Long-term compartment syndrome: signs, emergency care. Providing first aid for long-term compartment syndrome First aid for SDS includes

CHAPTER 9 LONG-TERM COMPRESSION SYNDROME

CHAPTER 9 LONG-TERM COMPRESSION SYNDROME

The first descriptions of the SDS clinic for earthquake victims date back to the beginning of the 20th century. During the Second World War E. Byuo-ters presented a detailed description of a specific pathology in the wounded recovered from the ruins after the bombing of London, calling it “crash syndrome” (from English word“crush” - crush, crush). In our country, the most famous researchers of SDS were AND I. Pytel(observations of the wounded during the bombing of Stalingrad), M.I. Kuzin(earthquake in Ashgabat 1948), E. A. N echaev, G. G. Savitsky(earthquake in Armenia 1988).

9.1. TERMINOLOGY, PATHOGENESIS

AND CLASSIFICATION OF THE SYNDROME

PROLONGED COMPRESSION

A complex of specific pathological disorders that develops after the release of the wounded from the rubble, where they long time(for 1 hour or more) were crushed by heavy debris, called long-term compartment syndrome. The emergence of SDS, which is described under different names ( long-term crush syndrome, crush syndrome, traumatic toxicosis, traumatic rhabdomyolysis etc.), is associated with the resumption of blood circulation in damaged and long-term ischemic tissues. In a large-scale war, the frequency of development of SDS can reach 5-20%.

In wounded people with SDS, damage to the extremities is mainly observed (more than 90% of cases), because Compression of the head and torso due to damage to internal organs is often fatal.

In injury surgery, in addition to SDS, there is also positional compression syndrome as a result of ischemia of parts of the body (limb, shoulder blade area, buttocks, etc.) from prolonged compression by the victim’s own weight lying in one position (coma, alcohol intoxication). Recirculation syndrome develops after restoration of a damaged artery in a long-term ischemic limb or removal of a long-term tourniquet.

Basis pathogenesis the above similar pathological conditions is endogenous intoxication products of tissue ischemia and reperfusion . In compressed tissues, along with areas of direct traumatic necrosis, ischemic zones are formed, where acidic products of anaerobic metabolism accumulate. After the wounded are released from compression, blood and lymph circulation is resumed in ischemic tissues, characterized by increased capillary permeability. This is called tissue reperfusion. In this case, toxic substances (myoglobin, products of impaired lipid peroxidation, potassium, phosphorus, polypeptides, tissue enzymes - histamine, bradykinin, etc.) enter the general bloodstream.

Happening toxic damage internal organs , primarily the lungs, with the formation of ARF.

Hyperkalemia may lead to acute cardiac dysfunction.

Under-oxidized products of anaerobic metabolism (lactic acid, etc.) are also washed out from ischemic tissues, which cause pronounced metabolic acidosis.

The most dangerous thing is the release of large amounts of protein into the blood from ischemic striated muscles. myoglobin. Myoglobin is freely filtered in the renal glomeruli, but clogs the renal tubules, forming insoluble hydrochloric acid hematin under conditions of metabolic acidosis (if the urine pH is more than 6, the likelihood of developing renal failure decreases with SDS). In addition, myoglobin has a direct toxic effect on the epithelium of the renal tubules, which together leads to myoglobinuric nephrosis and acute renal failure(OP N).

Rapidly developing post-ischemic edema of damaged and long-term compressed tissues causes acute hypovolemia with hemo concentration (BCV decreases by 20-40% or more). This is accompanied by a clinical picture of shock and, ultimately, also contributes to the deterioration of kidney function.

oliguria stops after a few days. The prognosis for mild DFS with proper treatment is favorable.

Moderate SDS develops with larger areas of compression of the limb for up to 6 hours. It is accompanied by endotoxicosis and impaired renal function for a week or more after the injury. The prognosis of moderate SDS is determined by the timing and quality of first aid, as well as subsequent treatment with the early use of extracorporeal detoxification.

Severe SDS develops when one or two limbs are compressed for more than 6 hours. With severe DFS, endogenous intoxication quickly increases, acute renal failure, MODS and other life-threatening complications develop. In the absence of timely intensive treatment using hemodialysis, the prognosis is unfavorable.

It should be noted that full compliance with the severity of vital function disorders important organs the scale and duration of tissue compression are not known. Mild SDS with untimely or inadequate medical care may lead to anuria or other fatal complications. On the other hand, with very long periods of compression of the extremities (more than 2-3 days), DFS may not develop due to the lack of restoration of blood circulation in necrotic tissues.

9.2. PERIODIZATION, CLINICAL SYMPTOMATICS OF LONG-TERM COMPRESSION SYNDROME

Early, intermediate and late periods of the course of SDS are distinguished (Table 9.2).

Table 9.2. Periodization of long-term compartment syndrome

9.2.1. Early period of compartment syndrome

Early period clinic (1-3 days) varies significantly among different wounded people. With moderate and severe SDS, after release from compression, a picture of traumatic shock may develop: general weakness, pallor, arterial hypotension and tachycardia.

Due to hyperkalemia, cardiac arrhythmias are recorded (sometimes up to cardiac arrest). In the next 1-2 days, the clinical picture manifests itself as instability in the respiratory and circulatory systems. With severe DFS, symptoms develop already in the first days acute renal failure and swelling of the lungs x(the earlier signs of anuria appear, the more dangerous they are prognostically).

