Freezing to Death Frostbite and Hypothermia

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Freezing to DeathFrostbite and Hypothermia
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• Cold injuries result from our inability to
  properly protect ourselves from the environment.
• Factors such as temperature, length of exposure,
  windchill, humidity and wetness play important
  roles in these processes.
• The majority of cold injuries encountered today
  affect the homeless and wilderness and sports
  enthusiasts.

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Frostbite
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Pathophysiology

• Frostbite represents a localized ischemic injury,
  and skin circulation is the critical factor
• To preserve the body's core temperature, the
  skin's blood flow can vary from 20 ml/min when
  the skin temperature is 15 C (59F) up to 8,000
  ml/min when the skin temperature is 41C (106F).
  Blood flow through the apical structures (i.e.
  hands, feet, nose and ears) varies the most
  markedly.

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• Our core temperature is defended by
  vasoconstriction and shunting of blood away from
  these structures thus your body will sacrifice
  fingers and toes to maintain its core
  temperature. This has been called the
  "life-or-limb" response
• Vascular tone is controlled by direct local
  temperature and indirect reflex temperature
  effects. An illustration of the latter would be
  that a cold head will cause vasoconstriction of
  the hands!

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• Maximal peripheral vasoconstriction and minimal
  blood flow occur when the extremities are cooled
  to 15C (59F).
• At 10C (50F), vasoconstriction is interrupted
  by periods of vasodilatation, termed cold-induced
  vasodilatation (CIVD) or the "hunting response."
  This protects the area from cold injury at the
  expense of increasing heat loss. It occurs in
  5-10-minute cycles, and individual variation may
  explain susceptibility to frostbite.
• Prolonged and repeated cold exposures increase
  the degree of CIVD

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• Eskimos, Lapps and Nordic fishermen have a strong
  CIVD with rapid cycling, which helps them
  maintain hand function in the cold. This response
  is impaired by altitude, hypoxia, dehydration and
  alcohol.

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• Humans are basically adapted to warm climates.
  Since humans do not adapt well to the cold,
  behavioral responses such as putting on
  additional clothing and seeking shelter are key
  to preventing frostbite.
• Factors such as mental illness and drug and
  alcohol use interfere with these behavioral
  responses.

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• Hypovolemia, hypothermia and the presence of
  other injuries all add to the severity of
  frostbite. Diabetes, atherosclerosis, vasculitis,
  Raynaud's phenomenon, hypotension and the use of
  vasoconstrictors or vasodilators increase the
  risk and seriousness of frostbite.
• Tight clothing increases the risk of cold injury
  by impairing circulation. Sweating accelerates
  heat loss. Individuals with previous cold injury
  are more susceptible to reinjury.

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• Local cold injury produces a succession of
  changes. Skin sensation is lost at about 10C
  (50F). With further cooling, blood becomes more
  viscous, and blood vessels constrict and begin to
  leak plasma.
• As skin cools further, freezing occurs and ice
  crystals form in the cells. This leads to
  cellular dehydration, shrinkage and damage to
  cell walls. Blood vessels and nerves are the most
  susceptible tissues.

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• Thawing results in additional injury, referred to
  as reperfusion injury.
• Blood flow becomes stagnant and contributes to
  further tissue hypoxia.
• There is also release of harmful substances from
  injured cells, leading to further cellular
  damage. The degree of microvascular damage
  determines whether circulation will recover or if
  the tissue will be lost. Tissue damage is
  dependent upon the rate and duration of freezing
  and the rate of thawing.

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• Refreezing after thawing causes more severe
  damage to the tissue involved

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Clinical Presentation and Prognosis

• Symptoms are related to the severity of the
  injury. Initial symptoms of frostbite include
  coldness, numbness and a "clumsy" extremity.
• Thawing and reperfusion are often accompanied by
  intense pain.
• Throbbing, burning or tingling sensations begin
  in 2-3 days after rewarming and may persist for
  weeks or months

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• These symptoms are intensified by heat. All
  patients experience some degree of sensory loss,
  which can last for years and may become
  permanent.

