Antibiotics (Properties, Administration, Interactions) - M.P. Cherenko 1999

Frostbite, Hypothermia

Normally, body Temperature ranges between 36—37 °С. The Main sources of heat production are the Muscles and the Liver, from which heat is transported throughout the body via the bloodstream. Heat dissipation is 80—90 % accounted for by the Skin. Body temperature can change under METABOLISM/18.html">The Influence of high and low temperatures. When the body is exposed to extremely low temperatures, primarily two pathological conditions develop—frostbite and generalized hypothermia (freezing).

In frostbite, specific areas of the body (extremities, Nose, ears, etc.) are affected by The impact of cold. In generalized hypothermia, the entire body is affected. However, this division is somewhat arbitrary, since frostbite is accompanied by systemic Disorders of the entire body in most cases.

FROSTBITE

Frostbite (congelatio) is damage to Tissues or specific body parts caused by exposure to low temperatures against the Background of various contributing factors.

During wartime, frostbite presents as a mass injury.

In peacetime, it occurs rarely, most commonly in individuals in a state of alcohol intoxication or during snowstorms and blizzards.

According to statistical data, the frequency of frostbite in specific PARTS OF THE body follows this sequence: lower extremities — 90.6 %, upper extremities — 6.2 %, both upper and lower extremities — 2.8 %, face — 0.2 %, and other body areas — 0.2 %.

Although the Blood supply to the facial skin is much better than that of the extremities, and the thermoregulation of these areas is more advanced, the frequency of facial frostbite is quite high. These injuries are usually superficial, although they can occasionally be significant. For instance, the literature describes a case of 4th-degree frostbite of the nose in a soldier who was breaking out of encirclement during severe frost. After a few days, the nose turned black and sloughed off. Cases of frostbite involving all extremities leading to death have also been documented. Frostbite of the male genitalia is rare (0.02 %).

Classification. V. Kotelnikov provides the following classification of cold injuries: 1) acute (frostbite, generalized hypothermia); 2) chronic (pernio/chilblains, cold neurovasculitis).

Depending on the intensity and Nature of the traumatic agent, Three types of frostbite are distinguished: 1) frostbite caused by air temperatures close to zero or moderately low; 2) frostbite caused by ambient temperatures below — 30°С; 3) contact frostbite—damage to specific body areas upon direct contact with a cold agent, most commonly a metal object (observed in pilots, tank crewmen, and tractor drivers).

The clinical course of frostbite comprises two periods: I — the pre-reactive, or hypothermia period (starting from the moment of cold exposure until the beginning of rewarming); II — the reactive period (beginning after rewarming).

Local tissue changes in frostbite depend on the depth of tissue damage. Taking this factor into account, a four-degree classification of frostbite is currently used (discussed below).

Regardless of the affected area and degree, pathoanatomically and clinically, frostbite progresses through three phases: 1) inflammation; 2) necrosis development and demarcation; 3) scarring and wound epithelialization.

To better understand the Clinical presentation of frostbite, it is worthwhile to examine the Etiology AND Pathogenesis of this type of injury.

Etiology. Low temperature is considered the primary and decisive factor in the etiology of frostbite, most frequently resulting from the action of cold dry air on tissues and Organs. The skin pallor observed in such cases served as the basis for the Conclusion that tissue temperature drops below zero and tissue fluid freezes. At one time, this was the leading theory of frostbite pathogenesis, viewing Cell death from freezing as the main cause of pathological changes. To support this, observations were cited of a person whose frozen fingers broke off like a dry twig due to careless movements.

At the same time, some scientists categorically deny the possibility of tissue freezing in frostbite.

There are no exact data in the literature regarding the lower temperature threshold at which living tissues perish, but undoubtedly, extremely low temperatures in contact frostbites cause more rapid tissue damage.

Low temperature is an important, but not the only factor in the occurrence of frostbite. An equally significant role is played by other contributing factors, primarily related to meteorological conditions. Air humidity (dampness) plays a major role in The Development of frostbite. During wartime, FOOT frostbite was observed even at positive temperatures when combined with high air humidity ("trench foot"). The Role of humidity in causing frostbite lies in the fact that wet skin dissipates 4 times more heat than dry skin.

Wind and blizzards are no less important than air humidity. During the transportation of the wounded in open vehicles or flatbed trucks, frostbite occurs even at positive temperatures.

