Transcript Environmental Emergencies A medical condition caused or

Environmental Emergencies
Paramedic Program
Chemeketa Community College
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Objectives
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Describe the physiology
of thermoregulation
Discuss the risk factors,
pathophysiology,
assessment findings, and
management of specific
hypothermic conditions
and frostbite.
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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 highaltitude illness
Terms
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Acute mountain sickness
Afterdrop
Boyle’s law
Core body temperature
Dalton’s law
Decompression sickness
Drowning
Frostbite
Frostnip
Heat cramps
Heat exhaustion
Heat stroke
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Henry’s law
High-altitude pulmonary
edema
High-altitude cerebral
edema
Homeostatis
Near drowning
Nitrogen narcosis
Thermal gradient
Thermogenesis
Thermolysis
Thermoregulation
Trenchfoot
Environmental Emergencies
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A medical condition caused or exacerbated
by the weather, terrain, atmospheric
pressure or other local factors
Risk Factors
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Age
General health
Fatigue
Predisposing medical conditions
Medications - Rx/OTC
Environmental factors
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Climate
Season
Weather
Atmospheric pressure
Terrain
Types of environmental illnesses
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Heat
Cold
Pressurization
Localized injuries
General Pathophysiology,
Assessment, Management
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Homeostasis
 Normal
 Evaluation
 Oral
 Axillary
 Tympanic
 Rectal
 Tactile
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Thermoregulation
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Regulatory center – Posterior hypothalamus
Peripheral thermoreceptors
 Central thermoreceptors
 Metabolic rate
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Core temperature
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Basal
Exertional
Caloric requirements
37 deg. Celsius
98.6 deg. Fahrenheit
Thermal gradient
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The difference in temperature between
environment and body
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Ambient temperature
Infrared radiation
Relative humidity
Thermogenesis
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Muscular
Baseline
 Exertion
 Shivering
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Metabolic
Sympathetic stimulation
 Processing of food and nutrients
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Endocrine
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Role of hormones in setting basal rate
Thermolysis
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Vasodilation
Perspiration
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Ineffective if relative humidity is 75% or greater.
Decrease in heat production
Increased cardiac output
Increased respiratory rate
Conduction, Convection, Radiation,
Evaporation, Respiration
Heat controlling mechanisms
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Nervous feedback mechanisms regulate body
temperature
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Hypothalamus
Skin
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Mucous membranes
Selected deep tissues
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Mostly cold receptors
Spinal cord
Abdominal viscera
Great veins
Heat Illness
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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
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Heat gain
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Metabolic heat production
 Increased
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Environmental heat gain
 Heat
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metabolic activity
transfer from environment
Heat
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Heat Loss
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Metabolic heat loss
 Increased
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Environmental heat loss
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thermolysis from vasodilation
thermolysis from heat transfer
Heat
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Predisposing factors
 Age
 Peds
 Elders
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General health and meds
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Diabetes
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Antihypertensive meds
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Diuretics - predispose to dehydration
Beta blockers - interfere with vasodilation; reduce
capacity to increase heart rate; may interfere with
thermoregulatory input
Psychotropic medications and antihistamines
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Autonomic neuropathy interferes with vasodilation and
perspiration - may interfere with thermoregulatory input
All interfere with central thermoregulation
Antipsychotics
Antihistamines
Phenothiazines
Heat
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Length of exposure
Intensity of exposure
Environmental
Humidity
 Wind
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Preventative measures
Adequate fluid intake
 Acclimatize; results in more perspiration with
lower salt concentration; increases fluid volume
in body.
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Hyperthermia
Heat cramps
Muscle cramps; 2ndary to rapid change in
extracellular fluid osmolarity resulting from
sodium and water losses.
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Due to dehydration and overexertion
Presents with
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Cramps in fingers, arms, legs, abdominal muscles.
Generally good mentation,
Hot sweaty skin,
Tachycardia,
Normal BP
Normal core temperature
Heat (cont.)
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Treatment
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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 Exhaustion
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Most common heat-related illness
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History of exposure to hot weather
necessary for accurate assessment
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Person may lose 1 – 2 liters of water/hour.
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Each liter lost contains 20-50 mEq of sodium
Heat Exhaustion
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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
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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
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S/S that don’t resolve are predictive of
impending heatstroke
Heat Stroke
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Increased CBT with significant neuro deficit
Organ damage
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Brain, liver, kidneys
Predisposing conditions include age,
diabetes, other medical conditions
increased CBT due to deficient
thermoregulatory function
Heat Stroke
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Exertional
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presents in people in good
health
 Increased
CBT due to overwhelming heat
stress
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 Excessive
ambient temp.
