Amy Gutman MD [email protected] / .

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Amy Gutman MD [email protected] / www.TEAEMS.com

Transcript of Amy Gutman MD [email protected] / .

Amy Gutman [email protected] /

www.TEAEMS.com

OVERVIEWOVERVIEW

Heat Related Illnesses

High Altitude Illnesses

Lightening Injuries

DEFINITIONSDEFINITIONS

“Normal” temperature98.6oF (37oC)

HypothermiaCore temp <95oF (35oC)

HyperthermiaCore temp >105oF (45oC)

HOMEOSTASIS: HOMEOSTASIS: THERMOREGULATIOTHERMOREGULATIO

NN Body’s desire to maintain a steady

internal environment

Maintain enzyme / cell activities & organ functions

Body temp maintained by multiple interconnected mechanismsPrimarily set by hypothalamus acting as a thermostatPeripheral & central thermoreceptors shunt blood to

core to maintain homeostasis

THERMOREGULATION THERMOREGULATION METHODSMETHODS

Body Temperature Core & Peripheral

Hypothalamus

Heat Dissipation Sweating, vasodilatation

Heat Conservation Shivering,

vasoconstriction

Thermoreceptors Central Peripheral

Metabolic Rate Basic metabolic rate Exertional metabolic rate Core temperature

HOMEOSTASIS: HOMEOSTASIS: THERMOLYSISTHERMOLYSIS

Conduction Direct loss of heat from one object to another

Convection Direct heat loss to air currents

Radiation Heat loss to nearby objects without direct contact

Evaporation Heat loss secondary to water evaporation from skin

Respiration Convection, radiation & evaporation

HOMEOSTASIS: HOMEOSTASIS: THERMOREGULATIONTHERMOREGULATION

Body generates cellullar level heat via mitochondrial metabolism

○ Basal metabolic rate○ Exertion metabolic rate

Shivering is an autonomic / automatic heat forming mechanism via muscle contraction

THERMAL REGULATIONTHERMAL REGULATION

Heat flows from area of high to low temperature

A body in warm environment gains heat, a body in a cool environment gives off heat

Other factors: Wind Relative humidity

Humidity Humidity IndexIndex

RISK FACTORSRISK FACTORS Age

Age extremes less able to tolerate temp shifts

Poor Health & Predisposing PMH IDDM: autonomic dysfunction reduces ability to vasodilate &

sweat Cardiac: fluid shifts not tolerated well

Medications Beta blockers, Diuretics, Antipsychotics

Environmental Factors Acclimitization, exposure time, ambient temperature, Humidity,

Wind

PREVENTATIVE PREVENTATIVE MEASURESMEASURES

Adequate fluid intake Dehydration prevents thermolysis

Recognizing SSX Early: N / V / abd pain, vision disturbances, decreased urine

output, poor skin turgor, hypovolemic shock

Treatment Hydration Gradual acclimatization Limited exposure to hostile environments

HEAT EMERGENCIES HEAT EMERGENCIES SPECTRUMSPECTRUM

Heat Cramps: Muscle cramps relieved by salt & hydration

Heat Edema: Swollen ankles relieved by leg elevation

Heat Syncope: LOC from vasodilation; must r/o serious etiologies

Heat Exhaustion: Volume depletion with vague, non-specific SSX

Heat Stroke: CNS dysfunction is hallmark

HYPERTHERMIAHYPERTHERMIA

Abnormal elevation of core temperature typically caused by elevated external temperatures

Must differentiate from fever (“pyrexia”) Fever: normal response to infection caused by pyrogens

which reset hypothalamic thermostat & increase BMR

Fever makes body environment less hospitable to infectious organisms

Fever treatable with anti-pyretics, hyperthermia is not

HEAT CRAMPSHEAT CRAMPS

Painful “non-emergency” that must be differentiated from other disorders

Hyperthermia causes sweating Sweat consists of water & salt Sodium loss causes muscle cramping

Symptoms: Extremity muscle cramping A & O, though weak, faint or dizzy Skin is warm & moist Temp normal to mildly elevated Vitals “reasonably” normal, often with tachycardia

HEAT EXHAUSTIONHEAT EXHAUSTION Most common heat illness seen by EMS

Etiology: Sweat & sodium loss creates loss of blood volume Vasodilation worsens problem ultimately causing a drop in cardiac

output /BP with a rise in heart rate to compensate

SSX: Body temp >100F (37.8) Cool & clammy skin Tachypnea, tachycardia, hypotension Muscle cramping & generalized weakness CNS: Headache, Anxiety, Impaired judgment

