FrostBite & Cold Injury seminar Flashcards

1
Q

What is cold injury?

A

Spectrum of injury secondary to heat loss

NONfreezing

  • Frost-nip
    • reversible superficial freezing; reversible pallor with resultant erythema and pain w rewarming
  • Trench foot
    • acute prolonged exposure to direct wetness (1-10C); resultant cold sensitivty, blistering, hyperhidrosis
  • Chilbain
    • chronic prolonged exposure to cool humid air (1-10C); resultant red painful patches, =>chronic vasculitis

FREEZING

  • Frostbite: ice crytal formation in tissue
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2
Q

What are risk factors for frostbite

A
  • Altered LOC
  • military
  • homeless
  • intoxication
  • elderly
  • comorbidity - atherosclerosis, PVD, smoking
  • improper clothing
  • outdoor activity/employment
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3
Q

What is the etiology of frostbite?

A

environmental

  • temperature : degree and length of exposure
  • conductive heat loss (metal/liquid nitrogen, wet clothes
  • convective heat loss (high wind)
  • decreased tissue oxygenation (high altitude)

host

  • compromised circulation (PVD, tight clothes)
  • previous Frostbite
  • africains
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4
Q

Describe the pathophysiology of frostbite

A

3 paths

4 phases

MANSONS DOUBLE VASCULAR LESION = direct injury w crystal intra/extracellular + indirect vasopasm/rbc sludge

PATHWAYS

  • cellular death
  • dermal ischemia
  • inflammatory mediators released

PHASES

  • Cooling & Freezing
    • ​Usual response to cold -> perpheral vasoconstriction to maintain core T ->skin temp drop ->ICE CRYSTAL FORMATION ->skin ischemia
    • DIRECT cellular injury
      • ​Intracellular: freezing causes PM lipoprotein disruption->cell death
      • Extracellular: increased ISFosmolarity->cell dehydration
    • INDIRECT
      • ​vasospasm and RBC sludge ->ischemia
  • Rewarming & Thawing
    • Crystals melt
    • Edema & reperfusion injury (ROS, TXA2, vasoconstriciton and plat agrgegation)
  • Progressive injury
    • PG accumulate in blisters
      • ​PGE2alpha + TXA2 - vasocontrict + plat agg
      • = increased depth and SA
  • Resolution
    • ​complete, incomplete or no spontaneous healing
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5
Q

How do you classify frostbite injury

A
  • 1st degree = partial thickness freezing
    • Sx: throbbing, aching pain - TRANSIENT
    • Sn: erythema, edema. desqaumation may occur
  • 2nd degree = Full thickness freezing
    • Sx: Numb
    • Sn: clear blisters, erythema with marked edema, usually develop wihtin 8hrs
  • 3rd degree = FT with Subcutaneous freezing
    • Sx: thrombbing aching shooting pain
    • Sn: blueish violet discoloration, hemorrhagic blisters, block of wood appearance
  • 4th degree = FT with Sq and tendon/muscle/bone
    • ​Sx: numb, +/- jt pain
    • Sn: mottled, deep red/cyanotic then black areas, no edema
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6
Q

How do you manage frostbite?

A
  • Hx: environmental etiologies, duration, comorbidities
  • PE: 6-24hrs for clear blisters- wiat 48hrs before classifying

TREATMENT

  • IN field - NO rewarmign unless can be competed - trasnfer
  • In ER
    • ABCs
    • rapid rewarm - 40-42C bath 20-40mins with AROM joints
    • analgesia, tetanus, elevation
    • escharotomy
  • Acute
    • Debride clear blisters (contrain TXA2)
    • Aloe vera q6h (antiPG, stops thromboxane synthase)
      • *preserves subdermal plexus
    • NSAIDS 12mg/kg q6h (antiPG)
      • COX inh - reduced PGE2 production
    • Wound care dialy - flamazine BID
    • Analgesia
    • antibiotics if indicated
    • thrombolysis - if risk lifealtering amputation and no CI to TpA
  • Late
    • allow tissue to mummify, eschar to separate
    • dressing daily
    • debride 1-3mths
    • Only timeto amputation early ->frank infection
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7
Q

What are complications of frostbite

A
  • amputation
  • Skin and NV
    • hyperhidrosis
    • altered pigment
    • cold sensitivity
    • chronic pain
  • Muscle/bone
    • HO
    • intrinsic muscle atrophy
    • stiffness
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8
Q

What is hypothermia

A

Core temperature <35C

Mild: 32-35

Moderate 32-28

Severe <28

* lifethreatening hypothermia is below 32

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9
Q

What is the etiology of hypothermia

A

Loss of heat

  • environmental
  • iatrogenic (CV pump/shunt)
  • skin disorder (psoriasis, burns, exfoliative dermatitis)
  • vasodilation (Etoh,drugs)

Reduced heat production

  • malnutrition
  • endocrine (hypoT,P,adrenal)

Reduced perfusion control

  • DM
  • SCI
  • CVA/SAH

Other

  • sepsis, pancratitis, uremia
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10
Q

How do you manage hypothermia

A
  • Hx: environment, comorbidities, confusion
  • PE
    • CNS: confusion->coma
    • CV: Afiv/Vfib/asystole/bradycardia
    • PVS: constricted ->central volume overload ->cold diuresis ->hypovolemia->RTdysfx->more diuresis
    • Resp: hyperventilation->meduallry depression->resp depression, noncardiogenic pulm edema
    • MSK: paresis
    • Hematologic: Hb curve shift left - less offloading at tissue, DIC, MetACid + Resp Alk
  • Treatment
  • A- airway Cspine
  • B- breathing - vent (PEEP for noncardiogenic pulm edema)
  • C- chest compression + volume expansion (PRIOR to rewarm)
  • D- Defib only once
  • E - Rewarming
    • PASSIVE - remove wet clothes, blankets
    • ACTIVE
      • External: heat lamp on core, heating pads, water bath 42-45
      • Internal: 45C iv fluid, vent hum air 47C, Lavage gastric NG/colonic/rectal, foley/peritoneal/pleural, Ecmo
  • If mild (32-35) -> passive and active external
  • if moderate (32-28) ->passive+active external COre only
  • if severe - active internal directly
    • iv lfuids
    • vent warm air
    • NG
    • foley
    • ECMO
    • pleural/peritonela lavage
  • continue until >35
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