1. Environmental Emergencies
(submersion, body temp extremes,
thermal injuries)

2. Submersion
Drowning: asphyxiation caused by submersion
in a liquid that causes interruption of the body’s
oxygen absorption
Near-drowning: a term formerly used to describe
victim’s survival at least 24 hours after submersion
• salt versus fresh water is no longer emphasized as
degree of pulmonary insult is determined by quantity
aspirated
• Epidemiology: 8000 deaths per year in the United
States
– 20% to 25% are children

3. Pathophysiology
• Wet drowning: Aspiration of water into airways
and lungs (85%)
– 1 to 3 cc of aspirated water will lead to destruction of
surfactant, alveolar instability, noncardiogenic
pulmonary edema, and impaired gas exchange
• Dry drowning: Severe parasympathetically
mediated laryngospasm (15%)
• Both types result in common pathway of hypoxia
which leads to acidosis, cardiac arrest, and brain
death

4. Risk factors
1. Drug and alcohol intoxication
2. Cardiac arrest
3. Hypoglycemia
4. Seizure
5. Suicidal or homicidal behavior
6. Child abuse

5. Symptoms and signs
• Hypoxia: Key factors predicting outcome are duration
and severity of hypoxia
• Vomiting:
– 66% of victims who receive rescue breaths vomit
– 86% of victims who require chest compressions and
ventilations vomit
• Mental status changes, tachycardia, cardiac
dysrhythmias, tachypnea, wheezing, pulmonary
edema, cyanosis, apnea
• Diving injuries:
– Potential head or cervical spine injury must be considered

6. Studies
• Arterial blood gas (ABG)
– Hypoxemia may be out of proportion to patient’s
clinical presentation
• Electrolyte panel
• Chest x-ray (CXR)

7. Managment
• Routine stabilization of cervical spine unnecessary unless
–
–
–
–
History of diving
Use of water slide
Signs of injury
Signs of alcohol intoxication
• Rescue breathing
– No need to clear airway of aspirated water as it does not obstruct the
trachea
• Heimlich maneuver/abdominal thrusts unnecessary
• Airway management
– Endotracheal intubation as necessary
– Noninvasive ventilatory support as necessary
– Serial ABGs traditionally used to guide need for ventilatory support

8. Extremes of Body Temperature
• Thermoregulation: ability to maintain normal
body temperature physiologic levels despite
external environmental temperature

9. Mechanism of action
• Heat conservation
– Shivering, vasoconstriction, and piloerection
• Cooling
– Radiation (60%)
• Transfer of heat via electromagnetic waves from body to cooler air
• Greatest source of heat loss
• Evaporation (30%)
– Heat loss by perspiration, breathing, saliva
– Acetylcholine regulates sweat glands and is impaired by anticholinergic drugs
• Convection (8%)
– Transfer of heat from body to fluid, surrounding air or water vapor
– Wind or “wind chill” is an example
• Conduction (2%)
– Direct transfer of heat via physical contact

10. Hypothermia
•
•
•
•
Normal: 97.7°F to 98.6°F (36.5°C to 37°C)
Mild: 93.2°F to 96.8°F (34°C to 36°C)
Moderate: 86°F to 93.2°F (30°C to 34°C)
Severe: <86°F (<30°C)

11. Etiology
• Environmental exposure
• Toxicologic—mnemonic COOLS
– Carbon monoxide, oral hypoglycemics, opioids,
liquors, sedatives (eg, benzodiazepines)
– Alcohol intoxication may lead to impaired decision
making and prolonged environmental exposure
• Systemic
– Sepsis, hypothyroid, hypoadrenalism,
malnutrition, central nervous system (CNS) injury

12. Symptoms and signs
• Mild hypothermia 93.2°F to 96.8°F (34°C to 36°C)
– Shivering
• Moderate hypothermia 86°F to 93.2°F (30°C to 34°C)
– Confusion
– poor judgment
– Paradoxical undressing
•
–
–
–
–
Prolonged vasoconstriction becomes overwhelmed and vasodilates, causing the skin to
feel “hot”
Tachycardia and tachypnea
Dilated pupils
“Shivering” reflex no longer present at 86°F (30°C)
Cold diuresis
• Severe hypothermia <86°F (<30°C)
– Bradycardia and slow atrial fibrillation
– <82°F (<28°C)—patient may appear dead (unresponsive, fixed pupils, apneic)
– Asystole and ventricular fibrillation common