Frostbite can also set in during sharp temperature fluctuations.

Mechanical factors contributing to frostbite include all those that impair Blood Circulation in the extremities (tight clothing, tight footwear).

An important role in frostbite is played by a decrease in the body's overall resistance, most commonly caused by wounds and blood loss. Shock accompanying wounds frequently leads to hypothermia as well. Blood loss, by inducing peripheral vasospasm, worsens the blood supply to the extremities. Against the background of tissue ischemia, frostbite occurs more readily.

The body's resistance is diminished by illness, fatigue, exhaustion, and hunger.

Some authors attach certain significance to acute infectious diseases (enteritis, colitis, dysentery) in the development of frostbite.

Smoking also contributes to frostbite. Nicotine, by causing vasospasm, leads to tissue ischemia, which in turn predisposes to frostbite.

Pathogenesis of frostbite. Despite the extensive literature on the pathogenesis of frostbite, this issue remains not fully elucidated to this day. This may be due to the fact that patients with frostbite seek medical attention at various stages of rewarming, meaning the pathogenesis is studied only after tissue temperature has been restored.

Among the theories regarding the pathogenesis of frostbite, the following can be distinguished.

1. The Theory of direct low-temperature impact on tissues. Proponents of this theory believe that vascular changes in frostbite occur secondarily, and the core of the pathogenesis is the direct damaging effect of cold on tissues, especially Muscle tissue.

2. The neuro-reflex theory. An important role in the pathogenesis of frostbite is attributed to the excitation of the sympathoadrenal system. Consequently, pressor substances are released into the systemic circulation, which increase vascular tone and lead to hemodynamic disorders.

3. The theory of local circulatory impairment in tissues. Primary significance in the pathogenesis of frostbite is attributed to vascular spasm and ischemia. Conversely, some authors assign the main role to vascular paralysis, which is why they termed gangrene in frostbite as neuroparalytic. Necrosis occurring in tissues during frostbite is considered secondary.

Of all the aforementioned theories, the least realistic is the theory of direct low-temperature impact on tissues. Frostbite in such cases usually occurs due to direct contact of a cold object with the tissues. There is much in common between the neuro-reflex and vascular theories: neuro-reflex influences are ultimately mediated through The Vascular System.

How is the pathogenesis of frostbite explained today? What changes occur in tissues during this type of injury?

The literature describes a case that occurred many years ago. In a field near Leningrad, the corpse of a frozen peasant was found. An investigation was launched. The investigator asked the prosector: what changes were discovered in the body? What was the cause of death? The autopsy was performed by an experienced pathologist. The only abnormality he found in the deceased's body was the absence of one eye. However, the deceased had been monocular since childhood. All other Internal Organs were unchanged. The prosector was unable to answer the question of what caused the peasant's death.

Physicians performing autopsies invariably observe a similar picture: no morbid changes or pathological phenomena are detected in cases of freezing (and not only in freezing, but also in cases where a particular part of the body has suffered frostbite).

Subsequent observations demonstrated that Changes in the body and individual organs occur only when the action of cold ceases and the action of heat begins.

Currently, the majority of authors believe that vascular and neural system reactions within supercooled tissues play a decisive role in the development of local frostbite manifestations. Cold induces angiospasm, the manifestations of which progress from the periphery toward The Heart. As a result, metabolism is inhibited in the supercooled tissues, and oxygen supply is impaired. Local tissue Hypoxia develops. At the same time, the minimal metabolism that persists in these tissues is sufficient to maintain viability at a certain level.

The danger arises when the frostbitten areas of the body begin to thaw. This leads to an increased metabolic rate in the tissues. Concurrently, the spastic arterioles and Arteries are unable to supply the necessary volume of blood to the tissues. All of this causes pronounced hypoxia and tissue necrosis. The duration of vascular spasm influences the subsequent fate of the tissues.

Only after the frostbitten areas have been warmed and blood circulation within them has been restored can the depth of tissue damage be determined.

Some time after warming, the Blood Vessels in the frostbitten area dilate, which is accompanied by a slowing of Blood flow through the vessels. Along with increased blood coagulability and altered rheological properties, this promotes intravascular blood clotting.

