Post on 21-Dec-2015
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Environmental Emergencies
Paramedic Program
Chemeketa Community College
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Objectives
Describe the physiology of thermoregulation
Discuss the risk factors, pathophysiology, assessment findings, and management of specific hypothermic conditions and frostbite.
Discuss the risk factors, pathophysiology, assessment findings, and management of drowning and near-drowning
Discuss the risk factors, pathophysiology, assessment findings, and management of diving emergencies and high-altitude illness
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Terms
Acute mountain sickness Afterdrop Boyle’s law Core body temperature Dalton’s law Decompression sickness Drowning Frostbite Frostnip Heat cramps Heat exhaustion Heat stroke
Henry’s law High-altitude pulmonary
edema High-altitude cerebral
edema Homeostatis Near drowning Nitrogen narcosis Thermal gradient Thermogenesis Thermolysis Thermoregulation Trenchfoot
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Environmental Emergencies
A medical condition caused or exacerbated by the weather, terrain, atmospheric pressure or other local factors
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Risk Factors
Age General health Fatigue Predisposing medical conditions Medications - Rx/OTC
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Environmental factors
Climate Season Weather Atmospheric pressure Terrain
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Types of environmental illnesses
Heat Cold Pressurization Localized injuries
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General Pathophysiology, Assessment, Management
Homeostasis Normal Evaluation
Oral Axillary Tympanic Rectal Tactile
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Thermoregulation
Regulatory center – Posterior hypothalamus Peripheral thermoreceptors Central thermoreceptors Metabolic rate
Basal Exertional Caloric requirements
Core temperature 37 deg. Celsius 98.6 deg. Fahrenheit
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Thermal gradient
The difference in temperature between environment and body Ambient temperature Infrared radiation Relative humidity
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Thermogenesis
Muscular Baseline Exertion Shivering
Metabolic Sympathetic stimulation Processing of food and nutrients
Endocrine Role of hormones in setting basal rate
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Thermolysis
Vasodilation Perspiration
Ineffective if relative humidity is 75% or greater. Decrease in heat production Increased cardiac output Increased respiratory rate
Conduction, Convection, Radiation, Evaporation, Respiration
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Heat controlling mechanisms
Nervous feedback mechanisms regulate body temperature Hypothalamus Skin
Mostly cold receptors Mucous membranes Selected deep tissues
Spinal cord Abdominal viscera Great veins
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Heat Illness
General signs and symptoms Diaphoresis Posture Increased skin temp. Flushing Altered mentation Altered level of consciousness
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Physiology of Heat Gain And Loss
Heat gain
Metabolic heat production Increased metabolic activity
Environmental heat gain Heat transfer from environment
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Heat Loss Metabolic heat loss
Increased thermolysis from vasodilation
Environmental heat loss Increased thermolysis from heat transfer
Heat
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Predisposing factors Age
Peds Elders
Heat
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General health and meds
Diabetes Autonomic neuropathy interferes with vasodilation and
perspiration - may interfere with thermoregulatory input Antihypertensive meds
Diuretics - predispose to dehydration Beta blockers - interfere with vasodilation; reduce
capacity to increase heart rate; may interfere with thermoregulatory input
Psychotropic medications and antihistamines All interfere with central thermoregulation Antipsychotics Antihistamines Phenothiazines
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Length of exposure Intensity of exposure Environmental
Humidity Wind
Preventative measures Adequate fluid intake Acclimatize; results in more perspiration with
lower salt concentration; increases fluid volume in body.
Heat
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Hyperthermia Heat cramps
Muscle cramps; 2ndary to rapid change in extracellular fluid osmolarity resulting from sodium and water losses. Due to dehydration and overexertion Presents with
Cramps in fingers, arms, legs, abdominal muscles. Generally good mentation, Hot sweaty skin, Tachycardia, Normal BP Normal core temperature
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Treatment Remove from environment Massage cramped muscle Apply moist towels to forehead and over
cramped muscles Increase fluid and sodium intake Consider IV with NS or LR, transport if s/s
persist
Heat (cont.)
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Heat Exhaustion
Most common heat-related illness
History of exposure to hot weather
necessary for accurate assessment
Person may lose 1 – 2 liters of water/hour.
