Paul Zammit

Geriatrician

Elevation of core body temperature above the normal diurnal range of 36ºC to 37.5ºC due to failure of thermoregulation

Hyperthermia is not synonymous with the more common sign of fever, which is induced by cytokine activation during inflammation, and regulated at the level of the hypothalamus

The most important causes of severe hyperthermia (greater than 40ºC or 104ºF) caused by failure of thermoregulation are: ◦ Heat stroke

◦ Neuroleptic malignant syndrome

◦ Malignant hyperthermia

Body temperature is maintained within a narrow range by balancing heat load with heat dissipation

Body's heat load results from both metabolic processes and absorption of heat from the environment

As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the ANS to produce sweating and cutaneous vasodilation

Evaporation is the principal mechanism of heat loss in a hot environment, but this becomes ineffective above a relative humidity of 75%

Other methods of heat dissipation ◦ Radiation- emission of infrared electromagnetic

energy ◦ Conduction- direct transfer of heat to an

adjacent, cooler object ◦ Convection-direct transfer of heat to convective

air currents These methods cannot efficiently transfer

heat when environmental temperature exceeds skin temperature

Temperature elevation ↑ O2 consumption and metabolic rate hyperpnea and tachycardia

Above 42ºC (108ºF), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function

Hepatocytes, vascular endothelium, and neural tissue are most sensitive to these effects, but all organs may be involved

As a result, these patients are at risk of multiorgan system failure

The regulation of body temperature involves three distinct functions:

Thermosensors

Central integrative area

Thermoregulatory effectors

Temperature-sensitive structures are located both peripherally in the skin and centrally in the body

Skin temperature changes, correlate poorly with changes in the rate of heat loss

Thermosensitive neurons are in the preoptic area of the anterior hypothalamus. They are activated when the temperature of the blood circulating through that area exceeds a certain “set point”

The skin temperature affects heat loss, since a person resting in a warm environment initiates sweating, even though the core temperature remains constant

In contrast, changes in core temperature are more potent in producing heat-dissipating responses

The CNS interprets information received from the thermosensors to properly instruct thermoregulatory effectors

The concept of a central thermostat by which an alteration shifts effector thresholds in the same direction fits a variety of clinical situations

For example, fever, the circadian rhythm of temperature variation, and the 0.5° C difference in rectal temperature after ovulation can be explained by variation of a thermal set-point

Sweating and peripheral vasodilation are the major mechanisms by which heat loss can be accelerated

In a warm environment, evaporation of sweat from the skin is the most important mechanism of heat dissipation

Heat loss from the skin by convection and radiation is maximized by increased skin blood flow to facilitate sweating

Humans possess apocrine and eccrine sweat glands

Apocrine glands are concentrated in the axillae and produce milky sweat rich in carbohydrate and protein. They are adrenergically innervated and respond to emotional stress as well as to heat

Most glands producing “thermal sweat” are eccrine glands. These are cholinergically innervated and distributed over the entire body, with the largest number on the palms and soles. Eccrine sweat is colorless, odorless, and devoid of protein

Individuals exercising in hot environments commonly lose 1 to 2 L/hr of sweat; loss of 4 L/hr for short periods is possible

Cooling is best achieved by evaporation from the body surface; sweat that drips from the skin does not cool the body, and sweat evaporated from clothing is considerably less efficient

Each liter of completely evaporated sweat consumes 580 kcal of heat

The ability of the environment to evaporate sweat is termed atmospheric cooling power and varies primarily with humidity, but also with wind velocity

As humidity approaches 100%, evaporative heat loss ceases

University of California Office of the President

August 2009 Safety Meeting

The vascular response to heat stress is cutaneous vasodilation and compensatory vasoconstriction of splanchnic and renal beds

These vascular changes are under neurogenic control and allow heat to be dissipated quickly and efficiently, but they place a tremendous burden on the heart

To maintain blood pressure, cardiac output must increase dramatically. For this reason, saunas and hot tubs may be dangerous for patients with cardiac disease

Cardiovascular and baroreceptor reflexes also affect skin blood flow. Reduced forearm sweating and vasodilation are observed in severely dehydrated subjects exercising in a warm environment

Elderly patients or those with chronic diseases who are taking medications predisposing to heat illness are prone to classic heatstroke during periods of high ambient heat and humidity. Adequate fluid intake is essential.

