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Emergency Medicine > Environmental Emergencies (Elkins Slides) > Flashcards

Environmental Emergencies (Elkins Slides) Flashcards

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1
Q

When does heat illness occur?

A

When one is unable to adequately regulate body temperature

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2
Q

Who is at risk for heat illness?

A
  • Young/elderly
  • Obese
  • Chronic physical/mental illness
  • Impaired by drugs/ETOH
  • Anyone denied access to hydration/nutrition
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3
Q

What is heat edema?

A
  • Mild swelling of dependent extremities due to heat exposure
  • Results from muscular and cutaneous vasodilation combined with venous stasis
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4
Q

Management of heat edema

A
  • Self-limiting with elevation
  • Rest
  • Cooling
  • Oral rehydration
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5
Q

What is heat syncope?

A
  • Syncope after exertion in the heat
  • Results from vasodilation leading to intravascular volume redistribution
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6
Q

Clinical presentation of heat syncope

A
  • Core temp is normal
  • Skin cool and diaphoretic
  • Weak pulse
  • Transient hypotension
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7
Q

Management of heat syncope

A
  • 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
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8
Q

What are heat cramps?

A

Painful spasms of voluntary muscles of the abdomen and extremities resulting from salt depletion

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9
Q

Clinical presentation of heat cramps

A
  • Core temp normal or slightly elevated
  • +/- muscle fasciculations
  • Skin moist or dry and cool or warm
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10
Q

Diagnostic evaluation of heat cramps

A
  • Rarely indicated
  • May show hemoconcentration
  • Low-normal Na, +/- low K+, and Mg
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11
Q

Management of heat cramps

A
  • Remove from heat
  • Begin external cooling
  • Oral electrolyte solution or IV NS
  • Replace K+ and Mg if needed
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12
Q

Disposition of heat cramps

A
  • Discharge home
  • Rest for 1-3 days-avoid physical exertion and heat exposure
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13
Q

What is heat exhaustion?

A
  • Inability to maintain adequate cardiac output due to strenuous physical exercise and environmental heat stress
  • Rapidly evolves to heat strok if no intervention
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14
Q

What are the 2 types of heat exhaustion?

A
  • Hypernatremic: results from lack of water access
  • Hyponatremic: fluid loss replaced with water only
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15
Q

Clinical presentation of heat exhaustion

A
  • 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)
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16
Q

Work-up of heat exhaustion

A
  • BMP: assess electrolytes and renal function
  • UA: assess presence of myoglobinuria
  • Additional diagnostics based upon patient presentation: CK, LFT, ABG, EKG
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17
Q

Management of heat exhaustion

A
  • 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
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18
Q

Heat exhaustion disposition

A

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

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19
Q

What is heat stroke?

A
  • 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)
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20
Q

Clinical presentation of heat stroke

A
  • 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
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21
Q

Diagnosis of heat stroke

A
  • 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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22
Q

Management of heat stroke

A
  • 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
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23
Q

What should UO be in heat stroke?

A

50-100 mL/h

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24
Q

What is the disposition of heat stroke?

A
  • Admit to ICU if hemodynamic instability, severe LFT elevation or rhabdomyolysis
  • All others admit to general floor (med/surg)
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25
Q

What is frostbite?

A

Damage to tissue due to exposure to freezing temperatures

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26
Q

Clinical presentation of frostbite (before re-warming)

A

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

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27
Q

Clinical presentation of frostbite after rewarming

A
  • Stinging
  • Burning
  • Aching
  • Throbbing
  • Tenderness
  • Tissue discoloration
  • Loss of elasticity and mobility
  • Profound edema
  • Hemorrhagic blisters
  • Necrosis
  • Gangrene
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28
Q

What is 1st degree frostbite? 2nd?

A
  • 1st: erythema and edema without blister, skin peeling
  • 2nd degree: serous filled blister
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29
Q

What is 3rd degree frostbite? 4th?

A
  • 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
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30
Q

Treatment of frostbite

A
  • 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
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31
Q

What are components of extremity wound care?

