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Thermal Injury

Cold

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Thermal Injuries:- Cold

The normal set point for human core temperature is 37±0.5°C. The human body maintains this temperature whenever possible, using autonomic mechanisms to regulate heat loss and gain in response to environmental conditions. Nevertheless, the human body has limited physiologic capacity to respond to cold environmental conditions. Thus, behavioral adaptations such as clothing and shelter are critical to defend against hypothermia.
The hypothalamus receives input from central and peripheral thermal receptors. In response to a cold stress, the hypothalamus attempts to stimulate heat production through shivering and increased thyroid, catecholamine, and adrenal activity. Sympathetically mediated vasoconstriction minimizes heat loss by reducing blood flow to peripheral tissues, where cooling is greatest. Peripheral blood vessels also vasoconstrict in direct response to cold.
Neurologic function begins declining even above a core temperature of 35°C. Once the core temperature reaches 32°C, metabolism, ventilation, and cardiac output begin to decline and shivering becomes less effective until it finally ceases as core temperature continues to drop to 30C

Cooling decreases tissue metabolism and inhibits neural activity. During the initial phase of cooling, shivering in response to skin cooling produces heat and increases metabolism, ventilation, and cardiac output.

When the entire body is exposed to low temperatures over a long period, the result can be alarming. At first blood is diverted from the skin to deeper areas of the body to prevent heat loss and maintain core body temperature, but this results in anoxia (lack of oxygen) and damage to the skin and the tissues under the skin, including the walls of the small vessels. This damage to the small blood vessels leads to swelling of the tissues beneath the skin as fluid seeps out of the vessels. When exposure to cold is prolonged, it leads eventually to cooling of the blood itself and at 88° F (about 31° C) protective mechanisms like contraction of blood vessels of skin to prevent heat loss and heat generation by shivering stop working, and the body cannot warm itself. Once this has occurred, the results are catastrophic. All the vital organs become affected and below 83° F (about 28° C), death usually ensues. The skin and the tissues under it are kept at a constant temperature (about 98.6° F, or 37° C) by the circulating blood and other mechanisms.

normal temperature varies from a minimum of 97.7° Fahrenheit (36.5° Celsius) to a maximum of almost 99.5° Fahrenheit

Thermoregulatory function of skin — The most important physiologic function of skin is thermoregulation. Skin blood flow is under both central and local control. In cold conditions, vasoconstriction can decrease skin blood flow to approximately 10 percent of baseline values. Because the metabolic demands of skin are low, decreased blood flow alone does not cause ischemia. Skin blood flow can also be decreased during periods of immobility when limbs are below the level of the heart.

Cold-induced vasodilation — Maximal vasoconstriction occurs when a hand or foot is cooled to approximately 15°C (59°F). Further cooling causes increases in blood flow known as cold-induced vasodilation (CIVD) or the "hunting response." CIVD occurs in 5- to 10-minute cycles. Prolonged and repeated cold exposures increase the amplitude and frequency of CIVD. Eskimos, Lapps, and Nordic fisherman have large CIVD response with rapid cycling [18]. A strong CIVD response is thought to decrease susceptibility to NFCI, but scientific evidence is lacking. A study of 206 Dutch Marines has been characterized as showing that a weak CIVD response correlates with increased susceptibility to NFCI [19]. However, in the 11 subjects who later sustained cold injury, the injury was frostbite rather than NFCI.

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Injury Due to Cold

Cold injuries are divided into freezing and nonfreezing injuries (occur with ambient temperature above freezing generally 0 to 15°C or 32 to 59°F).
Nonfreezing cold injuries include chilblain, immersion foot( trench foot.) "sea boot foot" or "bridge foot" shelter foot (or shelter limb)

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Signs & Symptoms of NFCI

Feet and hands that sustain NFCI are initially white and numb, but later become red, edematous, and extremely painful. In severe cases, the extremity can develop hemorrhagic bullae and tissue necrosis.
White, gray, or blue-white skin.
Cold, hard skin.
Loss of feeling in body part.
Peeling skin.
Clear or blood-filled blisters.
Black skin (severe)
May cause Infection and gangrene acutely and cold intolerance and pain syndromes chronically

Nonfreezing cold injury (NFCI) is characterized by impaired control of circulation and direct damage to the microcirculation, but the mechanism is poorly understood.

