driving shivering during immune activation. TNF-α, released by macrophages in response to infection, enhances the production of PGE2 in the hypothalamus via cyclooxygenase-2 pathways, intensifying the pyrogenic signal and promoting sustained shivering to support the febrile state. This cytokine-mediated amplification is particularly pronounced in systemic infections, where it coordinates the thermoregulatory response to combat pathogen proliferation.^[53]^[54]^[55] In certain infections, shivering manifests as rigors—intense, coordinated episodes of muscle contractions that generate significant heat, typically lasting 15-30 minutes. Rigors are hallmark features in conditions like malaria, where cyclical release of parasites induces paroxysmal shivering followed by high fever, and in sepsis, where they signal rapid bacterial dissemination and cytokine storm. These episodes underscore shivering's role in the acute phase of infection, distinguishing it from milder thermogenic responses.^[56]^[57]^[58] Clinically, persistent shivering or rigors hold diagnostic value, often indicating a rising fever above 38.5°C and the need for early detection of underlying infections such as bacteremia. Their presence prompts targeted investigations like blood cultures, as they correlate with systemic inflammatory responses and higher risks of severe outcomes in febrile illnesses.^[59]^[58]^[50]

In Neurological and Other Disorders

In Parkinson's disease, basal ganglia dysfunction due to dopamine depletion often manifests as resting tremors that can be mistaken for shivering, particularly in the jaw where the rhythmic movements resemble slower shivering despite not being a true thermoregulatory response.^[60] These tremors affect approximately 70-80% of patients at some point in the disease course, with the enhanced oscillatory activity in basal ganglia-thalamo-cortical circuits contributing to the misperception.^[61] Distinguishing this from physiological shivering is crucial, as the tremor typically diminishes with voluntary movement or action, unlike cold-induced shivering.^[60] Multiple sclerosis involves demyelination that disrupts neural conduction in thermoregulatory pathways, leading to episodic, involuntary muscle contractions that mimic shivering bursts, independent of core body temperature. This dysfunction lowers the shivering threshold to around 31.8°C. Such symptoms arise from lesions in the hypothalamus or spinal cord, exacerbating fatigue and motor impairment during flares.^[62]^[63] Hyperthyroidism elevates basal metabolic rate through excess thyroid hormone (T3 and T4) production, which sensitizes beta-adrenergic receptors and increases catecholamine effects, often resulting in fine tremors that may be perceived as inappropriate shivering.^[64] These tremors, typically affecting the hands, face, or tongue, stem from heightened sympathetic activity rather than cold exposure, occurring in up to 90% of untreated cases and resolving with beta-blockers or antithyroid therapy.^[64] The metabolic acceleration disrupts normal homeostasis, occasionally leading to subjective sensations of chilliness or shakiness despite overall heat intolerance.^[64] Drug-induced shivering frequently arises from alterations in dopamine pathways, as seen with neuroleptics (antipsychotics) that block D2 receptors, provoking extrapyramidal symptoms including tremors resembling shivering in 20-30% of patients on typical agents.^[65] Lithium, used in bipolar disorder, similarly disrupts dopamine balance and can induce shivering, particularly in toxicity states (serum levels >1.5 mmol/L), where it combines with serotonergic effects to cause muscle rigidity and chills in moderate to severe cases.^[66] These reactions, often dose-dependent, require monitoring and dose adjustment to mitigate basal ganglia-like dysfunction without compromising therapeutic efficacy.^[65]