A
  • 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
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32
Q

Disposition of frostbite

A
  • Home: limited area with only 1st degree injury
  • Hospital: extensive area of 1st degree and all 2nd, 3rd, 4th degree
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33
Q

Prognosis of frostbite

A
  • Long term sequelae
  • Cold sensitivity
  • Loss of sensation
  • Hyperhidrosis
  • Loss of digit/limb
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34
Q

Definition of hypothermia

A

Core body temp <35 C (<95 F) by rectal, bladder, or esophageal thermometer

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35
Q

What are primary causes of hypothermia?

A
  • Environmental exposure: often associated with alcohol/drug use
  • Therapeutic: targeted termperature management
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36
Q

What are secondary causes of hypothermia?

A
  • Burns
  • Hypoglycemia
  • Hypothyroidism
  • Hypoadrenalism
  • Hypopituitarism
  • CNS dysfunction
  • Sepsis
  • Drug intoxication
  • Trauma
  • Impaired shivering
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37
Q

Who are persons at risk for impaired shivering?

A
  • Advanced or very young age
  • Malnutrition
  • Physical exhaustion
  • Neuromuscular disease
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38
Q

What is are clinical presentations of each stage of hypothermia?

A
  • 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)
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39
Q

Diagnostic work up for hypothermia

A
  • 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
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40
Q

Management of hypothermia general and mild

A

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

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41
Q

Management of moderate hypothermia

A
  • Rewarming: warm environment with chemical, electrical, or forced air heating packs or blankets
  • Warm IV fluids
  • Full-body insulation, horizontal position
  • Immobilization
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42
Q

Management of severe hypothermia

A
  • 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
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43
Q

Management of hypothermia IV

A
  • 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)
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44
Q

Additional considerations for hypothermia

A
  • 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
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45
Q

Disposition of hypothermia

A
  • Admit all patients unless all of the below criteria are met
  • No comorbidities
  • No AMS
  • Presenting core temp > 34 C (93.2 F)
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46
Q

Stinging results in envenomation causing what 3 presentation?

A
  • Localized reaction
  • Systemic reactions
  • Anaphylaxis
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47
Q

Clinical presentation of localized bee sting?

A
  • Small pruritic, painful, erythematous, edematous lesion at sting site
  • Occassionally lesion will be >5 cm
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48
Q

Clinical presentation of fire ant sting

A
  • Sterile pustule evolves of 6-24 hours
  • May result in necrosis and scarring
49
Q

Clinical presentation of systemic/toxic reaction to wasp, bees, and stinging ants

A
  • 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
50
Q

Clinical presentation of anaphylactic reaction

A
  • True allergic reaction
  • Occurs within 6 h
  • Itchy eyes
  • Urticaria
  • Cough
  • Respiratory failure
  • CV collapse
51
Q

Lab evaluation of wasp, bee, stinging ants

A
  • Do not delay life-saving intervention for labs!
  • Only for systemic and anaphylactic reactions
  • Labs directed by complications: CBC, CMP, coags, CK
52
Q

Management of anaphylaxis

A
  • 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
53
Q

Management of localized reaction to wasp, bees, or stinging ants

A
  • Oral diphenhydramine 25-50 mg
  • Oral pain control: NSAID, acetaminophen
54
Q

Management of wasp, bees, and stinging ants systemic reactions

A
  • IV methylprednisolone
  • Diphenhydramine
  • Famotidine
55
Q

Complications of wasp, bees, and stinging ants

A
  • May require blood products
  • Dialysis
  • Extensive hospital care
56
Q

Wound management of wasp, bees, and stinging ants

A
  • Do not delay tx of systemic reactions to care for wound
  • Remove stinger with scraping technique
  • Wash wound
  • Ice and elevation
  • Tetanus update
57
Q

Disposition of wasp, bees, and stinging ants

A
  • 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
58
Q

What is the reaction to most scorpion stings?

A

Localized reaction

59
Q

Only systemically toxic scorpion in US with highest risk of toxicity to infants and children, where is it found?

A
  • Bark scorpion
  • Southwestern US
60
Q

Clinical presentation of scorpion sting

A
  • Sting painful without initial erythema/swelling
  • Exquisite pain with light percussion “tap sign”
  • Neuromuscular excitation
  • Cardiovascular toxicity
61
Q

What is the clinical presentation of neuromuscular excitation due to a scorpion sting?

