Environmental Emergencies (Elkins Slides) Flashcards
When does heat illness occur?
When one is unable to adequately regulate body temperature
Who is at risk for heat illness?
- Young/elderly
- Obese
- Chronic physical/mental illness
- Impaired by drugs/ETOH
- Anyone denied access to hydration/nutrition
What is heat edema?
- Mild swelling of dependent extremities due to heat exposure
- Results from muscular and cutaneous vasodilation combined with venous stasis
Management of heat edema
- Self-limiting with elevation
- Rest
- Cooling
- Oral rehydration
What is heat syncope?
- Syncope after exertion in the heat
- Results from vasodilation leading to intravascular volume redistribution
Clinical presentation of heat syncope
- Core temp is normal
- Skin cool and diaphoretic
- Weak pulse
- Transient hypotension
Management of heat syncope
- Rule out other causes of syncope: hypoglycemia, arrhythmias, fixed myocardial or cerebrovascular lesions
- Lie patient supine with legs elevated, remove from heat
- +/- external cooling
- IV/oral rehydration
- Disposition home after appropriate tx and patient education
What are heat cramps?
Painful spasms of voluntary muscles of the abdomen and extremities resulting from salt depletion
Clinical presentation of heat cramps
- Core temp normal or slightly elevated
- +/- muscle fasciculations
- Skin moist or dry and cool or warm
Diagnostic evaluation of heat cramps
- Rarely indicated
- May show hemoconcentration
- Low-normal Na, +/- low K+, and Mg
Management of heat cramps
- Remove from heat
- Begin external cooling
- Oral electrolyte solution or IV NS
- Replace K+ and Mg if needed
Disposition of heat cramps
- Discharge home
- Rest for 1-3 days-avoid physical exertion and heat exposure
What is heat exhaustion?
- Inability to maintain adequate cardiac output due to strenuous physical exercise and environmental heat stress
- Rapidly evolves to heat strok if no intervention
What are the 2 types of heat exhaustion?
- Hypernatremic: results from lack of water access
- Hyponatremic: fluid loss replaced with water only
Clinical presentation of heat exhaustion
- Temperature often mildly elevated, usually not above 40 degrees C
- Diaphoresis
- HA
- N/V
- Malaise
- Weakness
- Tachycardia
- Hypotension
- No evidence of CNS dysfunction (differentiates from heat stroke)
Work-up of heat exhaustion
- BMP: assess electrolytes and renal function
- UA: assess presence of myoglobinuria
- Additional diagnostics based upon patient presentation: CK, LFT, ABG, EKG
Management of heat exhaustion
- Remove from heat +/- external cooling
- Oral electrolyte solution if able to tolerate PO intake
- Alt: IV NS or LR, hypertonic saline if marked hyponatrmia due to water intoxication
Heat exhaustion disposition
Home: mild cases who don’t meet criteria below
Admit:
* Moderate-severe symptoms
* Comorbid illnesses
* Patients at extremes of age
* Lab abnormalities: elevated CPK, creatinine, LFTs, cardiac abnormalities, hyponatremia, persistent acidosis
* Social concerns
What is heat stroke?
- Dysfunction of the heat regulating mechanism with hyperthermia (core body >104 F) and end-organ damage
- Neural tissue, hepatocytes, nephrons, and vascular endothelium are most sensitive to heat stress
- 2 types: exertional (rapid onset) and non-exertional (slow onset)
Clinical presentation of heat stroke
- HA
- Dizziness
- Nausea
- Diarrhea
- Visual disturbances
- Skin hot, flushed, dry
- CV: rapid, bounding pulse, hypotension –> CV collapse
- Neuro: confusion, seizure, delirium, ataxia, coma
- Signs of DIC: hematuria, hematemesis, bruising, petechiae, and oozing at sites of venipuncture
Diagnosis of heat stroke
- CBC, PT/PTT: evidence of hemoconcentration and DIC
- CMP: reassess electrolytes every hour assessing for elevated or depleted K+ and Na; elevated LFTs
- Hyperkalemia is seen with ARF secondary to rhabdomyolysis
- Phophate (hypophosphatemia)
- UA: concentrated with protein, myoglobin, and tubular casts
- CK
- EKG
- CXR
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Management of heat stroke
- Rapid cooling with ice water, disrobe and spray water on pt with fan blowing, cooling blanket with ice packs over great vessels
- Great vessels: axilla, neck, and inguinal areas
- Tx severe shivering with IV BZD
- Continuous temp monitoring (rectal): discontinue once core temp 101.5-102
- If unresponsive to above: internal lavage of peritoneal, gastric, bladder, and/or rectal
- CV support: IV fluids 1-2 L bolus NS if hypotension or rhabdo, maintenance fluid to maintain UO
- Supplement O2 if needed
- Significant AMS- ventilate intubate
What should UO be in heat stroke?