Variations in Populations

In the Elderly

In older adults over 65 years, the shivering response is blunted, with attenuated thermogenesis primarily due to sarcopenia, the age-related loss of skeletal muscle mass and function.^[67] This reduction impairs the ability to generate heat effectively, as shivering typically boosts metabolic heat production by 300-500% in younger individuals, but this capacity is significantly diminished in the elderly.^[67] Additionally, aging leads to decreased hypothalamic sensitivity to temperature changes, further compromising central thermoregulatory control and resulting in a less intense and delayed shivering initiation.^[67] Comorbid conditions such as diabetes and cardiovascular disease exacerbate these impairments by further disrupting vasoconstriction and promoting excessive heat loss. In type 2 diabetes, attenuated cutaneous vasodilation delays heat dissipation responses, while reduced sympathetic vasoconstrictor tone hinders conservation of body heat during cold exposure.^[68] Similarly, heart failure is associated with excessive baseline vasoconstriction and impaired vasodilatory capacity, leading to shivering fatigue and accelerated core temperature decline in cold environments.^[68] These factors collectively heighten vulnerability to hypothermia, with studies indicating that older patients face a substantially elevated incidence compared to younger adults, often linked to shivering cessation and rapid physiological deterioration.^[69] Postmenopausal women exhibit more pronounced alterations in shivering responses due to estrogen deficiency, which disrupts hypothalamic thermoregulatory set points. Estrogen loss narrows the thermoneutral zone—the range between heat loss and shivering thresholds—resulting in a higher mean body temperature at which shivering begins and increased thermal instability.^[70] This effect is particularly evident in women experiencing hot flashes, where the altered thresholds contribute to inefficient cold defense mechanisms and greater overall thermoregulatory inefficiency.^[70]

In Neonates and Children

Neonates exhibit immature thermoregulation, characterized by a limited capacity for shivering compared to adults, as their primary response to cold stress relies on non-shivering mechanisms rather than effective muscle-based heat production.^[71] This immaturity stems from underdeveloped neuromuscular systems, due to an immature neuromuscular system that prevents effective shivering. Neonates' limited glycogen stores in skeletal muscle and liver increase the risk of hypoglycemia and metabolic exhaustion during prolonged cold exposure.^[72] Prolonged cold exposure thus exacerbates energy depletion, increasing risks of hypoglycemia and metabolic exhaustion in the early postnatal period.^[71] In neonates, brown adipose tissue (BAT) predominates as the key site for non-shivering thermogenesis, mediated by uncoupling protein 1 (UCP1) in mitochondrial membranes, which dissipates the proton gradient to generate heat without ATP synthesis.^[73] This BAT-driven process, activated by sympathetic stimulation and norepinephrine, supplements or largely replaces shivering during the first months of life, when muscle mass and efficiency remain low.^[74] BAT depots, rich in UCP1 expression from late gestation and peaking around birth, can increase metabolic heat production up to approximately twice the basal rate through non-shivering thermogenesis, ensuring survival in cool environments before shivering matures.^[75]^[76] Premature infants born before 37 weeks gestation face heightened vulnerabilities, with significantly reduced heat production capacity—often 50% or less than term neonates—due to scant BAT (1-2% of body weight versus 4% in term infants) and immature enzyme systems for fatty acid oxidation.^[71] Additionally, sudden infant death syndrome (SIDS) has been linked to impaired thermoregulation during sleep, where failures in arousal responses may disrupt coordinated heat conservation and production, particularly in prone positioning or overheating scenarios.^[77] Developmental maturation occurs progressively, with shivering patterns becoming more adult-like by around 1 year of age, as BAT activity wanes and reliance shifts to voluntary muscle contractions supported by higher basal metabolic rates (1.5-2 times adult levels per kilogram).^[78]^[79] This transition enables sustained thermogenesis during cold exposure, reflecting gains in muscle mass, neural control, and energy reserves that enhance endurance beyond the fragile neonatal phase.^[80]

