VIOLATION OF THERMAL

METABOLISM. FEVER.

MARTA R. GERASYMCHUKM.D., PH.D., ASSOCIATE PROFESSOR

PATHOPHYSIOLOGY DEPARTMENT, IFNMU

FEVER IS A CLINICAL HALLMARK OF INFECTION AND INFLAMMATION.

ACTUALITYThe aim of thermoregulation is to maintain the actual core temperature of the body at the set level of about 37°C (with diurnal variations).In contrast to passive hyperthermia, the set level is raised in fever, and the thermoregulatory mechanisms are thus responsible for maintaining the raised temperature. This becomes noticeablewhen the fever rises: because the actual level deviates from the suddenly raised set level, heat loss is reduced by a decrease in cutaneous blood flow, resulting in cooling of the skin (feeling cold). Additionally, heat production is increased by shivering (tremor). This lasts until the actual level has approached the new set level (plateau). When the fever falls, the set level again falls, so that now the actual level is too high and cutaneous blood flow increases, resulting in the person feeling hot and sweating profusely.

CORE TEMPERATURE of most females increases approximately 0.5°C to 1.0°C during postovulation time of their menstrual cycle.

NORMAL BODY TEMPERATURES

CORE BODY TEMPERATURE (i.e., intracranial, intrathoracic, & intraabdominal) normally is maintained within a range of 36.0°C to 37.5°C (97.0°F to 99.5°F). Within this range, there are individual differences.

Indeed, a NUDE PERSON can be exposed to temperatures as low as 55°F (12,78 °C) or as high as 130°F (54,44 °C) in dry air and still maintain an almost constant core temperature.

The SKIN TEMPERATURE, in contrast to the CORE TEMPERATURE, rises and falls with the temperature of the surroundings. The skin temperature is the important temperature when we refer to the skin’s ability to lose heat to the surroundings.

Temperatures differ in various parts of the body, with core temperatures being higher than those at the skin surface.

The rectal temperature is used as a measure of core temperature and is considered the

most accurate parameter. Rectal temperatures usually range from 37.3°C (99.1°F) to 37.6°C

(99.6°F).

The oral temperature, taken sublingually, is usually 0.2°C (0.36°F) to 0.51°C (0.9°F) lower

than the rectal temperature.

The axillary temperature also can be used as an estimate of core temperature. However, the parts of the axillary fossa must be pressed closely together for an extended period (5 to 10 minutes for a glass thermometer) because this method requires considerable heat to accumulate before the final temperature is reached.

Ear-based thermometry uses an infrared sensor to measure the flow of heat from the

tympanic membrane and ear canal.

EXERCISE can increase metabolic heat production 10-fold. Thankfully, thermoregulatory responses such as sweating simultaneously increase heat loss, and thus keep body temperature from rising dangerously high.

Shivering increases metabolic heat production.

BODY TEMPERATURE reflects the difference between heat production and heat loss and varies with

exercise and extremes of environmental temperature.

ICE CRYSTALS can form in tissues exposed to very cold and damp ambient temperatures.

The failure to adequately manage heat production and/or loss results in devastating consequences.

Very high temperatures (+45°C, 113° F) cause proteins to coagulate and/or aggregate.

Systemic changes in body temperature can be equally devastating, leading to tissue damage, organ

failure, coma, and even death.

THE BASAL NUCLEI SOME OF THE NUCLEI OF THE HYPOTHALAMUS

HYPOTHALAMUS

The part of the brain which lies below the thalamus, forming the major portion of the ventral region of the diencephalon and which functions to regulate bodily temperature, water

balance, carbohydrate and fat metabolism among other metabolic processes, and autonomic activities and also contributes to the regulation of internal homeostasis by

neurosecretory functions which control the activity of the pituitary gland.

6 aspects of internal homeostasis coordinated by the hypothalamus:

1.  BODY TEMPERATURE

2.  food intake/hunge

5.  water and electrolyte balance6.  thirst

3.  biological rhythms and drives 4.  regulates output of pituitary gland = hypophysis

Temperature-regulating centers located in the hypothalamus: preoptic and anterior hypothalamic nuclei, posterior

hypothalamic area

The anterior hypothalamic preoptic area contain large numbers of heat-sensitive neurons as well as about one third as many cold-sensitive neurons (temperature sensors function for controlling body temperature).

The heat-sensitive neurons increase their firing rate 2- to 10-fold in response to a 10°C increase

in body temperature.

The cold-sensitive neurons, increase their firing rate when the body temperature falls.

Even though many °t sensory signals arise in peripheral receptors, these signals contribute to body °t control mainly through the hypothalamus. The area of the hypothalamus that they stimulate is located bilaterally in the posterior hypothalamus approximately at the level of the mammillary bodies. The °t sensory signals from the anterior hypothalamic-preoptic area are also transmitted into this posterior hypothalamic area. Here the signals from the preoptic area & the signals from elsewhere in the body are combined & integrated to control the heat-producing & heat-conserving reactions of the body.

The skin is endowed with both cold and warmth receptors. There are far more cold receptors than warmth receptors—in fact, 10 times as many in many parts of the skin.

Peripheral detection of °t mainly concerns detecting cool & cold instead of warm temperatures. When the skin is chilled over the entire body, immediate reflex effects are invoked and begin to increase the ºt of the body in several ways: 1) by providing a strong stimulus to cause shivering, with a resultant increase in the rate of body heat production;2) by inhibiting the process of sweating, if this is already occurring; 3) by promoting skin vasoconstriction to diminish loss of body heat from the skin. Deep body temperature receptors are found mainly in the spinal cord, in the abdominal viscera, and in or around the great veins in the upper abdomen and thorax. These deep receptors function differently from the skin receptors because they are exposed to the body core °t rather than the body surface temperature. Skin °t receptors, they detect mainly cold rather than warmth. It is probable that both the skin and the deep body receptors are concerned with preventing hypothermia—that is, preventing low body °t.

Detection of Temperature by Receptors in the Skin and Deep Body Tissues

BLOOD TEMPERATURE

INTERNALTHERMORECEPTORS

SKIN THERMORECEPTORS

THERMOSTAT

SET POINT

HEAT PRODUCTION

HEAT EMISSION

IL -1

HYPOTHALAMIC CONTROL OF TEMPERATURE

1) Neurons to the “THERMOSTAT” is a group of thermosensitive neurons, which perceive the temperature of blood which flows through

hypothalamus. The information from skin and organs thermoreceptors comes here too.

A “thermostat” provides the middle temperature of body core.

2) Neurons of the “SET LEVEL OF TEMPERATURE” are a group of thermosensitive neurons which program the level of temperature of body

core. Information from a “thermostat” comes to the neurons of the “set level of temperature”, where comparing of present temperature of core to the

programmed level.

3) HEAT PRODUCTION CENTER. It neurons are localized in dorso- and ventromedial nucleus of hypothalamus. Their irritation causes multiplying formation of heat.