In other cases, the general condition is initially satisfactory. In the absence of severe craniocerebral injuries, consciousness in all wounded patients with SDS is, as a rule, preserved.

The wounded, freed from the rubble, complain of severe pain in an injured limb that swells quickly. The skin of the limb becomes tense, pale or bluish, cold to the touch, and blisters appear. Pulsation of peripheral arteries due to edema may not be detected, sensitivity and active movements reduced or absent. More than half of the wounded with SDS also have fractures of the bones of the compressed limbs, Clinical signs which may complicate the early diagnosis of DFS.

Due to severe edema, tissue pressure in the muscles of the limbs, enclosed in dense osteofascial sheaths, can exceed the perfusion pressure in the capillaries (40 mm Hg) with further deepening of ischemia. This pathological condition, which can occur not only with SDS, is designated by the term compartment syndrome (from the English “compartment” - sheath, vagina) or the syndrome of “increased intracase pressure”.

In the majority of wounded people with moderate and mild SDS, with prompt medical care, the general condition is temporarily stabilized (“bright period” of SDS).

Laboratory research blood reveals signs of hemoconcentration (increased hemoglobin numbers, hematocrit, decreased BCC and CV), pronounced electrolyte disturbances (increased potassium and phosphorus content), increased levels of creatinine, urea, bilirubin, glucose. There is hyperfermentemia, hypoproteinemia, hypocalcemia, metabolic acidosis. There may be no changes in the first portions of urine, but then due to the release of myoglobin urine turns brown, is characterized by a high relative density with a pronounced shift in pH to the acidic side. Also detected in urine a large number of protein, erythrocytes, leukocytes, cylinders.

9.2.2. Intermediate period of long-term compartment syndrome

In the intermediate period of SDS (4-20 days) symptoms of endotoxemia and acute renal failure come to the fore. After short-term stabilization, the condition of the wounded worsens, and signs of toxic encephalopathy (profound stupor, stupor) appear.

For severe DFS dysfunction of vital organs increases rapidly. The development of acute renal failure is signaled by oligonuria (decrease in the rate of hourly diuresis less than 50 ml/h). Anuria can last up to 2-3 weeks with a transition in favorable cases to the polyuric phase of acute renal failure. Due to overhydration, overload of the pulmonary circulation is possible, up to pulmonary edema. Cerebral edema, toxic myocarditis, disseminated intravascular coagulation syndrome, intestinal paresis, persistent toxic anemia, and immunosuppression develop.

SDS of moderate and mild severity characterized mainly by signs of oligoanuria, endotoxemia and local manifestations.

Swelling of the injured limbs persists or increases even more. In the muscles of the compressed limbs, as well as in areas of positional compression, foci of progressive secondary necrosis are formed, supporting endogenous intoxication. In ischemic tissues, infectious (especially anaerobic) complications often develop, which tend to generalize.

Laboratory research with the development of oligoanuria, a significant increase in creatinine and urea is detected. Hyperkalemia, uncompensated metabolic acidosis, and severe anemia are noted. Under microscopy, urine sediment reveals cylindrical formations consisting of desquamated tubular epithelium, myoglobin and hematin crystals.

9.2.3. Late period of long-term compartment syndrome In the late (recovery) period of SDS - after 4 weeks and up to

up to 2-3 months after compression - in favorable cases, there is a gradual improvement in the general condition of the wounded. There is a slow restoration of the functions of the affected internal organs (kidneys, liver, lungs, heart, etc.). However, toxic and dystrophic disorders in them, as well as severe immunosuppression, can persist for a long time. The main threat to the life of the wounded with SDS during this period is generalized IO.

Local changes are expressed in long-term non-healing purulent and purulent-necrotic wounds of the extremities. The functional outcomes of treatment of limb injuries with DFS are often unsatisfactory: atrophy and connective tissue degeneration of muscles, joint contractures, and ischemic neuritis develop.

Examples of diagnosis of SDS:

1. Severe SDS of both lower limbs. Terminal state.

2. SDS of moderate degree in the left upper limb.

3. Severe SDS of the right lower limb. Gangrene of the right leg and foot. Traumatic shock of the third degree.

9.3. ASSISTANCE AT THE STAGES OF MEDICAL EVACUATION

First and first aid. The content of first aid to the wounded during SDS can vary significantly depending on the conditions of its provision, as well as on the forces and means of the medical service involved.

On the battlefield the wounded, pulled out of the rubble, are taken to a safe place. Orderlies or the military personnel themselves, in the form of mutual assistance, apply aseptic dressings to wounds (casualties) formed by compression of the limbs. In case of external bleeding, it is stopped (pressure bandage, tourniquet). An anesthetic is administered from a syringe tube (1 ml of a 2% pro-medol solution), and transport immobilization is performed using improvised means. If consciousness is preserved and there are no abdominal injuries, the wounded are provided with plenty of fluids.

Pre-medical care for wounded people suspected of having SDS must include: intravenous administration crystalloid solutions (0.9% sodium chloride solution, 5% glucose solution, etc.), which, if possible, continues during further evacuation. The paramedic corrects mistakes made during first aid, bandages wet bandages, and improves transport immobilization. In case of severe swelling, shoes are removed from the injured limb and uniforms are cut off. Give plenty of fluids.

In case of organizing assistance to the wounded outside the zone of direct enemy influence(removal of rubble after bombings, earthquakes or terrorist attacks), medical assistance is provided directly at the site of injury by medical and nursing teams. Depending on the training and equipment, such teams carry out emergency first medical and even qualified resuscitation care.