Under the influence of hypoxia, as well as the direct effect of the thermal factor, toxic products (histamine, serotonin, kinins, etc.) accumulate in the tissues, leading to acidosis. After some time, these toxic products enter the bloodstream, causing toxemia. Toxemia occurs immediately after tissue rewarming and is the cause of general clinical manifestations such as adynamia, insomnia, vomiting, and fever.

Pathoanatomical changes in frostbite are characterized by damage to nerve endings and circulatory disturbances, up to their complete cessation. Initially, the skin is hyperemic, sometimes turning purplish-blue and slightly edematous. As plasma leaks from damaged vessels, the epithelial cell layer lifts, forming blisters filled with bloody-serous content. The skin acquires a blue-red hue and becomes edematous.

With prolonged exposure of tissues to low temperatures, the pathological process extends to the subcutaneous tissue, tendons, muscles, bones, and joints, where degenerative and necrotic processes take place.

During the pre-reactive period, the Blood vessels of the extremity are in a spastic state, the degree of which depends on the pain reaction. After rewarming, they dilate significantly. Only as a result of prolonged cold exposure does the spasm of arterioles and arteries persist longer after warming. In the Arteries of the extremities following frostbite, phenomena similar to those in endarteritis develop: proliferation of the intima, Hypertrophy of the media, and sclerosis of the adventitia. This process affects only the arteries within the frostbite zone and does not spread proximally. Veins are affected less frequently.

Clinical picture. Frostbite can manifest with local and general signs.

The main local clinical manifestations appear in patients with frostbite during the reactive period. The pre-reactive period is rarely observed by physicians because in most cases, patients are hospitalized already In the second period.

An early symptom of the pre-reactive period is mild pain, sometimes combined with numbness in the affected area. At this time, patients exhibit sensory disturbances, skin pallor, cooling, and the absence of a pulse in peripheral vessels, along with a sensation of "pins and needles." Objectively, the skin is pale with a cyanotic tint. The extremities are cold to the Touch and noticeably edematous. Pain and tactile sensitivity in the affected tissues disappear. Tissue freezing is observed very rarely.

During the reactive period, three Phases of the course can be pathoxologically and clinically traced within the frostbite zone.

The inflammatory phase is characterized by all classical signs: pain, edema, redness, a local increase in skin temperature, and decreased function of the affected area. These changes appear after rewarming. The intensity of pain depends on the depth of the lesion and its extent. Pain is sometimes so severe that it can trigger shock.

Tissue edema is the result of microcirculatory disturbances caused by histamine- and serotonin-like substances.

The increase in local temperature and skin hyperemia are associated with aseptic inflammation.

Tissue function is impaired only after 3—4 days. During the first days following frostbite, the patient may still retain The ability to move their fingers. This is because tendons are less sensitive to cold exposure.

The necrotic phase, particularly in the absence of surgical intervention, is protracted, sometimes lasting several months. The depth and extent of necrosis depend on the intensity of the cold agent, as well as the degree of Regional Blood Flow impairment. Initially, assessing the depth of necrosis is difficult (similar to burn injuries). In weakened patients with depressed reactivity, the Introduction of a virulent infection promotes a purulent-infectious process in the tissues, which may lead to Sepsis.

Once necrotic masses have separated (either spontaneously or through surgical management), the phase of wound scarring and epithelialization begins.

Depending on the depth of tissue damage, frostbite is clinically classified into four degrees:

First degree (congelatio erythematosa). Tissue alterations are minimal. Patients may experience no pain; the frostbitten area loses sensation. The skin turns pale and subsequently acquires a hyperemic hue with cyanosis. Mild soft tissue edema is noted. If the frostbite is limited to the first degree, all these symptoms resolve within 4—6 days;

Second degree (congelatio bullosa). The frostbitten surface acquires a cyanotic tint, and after a few days, blisters filled with serosanguineous fluid form on the skin, indicating deep vascular damage. Skin sensitivity is reduced. In the absence of infection, these symptoms gradually resolve over 2—3 weeks; edema and redness disappear, the fluid is either reabsorbed or drains through a ruptured blister wall, and the epidermis regenerates;

Third degree (congelatio phlegmonosa) is characterized by Necrosis of the skin and underlying soft tissues. Necrosis develops in three stages: 1) skin necrosis with The formation of blisters filled with hemorrhagic contents; 2) Separation of necrotic areas (days 5—7);