13. Complications
a. Pancreatitis
b. Acute tubular necrosis
c. Rhabdomyolysis
d. Disseminated intravascular coagulopathy
(DIC)
e. Acute respiratory distress syndrome

14. Diagnosis
•
Temperature
– Rectal probe for continuous temperature monitoring
– Warm patients to normal or near normal body temperature before declaring them dead
•
Laboratory tests
– ABG
•
•
Elevated pH
PCO2 decreased
– Complete blood count (CBC)
•
•
–
–
–
–
•
Hematocrit levels rise 2% for every 1°C drop in temperature
False hemoconcentration such that a normal hematocrit could represent severe anemia
Coagulation profile prolonged
Evidence of DIC (low fibrinogen, elevated split products, abnormal coagulation profile)
Creatinine kinase may be elevated with rhabdomyolysis
Amylase or lipase may be elevated with pancreatitis
ECG: Osborn waves (Figure 7–1)
– Size of the wave correlates with degree of hypothermia
– Usually resolves with rewarming
– No prognostic value

16. Management
Rewarming methods
• All patients
–
–
–
–
Rewarming techniques
• Passive rewarming
– Cover with blanket
Remove wet and cold garments
Cover with warm blanket
• Active external rewarming
Cardiac monitoring
– Forced hot air, warming blanket
Handle gently as hypothermic
– Rewarm trunk
heart is irritable and prone to • Active internal rewarming
unstable dysrhythmias
– Warm IV fluids to 115°F (45°C)
– Warm humidified oxygen
– Peritoneal lavage
– Bladder lavage
• Extracorporeal rewarming
– Cardiopulmonary bypass

17. Management
Stable patients
• Mild hypothermia 93.2°F to
96.8°F (34°C to 36°C)
Unstable patients
• Start CPR
• Defibrillate ventricular
– Passive rewarming
tachycardia and fibrillatioN
– Active external rewarming
• Intubation with warm
humidified oxygen
• Moderate hypothermia 86°F to
93.2°F(30°C to 34°C)
• Warm IV fluids
– Passive rewarming
• Mild or moderate hypothermia
– Active external rewarming
• Severe hypothermia 86°F
(<30°C)
– Passive and active external
rewarming
– Active internal rewarming until
core temperature >95°F (35°C)
– As per ACLS protocol
• Severe hypothermia
– Withhold IV medications
– Active internal rewarming

18. ACLS
• The cornerstone of ACLS in the severely hypothermic
patient is active rewarming
• Hypothermic bradycardia is not caused by increased vagal
tone but rather slowing of automaticity, and unlikely to
respond to atropine
• Medications ineffective until patient is 82°F (>28°C) and
may accumulate to toxic levels if given indiscriminately
• Current 2005 ACLS recommendations for defibrillation
– 86°F to 88°F (30°C to 32°C): defibrillate once, then resume CPR
and rewarming
– No additional attempts to defibrillate should be made until the
patient is >86°F to 88° F (30°C to 32°C)

19. Hyperthermia
Epidemiology: The elderly, very young, or chronically ill are most vulnerable to hyperthermia
–
Exertional heat stroke is the second leading cause of sports-related mortality (secondly only to spinal cord injuries)
Etiology
•
Loss of radiation
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–
–
•
Radiation account for 60% of heat loss
Radiation of heat becomes less efficient with increasing ambient temperature
Ceases when ambient temperature > body temperature
Inefficient evaporation
–
–
–
–
–
Normally accounts for 30% of heat loss
Less efficient with increasing ambient humidity
Ceases when humidity approaches 100%
Lack of acclimatization (individual not used to hot climate) results in inefficient perspiration until days 7 to 10
Impaired sweating
•
•
•
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Toxicologic
•
•
•
•
•
Anticholinergics
Skin disorders—scleroderma, psoriasis, burns
Autonomic disorders—diabetes
Sympathomimetics (amphetamine, cocaine)
Neuroleptic malignant syndrome, serotonin syndrome, malignant hyperthermia
Anticholinergics
Salicylate poisoning
Systemic conditions
–
Hyperthyroid, infection, pheochromocytoma