For the wounded released from the rubble, intravenous administration of crystalloid solutions is immediately established in order to eliminate blood plasma loss (it is even better to start infusion therapy before liberation from the rubble). If the development of DFS is suspected, 4% sodium bicarbonate 200 ml is administered intravenously (“blind correction of acidosis”) to eliminate acidosis and alkalinization of urine, which prevents the formation of hematin hydrochloride and blockage of the renal tubules. Also, 10 ml of 10% calcium chloride solution is injected intravenously to neutralize toxic effect potassium ions on the heart muscle. In order to stabilize cell membranes, large doses of glucocorticoids are administered. Painkillers and sedatives are administered and symptomatic therapy is carried out.

Before freeing the wounded from the rubble (or immediately after extraction), rescuers apply a tourniquet above the area of ​​compression of the limb to prevent the development of collapse or cardiac arrest from hyperkalemia. Immediately after this, the wounded person is removed to assess the viability of the compressed area of ​​the limb by a doctor.

The tourniquet is left on the limb (or applied if it has not been applied previously) in the following cases:

limb destruction(extensive damage to soft tissues of more than half the circumference of the limb, bone fracture, injury great vessels); limb gangrene(distal to the demarcation line, the limb is pale or blue-spotted, cold, with wrinkled skin or desquamated epidermis; sensitivity and passive movements in distal joints completely absent). For the rest of the wounded, aseptic stickers are attached to the wounds of the extremities with adhesive tape (circular bandages can compress the limb and impair blood circulation), and transport immobilization is performed.

If possible, priority evacuation (preferably by helicopter) is provided for all wounded with SDS directly to the stage of providing specialized medical care.

First medical aid. Upon admission to the medical center (med), the wounded with signs of SDS are sent to the dressing room first.

1000-1500 ml of crystalloid solutions, 200 ml of 4% sodium bicarbonate solution, 10 ml of 10% calcium chloride solution are administered intravenously. Catheterization in progress Bladder By assessing the color and amount of urine, diuresis control is established.

A long-term compressed limb is examined. If available destruction or gangrene- a tourniquet is applied. If in these cases the tourniquet was applied earlier, it is not removed.

In the rest of the wounded with SDS, against the background of infusion therapy, administration of cardiovascular and antihistamines The tourniquet is removed, novocaine blockade is performed (conductor or cross-sectional above the area of ​​compression), transport immobilization.

Cooling of the injured limb is provided (ice packs, cryopacks). If the condition of the wounded allows, an alkaline-salt drink is given (made at the rate of a teaspoon of baking soda and table salt per 1 liter of water). Urgent evacuation, preferably by helicopter, preferably immediately to the stage of specialized medical care, where there are conditions for the use of modern methods of extracorporeal detoxification.

Qualified medical care. In armed conflict

with established aeromedical evacuation of the wounded from medical companies directly to the 1st echelon MVG, when delivering the wounded from the SDS to the Omedb (Omedo Special Forces) - they only carry out pre-evacuation preparation in the scope of first medical aid. CCP is provided only for health reasons.

In conditions of large-scale war or when the evacuation of the wounded is disrupted The medical hospital (omedo) provides clinical and clinical care. Already during selective triage, the wounded with SDS are first of all sent to the intensive care ward for the wounded in order to assess their condition and identify life-threatening consequences.

In the event of massive sanitary losses, a number of wounded with severe SDS, unstable hemodynamics and severe endotoxemia (coma, pulmonary edema, oligoanuria) can be classified as agonizing.

In the intensive care ward To compensate for plasma loss, crystalloids (do not inject potassium!) and low-molecular colloid solutions are administered intravenously, while stimulating urination with Lasix and maintaining diuresis of at least 300 ml/h. For every 500 ml of blood substitutes, in order to eliminate acidosis, 100 ml of 4% sodium bicarbonate solution is administered to achieve a urine pH of at least 6.5. With the development of oliguria, the volume of infusion therapy is limited according to the amount of urine excreted. A 10% calcium chloride solution, glucocorticoids, painkillers and sedatives are administered.

In case of DFS, the administration of nephrotoxic antibiotics is contraindicated: aminoglycosides (streptomycin, kanamycin) and tetracyclines. Non-toxic antibiotics (penicillins, cephalosporins, chloramphenicol) are administered in half doses and only for the treatment of developed wound infections (but not for prophylactic purposes).

After stabilization of hemodynamic parameters, the wounded with SDS are examined in the dressing room for the seriously wounded(Table 9.3).

For signs of compartment syndrome(intense swelling of the limb with the absence of pulsation of the peripheral arteries, coldness of the skin, decreased or absent sensitivity and active movements) is indicated wide open fasciotomy . Indications for fasciotomy for SDS should not be expanded, because incisions are the gateway to wound infection. In the absence of signs of compartment syndrome, dynamic monitoring of the condition of the limb is carried out.

Fasciotomy is performed from 2-3 longitudinal skin incisions (above each osteofascial sheath) at least 10-15 cm long with dissection of dense fascial plates with long scissors throughout the entire segment of the limb. Wounds after fasciotomy are not sutured, because with significant tissue edema, this can impair blood circulation, and they are covered with napkins with water-soluble ointment. Immobilization is carried out with plaster splints.

“Lampas” incisions to the bone along the lateral surface of the limb or “subcutaneous” fasciotomy from small incisions are not used for DFS.

