hyperthermia class

7/28/2019 Hyperthermia Class

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Definition

Elevation of core body temperature above the

normal diurnal range of 36C to 37.5C 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 thehypothalamus


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Hyperthermia

The most important causes of severe

hyperthermia (greater than 40C or 104F)

caused by failure of thermoregulation are:

Heat stroke

Neuroleptic malignant syndrome

Malignant hyperthermia

Drug Induced


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Physiology

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 theenvironment

As core temperature rises, the preoptic nucleus of

the anterior hypothalamus stimulates efferent fibers

of the ANS to produce sweating and cutaneous

vasodilation.


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Hipertermia - Murdin Amit 5

Thermoregulation

ColdBehavioural

Cutaneous vasoconstriction

Shivering, non-shivering

WarmBehavioural

Cutaneous vasodilation

Sweating,Panting

Efferent Responses

Preoptic nucleiAnterior Hypothalamus

Thermal Receptorscold and warmSkin and viceral


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Physiology

Evaporation is the principal mechanism of heat lossin a hot environment, but this becomes ineffectiveabove 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 aircurrents

These methods cannot efficiently transfer heat whenenvironmental temperature exceeds skintemperature.


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Physiology

Temperature elevation O2 consumption andmetabolic rate hyperpnea and tachycardia

Above 42C (108F), oxidative phosphorylation

becomes uncoupled, and a variety of enzymes ceaseto function.

Hepatocytes, vascular endothelium, and neuraltissue are most sensitive to these effects, but all

organs may be involved. As a result, these patients are at risk of multiorgan

system failure.


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How does the newborn lose body heat?

Four ways a newborn may lose heat to the environment.

Most cooling of the newborn occurs during the first minutes after birth.


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Heat Regulation

Four mechanisms of heat loss/dissipation:

Radiation

Convection

Conduction

Evaporation


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Radiation

Physical transfer of heat between the body

and the environment by electromagnetic

waves

65% of heat transfer under normal

circumstances

Modified by insulation (clothing, fat layer),

cutaneous blood flow


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Convection

Energy transfer between the body and a gas or

liquid

Affected by temperature gradient, motion at

the interface, and liquid

Not usually a major source for heat loss or

dissipation, but this increases with wind and

body motion


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Conduction

Direct transfer of heat energy between two

surfaces

Responsible for only a small proportion of

heat loss under normal circumstances


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Levels of Hyperthermia

There are three levels of hyperthermia

- Heat cramps: painful muscle spasms/cramps

usually in legs, arms or abdomens.

- Heat exhaustion: when no action is taken

when a cramp becomes evident.

- Heat stroke: can cause impaired mental

function, leading to unconsciousness and

death.


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Signs & Symptoms

Heat Cramps Heat Exhaustion Heat Stroke

Pain Nausea, Vomiting Nausea, Vomiting

Muscle rigidity Muscle Cramps Irritable

Red, Sweaty, Hot Skin Pale, Cool, Clammy Skin Hot, Red, Dry Skin

Weak, Rapid Pulse Pounding, Rapid Pulse

that gradually weakens

Breathing Breathing

Faintness, Dizziness Dizziness, Delirium

Headache Headache

Confusion Altered consciousness

leading to convulsions

and unconsciousness

Thirst


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Heat Stroke

Core body temperature > 40.5C (105F) withassociated CNS dysfunction in the setting of alarge environmental heat load that cannot be

dissipated Complications include:

ARDS

DIC

Renal or hepatic failure

Hypoglycemia

Rhabdomyolysis

Seizures


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Exertional heat stroke

Occurs in young, otherwise healthy individuals engagedin heavy exercise during periods of high ambienttemperature and humidity

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

Labs: coagulopathy, ARF, elevated LFTs due to acutehepatic necrosis, respiratory alkalosis, and a

leukocytosis as high as 30,000 to 40,000/mm3 One series of 58 patients with heat stroke found an

acute mortality rate of 21 percent (Ann Intern Med1998 Aug 1;129(3):173-81)


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Menerangkan pengendalian hipertermia


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Menerangkan pengendalian hipertermia


