Military Surgery with Emergency Surgery - V.Ya. Bilyi 2004

Crush syndrome

Introduction. Crush syndrome (CS) is one of the primary focuses of research in trauma surgery, caused by severe specific traumatic injuries in the form of soft tissue crushing (destruction), vascular and neural lesions, and their prolonged compression. CS and its etiopathogenetic borderline states encompass both general and local bodily responses developing in reaction to pain, prolonged ischemia, plasma and Blood loss, intoxication, and degenerative-necrotic Changes in the damaged Tissues. The clinical manifestations of CS depend on the mechanism, the type of soft tissue injury, as well as the duration and severity of the trauma. Alternative names for CS—such as prolonged compression syndrome, traumatic toxicosis syndrome, release phenomenon, and positional syndrome—are not strict synonyms of CS, but rather its borderline etiopathogenetic variants. This is because CS typically involves compromised Muscle integrity, with long bone fractures occurring in the majority of cases (65%), whereas prolonged compression syndrome is characterized primarily by the prolonged ischemia of a large muscle mass. In recent years, another variation of this pathological process has become widespread: positional compression syndrome of the limb tissue masses. However, this syndrome should be viewed As a result of prolonged compression caused by the patient's own body weight.

Brief Historical Outline. The first reports of CS emerged at the early 20th century, although descriptions resembling CS can already be found in the works of N.I. Pirogov (1865), The Principles of General Field Surgery. The clinical picture of this syndrome was thoroughly described in 1909 by H. Colmers following a major earthquake in Sicily. Even back then, it was observed that several victims of this trauma who were subsequently rescued from the rubble in a satisfactory condition died a few days later from unknown causes. Maxim Gorky, having visited the area after the catastrophe, wrote: “...A man hangs upside down at the fourth-floor level, trapped by his leg; it is impossible to rescue him. The wind strips his shirt away, whipping his Hair, his arms dangling; he seems alive, convulsing from pain. He begs for help; his legs are crushed, but there is no way to free him from under the debris.” (Earthquake in Calabria and Sicily, St. Petersburg, Znanie Publishing House, 1909).

Recorded cases during World War I noted that wounded soldiers developed ACUTE RENAL FAILURE following severe closed trauma. A well-known case was described by Quenu (1923), who observed an officer whose both thighs had been pinned by logs. Following release, the patient's condition rapidly deteriorated and death soon ensued. This observation led Quenu to propose the toxemic theory of CS.

Similarly, CS was documented by personnel of the Ministry of Emergencies of Ukraine during rescue operations following the earthquake in Turkey (1999): “...When we pulled a living woman with a crushed arm from beneath the rubble, the Turks, overjoyed, pushed us aside, and we were unable to administer first aid. She asked where her child was, saw her alive, and... died.”

As a result of the London bombings during World War II, CS was diagnosed in 3.7% of casualties, while during the atomic bombings of Hiroshima and Nagasaki, it reached 60%.

In 1945, observations by A.Ya. Pitel were published, incorporating data from the Great Patriotic War period, titled “On Crush Syndrome and Traumatic Limb Compression.”

Equivalents commonly used for CS include terms such as “crush syndrome,” “ischemic muscle necrosis,” “traumatic limb compression syndrome,” “traumatic toxicosis,” “prolonged compression syndrome,” “release syndrome,” and “acute tubular nephropathy.”

In our view, the term “prolonged crush syndrome,” proposed by M.I. Kuzin, is the most apt in characterizing this condition, as it encompasses crushing, destruction, Various Forms of compression of human anatomical body parts, and combinations thereof.

Pathogenesis. The pathogenesis of CS is complex and comprises the following main factors: neurohumoral, toxemic, immunological, and plasma- and blood loss.

In etiopathogenesis, it is practical to distinguish between the direct destruction of anatomical structures (with and without soft tissue injury) and the prolonged compression of tissue masses resulting in ischemic muscle damage. Given that ischemic death of Muscle tissue occurs within 6 hours, the primary cause of early necrosis should be considered the direct traumatic impact on the tissues, whereas in the later period, it is edema and the blockade of Regional Blood Circulation.

The triggering mechanism in The Development of CS is pain (the neurohumoral factor). Even before the victim is extricated from compression, afferent nerve signals originating from the injury zone generate excitation in the Cerebral Cortex. This excitation is transmitted to the Hypothalamus—the central hub of humoral regulation—whereby a large volume of Hormones is released into the bloodstream via the adrenal system, causing centralization of blood circulation and an upregulation of all metabolic processes. Vasospasm induces ischemia in the renal cortex, reduced Glomerular Filtration, and the development of degenerative-necrotic changes in the epithelium of the renal convoluted tubules.

Thus, even prior to release from compression, neurohumoral influences establish the conditions for hemodynamic disturbances and lay the groundwork for the development of acute renal failure (ARF).