Although many authors attribute NFCI solely to prolonged vasoconstriction [14,15], the cause is likely more complex [22]. Animal experiments suggest that tissue damage is inversely proportional to tissue temperature and directly proportional to duration of exposure but that repeated exposure is likely to cause more damage than a single, longer exposure. The duration of a single exposure at a given temperature that is necessary to cause NFCI is not known, nor are there quantitative estimates of the effects of repeated exposure. Cold alone, without moisture, does not seem to be sufficient to cause NFCI. Immobility and malnutrition appear to contribute to injury in many cases.

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Chilblains (Erythema pernio)

Chilblains (erythema pernio) is a superficial tissue injury that occurs after prolonged or intermittent exposure to temperatures above freezing but with high humidity and high winds.
Initial pallor characterizes chilblains followed by erythema and pruritus of the affected area.
Women and young children are the most susceptible and chilblains commonly involve cheek and ears, fingers and toes.
The cold exposure causes damage to peripheral capillary beds, this damage is permanent and the redness and itching will return with re-exposure to cold. The condition is uncomfortable but not serious. Preventing exposure to cold is the best treatment..

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Trench foot

Trench foot & immersion syndrome are caused by prolonged exposure of the feet to cold, wet conditions. This can occur at temperatures as high as 60°F if the feet are constantly wet e.g. sea sports.

Since wet feet lose heat 25 times faster than dry, the body uses vasoconstriction to shut down peripheral circulation in the foot to prevent heat loss.
Skin tissue begins to die because of lack of oxygen and nutrients and due to buildup of toxic products.
The skin is initially reddened with numbness, tingling pain, and itching, then becomes pale and mottled and finally dark purple, grey or blue.

immobility, inadequate or wet clothing, constricting boots and clothing, inadequate fluid or caloric intake, and fatigue and stress, especially in combat. Associated injuries or underlying circulatory problems, including peripheral vascular disease or Raynaud phenomenon, may contribute to the risk or severity of NFCI. Diabetes causes circulatory problems that may predispose to NFCI. Smoking, older age, and ethnicity may play a role, but data are lacking. Mental illness and alcohol use are also likely risk factors. NFCI occurs most often during winter training in younger, less-experienced personnel. Risk factors included African-Caribbean ethnicity (higher risk than Caucasians), "feeling generally cold," performing static duties, wearing wet boots and clothing, and immersion of the affected limb in water.

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Trench foot (cont.)

The affected tissue generally dies and sloughs off. In severe cases trench foot can involve the toes, heels, or the entire foot.
If circulation is impaired for over 6 hours there will be permanent damage to tissue. If circulation is impaired for over 24 hours the victim may lose the entire foot. Trench foot causes permanent damage to the circulatory system making the person more prone to cold related injuries in that area.
A similar phenomenon can occur when hands are kept wet for long periods of time. The damage to the circulatory system manifests as Raynaud's phenomenon.

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WWIF

Warm water immersion foot (WWIF), or paddy- field foot is due to immersion in warm water (15 to 32°C; 59 to 90°F) for up to 72 hours. It manifests as painful, white, wrinkled soles.
Most patients with WWIF recover completely in one to three days with drying and elevation of the feet. Warm water immersion hand has also been described
"tropical immersion foot," is a more severe condition, characterized by symmetrical redness, edema, and tenderness of the skin of the ankles and the dorsa of the feet.
Jungle foot, sometimes referred to as "tropical jungle foot," "jungle rot," or "paddy foot,“ refer to TIF

Warm water immersion foot (WWIF) is a transient syndrome first described in soldiers in Vietnam. It manifests as painful, white, wrinkled soles of the feet due to immersion in warm water (15 to 32°C; 59 to 90°F) for up to 72 hours [8]. It has also been called paddy-field foot and, incorrectly and confusingly, "tropical immersion foot," which is a more severe condition also described in vietnum war [9]. Most patients with WWIF recover completely in one to three days with drying and elevation of the feet [10]. Warm water immersion hand has also been described

Jungle foot, sometimes referred to as "tropical jungle foot," "jungle rot," or "paddy foot," is a poorly defined condition seen in wars in Vietnam. Most, but not all, reports of jungle foot refer to TIF [10].