If necrosis of individual muscles or muscle groups of the limb is detected during wound inspection, their excision is performed - necrectomy .

Non-viable limbs with signs of dry or wet gangrene, as well as ischemic necrosis (muscle contracture, complete absence sensitivity), after diagnostic dissection

Table 9.3. Surgical tactics for DFS

skin lesions (muscles are dark or, conversely, discolored, yellowish, do not contract or bleed when cut) - are subject to amputation.

Amputation with SDS is performed above the level of the compression boundary, within healthy tissues. With a tourniquet applied, amputation is performed over the tourniquet. Lateral incisions on the limb stump being formed are used to monitor the viability of the overlying tissues. Wide subcutaneous fasciotomy of the limb stump is required. Primary sutures are not applied to the skin of the stump due to the threat of anaerobic infection and the high probability of the formation of new foci of necrosis.

If there is doubt about the non-viability of a limb, a relative indication for urgent amputation may be an increase in endotoxicosis and oligoanuria.

Injured with SDS of any severity, due to real threat acute renal failure and the need for specific detoxification methods, urgent evacuation is indicated. It is preferable to evacuate such wounded people to the stage of providing SCP by air, with the obligatory continuation of intensive care during the flight.

Specialized medical care wounded with SDS in the absence of surge arrester turns out in a general surgical hospital.

is a shock-like state that occurs after prolonged compression of the torso, limbs or their segments by heavy objects. Manifested by pain, deterioration, swelling of the affected parts of the body, acute renal failure. Without medical care, patients die from acute renal failure, increasing intoxication, pulmonary or cardiovascular failure. Treatment includes detoxification and plasma replacement infusion therapy, extracorporeal hemocorrection, antibiotic therapy, excision of areas of necrosis or amputation of a crushed limb.

ICD-10

T79.5 Traumatic anuria

General information

Long-term crush syndrome (CDS), other names - traumatic toxicosis, crash syndrome, Bywaters syndrome, myorenal syndrome - a pathological shock-like condition that occurs after prolonged compression of the torso, limbs or their segments by heavy objects. Crash syndrome develops immediately after the release of the patient and restoration of blood and lymph flow in the affected parts of the body. Accompanied by deterioration general condition, the development of toxemia and acute renal failure, with a large area of ​​damage, often ends in the death of the patient. In traumatology and orthopedics, a common type of crash syndrome is distinguished - the so-called positional compression syndrome (PCS), which develops as a result of prolonged (more than 8 hours) compression of body parts while a person is stationary on a hard surface.

Reasons for SDR

Typically, long-term crush syndrome occurs in victims of landslides, earthquakes, mine collapses, construction work, road accidents, logging, explosions and the destruction of buildings as a result of bombing.

Positional compression syndrome is usually detected in patients who were in a state of poisoning at the time of injury sleeping pills, narcotic or alcohol intoxication. Those tucked under the body are more likely to suffer upper limbs. For the reasons of development, symptoms and treatment methods, positional crush syndrome is practically no different from long-term crush syndrome, however, it usually proceeds more favorably due to the smaller area of ​​​​the lesion.

Pathogenesis

The occurrence of long-term crush syndrome is due to a combination of three factors:

• pain syndrome;
• massive loss of plasma caused by the release of the liquid part of the blood through the walls of blood vessels into damaged tissues;
• traumatic toxemia (intoxication of the body with tissue decay products).

Prolonged painful stimulation during crash syndrome leads to the development of traumatic shock. Loss of plasma causes blood thickening and causes thrombosis of small vessels. Traumatic toxemia in crash syndrome develops due to the absorption of tissue decay products of injured muscles into the blood. Immediately after the limb is released from the damaged tissue, a significant amount of potassium ions enters the vascular bed, which can cause arrhythmia, and in severe cases, cessation of the functioning of the lungs and heart.

Subsequently, the crushed muscle tissue of a patient with crush syndrome loses up to 66% of potassium, 75% of myoglobin, 75% of phosphorus and 70% of creatinine. Decomposition products enter the blood, causing acidosis and hemodynamic disturbances (including a sharp narrowing of the vessels of the renal glomeruli). Myoglobin damages and clogs the kidney tubules. All this leads to the development of acute renal failure, which threatens the life of a patient with crash syndrome.

Classification

By severity:

• Mild form of crash syndrome. Occurs when segments of a limb are crushed for 4 hours or less.
• Moderate form of crash syndrome. Develops as a result of crushing one limb within 4-6 hours. With timely initiation of treatment, the prognosis is favorable.
• Severe form of crash syndrome. Occurs when one limb is crushed for 6-8 hours. Accompanied by hemodynamic disorders and acute renal failure. With timely initiation of treatment, the prognosis is relatively favorable.
• An extremely severe form of crash syndrome. Develops as a result of crushing of two or more limbs for 6 or more hours. Accompanied by severe shock. The prognosis is unfavorable.

According to clinical symptoms:

• early period (from the moment of release to 3 days);
• toxic period (begins on days 4-5);
• period of late complications (develops 20-30 days after the injury).

Symptoms of SDR

Immediately after the compression is removed, the general condition of the victim improves. A patient with long-term crush syndrome experiences pain and limited movement in the crushed limb. During the first hours after release, swelling of the affected area gradually increases, becoming dense and woody. Blisters with serous-hemorrhagic contents form on the skin of the limb. When examining the damaged part of the body, a weakening of the pulsation of the arteries, a decrease in sensitivity and local temperature are revealed.

