Download - 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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Hipertermia - Murdin Amit 18
Menerangkan pengendalian hipertermia
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Hipertermia - Murdin Amit 19
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
Management of Heat Stroke
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D Intubate if needed
E Temperature should be measured by
oesophageal or rectal probe
Management of Heat Stroke
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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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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MALIGNANT HYPERTHERMIA
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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