Following release from compression, the second major factor in the pathogenesis of CS comes into play: toxemia. Prolonged compression of soft tissues is accompanied by impaired peripheral circulation distal to the level of compression, leading to tissue Hypoxia and metabolic acidosis. If CS were limited solely to these factors, it could be equated with the pathogenesis of disorders arising from the prolonged application of a tourniquet to a limb (tourniquet syndrome). However, CS is accompanied by significant tissue destruction, which facilitates the release of intracellular substances into the bloodstream—such as Lysosomes, Cell/35.html">Mitochondria, and, in compression-ischemic injuries, acidic metabolites of anaerobic Glycolysis. This exacerbates toxemia and drives the progression of ARF through the nephrotoxic action of Myoglobin, histamine, potassium, phosphorus, and other toxic agents. This gives rise to the so-called reperfusion phenomenon.

The ultimate result of prolonged crushing is mechanical tissue destruction combined with arterial insufficiency and venous stasis, leading to the generation of large amounts of toxic cellular metabolic products. The developing metabolic acidosis, coupled with myoglobin entering the bloodstream, blocks the renal tubules and impairs their reabsorptive capacity. Intravascular Blood Coagulation further impedes filtration. Myoglobin also obstructs the microvessels of the Lungs, Liver, and other Internal Organs, promoting dystrophic changes within them. Consequently, myoglobinemia and myoglobinuria are among the primary Factors Determining the severity of toxicosis in trauma victims. Toxemia is further amplified by the release of protein breakdown products from damaged Muscles, such as histamine, creatinine, potassium, and phosphorus.

Thus, in CS, muscles undergo ischemic-necrotic changes as a result of:

1) primary destruction and necrosis of muscles and Blood Vessels;

2) compression of muscles and vessels within fascial-muscle compartments by hematomas and interstitial fluid;

3) prolonged arterial vasospasm due to periarterial hemorrhages or a direct vascular reaction to trauma.

Following complete release from compression, another major pathogenetic factor manifests: plasma and blood loss. Notably, plasma loss occurs not only in the damaged tissues but also above the compression site due to generalized increased capillary permeability and electrolyte imbalances that drive extracellular fluid into the interstitial space. Plasma loss leads to pronounced hemoconcentration, manifested by a reduced circulating blood volume (CBV) and compromised renal hemodynamics in particular, which accelerates the progression of ARF.

Thus, the pathogenesis of CS is exceedingly complex and multi-component. Psycho-emotional stress experienced by victims during the period of compression (accompanied by diverse psychological reactions), pain, and forced immobility associated with the injury and early complications (blood loss) all influence the course of the syndrome and account for certain variations in clinical presentations. In response to prolonged and severe trauma, Traumatic Shock develops, proving fatal for many victims—especially when extrication from the rubble is delayed. Nonetheless, endogenous intoxication should be considered the cornerstone of CS pathogenesis following release.

The severity of CS largely depends on the degree of endotoxicosis.

Compensated endotoxicosis presents with the following clinical picture: a satisfactory condition of the victims; normal or subfebrile body Temperature; stable central hemodynamic parameters; absence of microcirculatory and respiratory disorders; satisfactory gastrointestinal and Urinary Tract function; absence of major and complicated wounds; and minimal deviation of laboratory parameters from normal values.

Subcompensated endotoxicosis is characterized by a moderate or severe general condition; Complaints of weakness, nausea, dizziness, and headache; elevated body temperature; unstable central hemodynamics; microcirculatory disturbances manifesting as circulatory centralization or vascular atonia; tachypnea up to 24–26 breaths/min; a subcompensated form of ARF; signs of paralytic ileus or diarrhea; large wounds or wounds complicated by purulent infection; a 3- to 4-fold increase in plasma creatinine, a 2- to 3-fold increase in urea, and a 1.5- to 2-fold increase in aminotransferases; hypoproteinemia, anemia, the presence of fibrinogen monomers in the plasma, and uncompensated metabolic acidosis with moderate base deficit.

In decompensated endotoxicosis, the patient's condition is extremely severe or critical, marked by encephalopathy manifested as mental inadequacy, euphoria or depression, somnolence, or stupor; victims suffer from nausea, vomiting, and headaches; body temperature rises to 39–40°C or drops below normal; blood pressure is unstable (80–60/40 mmHg); pronounced tachycardia (130–150 bpm) is present; central venous pressure drops to negative values, though it rises to 15–20 cm H₂O in the presence of hyperhydration; microcirculation and Respiration are severely impaired, as evidenced by an earthy (ashen) Skin color and marked tachypnea up to 35–40 breaths/min; major open or Closed Soft Tissue Injuries are present, including in areas of positional compression; acute hepatorenal syndrome develops; symptoms of myoglobin peritonism and paralytic ileus are possible; Laboratory tests reveal a 5-fold or greater increase in creatinine and urea levels, a 3- to 4-fold increase in bilirubin, a 3-fold increase in aminotransferases, pronounced anemia, hypoproteinemia, uncompensated metabolic acidosis with a significant base deficit; and blood coagulation disorders are generally detected.