Each liter lost contains 20-50 mEq of sodium
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Presents with: Increased CBT with some neuro deficit Sweating Decreased fluid intake Decreased urine output Tachycardia N/V/D Dizziness, transient syncope H/A Muscle cramps Dehydration Orthostatic hypotension
Heat Exhaustion
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Treatment Rest Remove enough clothing for cooling Fan skin 1 – 2 IV’s: IV Fluids; NS or LR High-flow oxygen Supine position Transport
S/S that don’t resolve are predictive of impending heatstroke
Heat Exhaustion
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Heat Stroke
Increased CBT with significant neuro deficit Organ damage
Brain, liver, kidneys Predisposing conditions include age,
diabetes, other medical conditions increased CBT due to deficient
thermoregulatory function
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Exertional
Commonly presents in people in good
health
Increased CBT due to overwhelming heat
stress
Excessive ambient temp.
Excessive exertion, prolonged exposure,
poor acclimatization
Heat Stroke
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Presents with: Hot, Red, Dry skin Irrational or unconscious Rectal temperature 105 deg. F or higher Tachycardia Bradycardia Hypotension with low or absent diastolic Rapid, shallow respirations Airway compromise Seizures Cardiac arrest
Heat Stroke
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Treatment Cool rapidly; pack in ice and/or wrap in wet
sheets Apply cold packs to armpits, groin, behind
knees, on wrists, ankles, behind neck High flow oxygen with airway management 1 – 2 IV’s: NS or LR, wide open Diazepam or Versed to control seizures Transport rapidly
Heat Stroke
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Dehydration in heat disorders
Common syndrome Leads to orthostatic hypotension
N/V/D Vision disturbances Decreased urine output Poor skin turgor Signs of hypovolemic shock May occur with s/s of heatstroke
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Treatment
High-flow oxygen
1 – 2 IV’s: NS or LR titrated to B/P, if BS
clear, dry
Dehydration
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Water Intoxication
Occurs when patient in hot environment
drinks water at a rate that exceeds fluid
loss from sweating and fails to replace
sodium losses.
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Presents with: Normal vitals with negative orthostatics Chills Loss of coordination N/V H/A Altered mentation Hx: greater than one liter/hour Urinary frequency, dilute urine
Water Intoxication
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Treatment
Encourage patient to eat foods high in sodium
Restrict further fluid intake
Unresponsive pt’s: follow protocol for
unconscious, unresponsive pt., IV tko.
Water Intoxication
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Pyrexia (Fever)
Body temperature above normal Hx of infection or illness Neuro sx may present If unsure, tx for heatstroke Treatment
Remove from environment Active cooling
Watch for reflex hypothermia Use tepid water
Fluid therapy Oral: Add some salt IV: 0.9% NaCl
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Hyperpyrexia
Core body temperature above 106 deg. F. Causes:
Hot baths Hot air Reaction to infection Some develop hyperpyrexia within 24 hours after
surgery Rare cause: Administration of succinylcholine
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Hypothermia - Body core temperature < 97.0 deg. F Environmental causes Other causes:
Hypothyroidism Brain tumors, head trauma MI, Diabetes, Hypoglycemia, Drugs, Poor
nutrition, Sepsis. Geriatrics also contribute Meds that interfere with thermogenesis
Narcotics, alcohol, barbiturates Antiseizure meds Antihistamines, other allergy meds Antipsychotics, sedatives, antidepressants Aspirin, acetaminophen, NSAIDs
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Fatigue, exhaustion Length of exposure Intensity of exposure Environmental
Humidity Wind Temperature
Hypothermia
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Hypothermia
Onset
Acute (immersion)
Subacute (exposure)
Chronic (urban)
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Mild hypothermia: Body core temp. 94 – 97 deg. F.
Presents with: Peripheral vasoconstriction Increase in sympathetic nervous discharge,
catecholamine release, basal metabolism. HR BP RR Shivering until CBT about 86 deg. F, Glucose
depleted Mood changes
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Treatment
Protect against heat loss and wind chill Add heat to head, neck, chest, groin Blankets Skin-skin contact
NO alcoholic or caffeine beverages or nicotine
Warm oral fluids and sugar
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Moderate hypothermia: Body core temp. 86 – 94 deg. F
Presents with: Peripheral vasoconstriction
Increase in sympathetic nervous discharge,
catecholamine release, basal metabolism.
