Cold Injury & Hypothermia

Question 1

Define frost bite

Answer 1

• Cold injury resulting from ice crystal formation in cells and tissues

Question 2

Discuss physiology of systemic/core temperature control

Answer 2

• Core temperature is maintained through heat production, heat conservation and heat loss
• Temperature receptors in skin (Raffini - hot temps; Krause - cool temps) communicate w/ posterior hypothalamus
• Posterior hypothalamus communicates with anterior hypothalamus to influence core heat:
  
  • heat production: shivering, thyroid hormone to increase oxidative metabolism
  • heat conservation: catecholamine release, vasoconstriction, inhibition of sweat production
• Heat loss primarily occurs through radiation (whereby heat protection mechanisms are not being utilized, vaso/venodilation in superficial venous system); also through sweat production and evaporation (convection) and conduction

Question 3

Discuss thermoregulatory role of SKIN

Answer 3

1. Vasomotor
   
   1. Vasocontriction/vasodilation
   2. Venous shunting - use superficial system whenhot and deep system when cold
   3. Glomus bodies - AV shunting
2. Dermis (and Subcutaneous fat) as insulation
3. Appendages
   
   1. Sebaceous glands - sebum prevents water loss
   2. Eccrine sweat glands - sweat production and evaporation (loss by convection)
4. Other: shivering, piloerection and increased density of hair distribution

Question 4

Describe the pathophysiology of cold injury

Answer 4

• 2 mechanisms, 3 pathways, 4 phases
• 2 Mechanisms:
  
  • Direct - cellular - ice crystal formation, extracellular dehydration and intracellular cell death
  • Indirect - vascular - progressive tissue ischemia, vasospasm and sludge
• 3 Pathways
  
  • Immediate - tissue freezing: cellular death d/t ice crystal
  • Progressive - tissue hypoxia: Necrosis 2’ progressive ischemia
  • Immediate & progressive - release of inflammatory mediators
• 4 Phases
  
  • Phase 1 - cooling & freezing
    
    • cold exposure, vasoconstriction, local ischemia
    • direct (celluar ice crystal formation) and indirect (ischemia & sludge)
  • Phase 2 - thawing and rewarming
    
    • ice crystals melt; intracellular and extracelluar edema; inflammation and release of thromboxane A2; secondary vasoconstriction and platelet aggregation
  • Phase 3 - progressive injury
    
    • accumulation of inflammatory markers
      
      • decrease prostaglandins associated wiht v.dil and antiplatelet
      • increase thromboxanes and PGs associated with v. const and plt aggregation
    • overall can increase surface area and depth of injury
  • Phase 4 - resolution
    
    • tissue demarcation
    • options are complete healing; complete healing w/ sequallae; no healing

Question 5

describe the principles of management of cold injury

Answer 5

Pre-hospital

• do not initiate re-warming unless it can be sustained (ie if there is risk of becoming cool)

Immediate (In emergency Dept)

• ATLS
• ABCs
• Assess core temperature / identify hypothermia
• Initiate rewarming
  
  • Systemic rewarming if indicated: active techniques like warm IV fluid, warm FOLEY irrigation; active aggressive techniques like gastric, peritoneal, pleural cavity lavage or bypass
  • Rapid rewarming of localized cold injury: with water bath immersion (39-41’C); passive techniques like warm room/blankets
• Analgesia
• Tetanus
• Fluid resus
• Elevation
• (rare to require escharotomy/fasciotomy)

Early

• Allow blisters to demarcate
  
  • clear blisters debride
  • hemorrhagic blisters keep
• Aloe Vera application
• NSAIDS
• Analgesia
• Antibiotics if indicated
• Consideration of:
  
  • dextran, heparin
  • thrombolytics
• Local wound care - SSD

Late (> 6 mos)

• allow area to declare itself
• delay amputation / surgery if eschar is dry (no infection)
• amputate / debride if infection

Question 6

define hypothermia

Answer 6

• core temp < 35’c (95’f)
• life threatening when < 32 ‘ c

Question 7

Summarize clinical manifestations of hypothermia

Answer 7

• CNS - depression –> coma
  
  • including paradoxical undressing, eventual EEG abnormalities, non-detection
• CVS - bradycardia –> a.fib, v.fib, asystole
• Resp - initial hyperventilation –> medullary depression & respiratory depression
• MSK - shivering - depletion of glycogen stores - nerve conduction block - paresis
• Fluid balance / GU - vasoconstriction - central volume expansion - cold diuresis - renal tubular dysfunction
• Heme - HbO2 dissociation curve shift left - decreased peripheral release of O2; decrease circulating thromboplastin –> DIC