Progresses to Heat Stroke if not treated

DEVELOPMENT OF HEAT DEVELOPMENT OF HEAT EXHAUSTIONEXHAUSTION

HeatHeat

Excessive Sweating

Excessive Sweating

HypovolemiaHypovolemia

Skin Arteriolar Dilation

Skin Arteriolar Dilation

Decreased Cardiac OutputDecreased Mean Arterial Pressure

Decreased Cardiac OutputDecreased Mean Arterial Pressure

Circulatory CollapseCirculatory Collapse

HEAT EXHAUSTION HEAT EXHAUSTION TREATMENTTREATMENT

Remove from environment

Remove clothing, active & passive cooling

Oral electrolytes or IV crystalloids

Resolves with hydration, rest & supine

If symptoms do not resolve consider other causes

HEAT STROKEHEAT STROKE

Environmental emergency with 80% mortality if late or inadequate treatment

Hallmark: hot dry skin without sweat plus AMS

Lack of hypothalamic thermoregulation causes uncontrolled hyperthermia

Core temp often >105 F Cellular death, protein denaturation Damage to brain, kidney & liver causes multi-system failure Rectal temperature is necessary to provide accurate reading

HEAT STROKE HEAT STROKE CATEGORIESCATEGORIES

“Classic” Secondary to altered thermoregulationElderly, chronically ill, patients with AMS

“Exertional”Healthy individuals with significant heat stressSkin initially moist due to exertional sweating

HEAT STROKE HEAT STROKE SSXSSX

Core temp >105F (40.5C)

Mental status changes / anxiety / Confusion

Hypotension

Tachypnea

Renal failure

DIC

Hypotension with bounding or thready tachycardia

Possible seizures

DEVELOPMENT OF HEAT DEVELOPMENT OF HEAT STROKESTROKE

Strenuous ExerciseHot, Humid Environment

Strenuous ExerciseHot, Humid Environment

Inadequate Temperature RegulationInadequate Temperature Regulation

Core Temperature ElevatesCore Temperature Elevates Impaired CNS FunctionImpaired CNS Function

Organ & Tissue DamageOrgan & Tissue Damage

Coma & DeathComa & Death

HEATSTROKHEATSTROKE E

TREATMENTTREATMENT

Transfer to cool environment

Remove clothing, start rapid active cooling Cover with moist sheets Mist with cool water

Target temperature 102F Overcooling may cause

reflex hypothermia

Administer O2 prn

IV rehydration

Cardiac monitor

AVOID vasopressors or anticholinergic drugs

Reassess vitals frequently

OEMS 2.3 HYPERTHERMIA /OEMS 2.3 HYPERTHERMIA /HEAT EMERGENCIESHEAT EMERGENCIES

Priorities: Rapid Recognition & Cooling! Scene safety, BSI Airway management, O2 as needed Continually assess & record LOC, ABCs, vitals SAMPLE history Loosen / remove clothing, move to cool environment If A&Ox3, give water or oral rehydration solution Rapid transport w/wo ALS in position of comfort Do not allow patient to exert themselves

OEMS 2.3 OEMS 2.3 MANAGEMENTMANAGEMENT

Rapid but not “over” cooling; If shivering occurs, discontinue active cooling

Cool packs to armpits, neck, groin and evaporation techniques (fans, windows)

Keep skin wet with towels or sponges Elevate legs if supine ALS intercept if necessary & available; Rapid transport w/wo ALS Notify receiving hospital

INTERMEDIATE AND PARAMEDIC Advanced airway management if necessary IV, O2, Monitor If SBP <100 give 250 bolus NS, titrate to hemodynamic status Medical Control for additional IVF boluses

HEAT HEAT EMERGENCIES EMERGENCIES

NOTESNOTES

No minimum temp for heat related illnesses Temperature severity does not

necessarily correlate with severity of heat illness Can be normothermic with heat cramps & exhaustion

Shivering begins when skin temperature drops, but core temp remains high Versed given to stop shivering and prevent core temperature

from rising despite cooling efforts

HEAT EMERGENCIES HEAT EMERGENCIES SUMMARYSUMMARY

Condition Muscle Cramps

Mental Status

Resp Pulse BP Core Temp Other

Heat Cramps

Yes Alert Normal Normal Normal Normal Weakness

Dizziness

‘Feel Faint’

Heat

Exhaustion

Possible Anxious, ALOC

Rapid, Shallow

Rapid, Weak

Normal Mildly Elevated

Headache

“Pins & Needles”

Diarrhea

Heat

Stroke

No ALOC, Delirium,

Coma

Deep & Rapid with

late Shallow Slowing

Rapid, Full with late slowing

Low Very High Seizures

LIGHTENING LIGHTENING INJURIESINJURIES

2nd largest US storm killer; mortality 45-50 persons/yr 

Injuries 10x more commonly than fatalities

10% lightening injuries are in persons who are indoors

Use of cell phones & portable electronic devices does not increase the risk of injury except via distracting

US LIGHTENING FACTS

1/3 lightening injuries work-related

Most common days: Sat, Sun & Weds

Most common times: 1200–1800, 1800–midnight

Irrational fear of lightning: “astraphobia”

Study of lightning: “fulminology” by a “fulminlogist”

WHAT IS LIGHTNING?WHAT IS LIGHTNING? Atmospheric electrostatic

discharge of a “leader” bolt travelling at >220,000 km/h (140,000 mph) reaches temps of 30,000 °C (54,000 °F)

Hot enough to fuse sand into glass (fulgurites)

Causes air ionisation leading to formation of NO & nitric acid which act as fertilizer to green plant life