Immunological examination of such patients reveals pronounced immunodepression, predominantly of the cellular type (a decrease in the count of T- and B-lymphocytes).

Thus, the crush syndrome (CS) is a polyetiopathogenetic, dynamic, phase-based process driven by neurohumoral and immunological alterations against the Background of toxemia, plasma and blood loss, and impaired vital bodily Functions, primarily hemodynamics and renal function.

It should be noted that the severity of CS is heavily influenced by concomitant injuries and early trauma complications (acting through the reciprocal aggravation phenomenon).

The clinical manifestations of CS vary widely across different periods of its clinical course, determined primarily by the type and severity of the trauma, as well as early complications.

Classification and clinical forms.

Based on its clinical manifestations, crush syndrome is divided into three periods:

1. Early period (traumatic shock phase) – observed During the first 24 hours.

2. Intermediate period (acute renal failure phase) – lasts up to days 8–12.

3. Late period (late complications or recovery phase) – extends beyond one month.

Early (shock) period. The clinical picture is driven by a shock state with

typical features of traumatic shock: following psycho-emotional agitation caused by severe pain, patients develop lethargy, torpor, somnolence, tachycardia, hypotension, and pallor of the skin. Blood coagulation disorders and a reduction in plasma volume can lead to a drop in blood pressure even without external blood loss. Cardiac rhythm disturbances (extrasystole, atrial fibrillation) are frequently observed, potentially progressing to diastolic cardiac arrest due to hyperkalemia and metabolic acidosis. Asystole may occur immediately after the victims are released from compression and microcirculation in the ischemic zone is restored. Pronounced changes in other organs and systems are rarely seen during the early period. Only in severe and extremely severe cases, accompanied by marked cardiovascular dysfunction, may pulmonary edema, acute hepato-renal syndrome, or toxic encephalopathy develop.

The clinical picture during this period resembles that of traumatic shock, yet it has several distinct features. These Specific features of the early CS period include:

1) more pronounced blood hypercoagulation;

2) progressive oliguria and anuria;

3) the complexity and unreliability of assessing the severity of traumatic shock in CS based solely on absolute values;

4) urinary abnormalities;

5) plasma loss and toxemia;

6) toxemia characterized by a malignant course.

Following the release from compression, the traumatized areas of the body exhibit the consequences of mechanical crushing or tissue destruction (see insert, Fig. 15): deformation, abrasions, and subepidermal blisters filled with serous or hemorrhagic fluid.

Skin indentations alternate with open tissue destruction, pale areas, and hyperemia; dense tissue edema progressively develops to the point where the peripheral pulse disappears. Sensation and mobility in the affected limbs depend on the degree of ischemia; the loss of active movement, along with the absence of pain and tactile sensitivity, are objective signs of uncompensated ischemia, whereas the inability to perform passive movements (rigor mortis-like muscle stiffness) indicates irreversible ischemia.

Thus, from a diagnostic, prognostic, and particularly tactical standpoint, it is crucial to determine the severity of ischemia in the compressed limb at an early stage. From this perspective, the most practical approach is the classification of ischemia grades, along with the Methods for its rapid assessment and prognosis of outcomes developed by V.A. Kornilov (Table 6).

Consequently, if passive and, all the more so, active movements in the distal joint relative to the site of prolonged crushing are preserved, the tourniquet should be removed. However, if flexion and extension in the joint are impossible (due to muscle stiffness), removing the tourniquet is contraindicated.

Already in the early period, in severe and extremely severe cases, the first signs of renal impairment appear: decreased diuresis, lacquer-brown urine, and the presence of Proteins, erythrocytes, casts, and myoglobin in the urinary sediment. Urine specific gravity increases, and its reaction becomes acidic.

With timely and comprehensive first aid delivered at the disaster site and rapid evacuation of victims to a medical facility, the aforementioned symptoms may disappear. This is primarily accompanied by an improvement in the patient's psycho-emotional status, followed by their somatic status. Breathing and blood pressure gradually normalize, pulse fullness improves, and tachycardia subsides. The brown color of the urine disappears, though its specific gravity remains elevated. A so-called "lucid interval" develops, which is prognostically dangerous as it may lead to the discontinuation of further therapeutic and diagnostic measures and the subsequent onset of acute renal failure.

Intermediate period. The intermediate period of CS (from the 4th to the 20th day) typically begins with a clinical deterioration driven by escalating endogenous intoxication and the development of acute renal failure.

Intoxication by Bacterial toxins increases sharply. Wound exudate typically yields staphylococcal strains associated with other pathogens, including *Pseudomonas aeruginosa*. The influx of gram-negative microflora toxins from natural microbial colonization sites increases as well. A major role in this process is played by "intestinal toxemia." Due to microcirculatory disturbances in the walls of the small and large intestines, their barrier function is compromised, allowing a significant amount of *E. coli* endotoxin to breach into the portal system. Upon contact with the endotoxin, hepatic stellate Cells (Kupffer cells) and leukocytes produce large amounts of BIOLOGICALLY ACTIVE SUBSTANCES—cytokines. Released in excess, these mediators trigger and sustain a cascade of pathological processes accompanied by symptoms of endogenous intoxication.