3) scarring and epithelialization (days 9—10). Following healing, a scar forms at the site of the frostbite. The average Treatment duration is 30—45 days;

Fourth degree (congelatio escharotica). The necrotic process involves all tissues, including bone. This degree comprises four stages. The First and Second stages are identical to those of third-degree frostbite. After some time, a demarcation line forms at the border between healthy and necrotic tissues; the devitalized part sloughs off or is surgically removed, and the process concludes with stump formation. The Third Stage is characterized by the development of granulation, and the fourth by scarring and epithelialization. In fourth-degree frostbite, radiographic findings may reveal signs of Osteoporosis and aseptic necrosis. The duration of treatment for fourth-degree frostbite varies.

If an infection develops, a demarcation line fails to form, necrosis proceeds via a wet pathway, and inflammation spreads to more proximal body regions. In such cases, body temperature rises, edema increases, pain intensifies, general well-being deteriorates, dyspeptic symptoms appear, and diarrhea sometimes occurs.

General clinical manifestations of frostbite during the pre-reactive period are mild. Pain in the affected area is slight; the patient experiences local numbness, tingling, and a sensation of cold.

General symptomatology emerges during the reactive period. Tissue edema promotes the accumulation of toxic products in the tissues, which eventually enter the bloodstream and trigger toxemia syndrome. Toxemia develops immediately after tissue warming and ceases once the demarcation line is formed. Only when complicated by infection and wet gangrene does it progressively worsen. The patient's condition deteriorates, body temperature rises, the pulse becomes rapid, and ARTERIAL BLOOD PRESSURE drops slightly.

The deeper the tissue damage and the larger the surface area of the frostbite, the more pronounced the toxemia. Intoxication leads to significant functional and morphological disorders affecting The Cardiovascular system, liver, and Kidneys. It should be noted that toxins are not released from the zone of absolute necrosis; they originate exclusively from tissues where blood circulation has not completely ceased and toxins can penetrate the bloodstream. Toxemia is particularly pronounced in third- and fourth-degree frostbites, as well as in extensive second-degree frostbites.

If infection supervenes, a purulent-inflammatory process develops in the affected areas, which may involve not only superficial layers but also deep tissue spaces. In cases of reduced reactivity, the condition is complicated by sepsis and septicopyemia.

Differentiating the degrees of frostbite during the pre-reactive period is extremely difficult. Infrared thermography can provide valuable assistance by yielding clear information across all phases of cold injury and detecting areas of circulatory impairment at early stages.

Complications of frostbite. First-degree frostbites are not accompanied by specific complications. They occur in cases of deep, extensive tissue damage (involving two, three, or four extremities). Such frostbites cause shock during the pre-reactive and early reactive periods. In the late reactive period, the condition may be complicated by lymphangitis, lymphadenitis, thrombophlebitis, Phlegmon, Osteomyelitis, neuritis, and sepsis. Local changes manifest proximal to the demarcation line. A rare complication of frostbite is the onset of an Acute Specific Infection—tetanus. During the regeneration and recovery period, skin and bone atrophy may persist, along with trophic ulcers, arteritis, arthrosis, joint contracture, hyperesthesia, cyanosis, and hyperhidrosis.

Prevention of frostbite. Preventive measures are categorized into individual and collective. Individual prevention includes protective gear (clothing, footwear), personal hygiene, body hardening, rational Nutrition and warming, and seeking timely medical assistance. Clothing should be warm, comfortable, loose, lightweight, and waterproof. In emergency situations, it should be easy to remove. In rainy or snowy weather, garments must be dried frequently.

Footwear must be intact, neither tight nor overly loose, and without laces. Excessively roomy footwear causes chafing and thereby contributes to frostbite. Warming footwear over an open fire is discouraged, as it damages the material and compromises waterproofness; treating it with grease is advisable. Socks should be dry and free of wrinkles. To prevent blood stasis in the fingers and toes, one should periodically flex and extend them. Dry feet are far less susceptible to frostbite than damp ones. Therefore, in cases of excessive sweating, daily foot washing with cold Water followed by rubbing until the skin reddens is recommended. Dusting the soles with boric acid, salicylic acid, tannin, or talcum powder is also beneficial.

Physical exercises, training, and cold-water rubs play a vital role in frostbite prevention.