50-100 mL/h
What is the disposition of heat stroke?
- Admit to ICU if hemodynamic instability, severe LFT elevation or rhabdomyolysis
- All others admit to general floor (med/surg)
What is frostbite?
Damage to tissue due to exposure to freezing temperatures
Clinical presentation of frostbite (before re-warming)
Mild
* Paresthesias
* Pruritis of tissue involved
* Loss of sensation and fine motor control
Mod-severe
* Decreased ROM
* Blister formation
* Edema
* Tissue appears white
* Firm/hard
* Cool to touch
Clinical presentation of frostbite after rewarming
- Stinging
- Burning
- Aching
- Throbbing
- Tenderness
- Tissue discoloration
- Loss of elasticity and mobility
- Profound edema
- Hemorrhagic blisters
- Necrosis
- Gangrene
What is 1st degree frostbite? 2nd?
- 1st: erythema and edema without blister, skin peeling
- 2nd degree: serous filled blister
What is 3rd degree frostbite? 4th?
- 3rd: skin necrosis; hemorrhagic blister with subcutaneous involvement
- 4th degree: full-thickness (including bone) non-blanching cyanosis; dry, black mummified eschar formation; loss or deformity of body part
Treatment of frostbite
- Treat systemic hypothermia before frostbite
- Avoid partial rewarming/refreezing
- Rapid rewarming in circulating water at 98.6-102.2 F
- 15-60 minutes; until a red-purple color appears and the skin becomes pliable- allow skin to air dry
- Avoid trauma
- Rewarming can be painful: pain management with parenteral NSAID and/or opiates (as needed)
- Warm oral/IV fluids if evidence of hypovolemia
- Extremity wound care
- Update tetanus
What are components of extremity wound care?
- Maintain sterile environment after rewarming
- Local wound care and dressing
- Topical aloe vera q6h
- Consult/refer to wound specialist: clean/debride superficial dead tissue in a whirlpoo BID x 3 weeks
- Abx prophylaxis is controversial
- Splint and elevate extremity
Disposition of frostbite
- Home: limited area with only 1st degree injury
- Hospital: extensive area of 1st degree and all 2nd, 3rd, 4th degree
Prognosis of frostbite
- Long term sequelae
- Cold sensitivity
- Loss of sensation
- Hyperhidrosis
- Loss of digit/limb
Definition of hypothermia
Core body temp <35 C (<95 F) by rectal, bladder, or esophageal thermometer
What are primary causes of hypothermia?
- Environmental exposure: often associated with alcohol/drug use
- Therapeutic: targeted termperature management
What are secondary causes of hypothermia?
- Burns
- Hypoglycemia
- Hypothyroidism
- Hypoadrenalism
- Hypopituitarism
- CNS dysfunction
- Sepsis
- Drug intoxication
- Trauma
- Impaired shivering
Who are persons at risk for impaired shivering?
- Advanced or very young age
- Malnutrition
- Physical exhaustion
- Neuromuscular disease
What is are clinical presentations of each stage of hypothermia?
