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High Acuity > Burns/Frostbite > Flashcards

Burns/Frostbite Flashcards

1
Q

Functions of the Skin

A
  • Protection
  • Barrier
  • Thermal regulator (36.5-37.5)
  • Sensation
  • Excretion & absorption
  • Vitamin D synthesis (D2 > D3 – active form)
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2
Q

Definition and 6 Types of Burns

A
  • Loss/disruption of tissue integrity: any layer(s)
  • Impedes normal skin function
  • Due to excessive exposure to: thermal, chemical, electrical, radiation, friction, or cold source.
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3
Q

4 Factors Affecting Burn Survival Rates

A
  1. Age
    > older adults have impaired sensation and reaction times
    > decreased risk assessment
    > thinner, more fragile skin with decreased circulation
    > impaired healing times
  2. Severity of burn = percentage of body service area (BSA) burned
    3 Depths of Burns
  3. Underlying Disease Processes
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4
Q

What 4 things determine burn severity?

A

o Depth of burn
o Extent of burn (TBSA)
o Location of burn
o Other patient risk factors

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5
Q

Causes of thermal burns

A

o Flame
o Scald
o Steam
o Smoke (Inhalation)

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6
Q

Causes of friction burn

A

Rug burn

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7
Q

Causes of radiation burn

A

o Sunburn
o Radiation therapy

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8
Q

Causes of electrical burn

A

o Lightning
o AC/DC current

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9
Q

Causes of chemical burn

A

o Acid
o Alkali

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10
Q

Electrical burns result from ______ transmission of ____, _____, or arcing

A
  • Result from direct transmission of current, flash or arcing
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11
Q

Explain why the outward appearance of electrical burns can be misleading

A
  • creates a burn where the current enters, and where it exits (entry and exit wounds)
  • created path entire way through body, most damage is internal
  • Only burn that TBSA not calculated because not accurately reflect damage
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12
Q

Where is most of the damage done in electrical burns, and what is key to monitor?

A
  • Most of the damage is done upon exit of the energy and within the tissues it passes
  • Current can impact major organs
    > Especially heart; electrical current can effect electrical current of heart; arrhythmias
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13
Q

Examples of acidic burn causative agents

A

bathroom cleaners, pool chemicals, car batteries, etc.

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14
Q

How does acid cause burns and what are the effects

A

o Tissue integrity damaged by coagulating cells & skin proteins; can limit depth of tissue damage
o Mild edema
o Charring, hard eschar
o Less dangerous

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15
Q

Examples of alkaline burn causative agents

A

oven cleaners, fertilizers, industrial cleaners, cement, firework sparklers, etc.

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16
Q

How do alkaline substances cause burns, what are the symptoms, and how does treatment differ?

A

Causes skin & its proteins to liquify = deeper injury. More severe.
++edema
No charring

Treatment and Number 1 Priority: decontamination; will continue to burn until neutralization with material described in WHMIS. If unknown, use water and soap.
> Neutralization before ABC’s – materials can harm healthcare workers if come into contact

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17
Q

What kind of treatment do radiation burns require?

A
  • Sun
  • Xray, MRI
  • Therapeutic radiation treatments
  • Superficial, requires typical first aid treatment
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18
Q

Sources of thermal burns and the type of burn they precipitate

A
  1. Flames > dry heat burns
    * Open flame, explosion
  2. Liquids > moist heat (scald) burns
    * Hot liquids, steam
  3. Hot object/substance > contact burn
    * Hot metal, tar, grease  often result in full-thickness injury
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19
Q

When should you suspect smoke inhalation burns?