Research into the pathophysiology of warm water immersion injuries is limited. Warm water immersion foot (WWIF) is thought to be due to hyperhydration (waterlogging) of the plantar stratum corneum when continuously exposed to warm water for up to 72 hours [10]. Tropical immersion foot (TIF) appears to be due to the passage of water through compromised epidermis into the dermis when the feet are continuously exposed to warm water for longer than 72 hours.

Risk factors continuous exposure of the feet to water at or above 15°C (59°F) without an opportunity for drying.

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Management of NFCI

Treat systemic hypothermia by rewarming. Do not actively rewarm extremities with isolated NFCI
Replace fluid losses, which may be substantial. Use isotonic intravenous fluids warmed to 42°C to both rehydrate and prevent hypothermia.
Extremities with NFCI should be allowed to rewarm gradually with bed rest, elevation of the legs or hands, and air drying at room temperature
Tetanus prophylaxis is recommended. There is no role for prophylactic antibiotics in the treatment of isolated NFCI.
During the prehyperemic stage, the extremity is numb. Once the hyperemic stage begins, it is necessary to control pain. Prophylactic treatment of pain prior to the hyperemic stage is ineffective.�

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Management of NFCI

Nonsteroidal antinflammatory drugs (NSAIDs) and opioids may be administered
Vasodilators, such as nifedipine, have not been shown to be helpful. Lumbar sympathectomy (regional anesthesia) may be helpful to control pain
Amitriptyline 50 to 100 mg orally at bedtime has been a standard treatment for pain in the United Kingdom
If amitriptyline is not effective, neuropathic pain medications such as gabapentin can be administered.
General care of the patient traditionally includes a high-protein diet and prohibition of smoking.
Antibiotic if cellulitis develops to cover staphylococci, streptococci, and pseudomonas species.
Surgical consultation if necrosis develops

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Hypothermia

Clinical staging scheme described by the International Commission for Mountain Emergency Medicine (this is sometimes referred to as "the Swiss system")
Mild (HT I) – Normal mental status with shivering. Estimated core temperature 32 to 35°C (90 to 95°F).
Moderate (HT II) – Altered mental status without shivering. Estimated core temperature 28 to 32°C (82 to 90°F).
Severe (HT III) – Unconscious. Estimated core temperature 24 to 28°C (75 to 82°F).
Severe (HT IV) – Apparent death. Core temperature 13.7 to 24°C (56.7 to 75°F) (resuscitation may be possible).
Death (HT V) – Death due to irreversible hypothermia. Core temperature <9 to 13.7°C (48.2 to 56.7°F) (resuscitation not possible).

Shivering may not cease until around 30°C in some patients. Vital signs and other evidences of life may be present at core temperatures below 24°C

Hypothermia is defined as decrease in the core body temperature below 35°C (95°F).

Mild hypothermia - core temperature 32 to 35°C (90 to 95°F) Shivering - not under voluntary control

Can't do complex motor functions (ice climbing or skiing), can still walk & talk

Vasoconstriction of peripheral vessels manifesting as pallor

Moderate hypothermia-core temperature 28 to 32°C (82 to 90°F)

Dazed consciousness and/or irrational behaviour e.g. paradoxical undressing - person starts to take off clothing, unaware he is cold

Loss of fine motor coordination - particularly in hands - e.g. can't zip up parka, due to restricted peripheral blood flow

Slurred speech

Violent shivering

“I don't care attitude” - flattened effect

Severe hypothermia - core temperature and below 28ºC (82°F) (immediately life threatening)

Unconscious. Not shivering.

Profound hypothermia- core temperature <24°C (75°F) or <20ºC (68°F)

In addition to hypothermia from environmental exposure, many medical conditions can cause hypothermia, including hypothyroidism, adrenal insufficiency, sepsis, neuromuscular disease, malnutrition, thiamine deficiency, and hypoglycemia. Ethanol abuse and carbon monoxide intoxication have been implicated in some cases of hypothermia [42]. Hypothermia has even been misdiagnosed as psychiatric illness, including attempted suicide. The differential diagnosis of hypothermia is summarized in the following table (table 6) [18,20,26,31,43-45].

Certain medications directly or indirectly cause hypothermia, either by impairing thermoregulatory mechanisms, decreasing awareness of cold, or clouding judgment. The most common medications that impair thermoregulation are anxiolytics, antidepressants, antipsychotics, and opioids. Medications that can impair a patient's ability to compensate for a low ambient temperature include oral antihyperglycemics, beta-blockers, alpha-adrenergic agonists (eg, clonidine), and general anesthetic agents [46].