Lightning has (+) and (-) bolt polarity (-) current 30,000 amperes, 500 megajoules of energy (+) current 300 kA , 10X greater than (-) bolts Average single bolt peak power output one trillion watts

(terawatt), lasting for 30 millionthsof a second

Voltage proportional to length bolt

Bolt heats vicinity air to 20,000 °C (36,000 °F), 3X temp of sun’s surface which causes a supersonic acoustic shock wave (thunder)

Return stroke follows a charge channel 1cm wide

• Upper cloud carries (+) charge, lower part carries (-) charge

• “Step leader" originates from cloud for 50ms then zig-zags gaining (-) charge

• High speed electrons ionize air, providing conducting path for bolt

• As step leader nears ground, strong electric field drives (+) ground charge to neutralize (-) charge in the "return stoke“

• Upper cloud carries (+) charge, lower part carries (-) charge

• “Step leader" originates from cloud for 50ms then zig-zags gaining (-) charge

• High speed electrons ionize air, providing conducting path for bolt

• As step leader nears ground, strong electric field drives (+) ground charge to neutralize (-) charge in the "return stoke“

LIGHTENING LIGHTENING INJURIESINJURIES

Not pure direct or alternating current

Most important difference between lightning & high-voltage electrical injuries is duration of current exposure

While energy briefly flows through person. vast majority of lightning energy flashes around body surface

Most energy mediated by other factors including surrounding objects that when are hit then transmits energy to person <1/3 of affected persons have burns When burns occur, they are usually superficial

Lightning strikes primarily neurologic injuries

LIGHTENING STRIKESLIGHTENING STRIKES

Direct 3-5% of injuries

Side splash 30% of injuries

Contact voltage from touching object that is struck 1-2% of injuries

Current effect as energy spreads across ground 40-50% of injuries

Upward leader does not connect w/downward leader 20-25% of injuries

CARDIAC CARDIAC INJURIESINJURIES

Massive defibrillation into VF (most common) or asystole, from which heart often spontaneously recovers

Respiratory arrest lasts longer than cardiac arrest

A secondary cardiac event arrest from hypoxia or CNS injury may occur

Most commonly ECG change is QT prolongation

NEUROLOGICAL NEUROLOGICAL INJURIESINJURIES

Neurocognitive deficits similar to TBIs: difficulty processing new information or multitasking

Chronic pain syndromes

Sympathetic nervous system injury: vascular spasm, paralysis, transient HTN, extremity mottling (keraunoparalysis), vertigo &/ or tinnitus

If found unconscious, suspect CNS & spinal injury

DERMATOLOGIC DERMATOLOGIC INJURIESINJURIES

Deep:Rare due to extremely brief skin

contact If burned treat like high-voltage

injury (i.e. rhabdomyolysis)

Superficial:Linear burns secondary to

vaporized sweat/ rainwater, pathognomonic fern pattern

Burns also secondary to heated metal such as necklaces, coins, cleats

BLUNT BLUNT TRAUMATRAUMA

Fractures more common in high-voltage injuries than directly related to lightning, but are common if patient fell or was thrown by the strike

Organ / cardiac / pulmonary contusions rare

Ear is sensory organ most commonly injured by lightningTM rupture from concussive or explosive force, direct

current entry, basilar skull fractureHearing loss, tinnitus, & CN 8 nerve symptoms

Eye injuries common: cataracts, macular holes, retinal separation, iritis

MANAGEMENTMANAGEMENT

Scene safety!

Resuscitation in the field if safe, otherwise evacuate

Spinal precautions if any LOC

ACLS protocols for specific arrythmia AEDs effectively used in a number of cases

LIGHTENING & START LIGHTENING & START TRIAGETRIAGE

Lethal initial arrhythmia usually asystole or VF

How does lightening asystole affect START triage?

ALTITUDE ALTITUDE RELATED ILLNESSRELATED ILLNESS

Elevations > 5000 ft produce physiologic consequences from low oxygen levels

Hypoxia results in spectrum of mild to critical illnesses

History: recent gain in altitude with complaints of headache PLUS one of: GI upset Fatigue Dizziness Insomnia

SPECTRUMSPECTRUM

Mild Nonspecific SSX similar to viral illness

High Altitude Pulmonary Edema (HAPE): Dyspnea, fatigue, dry cough

High Altitude Cerebral Edema (HACE): ALOC with neurological findings

High Altitude Retinal Hemorrhage (HARH)

General Treatment Guidelines: Immediately descend Acetazolamide (also preventative)

HIGH ALTITUDE PULMONARY HIGH ALTITUDE PULMONARY EDEMA (HAPE)EDEMA (HAPE)

Most common fatal high-altitude illness

Treatment: Descend Bed rest Oxygen HBO Nifedipine Intubation & diuresis

HIGH ALTITUDE CEREBRALHIGH ALTITUDE CEREBRALEDEMA (HACE)EDEMA (HACE)

Least common, most severe

Symptoms: Ataxia / Seizures Slurred speech Focal neurological deficits AMS

Treatment: Rapidly descend 100% Oxygen HBO

SUMMARYSUMMARY

Review of common environmental emergencies“Heat” “Height”“Holy Sh-t”

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