- Mild: conscious, shivering, HR/RR increase (temp 95-89.6 F)
- Moderate: mild alteration in consciousness, loss of shivering reflex, HR/RR drop (temp 89.6-82.4 F)
- Severe: unconscious, VS present, areflexia, fixed dilated pupils, hypotension, pulmonary edema, cardiac arrhythmia and arrest, coma (temp 82.4 F)
- HT IV: vital signs absent (75.2)
Diagnostic work up for hypothermia
- Do not delay treatment for laboratory evaluation
- CBC
- CMP: hypokalemia with mild HT, hyperkalemia with severe HT from cell death/ARF, evidence of organ damage
- TSH: severe untreated hypothyroidism
- Cortisol: look for signs of adrenal insufficiency
- Coags: elevated if complicated by coagulopathy
- Lactic acid: elevated with cell death
- Blood gas
- EKG
Management of hypothermia general and mild
All patients
* Continuous VS monitoring including core body thermometer
* Ventilate if needed
* Remove wet clothing, dry patient, and cover up
* Handle all patients gently to avoid fatal dysrhythmia
Mild (HT I)
* Place in warm environment at 82 F or above
* Encourage active movement
* Warm oral sugary drinks
* If significant trauma, comorbidities, or suspected secondary hypothermia treat as moderate
Management of moderate hypothermia
- Rewarming: warm environment with chemical, electrical, or forced air heating packs or blankets
- Warm IV fluids
- Full-body insulation, horizontal position
- Immobilization
Management of severe hypothermia
- Airway management likely needed
- Sinus bradycardia, a.fib, and a. flutter will resolve with rewarming
- V fib will not respond to therapy until pt is rewarmed
- AHA recommends one defibrillation attempt prior to rewarming
- Rewarming with external heating device and warm IV fluids
- Preferred rewarming treatment is ECMO if available due to high risk of cardiac arrest
Management of hypothermia IV
- Initiate CPR and provide airway management
- Transport to ECMO if available
- Prevent further heat loss (insulation, warm environment)
- Continue resuscitation until core temperature reaches 32 C (90F)
Additional considerations for hypothermia
- Coma cocktail: dextrose 50 mL IV, thiamine 100 mg IV/IM, naloxone 2 g IV
Treat underlying conditions - Hypothyroidism: levothyroxine 400 mcg IV + hydrocortisone 100 mg IV
- Hypoadrenalism: hydrocortisone 200 mg IV
- Sepsis: broad spectrum antibiotics
Disposition of hypothermia
- Admit all patients unless all of the below criteria are met
- No comorbidities
- No AMS
- Presenting core temp > 34 C (93.2 F)
Stinging results in envenomation causing what 3 presentation?
- Localized reaction
- Systemic reactions
- Anaphylaxis
Clinical presentation of localized bee sting?
- Small pruritic, painful, erythematous, edematous lesion at sting site
- Occassionally lesion will be >5 cm
Clinical presentation of fire ant sting
- Sterile pustule evolves of 6-24 hours
- May result in necrosis and scarring
Clinical presentation of systemic/toxic reaction to wasp, bees, and stinging ants
- More common with >50 stings
- N/V/D with urticarial lesions distant from site of sting
- Symptoms usually subside within 48 hrs
- Severe cases may lead to complications: rhabdomyolysis, hepatorenal failure, hemolysis, thrombocytopenia, DIC
Clinical presentation of anaphylactic reaction
- True allergic reaction
- Occurs within 6 h
- Itchy eyes
- Urticaria
- Cough
- Respiratory failure
- CV collapse
Lab evaluation of wasp, bee, stinging ants
- Do not delay life-saving intervention for labs!
- Only for systemic and anaphylactic reactions
- Labs directed by complications: CBC, CMP, coags, CK
Management of anaphylaxis
- Treated as anaphylactic shock
- Intubation if needed
- Epinephrine 1:1000 –> adults .3-.5 mL SC/IM; children .01 mg/kg (max .5 mg)
- IV methylprednisolone 2 mg/kg
- IV diphenhydramine 1 mg/kg
- IV famotidine .5 mg/kg IV
- Nebulized albuterol 2.5-5 mg for bronchospasm
Management of localized reaction to wasp, bees, or stinging ants
- Oral diphenhydramine 25-50 mg
- Oral pain control: NSAID, acetaminophen
Management of wasp, bees, and stinging ants systemic reactions
- IV methylprednisolone
- Diphenhydramine
- Famotidine
Complications of wasp, bees, and stinging ants
- May require blood products
- Dialysis
- Extensive hospital care
Wound management of wasp, bees, and stinging ants
- Do not delay tx of systemic reactions to care for wound
- Remove stinger with scraping technique
- Wash wound
- Ice and elevation
- Tetanus update
Disposition of wasp, bees, and stinging ants
- Local - discharge home
Systemic reactions - Admit if child, elderly, comorbidities, 50 or more stings, or prolonged reaction
- Otherwise healthy pts- observe for 6, if no rebound symptoms, repeat labs before discharge, Rx epipen, f/u with allergist
What is the reaction to most scorpion stings?