4) The center of HEAT EMISSION is disposed in the preoptic area of hypothalamus. At it irritation leads to calorification by an organism.

THE CENTER OF THERMOREGULATION

•• Metabolic rate of each cell•• Any factor that may the basal metabolic rate (BMR), such as that caused by muscle activity•• Extra metabolism caused by hormones (thyroxine, growth hormone, testosterone).

•• Any extra metabolism caused by the sympathetic nervous system (SNS) stimulation on cells•• Extra metabolism caused by cellular chemical activity•• Thermogenic effect of food digestion, absorption, or storage.

CHEMICAL REACTIONS OF METABOLISM The CHEMICAL REACTIONS that occur during the ingestion and metabolism of food & those required to maintain the body at rest (basal metabolism) require energy & produce heat. These processes occur in the body core (primarily the liver) & are in part responsible for the maintenance of core temperature.There is a 0.55°C (1°F) increase in body °t for every 7% increase in metabolism.

The sympathetic neurotransmitters, epinephrine and norepinephrine, which are released when an increase in body °t is needed, act at the cellular level to shift body metabolism to heat production rather than energy generation. This may be one of the reasons fever tends to produce feelings of weakness and fatigue. Thyroid hormone increases cellular metabolism, but this response usually requires several weeks to reach maximal effectiveness.

Metabolism is the body’s main source of heat production or thermogenesis.Many factors impact the metabolic rate, including:

MECHANISMS OF HEAT PRODUCTION

SKELETAL MUSCLE CONTRACTION MECHANISMS OF HEAT PRODUCTION

Skeletal muscles produce heat through two mechanisms:

GRADUAL INCREASE IN MUSCLE TONE

PRODUCTION OF RAPID MUSCLE OSCILLATIONS (SHIVERING— WHICH DOES NOT OCCUR IN NEONATES)

Both increasing muscle tone and shivering are controlled by the posterior hypothalamus and occur in response to cold. As peripheral temperature drops, muscle tone increases and shivering begins. Shivering is a fairly effective method for increasing heat production because no work is performed and all the energy produced is retained as heat, and increases the use of oxygen by approximately 40%.

The first muscle change that occurs with shivering is a general in muscle tone, followed by an oscillating rhythmic tremor involving the spinal-level reflex that controls muscle tone. Physical exertion body °t. Muscles convert most of the energy in the fuels they consume into heat rather than mechanical work. With strenuous exercise, more than ¾ of the metabolism resulting from muscle activity appears as heat within the body, and the remainder appears as mechanical work.

MECHANISMS OF HEAT PRODUCTION

Chemical thermogenesis, also called nonshivering thermogenesis or adrenergic thermogenesis, results from the release of epinephrine & norepinephrine. Epinephrine and norepinephrine produce a rapid, transient increase in heat production by raising the body’s basal metabolic rate. Chemical thermogenesis seems to be different from hormone-triggered increases in the basal metabolic rate. Chemical thermogenesis produces a quick, brief rise in basal metabolic rate, whereas the hormone thyroxine triggers a slow, prolonged rise. Chemical thermogenesis occurs in brown adipose tissue. Brown adipose tissue is rich with mitochondria and blood vessels & is essential for nonshivering thermogenesis. White and brown adipocytes are found together in visceral & subcutaneous tissue. White adipocytes store energy and brown adipocytes produce heat. Adipocytes demonstrate transdifferentiation & such plasticity allows direct conversion of one cell type into the other. With chronic cold exposure white-to-brown conversion increases thermogenesis, whereas excessive food consumption induces brown-to-white conversion to meet the need for energy storage..

CHEMICAL THERMOGENESIS

.

TEMPERATURE-DECREASING MECHANISMS WHEN THE BODY IS TOO HOT1. Vasodilation of skin blood vessels. In almost all areas of the body, the skin blood vessels become intensely dilated. This is caused by inhibition of the

sympathetic centers in the posterior hypothalamus that cause vasoconstriction. Full vasodilation can increase the rate of heat transfer to the

skin as much as eightfold.

3. Sweating. The effect of increased body temperature

shows a sharp increase in the rate of evaporative heat loss

resulting from sweating when the body core temperature

rises above the critical level of 37°C (98.6°F).

An additional 1°C increase in body temperature causes

enough sweating to remove 10 times the basal rate of

body heat production.

2. Decrease in heat production. The mechanisms that cause excess heat production, such as shivering and chemical thermogenesis, are strongly

inhibited.

MECHANISMS OF HEAT LOSSRADIATION

CONDUCTION

CONVECTION

VASODILATION

DECREASED MUSCLE TONE

EVAPORATION

INCREASED PULMONARY VENTILATION

VOLUNTARY MEASURES

ADAPTATION TO WARMER CLIMATES

Radiation is the transfer of heat through air or a vacuum. Heat from the sun is carried by radiation. Heat loss by radiation varies with the temperature of the environment. Environmental temperature must be less than that of the body for heat loss to occur. In a nude person sitting inside a normal-temperature room, approximately 60% of body heat typically is dissipated by radiation.

During strenuous physical activities, such as skiing (a) or running (c), the dermal blood vessels dilate and sweat secretion increases (b). These mechanisms prevent the body from overheating. In contrast, the dermal blood vessels constrict to minimize heat loss in response to low temperatures (b).

Conduction refers to heat loss by direct molecule-to-molecule transfer from one surface to another. Through conduction, the warmer surface loses heat to the cooler surface. Thus the skin loses heat through direct contact with cooler air, water, or another surface. In the same manner, the core of the body loses heat to the cooler body surface. Cooling blankets or mattresses that are used for reducing fever rely on conduction of heat from the skin to the cool surface of the mattress. Heat also can be conducted in the opposite direction—from the external environment to the body surface. For instance, body temperature may rise slightly after a hot bath.

Water has a specific heat several times greater than air, so water absorbs far greater amounts of heat than air does. The loss of body heat can be excessive and life threatening in situations of cold water immersion or cold exposure in damp or wet clothing. The conduction of heat to the body’s surface is influenced by blood volume. In hot weather, the body compensates by increasing blood volume as a means of dissipating heat. A mild swelling of the ankles during hot weather provides evidence of blood volume expansion. Exposure to cold produces a cold diuresis and a reduction in blood volume as a means of controlling the transfer of heat to the body’s surface.

CONDUCTION

Vasodilation. Peripheral vasodilation increases heat loss by diverting core-warmed blood to the surface of the body. As the core-warmed blood passes through the periphery, heat is transferred by conduction to the skin surface and from the skin to the surrounding environment. Because heat loss through conduction depends on the surrounding temperature, it is minimal to nonexistent if the surrounding air or water is warmer than the body surface.Vasodilation occurs in response to autonomic stimulation under the control of the hypothalamus. It is useful in instances of moderate temperature elevation. As core temperature increases, vasodilation increases until maximal dilation is achieved. At that point the body must use additional heat loss mechanisms.

