A condition in which exaggerated or abnormal changes in body temperature occur spontaneously or in response to environmental or internal stimuli. Poikilothermia refers to the inability to regulate core body temperature. Clinically, poikilothermia can be manifested by hypothermia (core temperature less than 35°C/95°F) or hyperthermia (core temperature > 37.8°C /100°F).
Impaired thermoregulation is a known complication seen in persons with spinal cord injury (SCI), particularly those with level of injury above T6, traumatic brain injury (TBI), stroke, and other conditions that cause damage to the brainstem. It also can be seen in patients who take certain medications such as anesthetic agents, tranquilizers, antihypertensive drugs, opioids, and sedatives, in addition to alcohol.
Epidemiology including risk factors and primary prevention
The frequency of impaired thermoregulation is not known. This problem is associated with spinal cord injury above level T6 and with severe traumatic brain injury. In SCI, it occurs often during extremes of ambient temperature. In patients with TBI or brainstem stroke, it can arise in the presence of noxious stimuli, although it frequently occurs spontaneously in the absence of environmental triggers.
In the normal state, powerful mechanisms exist to measure, assess, regulate, and adjust core temperatures. There are sensory, integrator/regulator, and effector components of thermoregulation.
The sensory components of the thermoregulatory control system derive from both internal and external sources. There are cutaneous cold and warm receptors located throughout the skin and superficial tissues, which are more concentrated in the fingers, face, and genitalia, and less concentrated proximally. There also are deep body thermal sensors, located in the abdomen and elsewhere. These sensors send impulses with thermal information through projections into the spinal cord, carried predominantly through C-fiber afferents. These fibers, with cell bodies in the dorsal root ganglion, enter the spinal cord and ascend contralaterally in the spinothalamic tracts through the medial lemniscus to the thalamus, which in turn, has fibers that project directly to the somatosensory cortex to enable conscious appreciation of temperature. The ascending fibers also have additional important projections to the hypothalamus to facilitate unconscious autonomic control of temperature. The preoptic hypothalamus receives and interprets the internal and external temperature information, generates the thermal set point, and integrates thermoregulatory responses.
Efferents from the hypothalamus control the body’s response to thermal changes through descending noradrenergic and cholinergic fibers exiting the spinal cord below the C7 level. The strategies which these effectors use to regulate core temperature include changes in vasomotor (causing peripheral vasoconstriction and vasodilatation) and sudomotor (causing sweating) tone, non-shivering and shivering thermogenesis, and piloerection. Conscious awareness of temperature changes, based in the cortex, enables behavioral adaptations to control temperature, including changing location, adjusting environmental temperatures (e.g., via heating or air conditioning), making postural adjustments, or changing clothing. When core body temperature decreases, sympathetic noradrenergic mechanisms normally induce piloerection, shivering, and vasoconstriction to produce body heat and to shunt blood away from the cool surface. Core body temperature is the result of the balance between heat production and heat loss, both of which are adjusted by the central hypothalamic thermoregulatory controller. When core body temperature rises, vasodilatation and sweating normally help the body to lose some of its internal heat. Medical and neurological problems that interfere with the flow of sensory information and/or motor output reduce the ability of the system to assess and mount a response to changes in temperature. Also, direct damage to the hypothalamus controller can result in dysregulation of temperature control.
In SCI, the normal connections are lost between the hypothalamus and both its motor and sensory projections. In high SCI, most of the skin is insensate, and so the person may have little or no sensitivity to heat or cold. In addition, the lack of sympathetic outflow on the effector side results in loss of vasoconstriction or vasodilatation, so heat cannot be conserved or lost in response to central temperature changes. In addition, heat production is limited in response to cold stimuli because of the loss of shivering ability resulting from motor deficits. Sweating is ineffective below the level of injury. With high SCI, heat production may increase only slightly over baseline, so central hypothermia in a cold environment is a significant risk for these patients. The amount of impairment of thermoregulation tends to vary according to level and possibly completeness of injury. Practically, the significant risk of hypothermia in cold external environments occurs more commonly in patients with SCI levels above T6 because of the large surface area for which sensation and shivering ability are lost in those patients.
The preoptic area of the anterior hypothalamus, which houses the main thermoregulatory center, can be damaged by trauma, leading to manifestations of thermodysregulation. Other causes of hyperthermia after TBI include post-traumatic cerebral inflammation and secondary infection. The development of post-traumatic hyperthermia (PTH) can be seen as a secondary effect of TBI that may negatively influence outcome. An increase in body temperature after injury is associated with increased cytokine release, and both hyperthermia itself and the cytokine release can exacerbate neuronal damage, through the mechanisms of increased oxidative stress, glutamate release, increased metabolic expenditure, increasing blood brain barrier permeability, cerebral edema, and raising intracranial pressure.
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
Thermodysregulation can arise early or late after spinal cord injury. Although it also can occur at any time after traumatic brain injury or brainstem damage, it tends to be more frequent during the early post-injury period. It is distinctly episodic.
Specific secondary or associated conditions and complications
Paroxysmal autonomic instability with dystonia (PAID), also known as central dysautonomia and central storming, is a clinical syndrome that develops from altered autonomic activity following TBI. Clinical manifestations are temperature typically greater than 38.5oC (fever), hypertension, heart rate greater than 130 beats per minute (tachycardia), rapid respiratory rate (tachypnea), pupillary dilation, associated with agitation, diaphoresis, rigidity, or decerebrate posturing.,
It arises from injury to the brainstem, but can also occur following brainstem hemorrhage, elevated pressure on the brainstem, and injury to select cortical areas (orbitofrontal, anterior temporal, and insula) that influence hypothalamic activity. Subcortical areas that may influence hypothalamic function are the amygdala, the periaqueductal gray matter, nucleus of tractus solitaries, and both the uvula and vermis of the cerebellum. Damage to these areas release control of vegetative function and results in dysregulation of autonomic balance.