Localized reaction
Only systemically toxic scorpion in US with highest risk of toxicity to infants and children, where is it found?
- Bark scorpion
- Southwestern US
Clinical presentation of scorpion sting
- Sting painful without initial erythema/swelling
- Exquisite pain with light percussion “tap sign”
- Neuromuscular excitation
- Cardiovascular toxicity
What is the clinical presentation of neuromuscular excitation due to a scorpion sting?
- Muscle spasms
- Cranial nerve dysfunction
- Roving eye movement
- Diplopia
- Difficulty swallowing
- Hypersalivation
What is the clinical presentation of cardiovascular toxicity due to scorpion sting?
- Tachycardia
- HTN
- Pulmonary edema
- Cardiogenic shock
Management of scorion sting
- Most managed symptomatically: oral or IV pain medication, benzodiazepine for motor control
More severe presentation
* Cardiac monitoring and IV access:; administer fluids and respiratory support if needed
* Antivenom (Anascorp)
MC SE of scorpion antivenom (Anascorp)
- Vomiting
- Pyrexia
- Rash
- Nausea
- Pruritis
- Anaphylaxis rare
What snakes are considered pit vipers and what is their appearance?
- Rattlesnakes
- Copperheads
- Water moccasin
- Large triangle shaped head with heat sensitive depression “pit” between their eyes
- Venom cytotoxic
Hallmark clinical presentation of pit viper bite
- Fang marks with pain
- Edema
- Hemorrhage
- Necrosis around bit
- Extending from bite if severe envenomation
- Usually within 30 minutes but may be delayed up to 12 h
- If no s/s after 12 h = dry bite
Systemic symptoms of pit vipers
- Nausea
- Vomiting
- Hemolysis
- Thrombocytopenia
- Coagulopathy
- Respiratory failure with CV instability and collapse
Management of pit vipers
- Consult poison control: 1-800-222-12222
- Cardiac monitoring and IV access: administer fluids and respiratory support if needed
- Immobilize bitten extremity and remove any constriction band applied proximal to bite (not effective)
- Serial (30 min) wound evaluations: measure above and below bite and mark border of edema, assess for symptoms of compartment syndrome
- Antivenom (CroFab)
- Td update if needed
Labs for pit viper bites
- CBC
- CMP
- Coags
- CK
- Urine myoglobin
- type and crossmatch
What can CroFab be used for?
- Rattlesnakes
- Copperheads
- Cottonmouths/water moccasins
MC SE of antivenom (CroFab)
- Urticaria
- Rash
- Nausea
- Pruritis
- Back pain
- Hypersensitivity in 5-19% patients
- Recurrent coagulopathy in 50% of patients
Disposition of pit viper bite
- Observe in ER for 8-12 hours - d/c home if no progression and all labs are WNL
- Admit (ICU) for severe reaction and those receiving antivenom
What is high altitude sickness?
- A spectrum of diseases that results from traveling to high elevations
- Most often seen at elevations at or >1500 m (4800 ft) with decreased partial pressures of oxygen at higher elevations
What is the underlying physiologic insult for high altitude sickness?
- Hypoxia
How does the body compensate for high altitude?
- Increased RR
- Renal excretion of HCO3
- Vascular changes
- Increasing the blood’s oxygen carrying capacity
Clinical presentation of acute mountain sickness
- Symptoms resembling a hangover
- Headache + one of the following:
- anorexia
- N/V
- Weakness
- Fatigue
- Dizziness
- Light-headed
- Fluid-retention
- Insomnia
- Oliguria
- Dyspnea
- Altered mental status
- Symptoms occur within 48 hours of rapid ascent
- Complications if left untreated: HAP (pulmonary)E (edema), HAC (cerebral) E (edema)
Management of acute mountain sickness
- Discontinue ascent until symptoms resolve completely
- Descent to lower elevation if no improvement in symptoms: descent of 300-1000 m can provide prompt relief
Symptomatic therapy
* Low-flow oxygen
* Acetaminophen or NSAID for HA
* Ondansetron for N/V
Mild presentation: improvement in 12-36 hours after cessation
Moderate presentation: hyperbaric oxygen therapy if available, acetazolamide + dexamethasone until symptoms resolve (acetazolamide can be used in prevention of acute mountain sickness)
Disposition of acute mountain sickness
- Discharge home if good response to intervention
- Pt education to avoid rapid ascents, overexertion, alcohol and respiratory depressants
- Use acetazolamide as prophylaxis starting 1 day prior to ascent and continue for 2 days after reaching highest altitude
What is HAPE?