Management

Prevention Strategies

Preventing shivering involves proactive measures to mitigate cold exposure and underlying health risks that trigger the response. In environmental contexts, wearing multiple layers of loose-fitting clothing is a primary strategy to enhance insulation and retain body heat, thereby reducing the likelihood of core temperature drops that induce shivering. ^[81] Organizations such as the Occupational Safety and Health Administration (OSHA) recommend at least three layers: an inner moisture-wicking layer, a middle insulating layer like wool or synthetic fleece, and an outer wind- and water-resistant shell. ^[81] Maintaining hydration is equally critical, as dehydration can impair thermoregulation and exacerbate cold stress; consuming warm, non-caffeinated fluids at regular intervals helps sustain plasma volume and core temperature stability during exposure. ^[82] Behavioral adaptations further bolster prevention, particularly for individuals like athletes or outdoor workers frequently in cold conditions. Cold acclimatization training, involving gradual exposure to low temperatures over several days to weeks, enhances metabolic efficiency and reduces the intensity of shivering by improving non-shivering thermogenesis and vascular responses. ^[83] Avoiding alcohol consumption is essential, as it causes vasodilation that impairs peripheral vasoconstriction—a key heat-conserving mechanism—and reduces shivering metabolic rate by approximately 13%, increasing the risk of hypothermia during cold exposure. ^[84] ^[85] Vaccinations and hygiene practices target non-thermal triggers like infections that cause febrile shivering. Annual influenza vaccination is recommended by the Centers for Disease Control and Prevention (CDC) to prevent flu-related fever and associated chills, with effectiveness estimates of 40-60% in reducing confirmed influenza cases among adults and children in well-matched seasons. ^[86] ^[87] Good hygiene, such as frequent handwashing and avoiding close contact with ill individuals, complements vaccination by lowering overall infection rates, including those from respiratory viruses that provoke shivering through fever. ^[86] Nutritionally, ensuring adequate calorie intake supports energy reserves to avert or delay shivering onset in cold settings. In cold environments, individuals may require an additional 500-1,000 kcal per day beyond basal needs to replenish glycogen stores depleted by thermogenic demands, with military rations often augmented by 1,000 kcal modules for Arctic operations to maintain metabolic heat production. ^[88] Prioritizing carbohydrate-rich foods (e.g., 50-60% of intake) helps sustain muscle glycogen, as depletion impairs shivering efficiency and accelerates core cooling. ^[89]

Treatment Interventions

Treatment of active shivering primarily focuses on addressing the underlying cause, such as hypothermia, while employing supportive and pharmacological methods to suppress the response and prevent complications. Passive rewarming is the initial approach for mild cases, involving the removal of wet clothing and application of insulating layers like dry blankets to minimize heat loss, which can raise core body temperature at a rate of 0.5 to 2 °C per hour without the need for medications.^[4] This method promotes endogenous heat production through preserved shivering until the core temperature stabilizes above the shivering threshold, typically around 32–35 °C, thereby suppressing shivers naturally as thermoregulation recovers.^[4] Administration of warm intravenous fluids may complement passive external techniques in hypothermic patients, further supporting gradual rewarming while avoiding rapid shifts that could exacerbate instability.^[4] Pharmacological interventions are indicated when shivering persists despite passive measures or in moderate to severe hypothermia, with meperidine serving as a first-line agent due to its potent antishivering effects. Meperidine, an opioid agonist at both μ- and κ-opioid receptors, reduces the shivering threshold by acting on thermoregulatory pathways in the hypothalamus, often at doses of 25–50 mg intravenously.^[90] This treatment achieves shivering resolution in approximately 80–90% of cases with a single dose, minimizing metabolic demands and oxygen consumption associated with intense shivering.^[91] Other opioids like morphine are less effective at equivalent doses, highlighting meperidine's unique κ-receptor mediated action in suppressing the response.^[92] For severe shivering unresponsive to passive or pharmacological methods, active external rewarming using forced-air warming devices, such as convective blankets, is employed to deliver controlled external heat directly to the skin, achieving rewarming rates of 0.5–4 °C per hour.^[93] These devices are preferred over immersion techniques, which can provoke afterdrop—a further decline in core temperature due to redistribution of cold peripheral blood upon rapid vasodilation—and increase risks of cardiac instability.^[94] Immersion is thus avoided in favor of surface methods to ensure safer progression.^[94] Throughout treatment, continuous monitoring is essential to guide interventions and detect complications from shivering. Core temperature should be assessed using reliable probes, such as esophageal or rectal thermometers, to track rewarming progress and confirm suppression of the shivering threshold.^[95] Electrocardiography (ECG) is critical for identifying arrhythmias, as intense shivering can produce tremor artifacts mimicking atrial fibrillation or other rhythms, while also elevating myocardial oxygen demand that may precipitate ventricular irregularities in hypothermic states.^[96]^[97]

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In our material this paradoxical undressing occurred in 25% of the cases and nearly all exhibited an additional phenomenon which has not yet been described in ...
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