During the same period, clinical manifestations of acute renal failure (ARF) progress, driven by hemodynamic disorders, severe metabolic disturbances, and endogenous intoxication. A particularly crucial role is played by myoglobin, which is readily filtered in the renal glomeruli but retained in the tubules because it converts into an insoluble form—acid hematin—in an acidic environment. In addition to mechanical tubular obstruction leading to oliguria or anuria, myoglobin exerts a toxic effect on the tubular endothelium, causing necrosis and shedding.

Thus, a typical acute myoglobinuric nephrosis develops, progressing to ARF. Hepatorenal syndrome, characterized by the simultaneous onset of acute renal and hepatic failure, is frequently observed. The pathogenesis of Liver failure is associated with endogenous intoxication, which leads to toxic hepatitis. In moderate and severe crush syndrome (CS), immune defense is virtually always compromised, resulting in pyogenic and septic complications.

The clinical picture of the intermediate period is characterized by complaints of weakness, headache, nausea, and vomiting. Pain appears in the lumbar region. Myoglobin excreted in the urine gives it a brownish color. Somnolence, sopor, and, in severe cases, a comatose state develop. Symptoms of ARF become more pronounced: diuresis drops down to anuria; hyperhydration increases; against the background of anasarca, pulmonary edema may occur, in the genesis of which, apart from hyperhydration, a crucial role is played by Heart failure, which worsens due to toxic myocarditis and the specific impact of hyperkalemia on the myocardium.

Local changes in the area of injured tissues may develop as aseptic necrosis under compression or as wound suppuration following crushing. During this period, victims with prolonged compression times (exceeding 8 hours typically exhibit foci of necrosis at the compression sites. These foci are difficult to diagnose due to Organism areactivity and the absence of local manifestations.

Laboratory tests reveal anemia, leukocytosis with a left shift in the leukocyte formula, toxic granularity of neutrophils, hypoproteinemia, hyperazotemia, hyperkalemia, Hyperbilirubinemia, and elevated Alanine and aspartate aminotransferases.

The course of ARF comprises 4 developmental stages:

Stage 1: initial stage, coinciding with the shock period of CS;

Stage 2: oligoanuric stage, coinciding with the intermediate period;

Stage 3: polyuric stage, coinciding with the late period of CS;

Stage 4: recovery.

Depending on the clinical severity and Treatment efficacy, Renal Dysfunction can be divided into 2 forms: subcompensated and decompensated.

The subcompensated form is characterized by incomplete renal impairment, whereas the decompensated form involves complete cessation of renal function.

To determine the degree of renal impairment, it is advisable to assess the Kidneys' response to Diuretics. In the subcompensated form, hourly diuresis increases after the administration of Lasix. In the decompensated form, it cannot be stimulated even by repeated administration of high doses of Lasix.

The most frequent complications of ARF include hyperhydration syndrome with pulmonary and cerebral edema, hyperkalemic cardiac arrest, uremic Hemorrhage, and uremic coma, which account for the high mortality rate among victims during the intermediate period of CS.

Late period. If the manifestations of vital organ dysfunction characteristic of the intermediate period are successfully compensated, the late or recovery period—often referred to as the period of local manifestations—begins 3 to 4 weeks after the trauma. By this time, rational treatment has significantly reduced the symptoms of endogenous intoxication, acute renal failure, and failure of other organs and systems, bringing local changes in the areas of prolonged tissue compression to the forefront: tissue Swelling subsides, the purplish-blue skin discoloration in the compression zone disappears, and the tissues feel warm to the Touch. Motor and sensory disorders gradually resolve. At the beginning of this period, pain in the injured limb sometimes intensifies, occasionally taking on a burning character as a result of concomitant neuritis—which, according to M.I. Kuzin, occurs in 56.5% of upper limb injuries and 35.7% of lower limb injuries. The skin and muscles in the compression area undergo necrosis and are sloughed off. In some cases, clostridial or non-clostridial anaerobic gangrene develops. Oligoanuria is replaced by polyuria. During this period, along with systemic disorders, local changes associated with the injury of specific body parts are typically observed, manifesting as wound suppuration, muscle atrophy, sensory disturbances, and contracture formation. In severe cases, pyogenic and septic complications may develop, such as Osteomyelitis, abscesses, Purulent Arthritis, etc., in the genesis of which immunosuppression plays a significant role.

The clinical severity of CS is directly dependent on the volume of traumatized tissues, as well as the duration and degree of their crushing. Accordingly, the following forms are distinguished (M.I. Kuzin):

1) Extremely severe form: resulting from compression of both lower limbs for more than 6 hours. Death occurs on the 1st day post-trauma in 90% of victims.

2) Severe form: resulting from compression of one or, occasionally, both lower or upper limbs for 6 hours. It proceeds with pronounced clinical manifestations throughout all Stages of the disease. Fatal outcomes are observed in both the early and intermediate periods.