PAID occurs in up to one-third of patients in coma or vegetative state. It is more common in patients with severe TBI, but also is seen in patients with hydrocephalus and CNS infection. It is possible to have electrocardiographic changes, arrhythmias, increased intracranial pressure, hypohidrosis, and cool limbs.
Essentials of Assessment
History should include time of onset, duration, triggering events, associated symptoms, and past treatments.
For patients with acute SCI, evaluation of autonomic dysfunction (including impaired thermoregulation) should be done as per the International Standards for Assessing Remaining Autonomic Function. Rectal temperature measurement is best if feasible, since skin temperature measurement is not as accurate for monitoring core body temperature, otherwise temperature can be monitored via oral or tympanic measurements.
A thorough examination should be performed looking for conditions that may serve as triggers. In particular, sources of infection should be sought as potential causes of fever before making a diagnosis of hyperthermia due to temperature dysregulation. Examination should include skin inspection, evaluation of the head & neck region, respiratory system, gastrointestinal tract, and genitourinary systems.
The febrile episode and associated symptoms may impair functional ability temporarily. Aging is also associated with an attenuated physiological ability to dissipate heat and the risk of heat-related illness in these individuals is elevated.
Unfortunately, there are no known biomarkers for impaired thermoregulation at this time. However, an autonomic test battery including parasympathetic and sympathetic cardiovascular function measures (deep breathing test, Valsalva maneuver, tilt, or pressor test), can be utilized. More specialized tests include carotid sinus massage, assessment of baroreceptor reflex function, pharmacological tests or cardiac, and regional hemodynamic measurements can also be considered.
A thorough fever workup, including complete blood count, urinalysis, urine culture, and chest x-ray should be performed to rule out infection. Testing for other causes of fever in SCI, such as deep vein thrombosis or heterotopic ossification should be considered.
Plain films to evaluate sources of fever might include those of the chest, abdomen, and limbs. Brain imaging may reveal evidence of severe brain injury.
Extremes of heat or cold in the environment may predispose the patient with impaired thermoregulation to hyperthermia or hypothermia, respectively.
Rehabilitation Management and Treatments
Available or current treatment guidelines
A section on management of temperature dysfunction after spinal cord injury is included in recent Consortium for Spinal Cord Medicine clinical practice guidelines on autonomic dysreflexia and other autonomic dysfunctions published by the Paralyzed Veterans of America.
It is necessary first to consider other causes of fever. Once other causes of fever are ruled out, then thermal dysregulation should be considered as a diagnosis.
In patients with SCI, treatment typically consists of behavioral and environmental strategies, such as changing the causative environment and avoidance of extremes in temperatures, with use of cooling devices, air-conditioned setting, and/or washing with tepid water to manage hyperthermia. Careful planning on amount and type of clothing is important. Ambient temperature regulation, insulated clothing, blankets, warm humidified air, and intake of warm fluids are measures to prevent or manage hypothermia.
For patients with TBI, it is often necessary to use medications. The most commonly used medications are beta blockers. Alpha adrenergic blocker medications have been tried less often. Bromocriptine may reduce hyperthermia and diaphoresis. Dantrolene may reduce extensor posturing. For extreme and refractory cases, judicious doses of morphine can be used to stop the episodes.
At different disease stages
Thermodysregulation is treated similarly at all stages of the condition.
Patient & family education
It is important to teach patients and families about common presenting symptoms, prevention strategies, and methods of immediate treatment. Measures to prevent hyperthermia include wearing appropriate light-weight and light-colored clothing, maintaining a proper temperature-controlled environment (e.g., use of air-conditioning), maintaining appropriate hydration, water spray or fan when exercising or in a hot environment. Since alcohol can cause vasodilation and heat loss, those prone to hypothermia should minimize alcohol intake in cold environments.
Trbovich, et al, concluded that cooling vests helped prevent exercise-induced hyperthermia in athletes with SCI. This small study did not find a significant difference with this intervention.
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
Episodes are considered resolved when the temperature returns to normal.
It is important to approach the patient with thermal dysregulation with a strong suspicion for infection. When, causes of fever have been ruled out, then impaired thermoregulation should be considered as a diagnosis.
Cutting Edge/ Emerging and Unique Concepts and Practice
Techniques to measure functional integrity of sudomotor nerves include the quantitative sudomotor axon reflex sweat test (QSART), analysis of the sympathetic skin response and the thermoregulatory sweat test (TST). In addition to these techniques, more recent developments have been introduced to reduce technical demands and interindividual variability such as the quantitative direct and indirect axon reflex testing or sudoscan. However, diagnostic accuracy of these tests remains to be determined.
Gaps in the Evidence- Based Knowledge
There is no specific evidence-based protocol or algorithm for behavioral or drug treatment for this condition.
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Ziemssen T, Siepmann T. The Investigation of the Cardiovascular and Sudomotor Autonomic Nervous System-A Review. Front Neurol. 2019 Feb 12;10:53. doi: 10.3389/fneur.2019.00053. PMID: 30809183; PMCID: PMC6380109.
Consortium for Spinal Cord Medicine Clinical Practice Guidelines: Evaluation and Management of Autonomic Dysreflexia and Other Autonomic Dysfunctions: Preventing the Highs and Lows. Management of Blood Pressure, Sweating, and Temperature Dysfunction. Paralyzed Veterans of America. Washington, DC. 2020.
Original Version of the Topic
Elliot J. Roth, MD. Impaired thermoregulation. 9/20/2013.
Previous Revision(s) of the Topic
Felicia Skelton, MD. Impaired thermoregulation. 8/17/2016.
Kareen Velez, MD
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