 Excessive
exertion, prolonged exposure,
poor acclimatization
Heat Stroke
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Presents with:
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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
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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
Dehydration in heat disorders
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Common syndrome
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Leads to orthostatic hypotension
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N/V/D
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Vision disturbances
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Decreased urine output
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Poor skin turgor
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Signs of hypovolemic shock
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May occur with s/s of heatstroke
Dehydration
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Treatment
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High-flow oxygen
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1 – 2 IV’s: NS or LR titrated to B/P, if BS clear,
dry
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Water Intoxication
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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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Water Intoxication
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Presents with:
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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
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Encourage patient to eat foods high in sodium
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Restrict further fluid intake
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Unresponsive pt’s: follow protocol for
unconscious, unresponsive pt., IV tko.
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Pyrexia (Fever)
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Body temperature above normal
Hx of infection or illness
Neuro sx may present
If unsure, tx for heatstroke
Treatment
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Remove from environment
Active cooling
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Fluid therapy
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Watch for reflex hypothermia
Use tepid water
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Oral: Add some salt
IV: 0.9% NaCl
Hyperpyrexia
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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
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Environmental causes
Other causes:
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Hypothyroidism
Brain tumors, head trauma
MI, Diabetes, Hypoglycemia, Drugs, Poor
nutrition, Sepsis. Geriatrics also contribute
Meds that interfere with thermogenesis
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Narcotics, alcohol, barbiturates
Antiseizure meds
Antihistamines, other allergy meds
Antipsychotics, sedatives, antidepressants
Aspirin, acetaminophen, NSAIDs
Hypothermia
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Fatigue, exhaustion
Length of exposure
Intensity of exposure
Environmental
Humidity
 Wind
 Temperature
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Hypothermia
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Onset
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Acute (immersion)
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Subacute (exposure)
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Chronic (urban)
Mild hypothermia: Body core
temp. 94 – 97 deg. F.
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Presents with:
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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
Treatment
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Protect against heat loss and wind chill
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Add heat to head, neck, chest, groin
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Blankets
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Skin-skin contact
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NO alcoholic or caffeine beverages or
nicotine
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Warm oral fluids and sugar
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Moderate hypothermia: Body
core temp. 86 – 94 deg. F
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Presents with:
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Peripheral vasoconstriction
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Increase in sympathetic nervous discharge,
catecholamine release, basal metabolism.
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 HR
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 BP
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 RR
Moderate hypothermia
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Significant ECG changes
Prolonged PR, QRS, QT intervals
 Absent P waves
 ST-segment, T-wave abnormalities
 J waves (Osborn waves)
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Shivering until CBT about 86 deg. F, Glucose
depleted
Mood changes
Treatment
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Remove all wet clothing; Rewarm
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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
Severe hypothermia: Body core
temp. less than 86 deg. F
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Presents with:
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Disorientation, confusion, irrational behavior
May become comatose
Shivering usually stops
May appear pulseless, apneic
Treatment
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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
Treatment
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Continue resuscitation efforts until pt. is
rewarmed to at least 86 deg. F. CBT
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Do not attempt warming in the field unless
the patient is more than 15 minutes from a
medical facility
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If rewarming, use water 103-105 deg.
A patient is not considered dead until warm!
Treatment (cont.)
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Rewarming shock - Afterdrop
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Resuscitation considerations
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Reflex vasodilation
BLS
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Take vitals longer
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CPR
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Oxygen
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AED
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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
Transport considerations
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Gentle
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Transport with head level or slightly down
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Destination considerations
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Frostbite
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Superficial - frostnip
Some freezing of epidermal tissue
 Initial redness followed by blanching
 Diminished sensation
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Deep
Freezing of epidermal and Subcutaneous Layers
 White, hard, loss of sensation
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Treatment
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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
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Don’t massage frozen area
Administer Morphine Sulfate, titrated to pain
relief
Trenchfoot
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Similar to frostbite but at temp. above freezing
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Assoc. w/ prolonged exposure to moisture
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S/S similar to frostbite
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Blisters may form; pain
Tx: Dry and warm; aerate
Near Drowning
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Statistics: 80,000 each year
85% male
 2/3 non-swimmers
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Submersion episode with at least transient
recovery
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Mammalian diving reflex
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Stages of drowning
Near 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
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Fresh vs. Salt water
No difference in metabolic result
 No difference in prehospital treatment
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AspirationFresh Water
Water rapidly
leaks to capillary
bed and
circulation
AspirationSalt Water
Salt Water
draws plasma fluid
into alveoli
Surfactant Destruction;
Alveolitis;
Destruction of capillary
membrane
Respiratory
Failure
Hospital Findings
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Salt water: hypertonic fluid
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Rapid shift of plasma and fluid into alveoli and
interstitial spaces
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Results in pulmonary edema, hypoxia
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Sx delayed 1 – 6 hours
Hospital Findings
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Fresh water
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Hypotonic to plasma and passes into
circulation.