General symptoms increase. The condition of the victim with crash syndrome is deteriorating. After a short period of excitement, the patient becomes lethargic and inhibited. There is a decrease in blood pressure and body temperature, arrhythmia, tachycardia, severe pallor skin. The skin of a patient with crash syndrome is covered with sticky cold sweat. Possible loss of consciousness, involuntary defecation and urination. Sometimes pulmonary edema develops. The amount of urine excreted decreases. Without adequate medical care, there is a risk of death within 1 or 2 days.

Foci of necrosis form on the crushed limb. As the dead tissue is sloughed off, muscle is exposed and has the characteristic appearance of cooked meat. Suppuration of wounds and eroded surfaces develops. Acute renal failure appears and gradually increases. On days 5-6, patients with prolonged crush syndrome develop uremic syndrome. An increase in potassium levels in the blood causes arrhythmia and bradycardia.

Signs appear on days 5-7 pulmonary insufficiency. Increasing intoxication, caused by the entry into the bloodstream of tissue decay products and bacterial toxins from a crushed limb, causes toxic hepatitis. Endotoxic shock is possible. The symptoms of multiple organ failure in patients with crash syndrome gradually decrease within 2-3 weeks.

Acute renal failure in crash syndrome resolves approximately a month after the injury. The patient's condition improves, his body temperature returns to normal. Pain and swelling of the limb are reduced. Necrotic muscles are replaced connective tissue, which leads to muscle atrophy and the development of contractures. In case of unfavorable development of events, local (suppuration) and general (sepsis) complications are possible.

Diagnostics

In order to compensate for metabolic acidosis, a patient with crash syndrome is given a 4% sodium bicarbonate solution by drip. Antibiotics are prescribed wide range actions intramuscularly. Conduct symptomatic therapy(diuretics, analgesics, antihistamines and antiarrhythmic drugs). In case of long-term crush syndrome, extracorporeal hemocorrection (hemodialysis, plasma and hemosorption) is carried out as early as possible.

If the viability of the muscle tissue is preserved and there is pronounced subfascial edema with impaired local circulation, the traumatologist performs a fasciotomy with revision and excision of necrotic muscle bundles. If there is no suppuration, the wound is sutured on the 3-4th day, after swelling has decreased and the general condition of the patient with crash syndrome has improved.

In cases of irreversible ischemia, amputation of the limb is performed above the site of application of the tourniquet. In other cases, excision of necrotic areas while preserving viable muscle bundles is indicated. Muscle viability is determined during surgical intervention. The criteria for viability are the preservation of normal color, the ability to bleed and contract. After tissue excision, the wound is washed generously with antiseptics. No stitches are required. The wound heals by secondary intention.

In the long term, patients with long-term crush syndrome are advised to take courses rehabilitation treatment(massage, exercise therapy) aimed at restoring muscle strength and eliminating contractures.

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Crash syndrome in the modern medical understanding is a symptomatic complex that develops with prolonged disruption of systemic circulation in soft tissues due to external pressure exerted on them. Quite often this pathology is also called Bywaters syndrome.

In addition to local problems, it is characterized by broad systemic pathological changes, including renal failure, hyperkalemia and so on. What actions should be taken in case of prolonged compression of the limbs? How does compartment syndrome develop? You will read about this and much more in our article.

First aid for compartment syndrome

Basic principles of providing first first aid for long-term compression syndrome (crash syndrome) includes:

• Proper analysis of rubble. When providing first aid, objects that cause compression must be lifted in parts, while quickly bandaging the limb with an elastic bandage in order to prevent the rapid development of shock and at the same time not to prolong the process of squeezing the arterial structures;
• Use of cold. Damaged areas are covered with bottles of cold water, ice and so on. It is advisable to place something soft under the limbs - for example, a blanket or clothing;
• Fastest possible transportation. The victim must be transported to the nearest intensive care unit of any hospital;
• Drink plenty of fluids. May be given during transportation with the addition baking soda, which will neutralize the negative effect on the kidneys. Such a procedure for providing assistance is possible only if there are no obvious symptoms of damage to internal organs, the abdomen is soft, and the person has all reflexes, including swallowing.

What not to do when providing assistance:

• Abruptly release the person from compression. Such a procedure will provoke an immediate shock and the development of the most acute negative consequences;
• Apply a tourniquet. During first aid, applying a tourniquet is justified only in cases where there is obvious non-viability of the limb or there is severe open bleeding. In all other situations, such a remedy will only prolong the compartment syndrome and ensure the appearance of more severe forms of the problem;

• Use medications.“Field” therapy for crash syndrome (except for anti-shock) does not have the desired effect, since real help can be provided to a person only in intensive care conditions, often with direct surgical intervention;
• Do not transport the person to the hospital. Regardless of the circumstances, the victim should be transferred to a hospital for treatment. complex diagnostics and implementation of the necessary measures that will not allow a potential crash syndrome to develop, even in situations where a person feels satisfactory after release and can walk, since most symptoms develop later.

Dr. Komarovsky will tell you how to provide first aid to children with compression of their limbs:

Emergency assistance to the victim

As part of the provision of primary emergency medical care, classical antishock therapy is most often performed.

Traumatic shock with prolonged compression syndrome develops after severe forms of the corresponding pathology and improper actions to free the person.