20. Symptoms and signs:
Continuum of illness ranging from heat cramps and heat exhaustion to heat
stroke
• Heat cramps
– Etiology: inadequate intake of fluids and electrolytes
– Symptoms and signs: muscle cramping usually affecting the calves and
abdomen
• Heat exhaustion
– Nonspecific weakness, headache, nausea and vomiting caused by dehydration
– Temperature <106°F (41°C) or normal
• Heat stroke
– Temperature >106°F (41°C)
– Organ damage (Table 7–1)
– Mental status change (irritability to coma)
• Presence of CNS dysfunction differentiates head exhaustion from heat stroke
– Anhidrosis (not universal)

21. Complications
•
•
•
•
•
•
Rhabdomyolysis
Compartment syndrome
Liver failure
Seizure
Dysrhythmias
Pulmonary edema and acute respiratory distress
syndrome (ARDS)
• Acute renal failure
• DIC

22. Diagnosis
•
Laboratory testing
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–
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CBC, CPK, glucose, BUN/creatinine, and LFTs
Hypoglycemia is a common occurrence
Abnormal liver function tests almost universal with heat stroke
•
•
CXR to rule out pulmonary edema
Head CT and lumbar puncture may be required to differentiate encephalitis/meningitis from heat
stroke
Management
• Hydration, but excessive fluids should be avoided to avoid pulmonary edema
• Rapid cooling
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–
•
Mechanical cooling
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•
Temperature 106°F (>41°C) requires immediate management
Cool to a target of 102°F (39°C) within 10 to 20 minutes
Remove clothing
Cool mist and fan (augments heat transfer via convection, radiation, and evaporation)
Ice water immersion advocated by some
Pharmacologic
–
Antipyretics (NSAIDs and acetaminophen) have no role in environmental heatstroke
•
–
Acetaminophen may be harmful with fulminant liver failure
Benzodiazepines to manage agitation and shivering

23. Clinical effects of heat stroke
•
•
Systemic inflammatory response Inflammatory mediators (ie, leukotrienes)
released, triggering inflammatory cascade
Cardiac Nonspecific electrocardiographic changes
– Myocardial enzyme elevations possible
•
Neurologic Mental status alteration
– Outcome related to time with elevated temperature
– Permanent cerebellar injury may result
•
Renal Acute renal failure in 10%
– Injury is secondary to myoglobinuria, direct injury to tubules, and volume depletion
•
Skeletal muscle Rhabdomyolysis
– Elevated CPK
– Hyperkalemia when myocytes destroyed
– Hypocalcemia
•
Gastrointestinal Vomiting
– Diarrhea
•
Coagulation Direct injury to clotting factors
– Disseminated intravascular coagulation (DIC)
– Acute liver injury, often

24. Thermal Injuries
• Frostbite: Tissue injury due to prolonged
exposure to below freezing temperatures (<32°F,
0°C)
• Frost nip: mild, reversible superficial cold injury
without tissue destruction or crystal formation
• Trench foot: prolonged wet, cold but nonfreezing
exposure causing reversible neurovascular injury
• Chilblain (pernio): skin injury consisting of painful
edema, erythema, and plaques caused by
repeated dry, cold but nonfreezing exposure

25. Pathophysiology
• Vasoconstriction leads to decreased delivery
of warm blood to extremities and formation of
ice crystals in tissue
• Leads to sludging at capillary level and
microvascular thrombosis
• Reperfusion injury occurs when frozen tissue
thaws