A
  • Muscle spasms
  • Cranial nerve dysfunction
  • Roving eye movement
  • Diplopia
  • Difficulty swallowing
  • Hypersalivation
62
Q

What is the clinical presentation of cardiovascular toxicity due to scorpion sting?

A
  • Tachycardia
  • HTN
  • Pulmonary edema
  • Cardiogenic shock
63
Q

Management of scorion sting

A
  • 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)

64
Q

MC SE of scorpion antivenom (Anascorp)

A
  • Vomiting
  • Pyrexia
  • Rash
  • Nausea
  • Pruritis
  • Anaphylaxis rare
65
Q

What snakes are considered pit vipers and what is their appearance?

A
  • Rattlesnakes
  • Copperheads
  • Water moccasin
  • Large triangle shaped head with heat sensitive depression “pit” between their eyes
  • Venom cytotoxic
66
Q

Hallmark clinical presentation of pit viper bite

A
  • 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
67
Q

Systemic symptoms of pit vipers

A
  • Nausea
  • Vomiting
  • Hemolysis
  • Thrombocytopenia
  • Coagulopathy
  • Respiratory failure with CV instability and collapse
68
Q

Management of pit vipers

A
  • 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
69
Q

Labs for pit viper bites

A
  • CBC
  • CMP
  • Coags
  • CK
  • Urine myoglobin
  • type and crossmatch
70
Q

What can CroFab be used for?

A
  • Rattlesnakes
  • Copperheads
  • Cottonmouths/water moccasins
71
Q

MC SE of antivenom (CroFab)

A
  • Urticaria
  • Rash
  • Nausea
  • Pruritis
  • Back pain
  • Hypersensitivity in 5-19% patients
  • Recurrent coagulopathy in 50% of patients
72
Q

Disposition of pit viper bite

A
  • 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
73
Q

What is high altitude sickness?

A
  • 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
74
Q

What is the underlying physiologic insult for high altitude sickness?

A
  • Hypoxia
75
Q

How does the body compensate for high altitude?

A
  • Increased RR
  • Renal excretion of HCO3
  • Vascular changes
  • Increasing the blood’s oxygen carrying capacity
76
Q

Clinical presentation of acute mountain sickness

A
  • 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)
77
Q

Management of acute mountain sickness

A
  • 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)

78
Q

Disposition of acute mountain sickness

A
  • 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
79
Q

What is HAPE?

A
  • 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
80
Q

Clinical presentation of HAPE

A
  • 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
81
Q

Diagnostic evaluation of HAPE

A
  • CXR: alveolar infiltrates, enlarged pulmonary arteries, normal cardiac size
82
Q

Management of HAPE

A
  • 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
83
Q

Discharge criteria for HAPE

A
  • O2 on room air is maintained >90%
  • Symptoms resolve
  • CXR has improved
84
Q

What is High Altitude Cerebral Edema (HACE)?

A
  • End-stage manifestation of AMS and HAPE
85
Q

Clinical presentation of HACE

A
  • S/s or history consistent with AMS
  • Altered mental status
  • Ataxia
  • Stupor Coma
  • Signs of increased ICP: retinal hemorrhage, papilledema
86
Q

Diagnostic evaluation of HACE

A
  • MRI reveals cerebral edema
87
Q

Management of HACE

A
  • 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
88
Q

Why does near drowning cause problems?

A

Water aspiration washes out surfactant –> diminished gas exchange –> V/Q mismatch and hypoxia

89
Q

Clinical presentation of near drowning

A
  • Minimal water aspiration –> pulmonary injury and ARDS up to 6-24 hours after aspiration
  • Prolonged hypoxia –> multiorgan failure
  • Hypothermia even in warm water submersions
90
Q

What causes most fire-related deaths?

A

Smoke inhalation

91
Q

Predisposing factors to inhalation injury

A
  • Closed-space fires
  • Conditions that decrease mentation ie etoh/drug intoxication, head injury
92
Q

Mechanisms of injury in inhalation

A
  • 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)
93
Q

Clinical presentation of inhalation injury

A
  • Facial burns
  • Singed nasal hair
  • Soot in nose or mouth
  • Hoarseness
  • Carbonaceous sputum
  • Wheezing
  • Symptoms of carbon monoxide poisoning may be present
94
Q

management of carbon monoxide poisoning

A
  • Humidified O2 via facemask
  • Prompt ET intubation
  • Bronchodilators
  • Pulmonary toilet
95
Q

What is the MOA of carbon monoxide?