Algorithm of actions for providing emergency care for crash syndrome (long-term compression syndrome):

• Temporary stop of bleeding. Performed in exceptional cases in the presence of gushing blood;
• Relief of pain syndrome. To help with pain, use any available painkillers in injection form;
• Correction of gas exchange disorders. Oxygenation, tracheal intubation, other actions;
• Resuscitation. When providing emergency care, basic resuscitation actions are performed to restore breathing and heartbeat ();
• Relief of shockogenic impulses. A combination of atropine, diazepam and tramadol is used. In addition, intravenous administration of glucocorticosteroids, the use of adrenomimetic drugs, and other drugs are rational. medicines according to symptomatic and vital signs.

Similar articles

What is crash syndrome

Crash syndrome is a special set of symptoms that develops as a consequence of long-term circulatory disorders in various soft tissues of the body - most often in the lower or upper extremities.

Similar pathological processes are diagnosed in victims of various disasters, including building collapses, earthquakes, and so on, as a result of which people find themselves sandwiched between hard surfaces for a long period of time.

Such a compression injury carries not only local risks of open or closed damage to structures, fractures, and so on, but can lead to short-, medium- and long-term serious consequences for the entire body.

Including leading to consequences associated with impaired functioning of the kidneys, liver, of cardio-vascular system and so on. Crash syndrome has three characteristic features:

• Direct compression of the limbs or body, followed by tissue necrosis over a fairly long period of time;
• Development of complex swelling together in places of compression at the local level;
• The formation of ischemic toxicosis and acute renal failure, as a rule, against the background of long-term compression of the main vessels and main nerves.

As a result, prolonged compression develops

For the first time, crash syndrome was described at the beginning of the 20th century, when soldiers participating in the First World War fell under various rubble, for example, in active street battles.

An accurate interpretation was carried out by British physicians Bywaters in the 40s of the last century: he studied and identified the syndrome as an independent nosological unit.

In the modern era, long-term compression syndrome most often develops as a result of an accident or the inability to get out of the rubble for a long period of time after earthquakes, building collapses, and other natural and man-made disasters.

The modern interpretation of the basic clinical picture of long-term compartment syndrome includes the following circumstances: prolonged exposure to soft fabrics forms the prerequisite for the accumulation of toxic products in the corresponding muscles.

After a sharp release of pressure, these substances in an altered form enter the bloodstream, causing severe acidosis (disorder of acid-base balance) and complex, extremely severe hemodynamic disorders (circulatory disorders).

Deep tissue necrosis in clear localizations, temporarily compressed by compression after the disappearance of the basic factor, leads to the entry of breakdown products into the main bloodstream with the development of self-poisoning of the body.

Symptoms of the pathological process

The specific manifestation of crash syndrome depends on the current clinical picture of the pathological process and the immediate form, as well as the duration of compression. In general, the following classification applies:

• Light form. It represents a pathology on a limb segment, with exposure for no more than 4 hours;
• Medium shape. Direct compression of part or all of a single limb for about 6 hours;
• Severe form. Pathological effects on several limbs for 6-7 hours;
• Extremely severe form. It is characterized by compression of all limbs, sometimes other parts of the body, for 8 hours or more.

Immediately after release, the patient may go into shock. If this does not happen, then starting from the third day after the incident, local complex symptoms begin to appear, from dense swelling, pallor of the skin and dysfunction of the limb to renal failure, oliguria, anuria, and so on.

Early symptoms are almost always erased, however, due to the low effectiveness of delayed treatment, acute clinical manifestations with rapid development of renal failure can last up to 2 weeks, which sometimes results in death for the patient.

If the victim was under the rubble or at the epicenter of the incident for a very long period of time, then Almost immediately after his release, he noted:

• Inability to move limbs;
• General condition is temporarily satisfactory;
• Weakness and nausea;
• Only slight tachycardia is noted.

Within a few hours after the event, the following increases rapidly:

• Body temperature rises;
• The pulse quickens;
• Blood pressure drops sharply;
• The skin acquires an uneven purplish-bluish coloration;
• Swelling;
• Bubbles with serous and serous-hemorrhagic contents form;
• Pulsation of peripheral arteries is noted;
• All types of sensitivity may be lost;
• The amount of urine excreted sharply decreases.

Diagnostic measures

The key feature for diagnosing compartment syndrome in humans is primary fee necessary data that would allow a qualitative and quantitative assessment of both the extent of the pathological process and the duration of its impact on individual areas of the body.

In the vast majority of cases, the first clinical manifestations external character occur after a certain period of time, from several hours to three days.

Without the information described above, it is almost impossible to recognize the presence of pathology, even using instrumental diagnostic techniques, before a clear clinical picture of the development of crash syndrome appears.

Treatment of crash syndrome

Any manifestations and consequences of crash syndrome are treated exclusively in a hospital setting - most often in the intensive care unit. Within the framework of primary care, anti-shock measures with the administration of analgesics, cardiovascular drugs and blood pressure normalizers. The next stage is intensive infusion therapy, which does not allow the formation and development of acute renal failure.

For moderate and severe degrees of crush syndrome, surgery is prescribed, for example, fasciotomy of the damaged limb, amputation of the distal parts and other measures as necessary.

At the same time, blood circulation is restored. After finishing the most acute period and stabilization of the victim's condition It is recommended to move to the rehabilitation stage, which includes:

• Strict drinking regime;
• Hemodialysis (method of extrarenal blood purification);
• Continuation of infusion therapy;
• Plasmapheresis (the procedure for collecting blood, purifying it and returning it back into the bloodstream);
• Physiotherapy and exercise therapy.