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• There are two classes of frostbite injury
  mild/superficial (no tissue loss) and severe/deep
  (loss of tissue).
• The initial appearance of frostbite may be
  deceptively benign
• Frozen tissue is numb, pale, hard and waxy

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• One cannot differentiate superficial from deep
  involvement at this stage
• Following rapid rewarming, there is an initial
  hyperemia.
• Partial sensation returns until blisters form.
  Favorable prognostic signs include normal
  sensation, color and warmth.

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• Edema should appear within three hours after
  thawing. Lack of edema is an unfavorable sign.
• Vesicles and bullae appear in 6-24 hours. Early
  formation of large, clear blisters that extend to
  the tip of an affected digit is a good indicator
  of tissue survival. Small, dark blebs that appear
  later and do not extend to the digit tip indicate
  damage to underlying vasculature and are
  associated with subsequent tissue loss.

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• In severe frostbite, a black, hard, dry eschar
  forms in 9-15 days postthaw.
• It takes 22-45 days after thawing to know the
  true extent of tissue loss.
• Most individuals will have persistent
  abnormalities of circulation even with minimal
  tissue loss. Long-term sequelae of frostbite may
  include excessive sweating, pain, coldness,
  numbness, abnormal skin color and joint
  stiffness. These symptoms tend to be worse in
  cold temperatures.

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Prehospital Treatment

• Treat hypothermia first, and avoid further heat
  loss from the patient
• Provide supportive care for any suspected trauma,
  remove constrictive clothing
• At all costs, thawed tissue must not be allowed
  to refreeze. If a part is still frozen and rescue
  is imminent, keep the part frozen, unless warm
  water thaw is available and there is no danger of
  refreezing.

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• For example, if a victim with frostbitten feet
  must walk to safety, it is better for him to walk
  out on frozen feet (delaying rewarming) rather
  than risk refreezing the feet.

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• Avoid excessive warming by hot water, campfire,
  car heater or any method gt48C (118F), which
  causes burning of the frozen part. Do not use
  friction massage, especially with ice or snow.
• leave blisters intact
• prevent tissue damage by applying a loose,
  sterile bandage.
• Splint the area and elevate the extremity.

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Prevention

• Adequate food and fluid intake, staying dry and
  avoiding fatigue are crucial to preventing
  frostbite. Clothing and shelter are necessary to
  provide a suitable micro-climate for the skin.
  Other important considerations include
• Trip planning Weather awareness Proper
  equipment Avoiding alcohol Avoiding reflex
  vasoconstriction---cover all skin Use of
  chemical warmers Check toes and fingers
  intermittently
• Buddy system for recognizing facial
  frostnip.

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Hypothermia

• Hypothermia is defined as a core temperature
  lt35C (95F)
• It occurs in all settings and in all seasons.
  Urban settings account for most cases in the
  United States
• Hypothermia is commonly associated with
  concurrent trauma. Elderly patients are often
  found indoors with underlying illnesses that can
  predispose them to hypothermia.

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Pathophysiology

• Humans are primarily tropically adapted
• The hypothalamus acts as the body's thermostat.
  Peripheral cooling of the blood activates the
  hypothalamus, which leads to an increase in
  metabolic rate, shivering and peripheral
  vasoconstriction

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• humans' main adaptations are behavioral, such as
  putting on clothes or seeking a warmer
  environment
• There are several mechanisms of heat loss

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• Radiation is heat loss to the surrounding
  environment and can be significant, depending on
  the amount of blood flow to the skin. It accounts
  for 60 of body heat loss at rest. A large amount
  of heat loss comes from the head. Radiant heat
  loss is reduced by wearing adequate
  clothing--especially a hat!

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• Conductive heat loss is heat transfer by direct
  contact with an object. It is reduced by
  insulation.

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• Heat loss from evaporation (i.e. respiration and
  perspiration) is affected by the relative
  humidity and ambient temperature of the
  environment.
• The body loses heat 25 times faster if the skin
  is wet. Evaporative loss is reduced by staying
  dry, using a vapor barrier and using mouth and
  nose moisture traps.
• Convection heat loss is determined by air
  movement over the skin (i.e. windchill) and is
  reduced by a windproof layer.

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• Predisposing factors to hypothermia can be
  divided into three groups. While there is some
  overlap, most can be categorized as those that
  decrease heat production, those that increase
  heat loss and those that impair thermoregulation.