3) Moderate severity: resulting from short-term compression (less than 6 hours) of both lower limbs or prolonged compression (6 hours) of only a limb segment.

4) Mild form: resulting from short-term compression (less than 4 hours). Renal dysfunction is masked, and changes in the traumatized body part predominate.

The clinical severity is also influenced by other factors: Burns (Combined Trauma), injuries to other anatomical and functional PARTS OF THE body (Polytrauma), hypothermia and overheating, Carbon monoxide poisoning, etc.

One of the latest working classifications of CS was proposed by E.O. Nechaev and P.G. Bryusov, according to which CS should be classified by:

1) type of compression: crushing, direct compression, and positional compression;

2) localization: forearm, arm, hand, lower leg, thigh, FOOT, chest, abdomen, pelvis;

3) combination of soft tissue injuries with damage to internal organs, Bones and joints, major blood vessels, and nerve trunks;

4) severity degree: extremely severe, severe, moderate, and mild;

5) phases: early (compression period and post-compression period), intermediate, and late;

6) complications: pyo-septic complications, as well as those involving internal organs and systems;

7) combination of injuries: accompanied by burns and frostbite, exposure to toxic agents, or nuclear blast factors.

Etiopathogenetic borderline states in the clinical course of PTS. One of the most specific variants of PTS in its clinical course is the development of crush syndrome (CS), a subtype of which is positional syndrome (PS). PS develops when a part of the body (typically one of the limbs) is compressed by its own weight during a prolonged stay in a forced, awkward posture, resulting in ischemia of the compressed limb followed by the manifestation of certain features characteristic of PTS.

In the vast majority of cases, PS occurs in individuals who have spent an extended period with parts of their bodies (usually a limb) under compression, typically due to body weight while trapped in a fixed, constrained position. Most frequently, this condition is triggered by the abuse of alcohol surrogates, narcotic substances, or poisoning by exhaust fumes or carbon monoxide.

Unlike CS, PS does not present with traumatic shock. Against the background of toxic or narcotic coma, collapse develops, while recovery from coma is marked by moderate pain, anemia, and tissue hyperesthesia. This indicates that in the pathogenesis of CS during the compression period, local factors outweigh systemic ones—namely hemodynamic disorders and impaired renal filtration. Furthermore, neither CS nor PS exhibits pronounced tissue destruction, edema and plasma loss develop slowly, and marked hemoconcentration is absent.

In severe forms of CS, the course of ARF is more favorable than in PTS. However, timely Diagnosis of this condition is rare, and patients are often admitted to hospitals with misdiagnoses such as tissue contusion, deep vein thrombophlebitis of the extremities, ARF of unclear Etiology, nephritis, or allergic edema.

According to A.K. Revsky (1990), CS is a complex symptom complex that arises primarily in response to acute tissue ischemia and pain resulting from compression. Its clinical course comprises a compression period and a decompression period. During the compression period, the victim's body undergoes pronounced functional and morphological alterations, primarily affecting The Cardiovascular system, which in turn can precipitate renal failure. During the decompression period, intoxication caused by disrupted metabolic products, microflora activation, and hemoconcentration may compound the clinical course of ARF with the manifestations of secondary multiple organ dysfunction syndrome.

A clinical picture similar to that of CS is observed when the patency of the main Arteries of a limb is restored after a prolonged period of ischemia—known as revascularization syndrome (Kornilov V.A., 1989). In such cases, despite the restoration of peripheral blood flow, ARF begins to develop, which can be fatal. A similar Clinical presentation may occur in victims following the removal of a tourniquet that has been applied to a limb for an extended period (tourniquet syndrome). The development of ARF may also accompany short-term, intensive compression of large muscle masses or their damage resulting from gunshot wounds or blunt trauma (traumatic endotoxemia syndrome).

Thus, despite a diverse etiology and differences in the pathogenesis of PTS and its borderline states (CS, PS, tourniquet syndrome, revascularization syndrome, and traumatic endotoxemia syndrome), they share similar Clinical Features—namely, various manifestations of ARF.

Principles of PTS treatment. Medical care should primarily focus on the Prevention and treatment of TS, mitigating intoxication and plasma loss, as well as averting ARF and purulent complications. During the provision of first medical aid, these objectives are achieved through effective pain management using narcotic and non-narcotic analgesics, administration of sedatives, transport immobilization, prevention of plasma loss (tight bandaging and, if possible, limb cooling), and the prevention of pyo-infectious complications. Victims are given alkaline-salt solutions to drink. Subsequently, The Scope of therapeutic measures expands to include differentiated infusion therapy, surgical interventions, and specialized treatments for ARF, such as extracorporeal detoxification methods.

Scope of care at the medical evacuation stage (MES). The proportion of self- and mutual aid in PTS is relatively small. Extricating an injured person from under rubble is not always a straightforward task and requires specialized rescue skills and technical equipment. Narcotic analgesics are administered intramuscularly using a syringe-tube (2 ml of a 2% promedol solution), immobilization is performed using improvised or standard-issue equipment if available at the scene, antibiotic tablets from the individual first-aid kit are administered orally, and an aseptic dressing is applied.