Elderly patients sometimes dress inappropriately for hot weather; heat loss is maximized by light, loose-fitting garments

Fluid intake is the most critical variable. Dehydration can be minimized by education on work-rest cycles and fluid consumption and through provision of cool, pleasantly flavored fluids

A weight loss of 5% to 6% represents a moderately severe deficit and usually is associated with intense thirst, scanty urine, tachycardia, and an increase in rectal temperature of about 2° C.

A loss of 7% or more of body weight represents severe water depletion

Evaporative cooling can be lost when clothing inhibits air convection and evaporation

Loose-fitting clothing or ventilated fishnet jerseys allow efficient evaporation

Light-colored clothing reflects rather than absorbs light

Water evaporated from clothing is much less efficient for body cooling than is water evaporated from the skin

The body's heat dissipation mechanisms are analogous to the cooling system of an automobile : Coolant (blood) is circulated by a pump (heart) from the hot inner core to a radiator (skin surface cooled by the evaporation of sweat). Temperature is sensed by a thermostat (CNS), which alters coolant flow by a system of pipes, valves, and reservoirs (vasculature)

Definition : constellation of physiologic adaptations that appear in a normal person as the result of repeated exposures to heat stress

Daily exposure to work and heat for 100 min/day results in near-maximal acclimatization in 7 to 14 days. This is characterized by an earlier onset of sweating (at a lower core temperature), increased sweat volume, and lowered sweat electrolyte concentration

Heat Cramps

Heat Edema

Heat Syncope

Heat Rash

HEAT EXHAUSTION

HEATSTROKE

Classic

Exertional

Brief, intermittent, and often severe muscular cramps occurring typically in muscles that are fatigued by heavy work

Heat cramps occur most commonly during the first days of work in a hot environment and develop in persons who produce large amounts of thermal sweat and subsequently drink copious amounts of hypotonic fluid

Heat cramps appear to be related to salt deficiency

The most commonly victims : athletes, roofers, steel workers, coal miners, field workers, and boiler operators

Heat cramps tend to occur after exercise when the victim has stopped working and is relaxing. In this respect, they differ from the cramps experienced by athletes during exercise, which tend to last for several minutes, are relieved by massage, and resolve spontaneously

Essentials of Diagnosis :

Cramps of most worked muscles

Usually occur after exertion

Copious sweating during exertion

Copious hypotonic fluid replacement during exertion

Hyperventilation not present in cool environment

Mild cases without concurrent dehydration may be treated orally with 0.1% to 0.2% salt solution (two to four 10-grain salt tablets [56 to 112 mEq] or ¼ to ½ teaspoon table salt dissolved in a quart of water), which is the general limit of palatability

Severe cases respond rapidly to intravenous isotonic solution (0.9% NaCl)

Salt tablets are gastric irritants and are not recommended

Swollen feet and ankles are often reported by nonacclimatized individuals, especially the elderly, who encounter climatic stresses of tropical and semitropical area

Such individuals often have no underlying cardiac, hepatic, venous, or lymphatic disease. They commonly have assumed rigorous schedules with long periods of sitting or standing

The edema is usually minimal, not accompanied by any significant impairment in function, and often resolves after several days of acclimatization

It is presumed that hydrostatic pressure and vasodilation of cutaneous vessels, combined with some degree of orthostatic pooling, lead to vascular leak and accumulation of interstitial fluid in the lower extremities

Aldosterone increases in response to the heat stress and perceived central volume deficit

Awareness of this clinical presentation prevents overly vigorous diagnostic and therapeutic intervention

In most individuals, the problem resolves either through adequate acclimatization or with the individual's return to a home climate

The elderly have a special predilection for this disorder

Individuals adapt to a hot, humid environment by dilation of cutaneous vessels to deliver heat to the body surface. Thus, an increased portion of the intravascular pool is located in the periphery at any given time

Increasing blood flow to compliant cutaneous veins raises skin vascular volume at the expense of thoracic blood volume. Individuals who stand for protracted periods tend to pool blood in the lower extremities

Combined with volume loss and peripheral vasodilation, this pooling can result in inadequate central venous return, a concomitant drop in cardiac output, and a cerebral perfusion inadequate to maintain consciousness

The disorder is self-limited, because assumption of a horizontal position is the cure

Individuals at risk for heat syncope should be warned to move often, flex leg muscles repeatedly when standing stationary, avoid protracted standing in hot environments, and assume a sitting or horizontal position when prodromal warning signs or symptoms occur

prodromal warning signs or symptoms :

scintillating scotomata

tunnel vision

Vertigo

Nausea

Diaphoresis

weakness

Adequate education prevents many serious injuries

Prickly heat, also known as miliaria rubra, lichen tropicus, and heat rash, is an acute inflammatory disorder of the skin that occurs in hot weather