26. Frostbite: Symptoms and signs
Numbness followed by anesthesia is suggestive of frostbite
• First-degree frostbite
– Definition injury is confined to the epidermis (conified epithelial cells)
– Symptoms and signs: erythema and edema
• Second-degree frostbite
– Definition: injury to epidermis and dermis (middle layer containing capillaries,
nerve endings, hair follicles)
– Symptoms and signs: hard edema and clear blisters
• Third-degree (full thickness) frostbite
– Definition: injury through and involving the hypodermis (connective tissue and
adipose connecting dermis to underlying structures)
– Symptoms and signs: hemorrhagic bullae, pale grey extremity
• Severe pain with rewarming
• Fourth-degree frostbite
– Definition: injury through to and involving the skin, muscles, tendons, bones
– Painless during rewarming

27. Management
•
Rewarming
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–
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Thawing in warm water 104°F to 108°F (40°C to 42°C)
Do not use dry heat such as a hair dryer
Do not rewarm if risk of refreezing exists as subsequent injuries worsen prognosis
Thawing requires 20 to 40 minutes for superficial injuries and up to 1 to 2 hours for deep
injuries (third- and Fourth-degree frostbite)
– Inadequate thawing often due to early stoppage because of inadequate analgesia
– Endpoint of thawing is a warm and soft extremity
•
Wound care
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–
–
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–
•
Unroof clear blisters rich in injurious thromboxane
Do not unroof hemorrhagic blisters
Topical aloe vera over all affected areas
Update tetanus status
Antibiotics if infection or penetrating wound
Consultation with surgery since tissue requires 6 to 8 weeks to determine need for
amputation

28. Thermal Burn
Degree
Thickness
Exam
1st
Epidermis
Erythema, tenderness, pain
Sunburn
No blisters
2nd
Epidermis/Dermis
Very painful unless deep second-degree burn
Superficial partial thickness : Skin is red and blanches
with pressure
Deep partial thickness: Blisters, which usually rupture
if not promptly cared for
3rd
All skin Layers
Pale, leathery appearance
Insensate secondary to destruction of nerve
endings and blood supply
4th
Skin, fascia,
muscle, tendon,
bone
Correlated to the severity and the extent of
involvement of underlying subcutaneous tissue

29. Diagnosis
• Carbon monoxide levels for all patients involved
in a fire
• Cyanide toxicity should be suspected in industrial
Fires
– Sources of cyanide include insecticides, internal
combustion engines, tobacco smoke, plastics made
from acrylonitrite
• Estimation of body surface area (BSA) involved
– Rule of nines (Figure 7–2)
• Pediatric version: patient’s palmar surface is 1% of BSA
• Note that the head is the highest percentage in pediatric
patients

30. Rule of Nines

31. Fluid management
• Parkland formula: 4 mL/kg × % total BSA burned (in pediatrics give 3
mL/kg)
– 50% given in the first 8 hours and remainder over 16 hours
– Ringer lactate is preferred IV fluid
• Maintain urine output at a minimum of 1 mL/kg/h
Transfer to burn center if
• >10% BSA of partial thickness degree burns Third-degree burn
(guidelines do not specify BSA)
• Second- or third-degree burns of hands, feet, genitalia, perineum,
or over joints
• Electrical, chemical, or inhalation injury
• Significant comorbid conditions

32. Management
Wound management
•
Blisters should be left intact (controversial)
•
Apply silver sulfadiazine or triple antibiotic ointments to burned areas
•
Deep burns require sterile management
•
Silver sulfadiazine should not be used on cartilaginous areas (eg, nose, ears) because of dark silver staining
•
Open wounds should be covered with sterile saline-soaked gauze as there is an increased risk of infection
•
Update tetanus status
•
Consider escharotomy for circumferential and full-thickness burns
•
Circumferential full thickness burns may cause vascular insufficiency in limbs and digits
•
Circumferential full thickness burns involving the chest may cause respiratory compromise
•
Consider securing airway if inhalation injury suspected
•
Suspect inhalation injury if:
–
–
–
–
–
•
•
•
Sore throat and dyspnea
Stridor with airway edema
Soot or burns to the nasopharynx
Singed facial or nasal hair
Carbonaceous sputum
Patient’s airway can unexpectedly and suddenly obstruct secondary to edema
Strongly consider prophylactic intubation as it is difficult to predict which patients will deteriorate
Consider fiberoptic laryngoscopy in patients with low suspicion for significant inhalation injury