Convection is the transfer of heat through currents of gases or liquids. It greatly aids heat loss through conduction by exchanging warmer air at the surface of the body with cooler air in the surrounding space. Convection occurs passively as warmer air at the surface of the body rises away from the body and is replaced by cooler air, but the process may be aided by fans or wind. (The combined effect of conduction and convection by wind is conventionally measured as the windchill factor.)

EVAPORATION

Evaporation of body water from the surface of the skin and the linings of the mucous membranes is a major source of heat reduction. Even when a person is not sweating, water still evaporates insensibly from the skin and lungs at a rate of about 600 to 700 ml/day. Heat is lost as surface fluid is converted to gas, so that heat loss by evaporation is increased if more fluids are available at the body surface. To speed this process, fluids are actively secreted through the sweat glands. As much as 2.2 L of fluid per hour may be lost by sweating. Electrolytes are lost with the water. Therefore, loss of large volumes through sweating may result in decreased plasma volume, decreased blood pressure, weakness, and fainting.

Like other heat reduction mechanisms, stimulation of sweating occurs in response to sympathetic neural activity and depends on a favorable temperature difference between the body and the environment. In addition, heat loss through evaporation is affected by the relative humidity of the air. If the humidity is low, sweat evaporates quickly, but if the humidity is high, sweat does not evaporate and instead remains on the skin or drips off.

Anything that prevents adequate evaporation when the surrounding temperature is higher than the skin temperature will cause the internal body temperature to rise. This occurs occasionally in human beings who are born with congenital absence of sweat glands. These people can stand cold temperatures as well as normal people can, but they are likely to die of heatstroke in tropical zones because without the evaporative refrigeration system, they cannot prevent a rise in body temperature when the air temperature is above that of the body.

DECREASED MUSCLE TONE. To decrease heat production, muscle tone may be moderately reduced and voluntary muscle activity curtailed. These mechanisms explain in part the “washed-out” feeling associated with high temperatures and warm weather. Decreased muscle tone and reduced activity have a limited effect on decreasing heat production, however, because muscle tone and heat production cannot be reduced below basal body requirements.

INCREASED PULMONARY VENTILATION. Exchanging air with the environment through the normal pulmonary ventilation provides some heat loss, although it is minimal in humans. As air is inhaled, the air draws heat from the upper respiratory tract. The air is further warmed in the alveoli by blood in the microcirculation. This warmed air then is exhaled into the environment. This normal process occurs faster at higher body temperatures through an increase in ventilatory rates. Thus hyperventilation is associated with hyperthermia.

VOLUNTARY MECHANISMS. In response to high body temperatures, people physically “stretch out,” thereby increasing the body surface area available for heat loss. They also “slow down” or “take it easy,” thereby decreasing skeletal muscle work, and they “dress for warm weather” with light-colored, loose-fitting garments to reflect heat and promote convection, conduction, and evaporation.

ADAPTATION TO WARMER CLIMATES. The body of an individual who moves from a cooler to a much warmer climate undergoes a period of adjustment, a process that takes several days to weeks. At first the individual experiences feelings of lassitude, weakness, and faintness with even moderate activity. Body temperatures rise with any work. Within several days, however, the individual experiences an earlier onset of sweating, the volume of sweat is increased, and the sodium content is lowered. Heart rate is decreased and stroke volume increased so that cardiac output remains unchanged. Extracellular fluid volume increases, as does plasma volume. These physiologic adaptations result in improved warm weather functioning and decreased symptoms of heat intolerance. People’s work output, endurance, and coordination increase, and their subjective feelings of discomfort decrease.

TEMPERATURE-INCREASING MECHANISMS WHEN THE BODY IS TOO

COLD1. Skin vasoconstriction throughout the body. This is caused by stimulation of the posterior hypothalamic sympathetic centers.

2. Piloerection. Piloerection means hairs “standing on end.” Sympathetic stimulation causes the arrector pili muscles attached to the hair follicles to contract, which brings the hairs to an upright stance. This is not important in human beings, but in lower animals, upright projection of the hairs allows them to entrap a thick layer of “insulator air” next to the

skin, so that transfer of heat to the surroundings is greatly depressed.

3. Increase in thermogenesis (heat production). Heat production by

the metabolic systems is increased by promoting shivering,

sympathetic excitation of heat production, and thyroxine

secretion. These methods of increasing heat

require additional explanation, which follows.

I. INCREASE OF TEMPERATURE

(ST. INCREMENTI)

II. SAVING OF THE PROMOTED TEMPERATURE

(ST. FASTIGII)

III. DECLINE OF TEMPERATURE

(ST. DECREMENTI).

Fever, or pyrexia, describes an elevation in body temperature that is caused by an upward displacement of the thermostatic set point of the hypothalamic thermoregulatory center. Temperature is one of the most frequent physiologic responses to be monitored during illness.

FEVER is a typical pathological process which arises up for higher warm-blooded animals and man at influence on the organism of pyrogenic irritants.

Fevers that are regulated by the hypothalamus usually do not rise above 41°C (105.8°F), suggesting a built-in thermostatic safety mechanism. Temperatures above

that level are usually the result of superimposed activity, such as convulsions, hyperthermic states, or direct impairment of the temperature control center.

PYROGENS ARE MATTERS WHICH ARE REASON OF DEVELOPMENT OF FEVER

INFECTIOUS UNINFECTIOUS NATURAL PRIMARYARTIFICIAL

SECONDARYEndotoxins(LPS)

Exotoxin

Products of activity of

pathogenic mushrooms

Rickettsia

Viruses

Components of the

incompatible blood

(transfusion fever)

Exogenous proteins

(protein of milk)

Products of disintegration

of tissues

Pyrogens exist in

nature or appear in

natural way from

unpyrogenic matters

Pyrogens get from bacterial

toxins and use with a medical purpose

(pyrotherapy)

Exogenous pyrogens entered

from outside

Endoenous pyrogens appear in an organism:

IL 1α, 1β, 6, 8, and 11, INFα2 & γ, TNFα (cachectin) & TNFβ (lymphotoxin), the macrophage-inflammatoryprotein MIP 1

S aureus strains growing on mucous membranes (eg, the vagina in association with menstruation) or

in wounds

TOXIC SHOCK SYNDROME

TOXIN-1 (TSST-1)

TOXIC SHOCK SYNDROME

•shock, high fever, •diffuse red rash that later desquamates; •Involved multiple other organ systems

characterized by

Super antigen stimulatesT-cells to produce large amounts of IL-2 & TNF

PYROGENIC EXOTOXIN A (similar/same as

streptococcal ERYTHROGENIC TOXIN

SCARLET FEVER

Clinical manifestations similar to staphylococcal

toxic shock syndrome

LPS (ENDOTOXIN) of gram-negative bacteria (bacterial

cell wall components that are often liberated

when the bacteria lyse)

In the bloodstream is initially bound to

circulating proteins, which then interact with receptors on

macrophages neutrophils & other reticuloendothelial

cells

IL-1, IL-6, IL-8, TNF-α, and other cytokines are released, & the complement & coagulation cascades are activated

fever, leukopenia, & hypoglycemia; hypotension &shock resulting in impaired perfusion of essential organs (eg, brain, heart, kidney); intravascular coagulation; & death from massive organ dysfunction.