It is the result of blockage of sweat gland pores

The following also increase ther risk:

illness and immobility – long periods of time spent in bed can make you sweat more, particularly if you have warm bedding

wearing too much clothing, particularly in the winter

sitting too close to a fire or heater

being overweight – which is more likely to lead to excessive sweating

The acute phase is characterized by vesicles in the malpighian layer of the skin caused by dilation and rupture of the obstructed sweat gland ducts

Clinically, this initially produces intensely pruritic vesicles on an erythematous base. The rash is confined to clothed areas, and the affected area is often completely anhidrotic

Over the next week or so, a keratin plug arises and fills these vesicles, causing a deeper obstruction of the sweat gland duct. The obstructed duct then ruptures a second time, producing a deeper vesicle within the dermis. This is known as the profunda stage, and it can persist for weeks. Profunda vesicles are not pruritic and closely resemble the white papules of piloerection

Chronic dermatitis is a common complication

Avoid excessive heat and humidity – if you need to go outside, spend time in the shade or take a small fan with you. Further exposure to the heat will cause you to sweat more and may make your rash worse. Drink plenty of fluids to avoid dehydration, especially in hot weather.

Wear loose cotton clothing – avoid wearing synthetic fibres, such as

polyester and nylon, which trap heat easier than natural fibres.

Keep your skin cool – a cool bath or shower will cool you down, soothe your skin and help prevent further sweating. Staying in an air-conditioned room for a few hours a day will also provide considerable relief. You can also use a cold compress, but don't leave it on the skin for longer than 20 minutes.

Use calamine lotion – this is available at most pharmacies and will help soothe sore and irritated skin.

hydrocortisone cream

Antihistamine medication may help control itching

Volume depletion that occurs under conditions of heat stress

Types: water depletion / salt depletion

Water depletion heat exhaustion results from inadequate fluid replacement by individuals working in a hot environment

This “voluntary dehydration” results in progressive hypovolemia

Salt depletion heat exhaustion takes longer to develop than the water depletion form. It occurs when large volumes of thermal sweat are replaced by water with too little salt

It differs from heat cramps in that systemic symptoms occur

This syndrome is characterized by hyponatremia, hypochloremia, and low urinary sodium and chloride concentrations

Body temperature usually remains near normal

Weakness

Fatigue

frontal headache

impaired judgment

Vertigo

nausea and vomiting

muscle cramps

Orthostatic dizziness and syncope

The core temperature is only moderately elevated, usually less than 40° C, and signs of severe CNS dysfunction are not present

Vague malaise, fatigue, headache

Core temperature often normal; if elevated, less than 40° C (104° F)

Mental function essentially intact; no coma or seizures

Tachycardia, orthostatic hypotension, clinical dehydration (may occur)

Other major illness ruled out

If in doubt, treat as heat stroke

Heat exhaustion is primarily a volume depletion problem, and rapid recovery generally follows fluid administration

Decisions regarding the type of fluid and electrolyte replacements should be based on serum electrolyte measurements and the estimation of hydration status by clinical and laboratory parameters

In mild cases, rest in a cool environment and an oral electrolyte solution, such as 0.1% saline, may suffice

Patients with significant volume depletion or electrolyte abnormalities generally require intravenous fluids

If the patient is orthostatic, normal saline should be administered until the patient is hemodynamically stable

Free water deficits should be replaced slowly over 48 hours

Overly rapid correction of hypernatremia is associated with seizures caused by cerebral edema

Older patients, particularly those with cardiovascular disease or other predisposing factors, require more cautious fluid and electrolyte replacement and frequent reassessment

Admission if patient is elderly, has significant electrolyte abnormalities, or would be at risk for recurrence if discharged

Rest

Cool environment

Assess volume status (orthostatic changes, renal profile, hematocrit, serum sodium)

Fluid replacement: normal saline to replete volume if patient orthostatic, replace free water deficits slowly to avoid cerebral edema

Body temperature rises with fails in homeostatic thermoregulatory mechanisms

This failure results in elevation of body temperature to extreme levels, usually greater than 40.5° C (105° F), producing multisystem tissue damage and organ dysfunction

Core body temperature > 40.5ºC (105ºF) with associated CNS dysfunction in the setting of a large environmental heat load that cannot be dissipated