Collective prevention in peacetime (during excursions or hiking trips) involves organizing work breaks, providing periodic warming in tents or sleeping bags, supplying hot beverages, and ensuring adequate nutrition. Cold food is poorly assimilated and requires increased Energy Expenditure for Digestion. During the cold season, incorporating higher amounts of CARBOHYDRATES and animal fats into the diet is recommended. Consuming hot water and coffee for 30 minutes raises the skin temperature of the fingers by several degrees.

Harmful substances such as alcohol and nicotine exacerbate susceptibility to frostbite. A single cigarette smoked on an empty Stomach induces capillary spasm lasting 15—16 hours.

Professional screening is required for work in cold environments. Individuals with disorders of the Autonomic Nervous system, peripheral vessels, or nerves, as well as those suffering from Diabetes Mellitus, thyrotoxicosis, or Epilepsy, are disqualified from such work.

The treatment of frostbite is complex. Numerous Methods exist, yet none is universally accepted.

The objectives of frostbite treatment are: 1) to elevate the temperature of the affected tissues; 2) to restore blood circulation in the frostbitten areas; 3) to combat shock and intoxication; 4) to prevent infections; 5) to remove necrotic tissues; and 6) to perform reconstructive and plastic surgeries to restore the function of the injured body part.

Therapy for frostbite begins with the provision of first aid. During the pre-reactive period, its goals are to restore tissue temperature, combat shock, normalize blood circulation, and eliminate tissue hypoxia. Timely and adequate first aid is of paramount prognostic significance.

Patients are administered tetanus toxoid or PPS, as frostbite is considered an open injury.

The following first-aid regimen is recommended for patients with frostbite. The affected limb is wiped with 56% ethyl alcohol, ektericide, or another antiseptic agent, dried thoroughly, and a multi-layer thermal insulation bandage is applied: a layer of gauze, a thick layer of cotton wool, another layer of gauze, and an outer rubberized fabric covering the entire limb. Various auxiliary Materials (blankets, rugs) can be used at the pre-hospital stage.

In cases of frostbite to the Cheeks, auricles, or nose, they should be rubbed with a warm hand smeared with petroleum jelly until the skin reddens (rubbing with snow is not recommended, as ice crystals can injure the skin and promote infection). Patients should be given hot drinks and small doses of alcohol to consume.

Inpatient treatment of patients should begin with active warming of the affected areas (limbs). The limb is immersed in a bath with a weak solution of potassium permanganate. The water temperature is gradually increased from 18 °C to 35 °C. Afterward, the frostbitten area is covered with a dressing containing petroleum jelly or Vishnevsky ointment.

Favourable effects on the affected areas are achieved through UHF irradiation, hydrocortisone Electrophoresis, hydrocortisone and novocaine phonophoresis, and longitudinal diathermy. These Procedures help reduce pain and edema, and if gangrene develops, it proceeds as a dry type.

The aforementioned measures must necessarily be combined with the administration of anticoagulants, vasodilators, antiplatelet agents, and ganglionic blockers.

Novocaine blockades of the thoracic and lumbar sympathetic ganglia, as well as paranephral novocaine blockade, are indicated.

Important attention should be paid to the treatment of shock (administration of analgesics, narcotics, and hypnotics, intravenous administration of lactate solution, novocaine, and the prescription of antihistamines).

The main objective in treating frostbite during the reactive period is to restore blood circulation in the affected tissues and prevent vascular thrombosis. The complex of conservative therapeutic measures must include physiotherapeutic methods, antiplatelet, detoxification, desensitizing, and anti-inflammatory therapy, The Use of vasodilators, as well as vitamin and hormone therapy.

Anticoagulant therapy involves the use of heparin, fibrinolysin, streptokinase, and one of the indirect anticoagulants: neodicumarin, syncumar, or phenilin. Heparin is prescribed intravenously or intramuscularly at 5,000 IU 4–6 times a day. Heparin reduces pain, paresthesia, and the sensation of cold, increases skin temperature, and improves capillary blood flow. Fibrinolysin is administered at 20,000–30,000 IU 2–3 times per treatment course.

To improve blood rheological properties, the administration of rheopolyglucin is indicated, and for vasodilation—papaverine hydrochloride at 0.05 g 3 times a day orally or 2 ml of a 2% solution subcutaneously 2 times a day for 10–12 days. Drugs such as No-shpa, nicoshpan, galidor, aescin, ATP, and MAP are also used. They improve coronary and

1 cerebral circulation.