- Hypoxic vasoconstriction and elevated right heart pressures results in noncardiogenic pulmonary edema
- Continuum of untreated acute mountain sickness
- MC cause of death in high altitude sickness
- Can be fatal within hours of onset
- Can occur in as little as 2400 m (8000 ft) ascension
Clinical presentation of HAPE
- Onset: day 2-4 after ascent
- Decreased exercise capacity is first symptom noticed
2 of following must be present: - Dyspnea at rest
- Cough
- Rales
- Tachypnea
- Weakness
- Decreased performance
- Chest tightness
- Tachycardia
- Signs of pulmonary HTN
Diagnostic evaluation of HAPE
- CXR: alveolar infiltrates, enlarged pulmonary arteries, normal cardiac size
Management of HAPE
- Supplemental O2 to keep O2 saturation >90%
- Continue O2 for 72 hours after descent in severe cases
- Immediate descent is treatment of choice
- Avoid excessive exertion during descent
- Hyperbaric treatment if descent isn’t possible
- Pharmacologic pulmonary vasodilation if O2 or descent is unattainable: sildenafil, tadalafil, nifedipine
- Sildenafil, tadalafil, and nifedipine can also be used prophylactically in patients with previous HAPE
Discharge criteria for HAPE
- O2 on room air is maintained >90%
- Symptoms resolve
- CXR has improved
What is High Altitude Cerebral Edema (HACE)?
- End-stage manifestation of AMS and HAPE
Clinical presentation of HACE
- S/s or history consistent with AMS
- Altered mental status
- Ataxia
- Stupor Coma
- Signs of increased ICP: retinal hemorrhage, papilledema
Diagnostic evaluation of HACE
- MRI reveals cerebral edema
Management of HACE
- Supplemental O2 to keep O2 saturation >90%
- Intubation if severe altered mental status
- Immediate descent (alt hyperbaric therapy)
- Dexamethasone 8 mg (followed by 4 mg q6h) PO, IM, or IV
- Admit patients who remain symptomatic for >2 hours after descent
Why does near drowning cause problems?
Water aspiration washes out surfactant –> diminished gas exchange –> V/Q mismatch and hypoxia
Clinical presentation of near drowning
- Minimal water aspiration –> pulmonary injury and ARDS up to 6-24 hours after aspiration
- Prolonged hypoxia –> multiorgan failure
- Hypothermia even in warm water submersions
What causes most fire-related deaths?
Smoke inhalation
Predisposing factors to inhalation injury
- Closed-space fires
- Conditions that decrease mentation ie etoh/drug intoxication, head injury
Mechanisms of injury in inhalation
- Thermal injury: inhalation of heat affecting upper airway leading to acute airway compromise
- Inhalation of particulate matter: results in bronchospasm and edema
- Inhalation of toxic gases: carbon monoxide (fire inhalation injuries) or hydrogen cyanide (burned wool, silk, polyurethane, vinyl)
Clinical presentation of inhalation injury
- Facial burns
- Singed nasal hair
- Soot in nose or mouth
- Hoarseness
- Carbonaceous sputum
- Wheezing
- Symptoms of carbon monoxide poisoning may be present
management of carbon monoxide poisoning
- Humidified O2 via facemask
- Prompt ET intubation
- Bronchodilators
- Pulmonary toilet
What is the MOA of carbon monoxide?
- Colorless, odorless, non irritating gas
- Displaces O2 from hemoglobin = tissue hypoxia
- CO has affinity for hgb that is 260 x greater than O2
Clinical presentation of carbon monoxide poisoning
- Historical findings: exposure to gas heat or smoke inhalation (need to identify source), multiple pts with same presentation from same residence
Flu-like symptoms
* HA
* Dizziness
* N/V
* DOE
* Irritability
* Fatigue
* Vision changes
* Tachycardia
* Confusion
* Lethargy
* Syncope
* Convulsions
* Coma
Diagnostics for carbon monoxide?