Complications include: ARDS

DIC

Renal or hepatic failure

Hypoglycemia

Rhabdomyolysis

Seizures

The resultant damage to tissues depend on :

Body temperature

Exposure time

Work load

Tissue perfusion

Individual factors

Neurologic dysfunction is a hallmark of heatstroke, and cerebral edema is common

Other pathologic changes include :

petechiae in the walls of the third and fourth ventricles

marked cerebellar damage

The hypothalamus, the predominant site of central thermoregulatory control, is usually not damaged

Heat stress creates tremendous demands on the cardiovascular system, and signs of circulatory failure, increases in skin blood flow (peripheral vasodilation) and a reduction of the thermal gradient between the core and the skin

Compensatory vasoconstriction of the splanchnic and renal vasculature. The resulting splanchnic and renal ischemia may explain the nausea, vomiting, and diarrhea observed in postmarathon runners

Hepatic damage : centrilobular necrosis with extensive cholestasis

Exposure to heat stress, endogenous or exogenous

Signs of severe CNS dysfunction (coma,seizures, delirium)

Core temperature usually above 40.5° C (105° F), but may be lower

Dry, hot skin common, but sweating may persist

Marked elevation of hepatic transaminases

Affects individuals with underlying chronic medical conditions that either impair thermoregulation or prevent removal from a hot environment.

Conditions include: ◦ Cardiovascular disease

◦ Neurologic or psychiatric disorders

◦ Obesity

◦ Anhidrosis

◦ Extremes of age

◦ Anticholinergic agents or diuretics

Occurs during periods of sustained high ambient temperatures and humidity, as during summer heat waves

Victims are often elderly and poor and live in underventilated dwellings without air conditioning

Debilitated patients who have limited access to oral fluids may develop water-depletion heat exhaustion, which progresses to heatstroke if untreated

Victims of CHS commonly suffer from chronic diseases, alcoholism, or schizophrenia, which predispose to heat illness. Such patients are often prescribed medications (e.g., diuretics, antihypertensives, neuroleptics, and anticholinergics) that impair the ability to tolerate heat stress

Sweating is totally absent in the majority of CHS patients

Poor outcome critria :

Advanced age

Hypotension

Altered coagulation status

Decreased level of conciousness

Occurs in young, otherwise healthy individuals engaged in heavy exercise during periods of high ambient temperature and humidity

Findings include : cutaneous vasodilation, tachypnea, rales due to noncardiogenic pulmonary edema, excessive bleeding due to DIC, altered mentation or seizures

Labs: coagulopathy, ARF, elevated LFTs due to acute hepatic necrosis, respiratory alkalosis, and a leukocytosis as high as 30,000 to 40,000/mm3

Delirium or coma is characteristic, but virtually any neurologic abnormality, including bizarre behavior, opisthotonus, hallucinations, decerebrate rigidity, oculogyric crisis, and cerebellar dysfunction, can be seen

Convulsions occur in up to 75% of patients and can be precipitated by therapeutic maneuvers (such as ice water immersion)

Profound muscle rigidity with tonic contractions, coarse tremor, and dystonic movements can mimic seizures

Pupils may be fixed and dilated, and the electroencephalogram may be isoelectric

All these changes are potentially reversible, although permanent damage, including cerebellar deficits, hemiplegia, dementia, and personality changes, is common in severe cases

Patients with heatstroke usually have hyperdynamic cardiovascular systems with low peripheral vascular resistance, tachycardia (up to 180 beats/min), and an elevated cardiac index. These changes are expected because skin blood vessels dilate to dissipate heat; however, this low peripheral vascular resistance has persisted in patients treated with ice water immersion and reduction of body temperature to near normal

Aberrations in coagulation are common in patients with severe heatstroke, and their presence is a poor prognostic sign

Abnormal hemostasis is manifested clinically by purpura, conjunctival hemorrhage, melena, bloody diarrhea, hemoptysis, hematuria, myocardial bleeding, or hemorrhage into the CNS

Hepatic injury is evidenced by markedly elevated levels of hepatic aminotransferases (serum aspartate transaminase and alanine transaminase)

Jaundice typically appears 24 to 72 hours after the onset of severe heatstroke and gradually recedes if the victim survives

Survivors generally have no permanent impairment of liver function

Renal damage is common. The initial urine specimen, usually obtained by catheterization, is a scanty, brownish, turbid fluid

Diarrhea, probably caused by intense splanchnic vasoconstriction, is commonly seen

Cooling aggravates the diarrhea, creating an unpleasant treatment problem

Pancreatitis is described with elevated serum amylase and lipase levels

Thermometry :

