Freezing to Death Frostbite and Hypothermia - PowerPoint PPT Presentation

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Freezing to Death Frostbite and Hypothermia

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... encountered today affect the homeless and wilderness and sports enthusiasts. ... Urban settings account for most cases in the United States ... – PowerPoint PPT presentation

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Title: Freezing to Death Frostbite and Hypothermia


1
Freezing to DeathFrostbite and Hypothermia
2
  • 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.

3
Frostbite
4
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.

5
  • 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!

6
  • 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

7
  • 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.

8
  • 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.

9
  • 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.

10
  • 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.

11
  • 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.

12
  • Refreezing after thawing causes more severe
    damage to the tissue involved

13
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

14
  • These symptoms are intensified by heat. All
    patients experience some degree of sensory loss,
    which can last for years and may become
    permanent.

15
  • 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

16
  • 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.

17
  • 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.

18
  • 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.

19
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.

20
  • 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.

21
  • 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.

22
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.

23
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.

24
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

25
  • humans' main adaptations are behavioral, such as
    putting on clothes or seeking a warmer
    environment
  • There are several mechanisms of heat loss

26
  • 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!

27
  • Conductive heat loss is heat transfer by direct
    contact with an object. It is reduced by
    insulation.

28
  • 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.

29
  • 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.

30
  • 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.

31
  • 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.

32
  • 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.

33
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).

34
  • Respiratory volume initially increases however,
    with further cooling, it decreases.
    Cardiovascular changes include initial
    tachycardia with progressive bradycardia and
    cardiac irritability.

35
  • 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.

36
  • 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.

37
  • 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).

38
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

39
  • 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.

40
  • Field rewarming options include heated,
    humidified oxygen, warmed IV fluids and truncal
    heat application of hot water bottles or direct
    body-to-body heat.

41
  • 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.

42
  • 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.

43
  • 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.
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