- CO-oximetry: most reliable
- Pulse ox not reliable
- Labs: carboxyhemoglobin level - elevated and ABG
Management of carbon monoxide poisoning
- Do not wait for confirmation test
- High flow O2 via non-rebreather or ET intubation
- Hyperbaric O2 therapy for severe poisoning
What is considered severe carbon monoxide poisoning?
- LOC, AMS, MI, focal neuro deficit, pregnancy
Disposition of carbon monoxide poisoning
- Depends on severity of symptoms and safe discharge environment
- Asymptomatic: safe home environment and no suicide attempt- d/c home
- Moderate symptoms: HA, N/V: observe x 4 hours with 100% O2, assess home safety before discharge, d/c home if symptoms resolve
- Severe symptoms: CNS symptoms, chest pain, EKG changes –> admit and consult with hyperbaric specialist
MC causes of thermal burn
- Scalding, direct thermal and flame burns
How is burn described?
- % of body surface area affected
- Rule of 9s
- Lund and Browder
- Palmar method
How is depth of thermal burn described?
- Superficial partial-thickness
- Deep partial-thickness
- Full-thickness burns
What is rule of 9s used for?
- 2nd and 3rd degree burns
What is Lund and Browder used for?
- More accurate for infants and children
- Provides estimates of BSA based upon age
Palmar method for thermal burn
- Back of patients hand is 1% BSA
- Used for small burns
What is the anatomy, presentation, and healing of a superficial burn?
- Anatomy: epidermis
- Presentation: red, painful, tender skin, no blister
- Healing: 7 d; no scar
What is the anatomy, presentation, and healing of a superficial partial-thickness burn?
- Anatomy: epidermis and superficial dermis
- Presentation: blister, exposed dermis is red and moist, very painful
- Healing: 14-21 days, no scar
What is the anatomy, presenation, and healing of a deep partial-thickness burn?
- Anatomy: epidermis and deep dermis, sweat glands, and hair follicles
- Presentation: blister, exposed dermis is pale white to yellow in color; no blanching with pressure; absent pain sensation
- Healing: 3-8 week, permanent scar
What is the anatomy, presentation, and healing time of a full thickness (third degree) burn?
- Anatomy: entire epidermis and dermis
- Presentation: skin is charred, pale, leathery; no pain
- Healing: months, severe scarring, skin grafts
What is the anatomy and healing of a fourth degree burn?
- Anatomy: entire epidermis and dermis, as well as bone, fat, and/or muscle
- Healing: months, multiple surgeries; amputation or extensive reconstruction
Describe rule of 9s
- 9% head
- 18% front
- 18% back
- 9% each arm
- 1% genitalia
- 18% each leg
Management of thermal burn
- Supplemental O2 and early intubation if needed for complication of airway edema or inhalation injury
- Monitor VS: pulse ox readings may be falsely elevated by CO poisoning; BP monitoring via radial or femoral arterial cath if unable to utilize extremity cuff
- Assess and treat associated trauma, inhalation, CO poisoning
- IV opiates for pain control
- Urinary cath to measure I&Os: maintain UO at .5-1 mL/kg/h
- IV lactated ringer via 2 large bore needles in unburned area, use parkland formula to determine fluid amounts
Diagnostics for thermal burn
Lab evaluation to assess complications
* Frequent ABGs
* CBC, CK, CMP
* UA for myoglobin
* Carboxyhemoglobin level
* Imaging: CXR, EKG
Complications of thermal burn
- Inhalation injury
- Carbon monoxide poisoning
- Bacterial super-infection
- Sepsis
- Multiorgan failure
Management of minor burns
- Cleaned with mild soap and water
- Large bullae (>2 cm) or those over mobile joints: drain or debride and apply topical 1% silver sulfadiazine
- discharge to home with PCP follow up
- Update tetanus as indicated
Management of moderate and severe burns
- Cover with dry sterile sheet
- Admit
- Moderate burns: hospital
- Severe burns: burn center
- Update tetanus as indicated
What causes a chemical burn and what questions should you ask?
- Results from exposure to stong acids/alkalis
- Histoical information about type and concentration of chemical
- Duration of exposure
- Extent of penetration
Clinical presentation of acid chemical burns
- Coagulation necrosis leading to eschar formation limiting extent of damage
- Partial-thickness with erythema and erosion