HR
BP
RR
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Significant ECG changes Prolonged PR, QRS, QT intervals Absent P waves ST-segment, T-wave abnormalities J waves (Osborn waves)
Shivering until CBT about 86 deg. F, Glucose depleted
Mood changes
Moderate hypothermia
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Treatment Remove all wet clothing; Rewarm
Add heat to head, neck, chest, groin Consider respiratory rewarming Do not give alcohol, caffine, nicotine Protect against heat loss and wind chill
Maintain horizontal position Avoid rough movement and excess activity Monitor cardiac rhythm Provide warm oral fluids and sugar AFTER
uncontrolled shivering stops and pt. is rewarming
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Severe hypothermia: Body core temp. less than 86 deg. F
Presents with: Disorientation, confusion, irrational behavior May become comatose Shivering usually stops May appear pulseless, apneic
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Treatment Assess pulse, respirations for at least 30
seconds q 1-2 minutes Begin CPR if pulseless, apneic; follow ACLS
guidelines Provide warmed, humidified oxygen Warm IV fluids only <84 deg. F CBT; do not give IV meds >84 deg. F CBT; give IV meds at longer
intervals GENTLE handling, especially when rewarming
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Continue resuscitation efforts until pt. is rewarmed to at least 86 deg. F. CBT
Do not attempt warming in the field unless the patient is more than 15 minutes from a medical facility If rewarming, use water 103-105 deg.
A patient is not considered dead until warm!
Treatment
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Rewarming shock - Afterdrop Reflex vasodilation
Resuscitation considerations BLS
Take vitals longer
CPR
Oxygen
AED
Treatment (cont.)
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ACLS Effects of cold on meds Orotracheal intubation Risks of Vfib related to depth and duration
of hypothermia Be gentle Impossible to defibrillate a heart colder
than 86 degrees Lidocaine and procainamide paradoxically
lower fibrillatory threshold and increase resistance to defibrillation
Bretylium and Mag. Sulfate may be effective
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Transport considerations
Gentle
Transport with head level or slightly down
Destination considerations
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Frostbite
Superficial - frostnip Some freezing of epidermal tissue Initial redness followed by blanching Diminished sensation
Deep Freezing of epidermal and Subcutaneous Layers White, hard, loss of sensation
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Treatment
Transport Rewarm rapidly if transport delayed
104o max Don’t rewarm if danger of refreezing Immobilize, elevate Bandage with bulky, dry, sterile dressings Don’t puncture blisters
Don’t massage frozen area Administer Morphine Sulfate, titrated to pain
relief
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Trenchfoot
Similar to frostbite but at temp. above freezing
Assoc. w/ prolonged exposure to moisture
S/S similar to frostbite
Blisters may form; pain
Tx: Dry and warm; aerate
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Near Drowning
Statistics: 80,000 each year 85% male 2/3 non-swimmers
Submersion episode with at least transient
recovery
Mammalian diving reflex
Stages of drowning
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Wet vs. Dry drownings Fluid in posterior oropharynx stimulates
laryngospasm Aspiration occurs after muscle relaxation Suffocation occurs with or without aspiration Aspiration presents as airway obstruction 15% of drownings are dry
Fresh vs. Salt water No difference in metabolic result No difference in prehospital treatment
Near Drowning
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Salt Water draws plasma fluid
into alveoli
Surfactant Destruction;Alveolitis;
Destruction of capillarymembrane
Aspiration-Fresh Water
Aspiration-Salt Water
Water rapidly leaks to capillary
bed and circulation
RespiratoryRespiratoryFailureFailure
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Hospital Findings
Salt water: hypertonic fluid
Rapid shift of plasma and fluid into alveoli and
interstitial spaces
Results in pulmonary edema, hypoxia
Sx delayed 1 – 6 hours
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Fresh water Hypotonic to plasma and passes into
circulation. If >20 mL/kg, blood volume increases;
hemolysis Surfactant destruction = reduced compliance,
alveolar collapse, hypoxia Severe electrolyte abnormalities
Hospital Findings
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Hypothermic considerations in near-drownings
Common treatment in all near-drowning patients May be organ protective Always treat hypoxia first
Treatment Airway
Questionable data to support prophylactic abdominal thrusts
Trauma
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Post-resuscitation Complications
ARDS or renal failure
S/S may not appear for 24 hours
All near-drowning patients must be
transported
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Diving Emergencies
Boyle’s law At a constant temperature, volume of gas inversely
related to its pressure (PV=K) Dalton’s law
The pressure exerted by each gas in a mixture is the same as it would exert if alone (Pt=PO2+PN2+Px)
Henry’s law At a constant temperature, solubility of gas in a
liquid solution is proportionate to partial pressure of the gas (%X=Px/Pt x 100)
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Increased pressure dissolves gasses into blood
Oxygen metabolizes Nitrogen dissolves Primary etiology - rapid ascent
Decompression Excess nitrogen bubbles out of solution on
depressurization Occurs in joints, tendons, spinal cord, skin, brain,
inner ear
Diving Emergencies
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Diving Emergencies
Barotrauma Tissue damage results from
compression or expansion of gas spaces when gas pressure in the body is different from ambient pressure.