Clinical observations indicate that frostbite causes sensitization of the Organism; therefore, antihistamines are used in its treatment: diphenhydramine (0.05 g

2 times a day), diazolin, suprastin, tavegil, etc. They reduce edema, hyperemia, and pain. In the first 3–5 days of the reactive period, Steroid Hormones (hydrocortisone) are used, which possess desensitizing and anti-inflammatory effects.

Throughout the entire period of frostbite treatment, the patient must take Vitamins (ascorbic and nicotinic acids, B vitamins, E).

Great attention is paid to detoxifying the patient's body. This is achieved through infusion-Transfusion Therapy and Forced diuresis. Intravenous infusions of hemodez, rheopolyglucin, and a 5–10% glucose solution are indicated for patients. Forced diuresis is performed by administering lasix or furosemide. To combat acidosis, a 4–5% sodium bicarbonate solution is transfused. Due to potassium loss during forced diuresis, the administration of 300 ml of a 3% potassium chloride solution is indicated. To improve liver function, glucose, seripar, and carsil are prescribed.

To combat wound surface infection in cases of limited and shallow frostbite, acetylsalicylic acid (2–3 g per day), butadione (0.15 g 2 times a day), and sulfonamides are used. In cases of pronounced inflammatory reaction complicated by lymphangitis or thrombophlebitis, Antibiotics are prescribed orally (erythromycin, oletetrin, ampicillin).

From the first day of treatment, patients should receive staphylococcal toxoid According to the schedule.

Novocaine blockades should be utilized within the complex of therapeutic measures for frostbite. They exert analgesic, vasodilating, and anti-inflammatory effects, and stimulate Connective Tissue regeneration. Case, vagosympathetic, paranephral, and epidural novocaine blockades are employed. Novocaine solutions are used for this purpose.

Local treatment of frostbite begins with primary surgical debridement of the wound surfaces. In first-degree frostbite, after wiping the affected surface with 56% ethyl alcohol or another antiseptic that does not alter skin coloration, a warming cotton-gauze bandage is applied. In second-degree frostbite, blisters are excised, and a dressing with one of antiseptic solutions or their combination is applied. Numerous preparations have been proposed for this purpose: a weak solution of potassium permanganate, ammonia solution, Vishnevsky ointment, sulfidine ointment, xerofor ointment, vitaminized ointment with lanolin, fish oil, etc.

For Surgical treatment, fasciectomy, necrotomy, and necrectomy are employed.

Fasciotomy is usually performed at the end of the first day or on the second day after frostbite. The surgery consists of making incisions in the skin, subcutaneous tissue, and fascia along the course of the limb in the area of greatest edema. This reduces tissue tension and improves blood circulation within them.

Signs of tissue necrosis already appear by the 3rd–6th day. At this time, necrotomy is performed (Fig. 60, a). Incisions are made down to the full depth of the necrotic tissues. Since deeper tissues may prove viable, necrotomy must be performed cautiously. Incising dead tissues facilitates the outflow of toxic tissue fluid and reduces toxemia.

The next type of surgical intervention is necrectomy (Fig. 60, b). The timing of its performance is determined individually (from the 5th to the 14th day). The surgery consists of the complete removal of dead areas, stepping back 1–1.5 cm distal to the demarcation line. The incision is made within the dead tissues in such a way as to leave a strip of necrotic tissue that will later mummify. Necrectomy helps subside inflammatory phenomena, reduces intoxication, and prevents the development of purulent-inflammatory processes in the affected tissues. After the separation of dead tissue remnants and the development of granulations, treatment is carried out in the same manner as for ordinary purulent wounds.

The extreme measure in the treatment of frostbite is amputation or disarticulation of the limb.

Amputations are classified as primary, secondary, and late. Primary amputations are rarely performed solely for frostbite; they are more commonly indicated in cases of Combined Trauma (frostbite complicated by bone crushing). These are typically performed on days 4–5, once the viability of the traumatized tissues becomes evident.

Class="center">

Fig. 60. Necrotomy in frostbite: a — foot edema (before and after surgery); b — Gangrene of the foot (before and after surgery)

Secondary amputations are performed due to life-threatening complications, such as sepsis.