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Classical Occurs due to exposure to a high

environmental temperature

Exertional Occurs in the setting of strenuous

exercise

Heat stroke


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Oxidative phosphorylation stops at

temperatures > 42 C

Cell damage

Loss of thermoregulatory compensatory

mechanisms

Hypoxia, increased metabolic demands,

circulatory failure, coagulopathies and

inflammatory response

Pathophysiology


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Tachyarrythmias and hypotension

Two types exist with exertional heat stroke

Hyperdynamic group high cardiac output and

tachycardia

Hypodynamic group Low cardiac output,

increase peripheral vascular resistance

CVS Effects


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Cardinal features of heat stroke

Delirium, lethargy, coma and seizures

Can be permanent (up to 33%)

Neurological Effects


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Injured cells leak phosphate and calcium

Hypercalcaemia and Hyperphosphataemia

Hypokalaemia is seen early

Secondary to heat induce hyperventilation leading torespiratory alkalosis

Sweat and renal losses

Hyperkalaemia is seen later Potassium losses from damaged cells and renal failure

Hyperuricaemia develops secondary to therelease of purines from injured muscle

Rhabdomyolysis


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ARF in approx 30%

Direct thermal injury to kidneys

Pre-renal insult of volume depletion and renal

hypoperfusion

Rhabdomyolysis

Renal Effects


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Exertional heat stroke is associated with

haemorrhagic complications

Petechial haemorrhages or eccyhmosis

secondary to direct thermal injury or DIC

Haematological


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Similar to sepsis

The actions of inflammatory mediators

account for the multi organ dysfunction

Immunological


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Consider in patients with altered mental state andexposure to heat

Classic triad of hyperthermia, neurologicalabnormalities and dry skin

Measure temp with rectal/oesophageal probe Sweating can still be present

Hypotension and shock 25% Hypovolaemia, peripheral vasodilatation and cardiac

dysfunction Sinus tachy

Hyperventilation a universal finding in heat stroke

Assessment


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UEC

Hypokalaemia

Hyperphosphataemia and hypercalcaemia

Hyperkalaemia and hypocalcaemia may be

present if rhabdomyolysis has occurred

Renal impairment

Investigations


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Urate is frequently high and may play a role

in the development of acute renal failure

Glucose elevated in up to 70%

LFT

Almost always seen in exertional heat stroke

(AST and LDH most commonly elevated)

CK 10000 to 1000000 in rhabdomyolysis

Investigations


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FBC WCC as high as 30 -40,000

Coag routinely abnormal and DIC may occur

Acid Base: Lactic acidosis

Compensatory respiratory alkalosis

Myoglobin serum or urine myoglobin maybe elevated

Investigation


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ECG

Rhythm disturbances (sinus tachy, SVT + AF)

Conduction defects (RBBB and intraventricular

conduction defects)

QT prolongation (most common secondary to low

K+ , Ca 2+ and Mg 2+)

ST changes (secondary to myocardial ischaemia)

Investigation


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CXR:

ARDS

Aspiration

Investigations


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If prompt effective treatment not undertaken

mortality approaches 80%

A

ETT if needed

Consider early

Avoid suxamaethonium

Management of Heat Stroke


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B Monitor Resp Rate and O2 sats Look for evidence of aspiration if GCS decreased Check for ARDS and ventilate as per lung injury

protocolC May be a large fluid deficit N saline is probably best (CSL lactate and avoid K+

containing fluids) Monitor heart rate, BP, CVP and urine output Picco/Swan-Ganz pulmonary artery catheter may be

indicated Pressors may be needed but avoid adrenergic agents as

they can impair heat dissipation by causing peripheralvasoconstriction do amine



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D Intubate if needed

E Temperature should be measured by

oesophageal or rectal probe



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Mainstay of therapy and must be initiatedfrom the onset

Use prehospital may be lifesaving

Initially remove patient from heat source andremove all clothing

Evaporative cooling tepid water on the skin

with fans Ice water immersion most effective method

but practically difficult and cant usemonitors/equipment and uncomfortable for

the patient

Cooling Methods


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Ice packs to axilla, groin and neck