In a focus of mass casualties, when care is provided by specialized teams including a physician, tourniquets are applied to the compressed limbs prior to extricating the victims from beneath the rubble, and narcotic and non-narcotic analgesics are administered intramuscularly. Once the compression is relieved, the physician assesses the extent of the damage and determines the degree of tissue ischemia according to V.A. Kornilov. In cases of decompensated ischemia or necrosis, the tourniquets are not removed, but are instead reapplied (if necessary) as close to the injury zone as possible.

In cases of compensated and subcompensated ischemia, the tourniquets are removed. Prior to removal, 20 ml of a 10% calcium chloride solution, cordiamine, caffeine, and 5 ml of a 2.4% aminophylline solution are administered intravenously.

In the absence of a physician at the scene and when providing medical care via mutual aid, a tourniquet must be applied in all cases prior to extrication from the compression zone, since it is "better to lose a limb than a life." Clear indications for applying a tourniquet include limb destruction or injury to major blood vessels.

During pre-medical care, if pain relief has not yet been administered, narcotic analgesics are given intramuscularly, and improvised splints are replaced with standard-issue ones. Oxygen inhalation is performed using a KI-4M apparatus. In severe injuries, intravenous solutions (Ringer's solution, sorbilact, rheosorbilact, aminol), cardiovascular agents, and respiratory analeptics are administered. Alkaline-salt solutions are given to drink (1 teaspoon of table salt and baking soda per 1 liter of Water).

First medical aid. Following first aid and pre-medical care, some subjective and even objective improvement may occur: general well-being improves, and urine becomes less colored. This period is conventionally referred to as the "lucid interval." However, this improvement is typically short-lived and illusory; therefore, the scope of first medical aid must be adequate and depend on the severity of the Anatomical and morphological signs of injury. During sorting, all patients with PTS are sent to the dressing room. After exposing the injured limbs, the degree of ischemia is determined, and depending on the examination results, tourniquets are removed, left in place, or applied. Following the removal of tourniquets in the compressed areas, tight bandaging of the limbs is performed, and the limbs are cooled if possible. Narcotic analgesics, antihistamines, Antibiotics, and 0.5 ml of tetanus toxoid are administered intramuscularly. In severe shock, intravenous administration is performed using 400 ml of rheosorbilact (sorbilact, aminol, Ringer's solution, rheopolyglucukin, neogemodez); 800 ml of physiological saline, 40 ml of 40% glucose solution, 20 ml of 10% calcium chloride solution, 5 ml of 2.4% aminophylline solution, cordiamine, and caffeine. If available, a Carbonic anhydrase inhibitor diuretic—diacarb (250 mg)—is used, The Effect of which is based on altering the body's acid-base balance. When hemodynamic parameters are stable (maximum blood pressure above 100 mmHg), nerve blocks with novocaine are performed, and, if feasible, self-analgesia with methoxyflurane or trichloroethylene is administered using portable auto-analgesizers.

Alkaline-salt drinks are given orally (2-4 g of baking soda). For concomitant injuries, temporary arrest of external bleeding is performed, aseptic dressings and transport immobilization are checked, traumatic amputation of a limb hanging by a skin flap is carried out, and the Urinary Bladder is catheterized.

During sorting at the first medical aid stage, three sorting groups are distinguished:

1. Victims requiring urgent first medical aid measures: those with ongoing external bleeding, severe traumatic shock, or applied tourniquets. This group of victims is sent to the dressing room as a matter of priority.

2. Victims subject to evacuation to the next stage. After receiving first medical aid in the reception and sorting unit, they are prepared for evacuation.

3. Agonizing patients. This category is sent to a designated area.

Qualified surgical care. In medical facilities that provide

qualified surgical care, two groups of casualties with PTS are identified during medical sorting:

1. Casualties requiring emergency life-saving surgical intervention are treated in the shock room as a matter of first priority.

2. Casualties awaiting evacuation to the next echelon of care.

When delivering qualified medical care, casualties with severe and moderate manifestations of crush syndrome are sent to the anti-shock unit. During intra-triage sorting, patients with ongoing internal hemorrhage or irreversible limb ischemia requiring amputation are directed to the operating room as a first priority; those with severe, tension-induced tissue edema resulting from compression are sent to the dressing room for fasciotomy. The definitive decision regarding The Need for fasciotomy is made after the removal of dressings and a more thorough examination of the injury site. The shock ward receives casualties presenting with marked hemodynamic instability who do not currently require surgical intervention. All other casualties, following the administration of medical care, must be transferred to the specialized surgical care echelon as early as possible.

Qualified surgical care measures include:

1. Elimination or reduction of pain impulses in the traumatized body part (novocaine blocks, epidural anesthesia, neuroleptanalgesia or therapeutic inhalation anesthesia, intravenous administration of narcotic and non-narcotic analgesics, tranquilizers, sedatives).

