Freezing to Death     Frostbite and Hypothermia

Freezing to Death Frostbite and Hypothermia PowerPoint PPT Presentation

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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 a

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Freezing to Death Frostbite and Hypothermia

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1. Freezing to Death Frostbite 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 >48C (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 <35C (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 <50% 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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