CHILBLAINS (PERNIO)

The indications for late amputation include osteomyelitis in the frostbite area and marked limb deformity.

Prolonged or repeated (chronic) exposure of tissues to moderately low temperatures leads to a pathological condition known as chilblains (pernio, perniones). Dystrophic changes occur in the Superficial layer of the epidermis and nerve endings. Chilblains most commonly affect the fingers, but can also occur on the toes, earlobes, and nose.

This condition manifests during the cold season and is characterized by pain, cyanotic skin discoloration, edema, and severe itching. In rare cases, fissures and occasionally foci of necrosis develop. Small nodular infiltrates may appear on the dorsal surface of the hand; these eventually ulcerate and later scar. Chilblains are most frequently observed in individuals who spend long hours working in unheated, damp environments.

The disease is prolonged and follows a chronic course, exacerbating when working in the cold, in damp environments, or upon exposure to high heat. During periods of remission, chilblains remain entirely asymptomatic.

Treatment for patients with chilblains involves warming compresses, physical therapy (warm baths, d'Arsonval currents, UHF therapy), and the use of warm gloves and socks. Limb hypothermia must be avoided. Novocain blockades are indicated.

HYPOTHERMIA (FREEZING)

Prolonged exposure of The Human Body to low temperatures when heat production cannot compensate for heat loss may lead to general hypothermia—a pathological and potentially fatal lowering of core body temperature.

The pathogenesis of frostbite and systemic hypothermia is identical, although severe systemic hypothermia may be accompanied by only mild frostbite. In peacetime, severe hypothermia is rare, occurring predominantly in individuals abusing alcohol, as well as in exhausted, fatigued persons weakened by long journeys.

According to Jansen, the lower limit of body temperature compatible with the recovery of vital Functions ranges from 23 to 24 °C. The Central Nervous System reacts to temperature drops first, with varying sensitivity across its regions. The Functions of the cerebral hemispheres and thermoregulatory capacity decline initially. This leads to muscular excitation, resulting in shivering. After some time, muscular weakness and loss of motor coordination develop, the person loses consciousness, auditory, visual, and volitional reactions are extinguished, and vital centers are compromised. The clinical picture of severe hypothermia resembles apparent death.

During The process of hypothermia, individuals often experience euphoria—an elevated mood.

Clinically, hypothermia is divided into four degrees:

Degree I (adynamia). The patient is lethargic, speech is slurred, and shivering is present. The skin is pale, goosebumps (piloerection) are observed, and bradycardia is present. Rectal temperature drops to 35–33 °C;

Degree II (stupor). General rigidity, adynamia, and shivering are noted. The skin is cold, cyanotic, with a marbled appearance; acrocyanosis or pallor of the distal extremities is present. Bradycardia (heart rate 30–50 bpm). The pulse is palpable with difficulty. Blood pressure is slightly decreased, Respiration is slow (8 breaths per min) and shallow. Body temperature drops to 32 °C;

Degree III (convulsions). Body temperature drops to 30 °C; unconsciousness, convulsions, vomiting, marked bodily rigidity, and trismus occur. The limbs are in a semi-flexed position (as the body cools, an instinctive attempt to reduce surface area for heat loss leads to flexion), bradycardia is present, and peripheral arterial pulses are absent. Blood pressure is unmeasurable, and respiration is slow, presenting as Cheyne-Stokes breathing;

Degree IV (apparent death). Body temperature drops below 27 °C, all organ functions gradually cease, and Energy Metabolism sharply declines. Respiration, pulse, and blood pressure are nearly undetectable. Reflexes are absent, and the sensation of pain completely disappears.

Death from hypothermia typically occurs as a result of cardiac arrest and cerebral anemia.

Treatment for severely hypothermic patients must be carried out in intensive care units and consists of rapid rewarming. The patient is immersed in a water bath starting at a temperature of 36 °C, which is increased to 38–40 °C over 25–30 minutes. Rewarming continues until core body temperature reaches 35 °C. The patient is given hot tea or coffee, and administered 20–40% glucose solution, caffeine, camphor, and cordiamin. Simultaneously, reopolyglucukin infusions are given, and water-electrolyte balance is corrected. In the event of convulsions, sodium oxybutyrate is administered.