Cooling blankets and wet towels

Peritoneal lavage and cardiopulmonary bypass

can be considered in severe resistant cases

Shivering may occur in rapid cooling this will

increase oxygen consumption and heat

production Sedate

paralyse

Paracetamol and aspirin are ineffective and

Cooling Methods


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Mortality should be less than 10% with

prompt treatment

Most recover without sequalae

Residual neurological defects are reported

Outcome


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Heat exhaustion mild heat stroke

Same physiological process

Patients can still have the capacity to dissipate

heat and the CNS is not impaired

Volume depletion is still a problem

Heat Exhaustion


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Painful involuntary spasms of major muscles

Usually in heavily exercised muscle groups

Dehydration and salt loss also thought to plat

a role

Rest rehydrate and replace salts

Heat Cramps


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OBJECTIVES FOR MALIGNNANT HYPERTHERMIA

Describe the pathophysiology associated with malignant hyperthermia.

Discuss the signs and symptoms of malignant hyperthermia.

List triggering agents for malignant hyperthermia.

Describe the malignant hyperthermia treatment protocol.

Discuss the testing available to identify malignant hyperthermia patient. List differential diagnosis for malignant hyperthermia.

Identify the population at risk for developing malignant hyperthermia.

Describe the plan of care for a known malignant hyperthermia patient.


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Malignant Hyperthermia

Uncommon, life-threatening, hypermetabolic disorder of theskeletal muscle triggered by inhalation agents andsuccinylcholine.

First case was of an Australian family over 40 years ago.

Inherited in some families as a autosomal dominant patternwith variable penetrance.

52% of cases occur under the age of 15, with the mean age18.3 years.

Incidence- 1:50,000 adults and 1:15,000 children.

High incidence states-Wisconsin, West Virginia, and Michigan


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MALIGNANT HYPERTHERMIA

PATHOPHYSIOLOGY

Cause of MH is not yet known with certainty.

MH is an inherited disorder of the skeletal

muscle system in which a defect in the calcium

regulation is expressed by exposure to

triggering anesthetic agents; intracellular

hypercalcemia results.


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PATHOPHYSIOLOGY

The ryanodine receptor modulate calcium

release from the channels in the sarcoplasmic

reticulum, and much attention has been

focused on this receptor as a site of the MH

defect.

There is no evidence of primary defect incardiac or smooth muscle cells.


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PATHOPHYSIOLOGY

When MH is initiated-the concentration ofcalcium in the muscle cells increase.

Actomysin cross-bridging, sustain musclecontraction, and rigidity results.

Energy-dependent reuptake mechanisms

attempt to remove excess calcium from themuscle cells, increasing muscle metabolismtwofold to threefold.


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MALIGNANT HYPERTHERMAI

TRIGGERING AGENTS

ALL VOLITILE ANESTHETICS

SUCCINYLCHOLINE

NON TRIGGERING AGENTS- EVERYTHING ELSE


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MALIGNANT HYPERHTERMIA

CLINICAL EVENTS OF MH: TACHYCARDIA

TACHYPNEA

LIABILE B/P, ARRHYTHMIAS

RISE ETCO2, ABRUPT OR GRADUAL MASSETER MUSCLE OR GENERALIZED MUSCLE RIGIDITY (75%)

UNANTICIPATED RESPIRATORY OR METABOLIC ACIDOSIS

RISING PATIENT TEMPERATURE

COLA-COLORED URINE

MOTTLED, CYANOTIC SKIN, DECREASED SaO2


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LABORATORY FINDINGS:

ARTERIAL BLOOD GAS:PCO2>60mmHg BASEEXCESS MORE NEGATIVE THAN-

8mEq/L,Ph6mEq/L CK>10,000 IU/L,

AFTER ANESTHETIC WITHOUTSUCCINYLCHOLINE

SERUM MYOGLOBIN >170mcg/L

URINE MYOGLOBIN >60mcg/L


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Hyperthermia may climb 1 degree to 2

degrees C every 5 minutes and exceed 43.3 C

(110 degrees F). Often a late but confirming

sign of MH.