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If >20 mL/kg, blood volume increases;
hemolysis
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Surfactant destruction = reduced compliance,
alveolar collapse, hypoxia
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Severe electrolyte abnormalities
Hypothermic considerations in
near-drownings
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Common treatment in all near-drowning patients
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May be organ protective
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Always treat hypoxia first
Treatment
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Airway
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Questionable data to support prophylactic abdominal
thrusts
Trauma
Post-resuscitation Complications
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ARDS or renal failure
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S/S may not appear for 24 hours
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All near-drowning patients must be
transported
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Diving Emergencies
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Boyle’s law
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Dalton’s law
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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
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At a constant temperature, volume of gas inversely
related to its pressure (PV=K)
At a constant temperature, solubility of gas in a
liquid solution is proportionate to partial pressure
of the gas (%X=Px/Pt x 100)
Diving Emergencies
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Increased pressure dissolves gasses into
blood
Oxygen metabolizes
 Nitrogen dissolves
 Primary etiology - rapid ascent
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Decompression
Excess nitrogen bubbles out of solution on
depressurization
 Occurs in joints, tendons, spinal cord, skin, brain,
inner ear
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Diving Emergencies
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Barotrauma
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Tissue damage results from
compression or expansion of
gas spaces when gas
pressure in the body is
different from ambient
pressure.
Barotrauma of Descent
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(Squeeze) Usually results from blocked
eustachian tube.
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Air trapped in non-collapsable chambers is
compressed;
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Vascular engorgement
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Edema
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Hemorrhage of exposed tissue
Barotrauma of Descent
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Occurs in Ears, sinuses, lungs, airways, GI tract,
Thorax, Teeth
Presentation
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Pain - severe, sharp
Sensation of fullness
H/A
Disorientation
Vertigo
Nausea
Bleeding from nose or ears
Barotrauma of Descent
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Management of Barotrauma of descent
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Perform gradual ascent to shallower depths
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Prehospital care supportive
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Transport with head elevated
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Treat with rest, decongestants,
antihistamines, antibiotics, possibly surgical
repair
Barotrauma of Ascent
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Reverse squeeze
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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
Conditions resulting from
barotrauma of ascent
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Pulmonary Overpressurization Syndrome may
occur
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Presents with
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Leads to alveolar rupture and extravasation of air
Gradually increasing chest pain
Hoarseness
Neck fullness
Dyspnea
Dysphagia
Subcutaneous emphysema
Air Embolism
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Suspect when diver suddenly loses
consciousness immediately after surfacing
Pneumomediastinum
Subcutaneous Emphysema
Pneumopericardium
Pneumothorax
Pneumoperitoneum
Systemic arterial air embolism
Air Embolism
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Presents with
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Stroke-like sx: Focal paralysis or sensory
changes
Aphasia
Confusion
Blindness or other visual disturbances
Convulsions
Loss of consciousness
Management of conditions
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Tension pneumothorax
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Air embolism
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Hyperbaric recompression
If intubated, fill cuff with saline
Transport left lateral recumbent position with 15
degree elevation of thorax
Other management
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Needle chest decompression
Oxygen administration, observation, transport to
hyperbaric facility
Decompression Sickness
“The Bends”
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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
Decompression Sickness
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Suspect decompression sickness in any
diver with sx within 12-36 hours after dive.
Prehospital care
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Supportive
High flow oxygen
IV fluids
Recompression chamber
Nitrogen Narcosis
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Nitrogen becomes dissolved in solution;
crosses blood-brain barrier and produces
neurodepressant effects (mimics alcohol)
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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
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Exposure to high altitude may exacerbate
chronic medical conditions
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Etiology - over 8000 feet above sea level
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Prevention
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Gradual ascent,
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Limited exertion,
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High carbohydrate diet,
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Meds
Acute Mountain
Sickness (AMS)
H/A
Malaise
Anorexia
Vomiting
Dizziness
Irritability
Impaired memory
Dyspnea on exertion
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High-altitude
Pulmonary
Edema (HAPE)
SOB
Dyspnea
Cough (/c or /s
Frothy sputum)
Generalized weakness
Lethargy
Disorientation
High-altitude
Cerebral Edema
(HACE)
H/A
Ataxia
Altered mentation
Confusion
Hallucinations
Drowsiness
Stupor
Coma
High-Altitude
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AMS
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HAPE
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Sx in 24-72 hrs; often preceded by strenous
exercise
HACE
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Sx within 4-6 hrs
Attains maximum severity in 24-48 hrs
Abates on 3rd or 4th day
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Most severe form
Progression from AMS; onset 12 hrs to 3 days