A
  • If someone was trapped in burning space
  • Singed nasal/facial hair
  • Close proximity to explosions
  • Facial/neck burn = upper/lower airway injury
  • Cough = black/gray/bloody sputum
  • Hoarse voice
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20
Q

Treatment of Smoke Inhalation Injuries

A
  1. Stabilize C-spine
  2. 100% humidified oxygen; alveolar damage is suspected
  3. Early intubation; rapid airway closure
    > Majority of mortality of burns is due to smoke inhalation, not damage to rest of body
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21
Q

Concern with Carbon Monoxide with smoke inhalation, clinical S+S and treatment

A
  • Colorless, odorless, tasteless gas
  • Inability to detect
  • Released into air with fire
  • 200x higher affinity for hemoglobin; Hgb will bind to CO before O2
  • SpO2 monitor doesn’t differentiate between CO and O2 saturation – reads HEMOGLOBIN bound, not what it is bound to
  • Clinical S+S: cherry red in face (CO causes vasodilation), classic signs of low oxygen
  • Treatment: 100% oxygen 15L to flush CO out for hours
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22
Q

Concern with cyanide poisoning with smoke inhalation

A
  • Product of incomplete synthetic combustion (furniture)
  • Consider when in house fire
  • Difficult to detect, when it enters into cells they can not produce ATP and enter into anaerobic metabolism even with oxygen present
  • If suspected; antidote given.
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23
Q

4 Grades of Frostbite:

A

1: hyperemia and edema

  1. clear milky fluid filled blisters with partial thickness necrosis

3: dark fluid filled blisters, non-blanching, cool and bumb, full thickness and SC necrosis > requires debridement

4: blisters beyond digit, bloodless, full thickness into muscle and bone - gangrene

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24
Q

When does grade of frostbite become apparent?

A

When body part is thawed

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25
Q

Superficial frostbite care

A

rewarm with body heat
* Analgesia > rewarming is painful (Tylenol, Advil, Dilaudid)

26
Q

Severe (3-4) frostbite care

A
  1. slowly rewarmed with bath water (do not touch basin)
  2. elevate extremity above heart to reduce edema
  3. tetanus shot
  4. loose sterile dressing
  5. antibiotics
  6. iloprost (vasodilator + inhibits platelets)
27
Q

Zones of Injury: Jackson Model

A
  1. Zone of coagulation: centre of injury; most deep and damaged part
    * Point of maximum damage
    * Irreversible tissue loss
    * Coagulative necrosis
  2. Zone of stasis:
    * Decreased perfusion; can progress if not reversed
    * Potentially salvageable
    * Goal of treatment: treat and reverse zone of stasis
    * Increase circulation and perfusion
  3. Zone of hyperemia:
    * Tissue perfusion increased (from inflammatory process - vasodilation)
    * Damage is reversible
28
Q

Pathophysiology of Burns (Capillary Leak Syndrome)

A

Normal Blood Capillary: Water is the smallest molecule that can pass through the capillary

Postburn Blood Capillary: Permeability is drastically increased due to mass vasodilation and inflammation response, which allows large molecules such as protein to pass through capillaries pores easily.
>Commonly results in hypovolemic shock – fluid lost to interstitial spaces and evaporates off
> Some distributive shock properties

29
Q

3 Factors Contributing to Shock in Burns and end result

A

1.Injury causing cell death (hyperkalemia and coagulopathy)

  1. Massive fluid shifts out of vessels due to increased permeability
    - hypovolemic shock due to sodium shift with fluid evaporation
  2. Collioid osmotic pressure decreases (edema and high HcT)

= intravascular volume
low BP
high HR

30
Q

4 Determinants of Burn Depth

A
  1. temperature of heat
  2. contact time
  3. medium of heat (water vs steam)
  4. thickness of skin
31
Q

Describe superficial burn

A
  • only epidermis
  • dry
  • pink/red
  • intact
  • blanches
  • no edema
  • no blisters
  • some pain
32
Q

Describe deep partial thickness burn

A
  • epidermis and dermis
  • wet
  • waxy
  • red-white
  • minimal blanching
  • ++ edema
  • less blistering
  • +pain
33
Q

Describe partial thickness burn

A
  • epidermis + papillary dermis
  • moist
  • weeping
  • pink-red
  • blanches
    • edema
    • blisters
  • ++ pain
34
Q

Describe full thickness burn

A
  • epidermis, dermis, and fat
  • dry
  • leathery
  • white
  • charred skin with eschar
  • absent hair
  • no blanching
  • no pain
  • no blisters
  • +++ edema