A
  • Colorless, odorless, non irritating gas
  • Displaces O2 from hemoglobin = tissue hypoxia
  • CO has affinity for hgb that is 260 x greater than O2
96
Q

Clinical presentation of carbon monoxide poisoning

A
  • 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

97
Q

Diagnostics for carbon monoxide?

A
  • CO-oximetry: most reliable
  • Pulse ox not reliable
  • Labs: carboxyhemoglobin level - elevated and ABG
98
Q

Management of carbon monoxide poisoning

A
  • Do not wait for confirmation test
  • High flow O2 via non-rebreather or ET intubation
  • Hyperbaric O2 therapy for severe poisoning
99
Q

What is considered severe carbon monoxide poisoning?

A
  • LOC, AMS, MI, focal neuro deficit, pregnancy
100
Q

Disposition of carbon monoxide poisoning

A
  • 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
101
Q

MC causes of thermal burn

A
  • Scalding, direct thermal and flame burns
102
Q

How is burn described?

A
  • % of body surface area affected
  • Rule of 9s
  • Lund and Browder
  • Palmar method
103
Q

How is depth of thermal burn described?

A
  • Superficial partial-thickness
  • Deep partial-thickness
  • Full-thickness burns
104
Q

What is rule of 9s used for?

A
  • 2nd and 3rd degree burns
105
Q

What is Lund and Browder used for?

A
  • More accurate for infants and children
  • Provides estimates of BSA based upon age
106
Q

Palmar method for thermal burn

A
  • Back of patients hand is 1% BSA
  • Used for small burns
107
Q

What is the anatomy, presentation, and healing of a superficial burn?

A
  • Anatomy: epidermis
  • Presentation: red, painful, tender skin, no blister
  • Healing: 7 d; no scar
108
Q

What is the anatomy, presentation, and healing of a superficial partial-thickness burn?

A
  • Anatomy: epidermis and superficial dermis
  • Presentation: blister, exposed dermis is red and moist, very painful
  • Healing: 14-21 days, no scar
109
Q

What is the anatomy, presenation, and healing of a deep partial-thickness burn?

A
  • 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
110
Q

What is the anatomy, presentation, and healing time of a full thickness (third degree) burn?

A
  • Anatomy: entire epidermis and dermis
  • Presentation: skin is charred, pale, leathery; no pain
  • Healing: months, severe scarring, skin grafts
111
Q

What is the anatomy and healing of a fourth degree burn?

A
  • Anatomy: entire epidermis and dermis, as well as bone, fat, and/or muscle
  • Healing: months, multiple surgeries; amputation or extensive reconstruction
112
Q

Describe rule of 9s

A
  • 9% head
  • 18% front
  • 18% back
  • 9% each arm
  • 1% genitalia
  • 18% each leg
113
Q

Management of thermal burn

A
  • 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
114
Q

Diagnostics for thermal burn

A

Lab evaluation to assess complications
* Frequent ABGs
* CBC, CK, CMP
* UA for myoglobin
* Carboxyhemoglobin level
* Imaging: CXR, EKG

115
Q

Complications of thermal burn

A
  • Inhalation injury
  • Carbon monoxide poisoning
  • Bacterial super-infection
  • Sepsis
  • Multiorgan failure
116
Q

Management of minor burns

A
  • 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
117
Q

Management of moderate and severe burns

A
  • Cover with dry sterile sheet
  • Admit
  • Moderate burns: hospital
  • Severe burns: burn center
  • Update tetanus as indicated
118
Q

What causes a chemical burn and what questions should you ask?

A
  • Results from exposure to stong acids/alkalis
  • Histoical information about type and concentration of chemical
  • Duration of exposure
  • Extent of penetration
119
Q

Clinical presentation of acid chemical burns

A
  • Coagulation necrosis leading to eschar formation limiting extent of damage
  • Partial-thickness with erythema and erosion

Emergency Medicine (13 decks)

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