Oral thermometry is affected by mouth breathing and is a poor approximation of the core

Rectal thermometry is less variable but responds to changes in core temperature slowly

Ensure ABCs, initiate rapid cooling, tx complications

Immediate cooling is the cornerstone of treatment

Cooling must be initiated as soon as possible, in conjunction with the initiation of stabilizing treatment

Mortality increases significantly when cooling is delayed

First Aid ◦ Call Emergency and Request Ambulance

◦ Move to Cool Area

◦ Cool with Wet Cloth and Fan the Victim to Increase Cooling

◦ If Conscious, Slowly Give Cool Water

Shaking chills suggest fever with an altered hypothalamic set point rather than heat illness (Meningitis and encephalitis)

In patients with thyroid storm, the clinical symptoms resemble those of heatstroke

It should be suspected if the thyroid gland is enlarged or nodular, but a normal thyroid gland does not exclude the diagnosis

Thyroid function test results are elevated, but these are not available on an emergency basis

Thyroid storm is rare, and some critical aspects of treatment, such as rapid cooling, coincide with those for heatstroke

Drug-induced heat illness is an important consideration, particularly anticholinergic poisoning

Differentiation may be difficult because both heatstroke and anticholinergic poisoning produce hyperpyrexia, hot and dry skin, tachycardia, and abnormal mental status

Constricted pupils are present in many heatstroke patients

Mydriasis should be present in patients with anticholinergic poisoning, and its absence argues strongly against this diagnosis

Typhoid fever, typhus, delirium tremens, and hypothalamic hemorrhage

Rare genetic disorder manifests after administration of anesthetic agents: succinylcholine and halothane

Onset is usually in 1 hour of the administration of anesthesia, rarely delayed up to 10 hours

½ of cases are inherited in as AD; Rest are inherited in different patterns

Early clinical findings in malignant hyperthermia include : muscle rigidity (especially masseter stiffness), sinus tachycardia, increased CO2 production, and skin cyanosis with mottling

Marked hyperthermia (up to 45ºC [113ºF]) occurs minutes to hours later; core body temperature tends to rise 1ºC every 5 to 60 minutes

Idiosyncratic reaction to antipsychotic agents

IN addition to hyperthermia, NMS is also characterized by "lead pipe" muscle rigidity, altered mental status, choreoathetosis, tremors, and evidence of autonomic dysfunction, such as diaphoresis, labile blood pressure, and dysrhythmias

Centers for Disease Control (CDC) ◦ Between 1999 to 2003 – 3442 Heat-Related

Fatalities in the U.S.

◦ Average Approximately 690 Deaths per Year

◦ Large Percentage of the Fatalities: Males

Elderly

Consume Plenty of Fluids ◦ 2 to 4 Glasses/Hour

Thirst – Unreliable Indicator of Dehydration

Avoid Alcohol, Caffeine, or High Sugar Beverages – Diuretics

Consult Physician If On a Limited Fluid Regiment or If Taking Water Pills

Acclimatization

◦ If you are continually are in a hot environment over several days, the body slowly conditions itself to the heat. This term is called “acclimatizaton”. The acclimation process takes several days, up to 10 days for some persons. Once you are not in a hot environment, the body may lose the acclimation in a matter of days.

Conditioning/General Health ◦ Stay in Shape, Exercise Regularly ◦ Watch Your Weight

Stay Indoors in an Air Conditioned (A/C) Place If Home is Not A/C - Go to A/C Public Place

Electric Fans - Effective Up to the mid-high 30 centigrade ◦ Cool Bath/Shower or Move to A/C Location

Wear Light Weight, Light Colored, Loose Fitting Clothes

Never Leave Anyone in Parked Closed Vehicles ◦ Temperatures Can Reach 120oF in 10 Minutes

◦ Since 1998, > 230 Child Fatalities

Try to Limit the Activities to Morning or Evening Hours

Do Not Engage in or Minimize Strenuous Activities

Consume 2 to 4 Glasses of Water Per Hour

Rest Often and Stay in Shady Areas

Wear Wide Brim Hats

To Prevent Heat Related Illnesses ◦ Stay Indoors (preferably with A/C) or In the Shade

If Possible Remain Indoors in the Heat of the Day

◦Drink Plenty of Fluids

◦ Rest & Minimize Strenuous Activities The Young and Elder are the Most

Susceptible to Heat-Related Illnesses ◦ Require Increased Monitoring During Extreme Heat

Conditions