Can also progress into muscle and bone

35
Q

Rule of 9’s

A

Used to calculate TBSA

Total (front and back)
Head: 9%
Arms: 9% each
Torso: 36%
Legs: 18% each
Groin 1%

36
Q

Primary Survey for Burns

A

STOP the burning process!
> By flushing all areas in contact with chemicals
1. Airway
* Burned airways swell rapidly
* Early intubation
2. Breathing
* Possible gas exposure (CO, cyanide)
* Circumferential burns around torso
3. Circulation/C-spine
* Cardiac status; shock treatment (>20% TBSA)
4. Disability
* Neurological status
5. Exposure & Evaluate
* Remove all rings, watches, jewelry r/t edema
* Remove all clothing from the area
* Cool the burn wound
6. Fluid resuscitation
* Calculate TBSA

37
Q

What does fluid resuscitation prevent in burn patients and when does it begin?

A

TBSA >20%

prevents the development of shock & maintains adequate perfusion/increase perfusion to zone of stasis

38
Q

Best indicator of adequate fluid replacement

A

Kidney Perfusion (urine output)

39
Q

Calculation of fluid resuscitation for burn victims

A

Parkland Formula

Weight in kg x 4ml x %TBSA= total amount of fluid infused in 24hrs from time of injury

40
Q

Explain timing of delivery and which fluid is used for resuscitation of burn victims

A
  • Give half during first 8hrs
  • Remaining half over the next 16hrs
  • Use Ringers Lactate
41
Q

How do you know fluid resuscitation has been achieved in burn victims and how does this differ for electrical burns

A
  • Maintain urinary output at 0.5ml/kg/hr (30-50 ml/hr).
  • For electrical burns (TBSA not calculated) with myoglobinuria, maintain urinary output at 1-1.5ml/kg/hr (~75-100 ml/hr) until urine is clear
  • Fluids can be increases if urine output is not meeting target
42
Q

Why do electrical burn victims require higher urine output?

A

Muscle damage (i.e. electrical burns traveling through body > entry/exit wounds)  myoglobin released into the bloodstream

Kidneys remove myoglobin from the body into the urine

In large amounts, myoglobin can damage the kidneys

Higher urine output/hr is required to help clear the myoglobin

43
Q

Cardiac complications emergent phase of burns

A
  • Increased capillary permeability  fluid leaks into interstitial space (edema)  hypovolemia  SHOCK
  • Tissue ischemia  anaerobic metabolism and necrosis  acidosis
  • Dysrhythmias (electrical burns, hyperkalemia, etc)
  • Electrolyte shifts   Na; hyper (or hypo) K+
  • Impaired circulation to extremities/organs
  • Impaired microcirculation and increased viscosity
44
Q

Urinary complications emergent phase of burns

A
  • Decreased blood flow to kidneys causes renal ischemia (AKI)
  • Myoglobin  Acute tubular necrosis (ATN)
45
Q

Respiratory complications emergent phase of burns

A

Upper resp tract injury
* Edema formation
* Mechanical airway obstruction & asphyxia
* Injury r/t length of exposure to smoke or toxic fumes
Lower airway (inhalation) injury
* Direct insult at the alveolar level
* Risk for ARDS

46
Q

Immunity complications emergent phase of burns

A
  • Loss of skin barrier & presence of eschar favor bacterial growth
  • Hypoxia, acidosis, thrombosis of vessels  impair resistance to bacteria
  • Risk for SIRS, sepsis, MODS
  • Blisters: sequestering of fluid & proteins
47
Q

GI changes that occur in emergent phase of burns

A
  • Shunting of blood to vital organs  decreased blood flow to gut  paralytic ileus (gastric distention, N/V)
  • Ischemia of gastric mucosa  duodenal/gastric ulcer; bleeding
48
Q

Hypermetabolic response in emergent phase of burns

A
  • Mediated by catecholamine release (epi, norepi)
  • Increased metabolic demand increases body temp
  • “Burn fever”=  temp
  • Shivering: further increases metabolic requirements
49
Q

Hematologic changes in emergent phase of burns

A
  • Release of thromboxane A2 by damaged cells  thrombocytopenia, abnormal platelet function,  fibrinogen levels, inhibition of fibrinolysis
  • Net deficit in plasma clotting factors (DIC)
  • Anemia  destruction of RBCs d/t burn injury
  • Blood loss
50
Q

Cognitive changes in emergent phases of burns

A
  • Hypoxia d/t smoke inhalation
  • Concomitant trauma, substance use/abuse, sedation or pain meds
51
Q

What is Eschar?