2. Correction of hemodynamic disorders through the administration of plasma volume expanders (rheopolyglucukin, sorbilact, rheosorbilact, Ringer's solution, aminol, 5 % glucose solution, physiological saline, plasma, albumin).

3. Prevention and management of acidosis, for which a 35 % sodium bicarbonate solution is administered intravenously in volumes of 300-500 ml. Sodium citrate is administered orally in large doses (up to 15-20 g of dry substance). Sodium citrate has the property of alkalizing urine, thereby facilitating the dissolution of salt and myoglobinuric conglomerates. Positive outcomes are also achieved by gastrointestinal lavage using alkaline solutions (drinking baking soda, high alkaline enemas).

4. To reduce plasma loss, limb immobilization is maintained by elevating the affected limbs and continuing local cooling. However, it must be borne in mind that cooling should be moderate and the skin temperature in the cooling area should not drop below 16-28 °C.

The development of tension tissue edema and the disappearance of the peripheral pulse serve as indications for subcutaneous dissection of the muscular-fascial compartments. In dubious cases, a limited diagnostic fasciotomy is permitted, in which the skin, subcutaneous tissue, and deep fascia are incised over a length of 5-7 cm to inspect the condition of the muscles. If necrosis or marked muscle edema is detected, the fascia is further widely dissected subcutaneously. Fasciotomy should not be considered a simple surgical Procedure, as a thorough knowledge of the TOPOGRAPHIC AND ANATOMICAL Features of the extremities is essential.

5. Correction of renal dysfunction and prevention of acute renal failure (ARF).

To this end, infusion therapy is administered, hemodynamic disorders are corrected through The Use of antispasmodics and diuretics, and peritoneal lavage, hemadsorption, and enterosorption are performed.

6. Restoration of METABOLISM through the use of a complex of Vitamins, polyionic solutions (Ringer's solution, sorbilact, rheosorbilact, aminol), and a 20 % glucose solution.

7. Management of hypoxia using Oxygen therapy, Hyperbaric Oxygenation, and intravenous administration of sodium hydroxybutyrate (GHB).

8. Surgical interventions:

a) emergency indications — definitive arrest of hemorrhage, limb amputation in cases of fulminant or rapidly progressing anaerobic infection, and limb amputation for necrosis in severe crush syndrome with progressive acute renal failure;

b) delayed interventions of the 1st priority — fasciotomy, limb amputation for ischemic necrosis or extensive soft tissue destruction;

c) delayed interventions of the 2nd priority — primary surgical debridement (PSD) of soft tissue wounds as indicated.

Thus, the indications for limb amputation at the stage of qualified surgical care are:

1. Extensive soft tissue destruction with signs of anaerobic infection.

2. Ischemic Gangrene of the extremity.

3. Extremely severe and severe forms of crush syndrome against the background of progressive acute renal failure.

4. Limb destruction.

5. Progressive wound infection.

Amputation in crush syndrome is performed under general anesthesia. If a tourniquet was applied to the limb, the amputation is performed without removing the tourniquet. If no tourniquet was applied, the amputation level is determined during surgery by assessing the viability of the soft tissues. The criteria for muscle viability are local bleeding and contractility. Non-viable tissues are excised. The wound is thoroughly washed with antiseptic solutions (dexasan solution, furacilin solution 1:5000; 0.02 % chlorhexidine solution; 1 % dioxidine solution). The operation is completed by applying sorbents or a gauze dressing soaked in antiseptic solutions to the wound. It is strictly forbidden to apply primary sutures to the wound. Only after 3-4 days, in the event of a favorable wound healing process, may primary delayed sutures be applied. In most cases, wounds following amputations for ischemic necrosis in crush syndrome heal by secondary intention. Repeated surgical debridement of wounds due to purulent-necrotic complications is frequently required.

The indication for fasciotomy in crush syndrome is pronounced subfascial edema causing impaired Blood Circulation in the limb. In most cases, fasciotomy is performed on the lower leg, where there are 3 dense fascial compartments. Fasciotomy can be performed under local (most commonly regional block) anesthesia. Initially, a 5-6 cm incision of the skin and fascia is made to assess the severity of subfascial edema and the condition of the muscles (see insert, Fig. 16).

In cases of significant muscle protrusion through a fascial incision of viable muscles, a subcutaneous Z-shaped fasciotomy is performed along the entire segment of the limb. An adsorbent dressing is applied to the wound. 3-4 days after fasciotomy, in the absence of local infectious complications, delayed primary sutures can be placed on the wound edges. If "diagnostic" fasciotomy reveals non-viable muscles, skin and fascial incisions are extended proximally to determine the amputation level at the boundary between viable and necrotic tissues.

Victims with severe and moderate crush syndrome (CS), who currently do not require surgery or will need it after anti-shock measures, are admitted to the shock trauma bay. They receive intensive care aimed at correcting hemodynamic disorders, preventing acute renal failure (ARF), and providing detoxification.