Some strains of group A β-hemolytic

streptococci

FEVER CAUSED BY BRAIN LESIONS

When a brain surgeon operates in the region of the hypothalamus: severe fever almost always occurs; rarely, hypothermia, occurs.

Demonstrate both the potency of the hypothalamic mechanisms for body

°t control & the ease with which abnormalities of the hypothalamus

can alter the set-point of temperature control.

Prolonged high ºt is compression of the hypothalamus by a brain tumor.

Brain damage from a fever generally will not occur unless the fever is over

107.6 °F (42 °C). Untreated fevers caused by infection will seldom go over 105 °F unless the child is overdressed

or trapped in a hot place.

During fever, arginine vasopressin (AVP), α-melanocytestimulating hormone (α-MSH), and corticotropin-releasing factor are released from the brain, and systemic anti-Inflammatory cytokines (i.e., IL-1 receptor agonist and IL-10) can act as endogenous cryogens or antipyretics to help diminish the febrile response. This antipyretic effect constitutes a negative-feedback loop. The antipyretic effect may help explain fluctuations in the febrile response. When the fever breaks, the set point is returned to normal. The hypothalamus responds by signaling a decrease in heat production and an increase in heat-reduction mechanisms. The result is decreased muscle tone, peripheral vasodilation, flushed skin, and sweating. The individual feels very warm, replaces warm clothing with cooler clothes, throws off the covers, and stretches out. Once the body has returned to a normal temperature, the individual feels more comfortable and the hypothalamus adjusts thermoregulatory mechanisms to maintain the new temperature.

At this point, PGE2 binds to receptors in the hypothalamus to induce in the thermostatic set point through the second messenger cyclic adenosine monophosphate (cAMP). In response to the in its thermostatic set point, the hypothalamus initiates shivering and vasoconstriction that raise the body’s core °t to the new set point, and fever is established. Peripheral vasoconstriction occurs with shunting of blood from the skin to the body core. Epinephrine release metabolic rate, and muscle tone . release of vasopressin reduces the volume of body fluid to be heated. Shivering also may occur. The individual dresses more warmly, body surface area by curling up, and may go to bed in an effort to get warm. Body °t is maintained at the new level until the fever “breaks.”

These cytokines induce prostaglandin E2 (PGE2), which is a metabolite of arachidonic acid (an intramembrane fatty 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.

These phagocytic cells digest the bacterial products and then release pyrogenic cytokines, principally interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), into the bloodstream for transport to the hypothalamus, where they exert their action.

When bacteria or breakdown products of bacteria are present in blood or tissues, phagocytic cells of the immune system

engulf them.

The endogenous pyrogens mediate a number of other responses. For example, IL-1 and TNF-α are inflammatory mediators that produce other signs of inflammation such as leukocytosis, anorexia, and malaise. Many noninfectious disorders, such as myocardial infarction, pulmonary emboli, and neoplasms, produce fever. In these conditions, the injured or abnormal cells incite the production of endogenous pyrogens. For example, trauma and surgery can be associated with up to 3 days of fever. Some malignant cells, such as those of leukemia and Hodgkin disease, secrete chemical mediators that function as endogenous pyrogens.

A fever that has its origin in the central nervous system is sometimes referred to as a NEUROGENIC FEVER. It usually is caused by damage to the hypothalamus due to central nervous system trauma, intracerebral bleeding, or an increase in intracranial pressure. NEUROGENIC FEVER is characterized by a high temperature that is resistant to antipyretic therapy and is not associated with sweating.

Characteristics of Febrile Conditions Chills.

When the set-point of the hypothalamic temperature-control center is suddenly changed from the normal level to higher than normal (as a result of tissue destruction, pyrogenic substances, or dehydration), the body temperature usually takes several hours to reach the new temperature set-point. Because the blood temperature is now less than the set-point of the hypothalamic temperature controller, the usual responses that cause elevation of body temperature occur. During this period, the person experiences chills and feels extremely cold, even though his or her body temperature may already be above normal. Also, the skin becomes cold because of vasoconstriction, and the person shivers. Chills can continue until the body temperature reaches the hypothalamic set-point of 103°F. Then the person no longer experiences chills but instead feels neither cold nor hot. As long as the factor that is causing the higher set-point of the hypothalamic temperature controller is present, the body temperature is regulated more or less in the normal manner, but at the high temperature set-point level.

Heat emission is more or less equal to thermoproduction. This balance of thermo regulative processes is set at more high level, as a norm, that provides maintenance of the promoted temperature of body.

Duration of fever can be a few hours, days and even years. After a level the increases of temperature distinguish the followings types of febris: a)mild pyrexia, (subfebrile) is an increase of temperature to 38ºC; b)moderate (febrile) - 38-39ºC; c)high (pyretic) - 39-41ºC;d)very high (hyperpyretic) - 41-42ºC.It is known that the temperature of body of man have day's (circadian) oscillation: maximal temperature in 5-7 hours of evening, minimum - in 4-6 hours of morning. This temperature rhythm is saved in most cases of fever.

II stage Stadium Fastigii

Forms of elevated temperature

36.6 °C (97.88 F) - NORMAL

37-38 °C (98.6 – 100.4 F) - SUBFEBRILE

39-41 °C (102.2 – 105.8 F) - PYRETIC

38-39 °C (100.4 – 102.2 F) - FEBRILE

over 41 °C (more than 105.8 F) - HYPERPYRETIC

Formulas for conversion of both Celsius to Fahrenheit and Fahrenheit to Celsius are as follows:

(X°C × 9/5) + 32 =Y°F;(X°F – 32) × 5/9 =Y°C

As a consequence of fever, heart rate is 8–12 min–1/ °C) and energy metabolism raised,

resulting in fatigue, joint aches and headaches

TYPES OF TEMPERATURE CURVESA. Febris Continua (Continous fever) in which the elevated °t for the some time persists at a high level, the difference between the morning and evening °t not exceed 1°C. (Typhoid fever, croupous pneumonia, typhus)

B. Febris Remittens (Remittent fever) in which the difference between the morning and evening °t exceeds 1°C, but the °t never falls to normal level. (Typhoid fever, catarrhal pneumonia, sepsis, etc.)