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• Both young and old extremes of age are
  susceptible to hypothermia from decreased heat
  production. Individuals with depleted glycogen
  stores or malnutrition have inadequate fuel to
  keep warm.
• Endocrine insufficiencies (pituitary, adrenal and
  thyroid) and certain drugs that impair shivering
  (alcohol) also play a role.

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• Ways of increasing heat loss were described
  earlier. The most common iatrogenic causes
  include the use of cold IV fluids and prolonged
  exposure of the patient for examination.
• Burns and other skin disruption (i.e. rashes)
  increase heat loss as well.

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• Thermoregulation can be impaired by diseases of
  the central or peripheral nervous systems, such
  as CVAs, neoplasms, Parkinson's, cord transection
  or neuropathies.
• Certain metabolic derangements (i.e. diabetes) or
  the pharmacologic effects of certain drugs (i.e.
  benzodiazepines, barbiturates, phenothiazines and
  cyclic antidepressants) also lead to impairment.

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Clinical Presentation

• The body's physiologic responses to cooling and
  clinical presentation vary widely between
  individuals. Initially, there is an increase in
  the metabolic rate and peripheral
  vasoconstriction
• Maximal shivering occurs at 35C (95F) and is
  extinguished as the core temperature drops to
  31-33C (88-92F).

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• Respiratory volume initially increases however,
  with further cooling, it decreases.
  Cardiovascular changes include initial
  tachycardia with progressive bradycardia and
  cardiac irritability.

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• There is a linear decline in mean arterial
  pressure, and cardiac output is lt50 at 25C
  (77F). The conduction system is preferentially
  affected, which leads to a prolongation of all
  ECG intervals. The ECG may also show a J-wave or
  Osborn wave.

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• The "hump" is present at the junction of the QRS
  complex and the ST-segment and can mimic acute
  myocardial injury. Arrhythmias are common below
  32 C (90F). Atrial arrhythmias are usually
  innocuous. Ventricular fibrillation is typically
  induced, and asystole is part of the natural
  progression.

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• Higher cerebral functions start to decline at
  core temperatures of 33-35C, and patients
  become unresponsive if cooling continues. The EEG
  is flat at 19C (66F).

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Prehospital Treatment

• Handle patients very gently, as the myocardium
  may be irritable and iatrogenic ventricular
  fibrillation could result.
• Prevent further heat loss with dry insulating
  materials
• If the patient is responsive, assume perfusion is
  present. Palpation of peripheral pulses is
  difficult in a vasocontricted bradycardic patient
  

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• Monitor the patient closely, oxygenate
• Shivering artifact is a common problem. Rewarming
  reverses vasoconstriction if the patient is not
  adequately fluid resuscitated, this can lead to
  irreversible and fatal shock, known as rewarming
  shock.

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• Field rewarming options include heated,
  humidified oxygen, warmed IV fluids and truncal
  heat application of hot water bottles or direct
  body-to-body heat.

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• Myth A hypothermic patient is a metabolic icebox
  and is therefore stable and should not be
  rewarmed in the field.
• Fact The patient is unstable and will continue
  to rapidly lose heat to the environment. Death is
  inevitable if temperature declines to a certain
  value. Rescuers should always attempt to at least
  stabilize the core body temperature.

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• Remember "No body is dead until it is warm and
  dead."
• Initiate CPR in severe hypothermia unless DNR
  status is documented and verified, obvious lethal
  injuries are present, chest wall decompression is
  impossible, any signs of life are present, or
  rescuers are endangered by conditions. Apparent
  rigor mortis, dependent lividity and fixed
  dilated pupils are not reliable criteria to
  withhold CPR.

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• Anticipate substandard activity of resuscitation
  drugs in hypothermic patients
• In v-fib or v-tach, defibrillation rarely
  succeeds below 30C (86F)
• Atrial arrhythmias are typically innocent and do
  not require treatment, as spontaneous conversion
  is usual with rewarming. Expect a slow
  ventricular response in hypothermic patients.
  Vasopressors can potentially cause arrythmias and
  are ineffective if the patient is already
  maximally vasoconstricted.