Possible complication and consequences

With moderate and severe degrees of prolonged compartment syndrome, the prognosis in most cases is unfavorable, and there is a high probability of death in the patient.

Even timely qualified medical care in some cases does not allow the compressed limbs to be kept intact, and the person may remain disabled.

The victim develops the prerequisites for the development of irreversible renal failure with the need for an organ transplant - in the absence of the latter procedure, lifelong hemodialysis is prescribed.

Stages and symptoms of the disease

There are four stages of the disease:

Toxic shock - immediately after compression, a painful shock occurs, which is usually not accompanied by a significant decrease in blood pressure (it is rarely below 90 mm Hg). Severe pain after compression lasts from several minutes to 2 hours. When the compression is eliminated, they can immediately collapse will occur and death. If this does not happen, you should determine the affected area, which is easily identified by the reduced temperature and density of the affected tissues. Characteristic purple-violet skin color. Approximately 1 hour after decompression, woody swelling appears and increases rapidly. If the urine discharged from the bladder is dirty-brown in color, this indicates a severe form of DFS. An even more unfavorable sign of anuria is when, after 200-300 ml of urine has been released, it ceases to be excreted altogether. In this situation, hyperkalemia is extremely dangerous. Ischemia a compressed limb leads to numbness and disappearance of pain. After decompression, toxemia occurs due to the entry of ischemic toxins into the bloodstream; myoglobinuria plays an important role, which leads to necrosis of the renal tubules and the development of acute renal failure. The level of potassium in the blood increases sharply, which can be a direct cause of death. Damage to internal organs may occur - erosive gastritis, enteritis, gangrene of the cecum or sigmoid colon. Victims are concerned about weakness, thirst, nausea, and may experience vomiting. There is little urine, it becomes yellow-brown or reddish in color. Swelling of areas of the body that have been subjected to compression appears and progresses; the skin over these areas is pale bluish, cold, shiny, easily wounded, the tissues are dense to the touch. Possible blisters, abrasions, hematomas, and often contaminated wounds. All this together creates a picture post-compression toxic shock with very high level mortality rate severe forms long-term compartment syndrome. This stage lasts up to 48 hours after the compression is released.

Light Gap- not always. After the patient’s condition has stabilized as a result of treatment, a short period of light (“imaginary well-being”) occurs, after which the condition worsens again.

Acute renal failure. Lasts from 3-4 days to 8-12 days. There is an increase in the extremities freed from compression. The composition of the blood changes, anemia increases, urine output sharply decreases, up to anuria. A sharp worsening of the condition, the patient is lethargic, apathetic. Vomit. Areas of necrosis of limb tissue. The pulse is frequent and weak. Blood pressure is reduced.

Recovery stage. Begins from the 3-4th week of the disease. Kidney function, protein content and blood composition are normalized. Infectious complications come to the fore. High risk of sepsis.

Possible complications:

1) Toxic damage to the liver, kidneys and other organs due to increasing intoxication.

2) Fat embolism - blockage with fat droplets from bone marrow vessels (pulmonary, renal, cerebral, etc.). Thromboembolism of the same vessels is possible. Consequently, necrosis (destruction) of the relevant organs may occur. That is, a heart attack.

3) Immediately after the injury, or after a light interval (hours to a day or more), a rash and small hemorrhages develop on the face, upper torso and limbs. The skin becomes purple-bluish in color, with blisters.

Long-term compartment syndrome (LCS) is a severe pathological condition, resulting from closed damage to large areas of soft tissue under the influence of large and/or long-acting mechanical force, accompanied by a complex of specific pathological disorders (shock, heart rhythm disturbances, acute kidney injury, compartment syndrome), most often in the extremities for a period of more than 2 hours.

SDS was first described by N. I. Pirogov in 1865 in “The Beginnings of General Military Field Surgery” as “local asphyxia” and “toxic tissue tension.” Special attention attracted the SDF during World War II. In 1941, English scientists Bywaters E. and Beall D., taking part in the treatment of victims of the bombing of London by German aircraft, identified this syndrome as a separate nosological unit. In London residents who suffered from fascist bombings, SDS was recorded in 3.5-5% of cases and was accompanied by high mortality. In 1944, Bywaters E. and Beall D. determined that myoglobin plays a leading role in the development of renal failure.

In the domestic literature, SDS was described for the first time under the name “crush syndrome and traumatic compression of the limbs” in 1945 by A. Ya. Pytel. Based on materials from the 1948 Ashgabat earthquake, N. N. Elansky in 1950 described in detail the clinical picture and treatment of prolonged crush syndrome, and an opinion was expressed about the leading role of toxicosis in the development of the clinical picture.

In peacetime, SDS most often occurs in victims of earthquakes and man-made disasters (Table 1).

Table 1

Frequency of SDS development during earthquakes

Most often (79.9% of cases) SDS occurs when closed injury soft tissues of the lower extremities, in 14% - with damage to the upper and in 6.1% - with simultaneous damage to the upper and lower extremities.

Table 2 shows the main reasons leading to SDS.

table 2

Main etiological factors of DFS

As a result of tissue compression, blood flow in the vessels is disrupted and tissue waste products accumulate. After blood flow is restored, cellular breakdown products (myoglobin, histamine, serotonin, oligo- and polypeptides, potassium) begin to enter the systemic circulation. Pathological products activate the blood coagulation system, which leads to the development of DIC syndrome. It should be noted that another damaging factor is the deposition of water in damaged tissues and the development of hypovolemic shock. A high concentration of myoglobin in the renal tubules under acidic conditions leads to the formation of insoluble globules, causing intratubular obstruction and acute tubular necrosis.