C. Febris Intermittens (Intermittent fever) which is characterized by regular alternation of brief attacks of fever (paroxysms) with feverless periods (apyrexia). High °t persists for several h, drops to normal and then rises again. The length of the feverless periods may vary (Malaria). Attacks – occurs every 3rd day (f. quartana), every 2nd day (f. tertiana) or every day (f. quotidiana)

D. Febris Recurrens (Recurrent fever) which is characterized by longer periods of pyrexia then intermittent f. (5-6 days). The duration of these periods corresponds to that of the periods of normal °t (Borreliosis – relapsing fever; Treponematoses, Tularemia, Meningococcemia, Malaria, rat-bite fever).

E. Febris Hectica (Hectic fever) in which the swings are 3 to 5 °C (Sepsis, severe Tbc, malignant tumors)

F. Febris Inversa (Inverse fever) is a fever with perverted course, for ex. elevation of °t in the morning and a drop in the evening (Sepsis, Tbc)

III STAGE DICREASE

TEMPERATURE (STADIUM

DECREMENTI)A mechanism of decline of body temperature in the III

stage of fever. As soon as an action is halted IL-1 on the

termoregulative center, maintenance of PgE diminishes in the neurons of the “set level of temperature”, that lead to restore sensitiveness of neurons to the "thermostat" signals.

The temperature of “core” begins to be perceived as promoted, as a result of what the center of heat emission is activated and the heat production center of is repressed.

Two types of physiologic reactions have most value: a)expansion of skin vessels and extremities vessels; b)multiplying hidropoiesis and sweating [sweat

secretion; perspiration]. These reactions are reason of multiplying heat emission and diminishing of body temperature.

Distinguish 2 variants of decline of temperature:1) critical decline is the sharp diminishing of temperature

during a few hours;2) a lytic decline is the gradual diminishing of

temperature during a few days.At the critical decline of temperature there is

hyperhidrosis with acute expansion of peripheral vessels, which can lead to falling of arterial pressure and development of acute vascular insufficiency (collapse).

DiagnosisMost febrile illnesses are due to common infections and are relatively easy to diagnose. In certain instances, however, it is difficult to establish the cause of a fever. A prolonged fever for which the cause is difficult to ascertain is often referred to as fever of unknown origin (FUO) or unexplained persistent fever. FUO is defined as a temperature elevation of 38.3°C (101°F) or higher that is present for 3 weeks or longer and includes 1 week of comprehensive diagnostic testing that does not identify a diagnosis. Among the causes of FUO are malignancies (i.e., lymphomas, metastases to the liver and central nervous system); infections such as human immunodeficiency virus, tuberculosis, or abscessed infections; and drug fever. Malignancies, particularly non-Hodgkin lymphoma, are important causes of FUO in the elderly. Cirrhosis of the liver is another cause of FUO.

Recurrent or periodic fevers may occur in predictable intervals or without any discernible time pattern. They may be associated with no discernible cause, or they can be the presenting symptom of several serious illnesses, often preceding the other symptoms of those diseases by weeks or months. Conditions in which recurrent fevers occur but do not follow a strictly periodic pattern include genetic disorders such as familial Mediterranean fever. FAMILIAL MEDITERRANEAN FEVER, an autosomal recessive disease, is characterized by an early age of onset (<20 years) of acute episodic bouts of peritonitis and high fever with an average duration of less than 2 days. In some cases pleuritis, pericarditis, and arthritis are present.The primary chronic complication is the presence of serum antibodies that can result in kidney or heart failure. Other conditions that present with recurrent fevers occurring at irregular intervals include repeated viral or bacterial infections, parasitic and fungal infections, and some inflammatory conditions, such as lupus erythematosus or Crohn disease. The clinical challenge is in the differential diagnosis of periodic or recurrent fever. The initial workup usually requires a thorough history and physical examination designed to rule out the more serious medical conditions that present initially with fever.

Diagnosis

Fever occurs frequently in infants and young children and is a common reason for visits to the emergency department. Infants and young children have decreased immunologic function and are more commonly infected with virulent organisms. Also, the mechanisms for controlling temperature are not as well developed in infants as they are in older children and adults. Even though infants with fever may not appear ill, this does not imply an absence of bacterial disease. In infants younger than 3 months, a mild elevation in temperature (i.e., rectal temperature of 38°C [100.4°F]) can indicate serious infection.Although the differential diagnosis of fever is quite broad and includes both infectious and noninfectious causes, the majority of febrile children have an underlying infection. The most common causes are minor or more serious infections of the respiratory system, gastrointestinal tract, urinary tract, or central nervous system. The epidemiology of serious bacterial disease has changed dramatically with the introduction of the Haemophilus influenzae and Streptococcus pneumoniae vaccines in developed countries. H. influenzae type b has been nearly eliminated, and the incidence of pneumococcal disease caused by vaccine and crossreactive vaccine serotypes has declined substantially. Fever in infants and children can be classified as low risk or high risk, depending on the probability of the infection progressing to bacteremia or meningitis and signs of toxicity. Infants between the ages of 1 and 28 days with a fever should be considered to have a bacterial infection that can cause bacteremia or meningitis. Signs of toxicity include lethargy, poor feeding, hypoventilation, poor tissue oxygenation, and cyanosis. A white blood cell count with differential and blood cultures usually is taken in high-risk infants and children to determine the cause of fever. A chest radiograph should be obtained in febrile infants younger than 3 months of age with at least one sign of a respiratory illness (e.g., tachypnea, crackles, decreased breath sounds, wheezing, coughing).Febrile children who are younger than 1 year of age and girls between 1 and 2 years of age should be considered at risk for a urinary tract infection.The approach to treatment of the young child who has a fever without a known source varies depending on the age of the child. High-risk infants and infants who are younger than 28 days are often hospitalized for evaluation of their fever and treatment.

Fever in Children

In the elderly, even slight elevations in temperature may indicate serious infection or disease, most often caused by bacteria. This is because the elderly often have a lower baseline temperature, and although they increase their temperature during an infection, it may fail to reach a level that is equated with significant fever. Normal body temperature and the circadian pattern of temperature variation often are altered in the elderly. Fever in the older adult does increase the older adult’s immunological response, but it is generally a much weaker response compared to younger people.It has been suggested that 20% to 30% of older adults with serious infections present with an absent or blunted febrile response. The probable mechanisms for the blunted fever response include a disturbance in sensing of temperature by the thermoregulatory center in the hypothalamus, alterations in release of endogenous pyrogens, and the failure to elicit responses such as vasoconstriction of skin vessels, increased heat production, and shivering that increase body temperature during a febrile response.Absence of fever may delay diagnosis and initiation of antimicrobial treatment. Therefore, it is important to perform a thorough history and physical examination focusing on other signs of infection and sepsis in older adults. Signs of infection in older adults when fever is absent include unexplained changes in functional capacity, worsening of mental status, weakness and fatigue, and weight loss.Another factor that may delay recognition of fever in older adults is the method of temperature measurement. It has been suggested that rectal and tympanic membrane methods are more effective in detecting fever in the elderly. This is because conditions such as mouth breathing, tongue tremors, and agitation often make it difficult to obtain accurate oral temperatures in older adults.

