[Clinical Skills] Elevated Body Temperature

April 3, 2016 Clinical Skills, Practice No comments , , , , , , , , ,

Regulation of Body Temperature

Internal body temperature is tightly regulated to maintain vital organ function, particularly the brain. Temperature deviation of more than 4 C above or below normal can produce life-threatening cellular dysfunction. Internal temperature is regulated be the hypothalamus, which maintains a temperature set point. The autonomic nervous system maintains body temperature by regulating blood flow, conducting heat from the internal organs to the skin, and innervating sweat glands. Increasing flow and dilating cutaneous capillaries radiate heat away by conductive loss whereas sweat increases evaporative heat loss. Behavioral adaptations are also important; in hot conditions, people become less active and seek shade or a cooler environment. Decreased body temperature is countered by shivering (increasing heat generation in muscles) and by behavioral adaptations such as putting on clothes and seeking warmer environs. Deviations of body temperature indicate changes in the set point, increased heat production, decreased heat dissipation, failure of regulatory system, or any combination of these.

  • Hypothalamus
  • ANS (blood flow [from internal to superficial; skin blood flow], sweat glands, and shivering)
  • Behavioral adaptations

Normal Body Temperature

Internal body temperature is maintained within a narrow range, +- 6 C, in each individual. However, the population range of this set point varies from 36.0 C to 37.5 C making it impossible to know an individual's normal temperature without an established baseline. Without a baseline it is reasonable to regard an oral temperature above 37.5 C and a rectal temperature over 38.0 C as fever. The minimum normal temperature is more difficult to define; the oral temperature often dips to 35.0 C during sleep.

Diurnal variation of body temperature. Daytime workers, who sleep at night, register their minimum temperature at 3 to 4 AM, whence it rises slowly to a maximum between 8 and 10 PM. This pattern is reversed in night-shift workers. The transition from one pattern to the other requires several days.

Simultaneous temperatures in various regions. Heat is produced by the chemical reactions of cellular metabolism, so a temperature gradient extends from a maximum in the liver to a minimum on the skin surface. Customarily, the body temperature is measured in the rectum, the mouth, the ear, the axilla, or the groin. Among these sites, the rectal temperature is approximately 0.3 C higher than that of the oral or groin reading; the axillary temperature is approximately 0.5 C less than the oral value.

Elevated Temperature

Increased body temperature results from excessive heat production or interference with heat dissipation. Each of these mechanisms may be physiologic (i.e., occurring as a normal response to a physiologic challenge) or pathologic (i.e., temperature elevation as a result of damage to the normal thermoregulatory pathways). Physiologic elevation of temperature results from an elevation of the hypothalamic physiologic point for body temperature, a feve. Pathologic elevations of body temperature, hyperthermia, result from unregulated heat generation and/or impairment of the normal mechanisms of heat exchange with the environment.

Physiologic Elevated Temperature – Fever

Release of endogenous pyrogens, particular interleukin (IL-1), triggered by tissue necrosis, infection, inflammation, and some tumors, elevates the hypothalamic set point leading to increased body temperature. Onset of fever may be marked by a chill with shivering and cutaneous vasoconstriction as the body begins generating increased heat and decreasing heat loss; particularly severe chills are called rigors. When the new set point is reached, the skin is usually warm, moist, and flushed; but absence of these signs does not exclude fever. Occasionally, the skin temperature may be subnormal or normal, while the core temperature is markedly elevated. Tachycardia usually accompanies fever, the increase in pulse rate being proportionate to the temperature elevation. During the fever, the patient usually feels more comfortable in a warm environment. The new set point and the pattern of the fever reflect the dynamics of particular pathophysiologic process. Return of the set point to normal, either temporarily or permanently, is marked by sweat and flushing as the body dissipates the accumulated heat. Night sweats occur in many chronic infections, inflammatory diseases, and some malignancies, particularly lymphomas. They represent an exaggeration of the normal diurnal variation in temperature, the sweat marking the decline of the temperature at night.

Fever Pattern

  • Continuous fever. The diurnal temperature fluctuation is 0.5 C to 1.0 C.
  • Remittent fever. The diurnal temperature fluctuation is more than 1.1 C without any normal readings.
  • Intermittent fever. Episodes of fever are separated by days of normal temperature.
  • Relapsing fever. Fevers occur every 5 to 7 days in borreliosis (Lyme disease) and Colorado tick fever.
  • Episodic fever. Fever lasts for days or longer following by remission of fever and clinical illness for at least 2 weeks.
  • Pel-Epstein fever. Several days of continuous or remittent fever are followed by afebrile remissions lasting an irregular number of days. This is characteristic of Hodgkin disease.

Clinical Occurrence

  • Congenital: familial Mediterranean fever, other familial periodic fevers, porphyrias
  • Endocrine: hyperthyroidism, pheochromocytoma
  • Infection: bacterial, viral, rickettsial, fungal, and parasitic infections either localized, or systemic
  • Inflammatory/Immune: systemic lupus erythematosus (SLE), acute rheumatic fever, Still disease, vasculitis, serum sickness, any severe local or systemic inflammatory process
  • Mechanical/Traumatic: tissue necrosis, exercise
  • Metabolic/Toxic: drug reactions, gout
  • Neoplastic: leukemia, lymphomas, and solid tumors
  • Neurologic: seizures
  • Psychosocial: factitious
  • Vascular: thrombophlebitis, tissue ischemia, and infarction, vasculitis, subarachnoid hemmorrhage

Fever of Unknown Origin/FUO

Fever of Unknown Origin. Three conditions define a fever of unknown origin (FUO): 1.the illness has lasted >3 weeks; 2.the temperature is repeatedly >38.3 C; and 3. >= three outpatient visits or >=3 days in the hospital have not yielded a diagnosis.