At patient presentation, beware of vital signs inconsistent with the degree of hypothermia. A relative tachycardia inconsistent with the core temperature suggests hypoglycemia, hypovolemia, or an overdose. Relative hyperventilation implies an underlying organic acidosis (eg, diabetic ketoacidosis, aspirin overdose), since CO2 production should be decreased in moderate or severe hypothermia.

The neurologic manifestations of hypothermia vary widely, but the level of consciousness should be consistent with the core temperature. If the level of consciousness is not proportional to the degree of hypothermia, suspect a head injury, central nervous system infection, or overdose.

Although the myriad secondary causes of hypothermia listed above may occur simultaneously with accidental hypothermia (eg, excessive alcohol use leading to prolonged environmental exposure), the latter can usually be distinguished on the basis of a history of exposure to cold without other complicating factors.

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Management of Hypothermia

Airway, breathing, circulation-

CPR if cardiac arrest. IV fluid at 40-42C
Low-dose (2 to 5 mcg/min) dopamine if BP continues to be low with fluid.

Prevention of further heat loss- Room temperature 28°C (82°F).
Initiation of rewarming appropriate to the degree of hypothermia

Passive external rewarming (PER)
Active external rewarming (AER)
Active internal (core) rewarming (ACR)

Treatment of complications: Low BP; Infection, adrenocortical and thyroid insufficiency

After wet clothing is removed, the patient is covered with blankets or other types of insulation. PER may be unsuccessful in the setting of glycogen depletion, sepsis, or hypovolemia, especially in elderly patients.

Active external rewarming (AER) — During active external rewarming, some combination of warm blankets, heating pads, radiant heat, warm baths, or forced warm air is applied directly to the patient's skin.

Active internal (core) rewarming (ACR) In addition to IV administration of warmed crystalloid (40 to 42°C), effective techniques include irrigation of the peritoneum or the thorax (via the pleural space) with warmed isotonic crystalloid, and extracorporeal blood rewarming.

Chest compressions should also not be started if cardiac contractions are seen on bedside echocardiogram or pulses can be detected with Doppler ultrasound. If pulses are not found after checking for one minute, CPR should be started immediately and provided continuously if possible. Continuous CPR may not be possible due to safety considerations or during evacuation of the patient. Mechanical chest-compression devices should be used, if available, to avoid interruption of CPR during transport. CPR can be delayed up to 10 minutes while rescuers move the patient to a safer location. In a patient with core temperature of 20 to 28°C, or if the core temperature is not known, administer CPR continuously for periods of at least 5 minutes, alternating with periods of no longer than 5 minutes without CPR. In patients with a core temperature below 20°C, administer CPR continuously for periods of at least 5 minutes, alternating with periods of no longer than 10 minutes without CPR

Blood pressure is supported with warmed (40 to 42°C) infusions of isotonic crystalloid. Large infusions may be necessary. Use of warmed crystalloid is critical. Infusion of room-temperature fluids can worsen hypothermia. Intraosseous (IO) access may be easier to obtain than intravenous access in cold, vasoconstricted patients. An indwelling bladder catheter is helpful to assess urinary output and fluid shifts. Because of the neuroprotective effects of hypothermia, complete recovery of patients with hypothermia and cardiac arrest has been well documented despite prolonged resuscitation [21,52-57]. Therefore, under usual circumstances, resuscitative efforts should only be withheld if there is a nonsurvivable injury or fatal illness, if the body is so frozen that chest compressions are impossible, or if the nose and mouth are blocked with snow or ice [9,58]. Efforts should be continued (occasionally for several hours) until the patient's core temperature reaches 32 to 35°C (90 to 95°F) [18]. Mild hypothermia is treated with passive external rewarming

●Moderate and refractory mild hypothermia are treated with active external rewarming

●Severe (and some cases of refractory moderate) hypothermia is treated with active internal rewarming and possibly extracorporeal rewarming