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Barotrauma of Descent
(Squeeze) Usually results from blocked eustachian tube.
Air trapped in non-collapsable chambers is compressed; Vascular engorgement Edema Hemorrhage of exposed tissue
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Barotrauma of Descent
Occurs in Ears, sinuses, lungs, airways, GI tract, Thorax, Teeth
Presentation Pain - severe, sharp Sensation of fullness H/A Disorientation Vertigo Nausea Bleeding from nose or ears
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Management of Barotrauma of descent Perform gradual ascent to shallower depths
Prehospital care supportive
Transport with head elevated
Treat with rest, decongestants,
antihistamines, antibiotics, possibly surgical
repair
Barotrauma of Descent
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Barotrauma of Ascent
Reverse squeeze Volume of air in pressurized spaces expands
as ambient pressure decreases (Boyle’s law) Compressed gas at 33 ft (2 atmospheres)
doubles at surface (1 atmosphere) because pressure is ½ of 33 ft.
Last 6 feet of ascent have greatest potential for volume expansion
Most common cause is breath-holding
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Conditions resulting from barotrauma of ascent
Pulmonary Overpressurization Syndrome may occur Leads to alveolar rupture and extravasation of air
Presents with Gradually increasing chest pain Hoarseness Neck fullness Dyspnea Dysphagia Subcutaneous emphysema
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Air Embolism
Suspect when diver suddenly loses consciousness immediately after surfacing
Pneumomediastinum Subcutaneous Emphysema Pneumopericardium Pneumothorax Pneumoperitoneum Systemic arterial air embolism
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Air Embolism
Presents with Stroke-like sx: Focal paralysis or sensory
changes Aphasia Confusion Blindness or other visual disturbances Convulsions Loss of consciousness
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Management of conditions
Tension pneumothorax Needle chest decompression
Air embolism Hyperbaric recompression If intubated, fill cuff with saline Transport left lateral recumbent position with 15
degree elevation of thorax Other management
Oxygen administration, observation, transport to hyperbaric facility
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Decompression Sickness“The Bends”
Multi-system disorder Nitrogen in compressed air converts from
solution to gas, forming bubbles (Henry’s law)
Results from too-rapid ascent Results in vascular occlusion, poor tissue
perfusion, ischemia Joints and spinal cord most often effected
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Decompression Sickness
Suspect decompression sickness in any diver with sx within 12-36 hours after dive.
Prehospital care Supportive High flow oxygen IV fluids Recompression chamber
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Nitrogen Narcosis
Nitrogen becomes dissolved in solution; crosses blood-brain barrier and produces neurodepressant effects (mimics alcohol) Most common at depths of 70-100 feet Intoxication Treatment
Self resolving Return to shallow depths Supportive care Transport for evaluation
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High-Altitude Illness
Exposure to high altitude may exacerbate
chronic medical conditions
Etiology - over 8000 feet above sea level
Prevention Gradual ascent,
Limited exertion,
High carbohydrate diet,
Meds
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Acute Mountain Sickness (AMS)
H/AMalaise
AnorexiaVomitingDizzinessIrritability
Impaired memoryDyspnea on exertion
High-altitudeCerebral Edema
(HACE)
H/AAtaxia
Altered mentationConfusion
HallucinationsDrowsiness
StuporComa
High-altitude Pulmonary
Edema (HAPE)
SOBDyspnea
Cough (/c or /sFrothy sputum)
Generalized weaknessLethargy
Disorientation
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AMS Sx within 4-6 hrs Attains maximum severity in 24-48 hrs Abates on 3rd or 4th day
HAPE Sx in 24-72 hrs; often preceded by strenous
exercise HACE
Most severe form Progression from AMS; onset 12 hrs to 3 days
High-Altitude