Clinical Occurrence

  • Nonifectious inflammatory diseases: still disease, SLE, sarcoidosis, Crohn disease, polymyalgia rheumatica, vasculitis (giant cell arteritis, Wegener disease, polyarteritis nodosa)
  • Infections: Endocarditis, tuberculosis, urinary tract infection, cytomegalovirus, Epstein-Barr virus, HIV, subphrenic abcess, cholangitis and cholecystitis
  • Neoplasms: Non-Hodgkin lymphoma, Hodgkin disease, leukemia, adenocarcinoma
  • Miscellaneous: habitual hyperthermia, subacute thyroiditis, Addison disease, drug fever

Pathologic Overproduction and Impaired Dissipation of Heat

  • Hyperthermia. Unregulated heat production or damage to the heat dissipation systems leads to rapid and severe uncompensated temperature elevations.

    • Impaired heat loss: high environmental temperature and humidity, moderately hot weather for a person with congenital absence of sweat glands, congestive heart failure, heat stroke, a ticholinergic drugs and toxins; poverty, homelessness, and psychosis all of which inhibit the ability to adapt to environmental challenges
    • Increased heat generation: malignant hyperthermia, neuroleptic malignant syndrome, heavy exertion in hot and humid environment.

Lowered Body Temperature


Decreased hypothalamic set point, insufficient heat generation, and excessive heat loss due to behaviors and environmental conditions all lead to a sustained decline in core temperature. Low body temperature impairs cellular metabolism and brain function, particularly judgement, and the combination prevents protection from continued exposure leading to fatal hypothermia. Hypothermia also protects the tissue from ischemic injury, so complete recovery is possible from rapid and sustained cooling even when the patient appears clinically dead. Relative or absolute hypothermia in situations where fever would be expected is a poor prognostic sign.

Clinical Occurrence

Endocrine: Hypothyroidism

Idiopathic: Advanced age

Infectious: Sepsis

Mechanical/Traumatic: Exposure and immersion, hypothalamic injury from trauma or hemorrhage, burns

Metabolic/Toxic: Antipyretics, hypoglycemia, drug overdoses

Neoplastic: Brain tumors

Neurologic: Stroke

Psychosocial: Poverty, homelessness, and psychosis

Vascular: Stroke


October 25, 2015 Infectious Diseases, Physiology and Pathophysiology No comments , , , , , , , ,

dreamstime_10999299high_feverBody Temperature System and Mechanisms could be found at thread "Mechanism of Thermoregulation" at

Body temperature, at any given point in time, represents a balance between heat gain and heat loss. Body heat is generated in the core tissues of the body, transferred to the skin surface by the blood, and released into the environment surrounding the body.

The thermostat

In the hypothalamus there is a thermostat, which controls and maintains the temperature of the individual. If the thermostat has been reset to a new point different from the normal value, the body would sense the difference between true body temperature and the new thermostat via temperature receptors, and after the signal being transmitted into the hypothalamus, the ratio of heat production to heat loss will be changed accordingly via temperature-regulating responses to make the body core temperature the same as the new thermostat. For example, if the thermostat had been reset to above 37℃, the temperature receptors then signal that the actual temperature is below the new set point, and the temperature-raising mechanisms are activated. Then the ratio of heat production to heat loss would increases and the actual body temperature starts to increase until the value equaling the new set point.


The body temperature of a health individual changes with circadian rhythm, with the lowest at 3 AM to 6 AM and highest at 3 PM to 6 PM. Generally a orally measured temperature higher than 37.2 C in the early morning or 37.7 in the late afternoon and evening is considered as fever.

Body temperature can be measured by several different methods and at many different sites. However, in critical ill patients the variability between sites may increase. For example, during open mouth breathing, sublingual temperature falls relative to tympanic membrane temperature. Likewise, skin temperature can fall relative to core temperature during cardiogenic shock due to a decrease in cutaneous blood flow. Because of this variability, mouth, skin, and axillary measurements are not recommended for use in critical ill patients.


Fever describes an elevation in body temperature that is caused by an upward displacement of the thermostatic set point of the hypothalamic thermoregulatory center. Many proteins, breakdown products of proteins, and certain other substances released from bacterial cell membranes can cause a change in the set point to rise. Fever is resolved when the condition that caused the increase in the set point is removed. Fevers that are regulated by the hypothalamus usually do not rise above 41 C, suggesting a built-in thermostatic safety mechanism.

Pyrogens are exogenous or endogenous substances that produce fever. Exgenous pyrogens are derived from outside the body and include such substances as bacterial products, bacterial toxins, or whole microorganisms. Exogenous pyrogens induce host cells to produce fever-producing mediators called endogenous pyrogens. When bacteria or breakdown products of bacteria are present in blood or tissues, phagocytic cells of the immune system engulf them. These phagocytic cells digest the bacterial products and then release pyrogenic cytokines (for information about inflammation mediators please refer to thread "Inflammation Mediators" at, principally interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha), into the bloodstream for transport to the hypothalamus, where they exert their action. These cytokines induce prostaglandin E2 (PGE2), which is a metabolite of arachidonic acid. It is hypothesized that when interleukin (IL-1B) interacts with the endothelial cells of the blood-brain barrier in the capillaries of the organum vasculosum laminae terminalis (OVLT), which is in the third ventricle above the optic chiasm, PGE2 is released into the hypothalamus.

At this point, PGE2 binds to receptors in the hypothalamus to induce increases in the thermostatic set point through the second messenger cyclic adenosine monophosphate (cAMP). In response to the increase in its thermostatic set point, the hypothalamus initiates shivering and vasoconstriction that raise the body's core temperature to the new set point, and fever is established.