As a result of hypovolemia, DIC syndrome, and cytolysis products entering the bloodstream, in particular myoglobin, multiple organ failure develops, the leading place in which is acute kidney injury (AKI).

Depending on the extent and duration of tissue compression, three degrees of severity of SDS are distinguished (Table 3).

Table 3

Classification of SDS by severity

The clinical picture of DFS has a clear periodicity.

The first period (from 24 to 48 hours after release from compression) is characterized by the development of tissue edema, hypovolemic shock and pain.

The second period of SDS (from days 3-4 to 8-12) is manifested by an increase in edema of compressed tissues, impaired microcirculation and the formation of AKI. IN laboratory tests blood, progressive anemia is detected, hemoconcentration is replaced by hemodilution, diuresis decreases, and the level of residual nitrogen increases. If treatment is ineffective, anuria and uremic coma develop. Mortality during this period reaches 35%.

In the third period (from 3-4 weeks of the disease), clinical manifestations of multiple organ failure are observed, including AKI, acute lung injury, heart failure, DIC and gastrointestinal bleeding. During this period, a purulent infection may occur, which can lead to the development of sepsis and death.

SDS ends with a period of convalescence and restoration of lost functions. This period begins with short-term polyuria, which indicates resolution of AKI. Homeostasis is gradually restored.

Diagnosis of DFS is based on anamnestic and clinical laboratory data.

Laboratory signs of DFS consist of increased levels of creatine phosphokinase, metabolic acidosis, hyperphosphatemia, uric acid and myoglobin. Evidence of severe kidney damage is acidic urine and the appearance of blood in the urine (gross hematuria). The urine becomes red, its relative density increases significantly, and protein is detected in the urine. Signs of AKI include a decrease in diuresis to oliguria (daily diuresis less than 400 ml), an increase in the level of urea, creatinine, and potassium in the blood serum.

Treatment measures should begin at prehospital stage and include pain relief, intravenous infusion fluids, heparin administration. The victim must be taken to the hospital as soon as possible. When observing and treating patients, it is necessary to take into account the risk of developing hyperkalemia soon after release of the affected limb, and conduct careful monitoring for the development of shock and metabolic disorders.

In the hospital, according to indications, surgical treatment of the affected areas is carried out, including “lamp” incisions with mandatory dissection of the skin, subcutaneous tissue and fascia within the edematous tissues. This is necessary to relieve secondary compression of the affected tissues. If necrosis of only part of the muscles of the limb is detected, their excision is performed - myectomy. Non-viable limbs with signs of dry or wet gangrene, as well as ischemic necrosis (muscle contracture, complete lack of sensitivity, during diagnostic dissection of the skin - the muscles are dark or, on the contrary, discolored, yellowish, do not contract or bleed when cut) are subject to amputation above the level of the compression limit, in within healthy tissues.

Massive infusion therapy is mandatory. Infusion therapy is aimed at correcting fluid and electrolyte disturbances, shock, metabolic acidosis, preventing DIC and reducing or preventing AKI.

Antibacterial therapy should begin as early as possible and be used not only for treatment, but, above all, for prevention infectious complications. In this case, it is necessary to exclude the use of nephro- and hepatotoxic drugs.

More than 10% of victims require extracorporeal detoxification. Anuria during the day with the ineffectiveness of conservative therapy, hyperazotemia (urea more than 25 mmol/l, creatinine more than 500 µmol/l), hyperkalemia (more than 6.5 mmol/l), persistent hyperhydration and metabolic acidosis require immediate initiation of renal replacement therapy - hemodialysis , hemofiltration, hemodiafiltration. Methods of renal replacement therapy make it possible to remove medium- and low-molecular toxic substances from the bloodstream and eliminate acid-base and water-electrolyte imbalances.

On the first day, plasmapheresis (PP) is indicated. According to the data presented by Vorobyov P.A. (2004), PF showed high efficiency in the treatment of sick victims of the earthquake in Armenia in 1988. Carrying out PF on the first day after decompression made it possible to reduce the incidence of AKI to 14.2%. The effectiveness of PF is associated with the rapid removal of myoglobin, tissue thromboplastin and other products of cellular breakdown.

VTS is currently trending upward throughout the world. This is due, among other things, to the increase in victims of road accidents. Predicting the course of the disease is quite difficult, since most of the data comes from earthquakes and other man-made disasters. According to available data, mortality depends on the timing of treatment and ranges from 3 to 50%. If AKI develops, the mortality rate can reach 90%. The use of renal replacement therapy methods has reduced mortality to 60%.

Literature

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2. Gumanenko E. K. Military field surgery of local wars and military conflicts. Guide for doctors / ed. Gumanenko E.K., Samokhvalova I.M. - M., GEOTAR-Media, 2011. - 672 p.
3. Genthon A., Wilcox S. R. Crush syndrome: a case report and review of the literature. // J. Emerg. Med. - 2014. - Vol. 46. ​​- No. 2. - P. 313 - 319.
4. Malinoski D. J., Slater M. S., Mullins R. J. Crush injury and rhabdomyolysis. // Crit. Care. - 2004. - Vol. 20 - P. 171 - 192.
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