FEVER IN OLDER ADULTS

TreatmentFever is a disease symptom, its manifestation suggests the need for diagnosis and treatment of the primary cause. Modification of the environment ensures that the environmental temperature facilitates heat transfer away from the body. Sponge baths with cool water or an alcohol solution can be used to increase evaporative heat losses, but caution is necessary so the person is not cooled too quickly. It is better to bring the person to a health care practice to obtain advice on whether the person may need intravenous lines for hydration and other medical attention. More profound cooling can be accomplished through the use of forced air blankets or a cooling mattress, which facilitates the conduction of heat from the body into the coolant solution that circulates through the mattress. Care must be taken so that the cooling method does not produce vasoconstriction and shivering that decrease heat loss and increase heat production.Adequate fluids and sufficient amounts of simple carbohydrates are needed to support the hypermetabolic state and prevent the tissue breakdown that is characteristic of fever. Additional replacement fluids are needed for sweating and to balance the insensible water losses from the lungs that accompany an increase in respiratory rate. Fluids also are needed to maintain an adequate vascular volume for heat transport to the skin surface.Antipyretic drugs, such as aspirin, ibuprofen, and acetaminophen, often are used to alleviate the discomforts of fever and protect vulnerable organs, such as the brain, from extreme elevations in body temperature. It is thought that these drugs act by resetting the set point of the temperature-regulating center in the hypothalamus to a lower level, presumably by blocking the activity of cyclooxygenase, an enzyme that is required for the conversion of arachidonic acid to PGE2. However, evidence suggests that the routine administration of antipyretics does not decrease the duration of the fever or illness. Because of the risk of Reye syndrome, the Centers for Disease Control and Prevention, U.S. Food and Drug Administration, and American Academy of Pediatrics Committee on Infectious Diseases advise against the use of aspirin and other salicylates in children with influenza or chickenpox.

THE MOST COMMON AND EFFECTIVE MEDICATIONS TO TREAT FEVERS ARE:

TYIENOL (Acetaminophen)Tylenol is approved for use in children as young as 2 months old, but should never be given to a child under 3 months without first speaking to a doctor.

ADVIL or MOTRIN (Ibuprofen)Ibuprofen is approved for use in children as young as 6 months.

AspirinAspirin should never be given to children under 18 years of age, unless

specifically recommended by a doctor, because of the risk of a rare but possibly fatal illness called Reye’s Syndrome.

Hyperthermia (marked warming of core temperature) can produce nerve damage, coagulation of cell proteins, and death. At 41° C (105.8° F), nerve damage produces convulsions in the adult. At 43° C (109.4° F), death results. Hyperthermia is not mediated by pyrogens, and there is no resetting of the hypothalamic set point. Hyperthermia may be accidental or therapeutic. Therapeutic hyperthermia is a form of local or general body-induced hyperthermia. Its purpose is to destroy pathologic microorganisms or tumor cells by facilitating the host’s natural immune process through elevated body temperature. As a form of treatment, it is generally controversial.

The four forms of accidental hyperthermia are:

1) HEAT CRAMPS,

2) HEAT EXHAUSTION,

3) HEAT STROKE,

4) MALIGNANT HYPERTHERMIA

DISORDERS OF TEMPERATURE REGULATIONHyperthermia

Heat CrampsHeat cramps are slow, painful, skeletal muscle cramps and spasms, usually occurring in the muscles that are most heavily used and lasting for 1 to 3 minutes. Cramping results from salt depletion that occurs when fluid losses from heavy sweating are replaced by water alone. The muscles are tender, and the skin usually is moist. Body temperature may be normal or slightly elevated. There almost always is a history of vigorous activity preceding the onset of symptoms.

Heat ExhaustionHeat exhaustion is related to a gradual loss of salt and water, usually after prolonged and heavy exertion in a hot environment.The symptoms include thirst, fatigue, nausea, oliguria, giddiness, and finally delirium. Gastrointestinal flulike symptoms are common. Hyperventilation in association with heat exhaustion may contribute to heat cramps and tetany by causing respiratory alkalosis. The skin is moist, the rectal temperature usually is higher than 37.8°C (100°F) but below 40°C (104°F), and the heart rate is elevated. Signs of heat cramps may accompany heat exhaustion.

HEAT STROKE is a potentially lethal result of a breakdown in control of an overstressed thermoregulatory center. The brain cannot tolerate temperatures over 40.5°C (104.9° F). When core temperature reaches or exceeds 40.5°C (104.9° F), the brain may be preferentially cooled by maximal blood flow through the veins of the head and face, specifically the forehead. Sweat production on the face is maintained even during dehydration. Evaporation of the sweat cools the blood in the veins of the face and forehead; the blood then is returned to the endocranial venous network and sinus cavernosus, cooling the blood in the cerebral arterial vessels that lie in proximity. Fanning the face enhances this mechanism. In this way the brain can be maintained temporarily at 40°C (104°F), even when core temperatures are higher. In instances of very high core temperatures (40° to 43°C [104° to 109.4° F]), the cardiovascular and thermoregulatory centers may cease to function appropriately. Sweating ceases, and the skin becomes dry and flushed. The individual may be irritable, confused, stuporous, or comatose. Visual disturbances may occur.As heat loss through the evaporation of sweat ceases, core temperatures increase rapidly. High core temperatures and vascular collapse produce cerebral edema, degeneration of the CNS, swollen dendrites, and renal tubular necrosis. Treatment: removing the person from the warm environment, if possible, and using a cooling blanket or cool water bath.

DEATH results unless immediate, effective treatment is initiated.

Children are more susceptible to heat stroke than adults because: 1) they produce more metabolic heat when exercising, 2) they have a greater surface area: mass ratio, 3) their sweating capacity is less than that of adults.

Drugs can induce fever by several mechanisms.:o interfere with heat dissipation, o alter temperature regulation by the hypothalamic centers, o act as direct pyrogens, o injure tissues directly/induce an immune response. Exogenous thyroid hormone increases the metabolic rate & can increase heat production & body temperature. PROPYLTHIOURACIL (PTU) has several side effects including fever & that use of PTU can induce fever and cause interstitial pneumonia. Peripheral heat dissipation can be impaired by ATROPINE & ANTICHOLINERGIC drugs, antihistamines, phenothiazine antipsychotic drugs, & tricyclic antidepressants, which sweating, or by AMPHETAMINEs (especially ecstasy), COCAINE, & sympathomimetic drugs, which produce peripheral vasoconstriction. Intravenously administered drugs can lead to infusion-related phlebitis with production of cellular pyrogens that produce fever.