Late complications: cerebral edema,

myoglobinuric renal failure, consumptive

coagulopathy, hepatic dysfunction, andpulmonary edema.


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Manifestations that mimic MH

TACHYCARDIA-hypoxia, hypercarbia, hypovolemia,light anesthesia, anticholinergics, sympathomimetics,cocaine, pheochromocytoma.

HYPERPYREXIA-heatstroke, blood transfusionreaction, infection, drug reaction, neurolepticmalignant syndrome, serontonin syndrome,hypermetabolic states-sepsis, thyroid storm,pheochromocytoma.


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Manifestations that mimic MH

Tachypnea, Hypercapnia-CHF, pulmonary edema,hypermetabolic states, intraperitoneal CO2insuflation, airway obstruction, pneumothorax,excessive dead space, low minute volume.

Masseter Muscle Rigidity-insufficient neuromuscularblockade, temporomandibular joint syndrome,neuroleptic malignant syndrome, myotonia.


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IN ADDITION TO BEING A TRIGGERING AGENT

FOR MH, SUCCINYLCHOLINE MAY ALSO

INDUCE A HYPERKALEMICMEDIATED

CARDIAC ARREST IN CHILDREN WITH OCCULTMYOPATHIES. PACKAGE INSERT WAS

MODIFIED TO WARN AGAINST THE ROUTINE

USE OF SUCCINYLCHOLINE IN CHILDREN.


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PREOP ASSESMENT Family history of muscle disorders

Unexpected intraoperative deaths

Family or personal muscle rigidity/stiffness or high feverunder anesthesia

History of heat stroke

Personal history of dark cola-colored urine following surgery

Absence of positive history does not preclude MHsusceptability

MH is linked to Duchennes and Beckers muscular dystrophy 50% of patients with unexplained CK elevation test positive

for MH on biopsy


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TREATMENT CALL FOR HELP-tell surgeon to conclude procedure

Discontinue volitile agent and succinylcholine

Hyperventilate 100% O2 at 10 L/min

Dantrolene 2.5mg/kg up to 10mg/kg (175mg in 70kgup to700mg) each vial 20mg mix in 60 cc of sterilewater

Dysrhythmias treat acidosis and hyperkalemia,

standard antiarrhythmic drugs. Avoid calciumchannel blockers


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FEVER- cooling lavage orogastric, bladder, open cavities,chilled IV fluid, ice packs, hypothermia blanket

ACIDOSIS- NA bicarbonate, send ABGs, lytes, glucose every

15minutes. Base line coagulation studies, CK, myoglobin, liverenzymes

HYPRERKALEMA-hyperventilation, 10 units regular insulin in50 ml 50% glucose titrated to potassium level

Maintain urine output 2ml/kg/hr by hydration and mannitol(300mg/kg) and/or furosemide (.5 to 1.0mg/kg)

Consider CVP/PA arterial monitoring


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Anesthesia for the MH-susceptible patient Standard monitoring equipment

Cooling blanket under patient at start of procedure

Preop anxiolytic

Local or regional if possible

Triggering agents removed from OR Anesthesia machine- change soda lime, circuit, removing or inactivating

vaporizers, flush 10L O2 for 20 minutes

3000 ml cold IV solution available

Ice available

ABG analysis available

36 VIAL OF DANTROLENE AVAILABLE


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DIAGNOSTIC TESTING

CAFFEINE HALOTHANE TEST

THIGH MUSCLE BIOPSY MEASURES THE

CONTRACTILE RESPONSE TO CAFFEINE,HALOTHANE, OR BOTH. THIS IS AUGMENT INTHE PATIENT WITH MH.

92% SENSITIVITY AND 78%SPECIFICITY


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GENETIC DIAGNOSTIC TESTING

RYR-1 gene

Has 28 mutations that are causal for MH

Blood test can be shipped to the lab

Limitation is sensitivity of approximately 25%


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GENETIC DIAGNOSTIC TESTING

Patients should consider genetic testing if: a)

they have a positive contracture test, b) afamily member has had a positive contracturetest, c)they suffered a MH episode, d) a familymember has been found to have a causalmutation


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hyperthermia class

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