Specific aspects of anti-shock therapy in CS include fluid resuscitation with protein preparations (200-400 ml of 10% albumin solution), improvement of blood rheological properties by administering 400 ml of sorbilact, reosorbilact, Ringer's solution, rheopolyglucukin, 5000-10000 IU of heparin, along with hemodilution (1600-2000 ml of 0.9% sodium chloride solution), correction of metabolic acidosis (400-800 ml of 4% sodium bicarbonate solution, aminol), stimulation of diuresis (40-500 mg of lasix), and, if necessary, management of hyperkalemia through calcium preparations (10-30 ml of 10% calcium chloride solution) and concentrated glucose with Insulin (20-40 ml of 40% glucose solution with 16-32 IU of insulin), hemodez, aminol, and reosorbilact. To prevent fluid overload, the volume of infusion therapy is controlled by urine output.

Following shock stabilization at the stage of qualified surgical care, patients are evacuated to specialized medical facilities. Patients with severe CS presenting with prominent signs of ARF should be referred to specialized hospitals equipped with an "artificial Kidney" unit (Fig. 17).

Class="center">

Fig. 17. Fresenius A 2008-C artificial kidney machine by Fresenius.

Patients with moderate CS should preferably be directed to designated hospitals reinforced with equipment and specialists in extracorporeal detoxification. Only comprehensive treatment utilizing various detoxification methods (hemo-, plasmo-, lymphosorption, plasmapheresis, etc.) can ensure a favorable clinical course of the pathological process.

Patients will arrive at the specialized care stage at the beginning of the intermediate period, when clinical signs of ARF begin to manifest. At this stage, therapeutic measures aim to prevent and treat ARF and include balanced infusion therapy, Forced diuresis (provided renal excretory function is preserved), correction of Water and Electrolyte balance, transfusion of plasma and protein plasma substitutes, correction of hyperkalemia and acidosis, as well as the administration of anticoagulants and protease inhibitors.

Promising agents for detoxification include enterodez, enterosorb, and enterosgel, which are considered non-toxic and intended for oral administration. These drugs bind toxic substances and eliminate them via the gastrointestinal tract. The therapeutic effect manifests 40-60 minutes after administration. The oral route of administration and elimination along with sorbed substances through the intestinal tract make these agents particularly valuable in ARF complicated by oligoanuria, as infusion therapy is restricted in these conditions, especially in the presence of fluid overload.

In such cases, progressive endotoxemia can be managed using methods of extracorporeal detoxification—the removal of toxic substances and excess fluid from the body. This approach allows for the expansion of infusion-Transfusion Therapy by enhancing its efficacy, overcoming transfusion volume limits, and reducing the risk of post-transfusion reactions and complications.

Fig. 18. COBE-Spectra blood cell separator for extracorporeal plasmapheresis.

Extracorporeal detoxification (ED) methods include membrane techniques (hemodialysis, hemofiltration), sorption techniques (hemosorption, plasmasorption, lymphosorption), and gravitational techniques (plasmapheresis), which simulate biological detoxification mechanisms. However, none of the ED methods is universal; therefore, combined techniques that are most effective for traumatic endotoxemia should be employed. Such combinations may include hemosorption coupled with extracorporeal oxygenation, plasmapheresis with plasmasorption, or blood ultrafiltration with hemosorption, performed sequentially in a single extracorporeal circuit (Fig. 18).

The most thoroughly validated approach utilizing combined Procedures is gravitational (centrifugal) automated plasmapheresis. Combining plasmapheresis with plasmasorption and blood oxygenation is considered the most effective strategy (Fig. 19).

However, in mass casualty incidents and delayed admissions of patients to specialized medical care, these therapeutic measures will be severely limited and not always effective. Therefore, it is necessary to focus on simpler methods for managing ARF. Such methods include peritoneal lavage and enterosorption, which can practically be implemented from the stage of qualified surgical care or in any hospital staffed with a surgeon.

Considering immunosuppression and the risk of infectious complications in the injured body part, immune stimulation (non-specific defense mechanisms) and antibiotic therapy are administered. If purulent complications occur, abscesses are opened, and necrotic tissues are excised as part of repeat surgical debridement. When late complications develop (purulent osteomyelitis, purulent fistulas, Sepsis, etc.), appropriate treatment is administered.

At the specialized care stage, limb amputations are performed if secondary indications arise. In the late period of CS, local disorders come to the forefront—muscle atrophy, joint stiffness, traumatic neuritis, paresis, paralysis, etc. Reconstructive surgery (see insert, Fig. 20), physical therapy, and physical rehabilitation are performed during this period.

Fig. 19. OS-6 refrigerated centrifuge for automated gravitational plasmapheresis.

Conclusion. Crush syndrome is one of the most severe challenges in disaster and emergency surgery. The high volume of casualties, The complexity of organizing first aid and primary medical care, the severity of the clinical course, the difficulties in delivering early qualified and specialized care, and the unsatisfactory treatment outcomes and sequelae necessitate continuous improvement of organizational and therapeutic approaches for this pathology.