Drug fever

TREATMENT with anticancer drugs → release of endogenous pyrogen from destroyed cancer cells. Overdoses of serotonin reuptake inhibitors or use in people taking monoamine oxidase (MOA) inhibitors can cause agitation, hyperactivity, and hyperthermia (Serotonin syndrome).The most common cause of drug fever is a hypersensitivity reaction. Hypersensitivity drug fevers signs: arthralgias, urticaria, myalgias, gastrointestinal discomfort, and rashes.Temperatures of 38.9°C to 40.0°C (101.8°F to 104.0°F) are common in drug fever.

coinciding with the administration of a drug & disappearing after the

drug has been discontinued

autosomal dominant metabolic disorder; heat generated by uncontrolled skeletal muscle contraction can produce severe & potentially fatal hyperthermia; mutation involves the RYR1 gene on chr. 19q13.1.2; muscle contraction is caused by an abnormal release of intracellular Ca2+ from the sarcoplasmic reticulum through calcium release channels. Ca2+ leads to a sustained hypermetabolic rate & a subsequent loss of cellular integrity: excess lactate production, high adenosine triphosphate (ATP) consumption, increased oxygen consumption; carbon dioxide production; elevated heat production. An episode of malignant hyperthermia is triggered by exposure to certain stresses or general anesthetic agents (acute/insidious onset of symptoms). MH is associated with the halogenated anesthetic agents (halothane) & the depolarizing muscle relaxant succinylcholine. Nonoperative precipitating factors: trauma, exercise, environmental heat stress, & infection. Dangerous in a young person (large muscle mass to generate heat). Steady in end-tidal carbon dioxide levels (initial sign, when the condition occurs during anesthesia, is skeletal muscle rigidity). Cardiac arrhythmias and a hypermetabolic state; TREATMENT: measures to cool the body, cardiopulmonary support, & the administration of dantrolene, a muscle relaxant drug that acts by blocking the release of calcium from the sarcoplasmic reticulum.

Malignant Hyperthermia (MH)

BROMOCRIPTINE (a dopamine agonist) & DANTROLENE (a muscle relaxant) may be used as part of the treatment regimen.

Type of burns

The extent of the total body surface area (TBSA) burn is estimated using the “rule of nines. First-degree burns are not included in the TBSA estimate. The surface area of the palm, including palmar finger surface, averages 1% of the body surface area over a wide range of ages; thus it can be used to estimate burn areas of irregular size and shape.

Rule of nines

SECOND DEGREE THIRD DEGREE

CHARACTE-RISTIC

FIRST DEGREE

SUPERFICIAL PARTIALTHICKNESS

DEEP PARTIAL THICKNESS FULL THICKNESS

MORPHOLOGY Destruction of epidermis only

Destruction of epidermis & some dermis

Destruction of epidermis & dermis, leaving only skin appendages

Destruction of epidermis, dermis, & underlyingsubcutaneous tissue

SKIN FUNCTION Intact Absent Absent Absent

TACTILE AND PAIN SENSORS

Intact Intact Intact but diminished Absent

BLISTERS Present only after first 24 hr

Present within minutes, thin walled and fluid filled

May appear as fluid-filled blisters; often is layer of flat, dehydrated “tissue paper” that lifts off in sheets

Blisters rare; usually is a layer of flat, dehydrated “tissue paper” that lifts off easily

APPEARANCE OF WOUND AFTER INITIAL DÉBRIDEMENT

Skin peels at 24-48 hr, normal or slightly red underneath

Red to pale ivory, moist surface

Mottled with areas of waxy white, dry surface

White, cherry red, or black; may contain visible thrombosed veins; dry, hard leathery surface

HEALING TIME 3-5 days 21-28 days 30 days to many monthsWill not heal; may close from edges as secondary healing if wound is small

SCARRING None

May be present; low incidenceinfluenced byGenetic predisposition

Highest incidence because of slow healing rate promoting scar tissue development; also influenced by genetic predisposition

Skin graft; scarring minimized by early excision and grafting; influenced by genetic predisposition

DEPTH OF BURN INJURY

IMMEDIATE CELLULAR AND IMMUNOLOGIC ALTERATIONS OF BURN

SHOCKAcute Burn

InjuryDirect tissue

injuryIncreased capillary

permeability

Systemic injury response

Increased capillary

permeability

Tissue injury

Endothelial injury

Leukocytesequestratio

n

Acidosis Depressed cardiac function Multiorgan dysfunction

Edema

Tissue ischemia

Hypovolemia and

hyperviscosity

Hypothermia is defined as a core temperature (i.e., rectal, esophageal, or tympanic) less than 35°C (95°F). Accidental hypothermia may be defined as a spontaneous decrease in core temperature, usually in a cold environment and associated with an acute problem but without a primary disorder of the temperature-regulating center. In children, the rapid cooling process, in addition to the diving reflex that triggers apnea and circulatory shunting to establish a heart–brain circulation, may account for the surprisingly high survival rate after submersion. The diving reflex is greatly diminished in adults.Systemic hypothermia may result from exposure to prolonged cold (atmospheric or submersion). The condition may develop in otherwise healthy people in the course of accidental exposure. Because water conducts heat more readily than air, body temperature drops rapidly when the body is submerged in cold water or when clothing becomes wet. In people with altered homeostasis due to debility or disease, hypothermia may follow exposure to relatively small decreases in atmospheric temperature.Many underlying conditions can contribute to the development of hypothermia. Malnutrition decreases the fuel available for heat generation, and loss of body fat decreases tissue insulation. Alcohol and sedative drugs dull mental awareness to cold and impair judgment to seek shelter or put on additional clothing. Alcohol also inhibits shivering. People with cardiovascular disease, cerebrovascular disease, spinal cord injury, and hypothyroidism also are predisposed to hypothermia.

Hypothermia

HYPOTHERMIA

I Stage of excitement (mild hypothermia, 32–35°C): maximal muscle tremor, resulting in a marked increase in resting metabolic rate, all sources of glucose are utilized (hyperglycemia), and O2 consumption is increased up to six fold. Tachycardia and vasoconstriction cause a rise in blood pressure; sacral vasoconstriction causes pain. The person is at first fully awake, later confused and even apathetic, and ultimately judgment becomes impaired.

II Stage of exhaustion (moderate hypothermia, 32-28°C): the sources of glucose become exhausted (hypoglycemia); bradycardia, arrhythmia, and depressed breathing occur and the person begins to hallucinate and to behave perplexingly, soon losing consciousness and no longer feeling pain.

III Stage of paralysis (severe hypothermia, < ca.28°C): coma; no pupillary reflexes (but no sign of brain death); ultimately ventricular fibrillation, asystole, and apnea. The lower the temperature until cerebral blood flow ceases, the longer the brain will tolerate circulatory arrest (30°C: 10–15min; 18°C: 60–90 min). This is why some persons have survived extreme hypothermia (< 20°C). The long time of circulatory arrest tolerated at low temperature is also of use in induced therapeutic hypothermia (during open-heart surgery and preservation of organs for transplantation).