Passive external rewarming (PER) — Passive external rewarming is the treatment of choice for mild hypothermia. It is also used as a supplemental method, when feasible, in patients undergoing aggressive rewarming for moderate to severe hypothermia. After wet clothing is removed, the patient is covered with blankets or other types of insulation. The resulting reduction in heat loss combines with the patient's intrinsic heat production to produce rewarming. Room temperature should be maintained at approximately 28°C (82°F), if possible. The combination of ACR, using heated IV infusions and warmed humidified oxygen, and AER provides an effective initial strategy for most spontaneously perfusing, severely hypothermic patients

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Freezing Injury by Cold

Frostnip and frostbite.
Prolonged exposure to freezing temperature causes tissue damage known as frostnip in milder form
Factors predisposing the body to frostbite,

Malnutrition or emaciation leading to a loss of the fatty layer under the skin,
lack of adequate clothing, a wet body or limbs which loses heat faster than dry body
Any type of insufficiency of the peripheral blood vessels.

All of these increase the loss of body heat.

Normally the body temperature (about 98.6° F, or 37° C) is maintained by the energy produced by cells by metabolizing food that requires a steady supply of food and oxygen. In response to low environmental temperature the body uses several protective mechanisms to generate additional heat to maintain body temperature. The small blood vessels in the skin contract, to prevent heat loss and maintain core body temperature and blood supply to vital organs, such as the heart and brain. In case needed muscles produce additional heat through shivering. But if body temperature continues to fall and reaches about 88° F (about 31° C), these protective mechanisms stop working, and the body cannot warm itself. However, as less warm blood reaches the skin, body parts such as the fingers, toes, ears, and nose cool more rapidly and with low body temperature, most organs, especially the heart and brain, become sluggish and eventually stop working.

If body temperature falls below 83° F (about 28° C), death may occur.

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Frostnip

Frostnip is the freezing of top layers of skin tissue. It is generally reversible and manifests with numbness, white, waxy skin-top layer feels hard, rubbery but deeper tissue is still soft.
It occurs typically on cheek, ear lobes, nose, fingers and toes.
Frostnip is managed by gentle rewarming e.g. by blowing warm air on it or placing the area against a warm body part (partner's stomach or armpit).
Avoid rubbing as this can damage the tissue by having ice crystals tear the cells.

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Frostbite

Frostbite is more severe than frostnip and includes all layers of skin.
The skin appears white and has a “wooden” feel all the way through with numbness and possibly anaesthesia.
Deep frostbite can include freezing of muscle and/or bone, it is very difficult to rewarm the appendage without some damage occurring.
Like frostnip- exposed parts of the body with thin covering of skin and soft tissue are particularly at risk.

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First Degree Frostbite

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Second degree frostbite is characterized by blistering and desquamation

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Third Degree Frostbite

24 h cold exposure following road accident with delayed rescue

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Third degree frostbite is associated with necrosis of skin and subcutaneous tissue with ulceration

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Fourth degree frostbite includes destruction of connective tissues and bone, with gangrene

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Fourth –Degree Frostbite:- Livid discoloration, Thrombosed subcutaneous veins, Lack of sensation with slight oedema

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Fourth-degree frostbite of the extremities requires amputation in most cases

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Eye Injuries

Freezing of cornea:

Caused by forcing the eyes open during strong cold winds without goggles.
Treatment is very controlled, rapid rewarming e.g. placing a warm hand or compress over the closed eye. After rewarming the eyes must be completely covered with patches for 24-48 hours.

Eyelashes freezing together: Put hand over eye until ice melts, then open the eye.

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Snowblindness (sunburn of the eyes)

Snowblindness (sunburn of the eyes):

Eye protection from sun is just as necessary on cloudy or overcast days as it is in full sunlight when on snow.
Snow blindness can occur during a snow storm if the cloud is thin. The eyes feel dry, irritated and gritty and moving or blinking becomes extremely painful. Photophobia occurs, eyelids may swell, with erythema and epiphora.
Treatment involves cold compresses and dark environment while avoiding rubbing the eyes.
Prevention by wearing good sunglasses with side shields or goggles.

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Key Messages

Protracted exposure to low temperatures with slow cooling can lead to non-freezing cold injuries.
Frostbite arises from formation of ice crystals in tissue.
Particularly in the acute stage, frostbite should be treated at burn centers if at all possible
The affected parts of the body should not be warmed until renewed exposure to cold can be ruled out.
The treatment of frostbite and non-freezing cold injuries is barely standardized; there are no studies with large case numbers and no authoritative treatment guidelines.