A
  • A scab or dry crust that results from trauma, such as a burn, infection, or excoriating skin disease
  • DEAD skin
  • Potentially dangerous:
  • risk for compartment syndrome
  • chest restriction (can be hard; if burns circumferential)
  • sub-eschar edema
  • Extensive circumferential full-thickness burn of a limb or chest eschar may cause problems it is unyielding/rigid
  • Escharotomy may be necessary
52
Q

What do we do about the burn after initial stabilization?

A
  1. pain management
  2. promote wound healing
  3. PT/OT
  4. Nutritional therapy
  5. psychological
53
Q

Healing/Treatment of Superficial Burns

A

Superficial/uncomplicated burns heal by regeneration (cell division and replenishing the epidermis) within a few weeks
o Topical abx (i.e. Polysporin) and gauze

54
Q

Healing/Treatment of Complicated Burns

A

Full-thickness requires surgery
 Debridement and grafting or permanent injury and scarring can occur; will not heal by themselves

Advanced dressing in partial thickness & deep partial thickness burns
 “advanced dressing”= something with antimicrobial ex) silver

55
Q

4 Purposes of Burn Dressings

A
  1. Absorb & contain the drainage
  2. Provide protection for the wound from the environment
    o Pts with burns are at increased risk for infection
    o Infected wounds take longer to heal & will increase scar tissue formation
  3. Decrease wound pain
    o Initially, superficial burns are very sensitive to air currents
    o Deeper burns become more sensitive to air as the heal and nerves are re-enervated
    o Wound coverings eliminate air currents from the wound surface
  4. Permit high humidity at the wound site
    o A moist environment is critical for epithelial cells to migrate and spread
    o Re-epithelialization can occur on a dry surface; however, it is slowed down
    o moist wound healing is NOT usually used for infected burns or burns with eschar
56
Q

Purpose of cleansing/debridement

A
  • All dressings are done as a sterile procedure
  • Always soak the inner dressing with sterile NS or water prior to removing the old dressing
  • You do not want old dressing to adhere to wound because healthy tissue may be removed inadvertently
  • Cleanse wound with warm sterile cleansing solution. Wipe burn from center toward outer edges
  • Remove excess exudate, topical ointments and loose eschar using a light scrub
  • If necessary, lift loose skin/eschar with sterile forceps and trim with sterile scissors, this process should not cause pain or bleeding
57
Q

Pro Removing Blisters

A
  • Fluid inside the blisters depresses immune function, affects neutrophils job of killing foreign cells, and enhances inflammation
58
Q

Pro Leaving Blisters Intact

A
  • Blister is a protective cover for the burn
  • The blistered skin will gradually wrinkle and collapse onto the healing wound: this skin is a protective layer
  • If the blister is removed, the wound can become very painful
  • Spontaneous re-absorption of the fluid will take place in ~ 1 week
59
Q

Grafting

A
  • Surgical procedure: skin or skin substitute is placed over a burn or non-healing wound to permanently replace damaged or missing skin or provide a temporary wound covering
  • Use of patient’s own skin to close the wound (autologous)
  • Cadaver skin, pigskin, or type of biobrane (expensive) to close the wound
  • Surgical debridement of full-thickness burns is necessary to prepare the wound for grafting
60
Q

Contractures

A
  • An area of skin that has undergone excessive scarring from a deep burn
  • Caused from thick bands of hypertrophic scaring that restrict joint movement  loss of joint mobility  permanently impair function
  • Some are unavoidable… but many can be prevented:
  • Early excision and grafting for full-thickness burns
  • Stretching, minimum of 5-6 times a day; painful, patients may not adhere
  • Casting or splinting to position potential contracture area in a stretched position
  • Having patient do as much for themselves as possible (ie. Self-grooming, eating etc.)
61
Q
A

High Acuity (20 decks)

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