THE ACUTE SEQUELAE AND SYMPTOMS OF HYPOTHERMIA CAN BE DIVIDED INTO THREE STAGES (I–III):

Infants are particularly at risk for hypothermia because of their high ratio of surface area to body mass. Relative to body weight, the body surface area of an infant is three times that of an adult, and in infants with low birth weight, the insulating layer of subcutaneous fat is thinner. The newborn infant is particularly at risk, but the premature newborn is at greatest risk for heat loss and hypothermia. Under the usual delivery room conditions (20°C to 25°C [68°F to 77°F]), an infant’s skin temperature falls approximately 0.3°C/minute and deep body temperature by approximately 0.1°C/minute. The heat loss occurs by convection to the cooler surrounding air, by conduction to cooler materials on which the infant is resting, by radiation to nearby cooler solid objects, and by evaporation from the moist skin. The unstable body temperature of a preterm infant can drop precipitously after delivery, and this hypothermia is associated with an increase in morbidity and mortality.

Neonatal Hypothermia

The newborn infant does have one important process to fight against hypothermia. This process is called nonshivering thermogenesis, and it occurs primarily in the liver, brown fat tissue, and brain. Brown fat differs from regular adipose tissue because it has a high number of mitochondria. Newborns have this brown fat tissue in their necks and upper back. The brown fat has an uncoupling protein called UCP1 (thermogenin), which allows oxidation of fatty acids to produce heat. The extreme cold temperature stimulates a release of epinephrine & TSH, which causes a release of T3 and T4. Epinephrine activates the 5´/3´-monodeiodinase, which assists with the conversion of T4 to the more rapid-acting T3. The T3 acts in the brown fat to release the mitochondrial oxidation from phosphorylation. This, in turn, causes more heat production.

Neonatal Hypothermia

Used to slow metabolism;Preserve ischemic tissue after brain trauma or during brain surgery; After cardiac arrest; In neonatal hypoxic encephalopathy.Hypothermia protects the brain by:Reduction in metabolic rate; ATP consumption and oxidative stress;Reduction of the critical threshold for oxygen delivery; Modulation of excitotoxic neurotransmitters; Calcium antagonism;Preservation of protein synthesis;Preservation of the blood-brain barrier;Decreased edema formation;Modulation of the inflammatory response. Survival from accidental hypothermia has been reported in individuals with core °t at 16° C (60.8° F) & from therapeutic hypothermia with °t at 9° C (48.2° F).

Therapeutic Hypothermia

Aneurysm opened with hypothermia & distal anastamosis completed

COMPLICATION MECHANISM

Acidosis

Rewarming stimulates peripheral vasodilation; peripheral blood, returning to the core from the ischemic peripheral tissues, causes a reduction in the pH of core blood

Rewarming shock

As rewarming and vasodilation progress, the body is unable to maintain blood pressure because of reduced fluid volume (from “cold diuresis”), catecholamine depletion (prolonged shivering), and myocardial injury

Deep-ended hypothermia

As colder surface blood is returned to the core, core temperature may drop; this is also referred to as “after fall” or “after drop”

DysrhythmiaRewarming places an additional stress on an already severely stressed myocardium

Accidental Hypothermia: Complications of Rewarming

TRAUMA

CNS TRAUMA

ACCIDENTAL INJURY

THERMAL BURNS

HEMORRHAGIC SHOCK

MAJOR SURGERY

Major body trauma has varying effects on temperature

regulation, depending on the body systems involved.

Central Nervous System Trauma

CNS damage, inflammation

intracranial pressures, or intracranial bleeding

Fever greater than 39°C (102.2°F)

NEUROGENIC FEVER

with/ without relative bradycardia & is not caused by infection

°t is sustained, not induce sweating, resistant to

antipyretic therapy

ACCIDENTAL INJURIES

Slight elevation in core temperature

Severe injuries result in peripheral vasoconstriction with decreased surface and

core temperatures

Core °t is inversely related to the severity of the

injury &may be a result of decreased oxygen

transport to the tissues In severe injuries,

shivering is absent & some alteration in

thermoregulation is evident

Volume expansion with warmed solutions is recommended to prevent

the deleterious effects of hypothermia on cardiac output, cardiac rhythm, and the immune

system

HEMORRHAGIC SHOCK

Loss of blood volume in

hemorrhagePeripheral

vasoconstriction & hypoxia contributing to

hypothermia

Risk for subsequent in core °t occurs treated with unwarmed, volume-expanding solutions &

surgery

Significant hypothermia through exposure of body cavities to the relatively cool operating room environment; Irrigation of body cavities with room °t solutions; Infusion of room °t intravenous solutions; Use of drugs that impair thermoregulatory mechanisms;Inhalation of unwarmed anesthetic agents.

MAJOR SURGER

Y

Anesthesia

Induces hypothermia

Reduces platelet function

Impairs the coagulation cascade contributing to

transfusion requirements & postoperative complications

Reduces intraoperati

ve hypothermia

& postoperativ

e complication

s

Use of irrigating;warmed intravenous solutions;perioperative forced air;other warming procedure.

Large burn injuries produce significant

hypothermia because of the loss of the skin barrier to fluid evaporation & the

loss of control of the microcirculation in the

skin. Severe burns also

compromise the normal insulation of the skin & subcutaneous tissues.

Thermal Burns

Even with mild hypothermia and/or low ambient temperature the perfusion of skin and limbs is markedly reduced, with intermittent and brief increases (Lewis reaction: about every 20 min at a skin temperature < 10°C). None the less, frostbite may occur:1st degree (at first pallor and loss of sensation;swelling and pain after rewarming); 2nd degree (blister formation after 12–24 h followed later by healing); 3rd degree (after days and weeks: extensive tissue necrosis with healing by scar).

FROSTBITE

FROSTBITE

Mapping How Emotions Manifest in the Body

The mapping exercise produced what you might expect: an angry hot-head, a happy person lighting up all the way through their fingers and toes, a depressed figurine that was literally blue (meaning they felt little sensation in their limbs). Almost all of the emotions generated changes in the head area, suggesting smiling, frowning, or skin temperature changes, while feelings like joy and anger saw upticks in the limbs—perhaps because you’re ready to hug, or punch, your interlocutor. Meanwhile, “sensations in the digestive system and around the throat region were mainly found in disgust,” the authors wrote. It's worth noting that the bodily sensations weren't blood flow, heat, or anything else that could be measured objectively—they were based solely on physical twinges subjects said they experienced.

•Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.– New York, Milwaukee. – 2009. •Essentials of Pathophysiology: Concepts of Altered Health States

(Lippincott Williams & Wilkins), Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapter 9•General and clinical pathophysiology. Edited by prof. A.V. Kubyskin.

Simf. – 2011. •Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang //

Thieme. Stuttgart. New York. – 2000. •Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead,

Jacquelyn L. Banasic // Elsevier Inc. – 2010. •Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS

medicine Publishing. – 2010.

Literature:

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