Prolonged positional compression syndrome. Long-term compartment syndrome, cause, symptoms, first aid First aid for prolonged compartment syndrome

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Lesson 1, 2. Definition, causes, severity and signs of long-term compartment syndrome. Compression periods: early, intermediate, late. Dependence of the severity of the syndrome on time and localization of compression (chest, abdomen, pelvis, hand, forearm, foot, lower leg, thigh). Features of the manifestation of long-term compression syndrome in children. Tactics for releasing a compressed limb. Bandaging, immobilization and cooling of a compressed limb using standard and improvised means. Warming the victim. The procedure for medical evacuation of a victim. Help with compression of a limb from which release is impossible. Forced amputation of limbs.

Compartment syndrome or traumatic toxicosis is a disease that occurs as a result of long-term and sometimes short-term extensive compression of one or several large segments of the limbs, which have a pronounced mass (lower leg, thigh, gluteal region).

Long-term compartment syndrome (LCS) is the body's reaction to endotoxemia that develops as a result of ischemic tissue damage due to mechanical compression.

Causes of ischemic tissue damage

The basis of pathological changes in DFS is circulatory insufficiency of tissues, leading to their hypoxia, dysfunction and death (necrosis).

The duration of tissue hypoxia should not exceed the period after which, when adequate blood supply is restored, it is still possible to maintain their viability. The duration of this period can be increased by reducing the oxygen demand of tissues (for example, when they are cooled) or reduced by increasing these demands (intense muscle work).

Tissues have different resistance to hypoxia - from several minutes (brain, heart muscle) to several hours (skeletal muscles, skin).

The extent of ischemia can be different and affect the entire body, individual vital organs (brain, heart, kidneys) or be local in nature when organs and tissues that are not vitally important are affected (for example, limbs). At the same time, even local hypoxia can lead to both local and general complications. Local complications (necrosis) lead to local dysfunction. General complications are associated with cytolysis, the release of toxic products and their entry into the body from the source of ischemia (ischemic toxicosis), which can pose an immediate threat to life.

There are many reasons that can cause irreversible ischemic disorders in tissues. Among them, we can highlight those that are most characteristic of emergency conditions:

compression injury resulting from external compression of tissues (long-term compression syndrome itself);
injury to a great vessel with prolonged disruption of blood flow in the distal sections;
long-term presence of a hemostatic tourniquet on a limb exceeding the maximum permissible time (tourniquet injury);
prolonged immobility in an unnatural position with impaired blood supply (positional compression syndrome);
compression of the muscles of the limb in intact fascial sheaths against the background of severe edema with impaired blood supply (compartment syndrome).

Compression of the limbs occurs in peacetime and military situations during landslides, car accidents, train crashes, earthquakes, and destruction of buildings.

Most often, SDS occurs as a result of victims falling under rubble. At the same time, compression of the extremities, as a rule, predominates in the localization of damage (60% of all cases of DFS develop with damage to the lower extremities and 20% to the upper extremities). The experience of eliminating the consequences of emergencies over the past 20 years has shown that emergency situations most often occur during earthquakes, when the share of such victims is up to 30-33% of their total number.

Due to prolonged compression, blood circulation in the tissues and the delivery of nutrients and oxygen to them are impaired. As a result, tissue necrosis occurs with the release of toxic waste products (autotoxins) into the body. Immediately after the limb is released from compression, a significant amount of toxins can enter the bloodstream. The condition of the victims noticeably worsens, even to the point of impaired cardiac activity and breathing. The effect of toxic products on the nervous system, kidneys and liver is especially harmful. Due to impaired renal function, urine output decreases sharply and then stops. In severe cases, death can occur in the next 2-4 days from impaired renal, liver, and cardiovascular function.

In the next few hours after release, edema of the damaged limb segment develops. The fabrics become dense to the touch. The pallor of the skin is subsequently replaced by a purplish-blue color with areas of small hemorrhages. Bubbles with light or bloody contents appear. The skin is cold, pain sensitivity is reduced. The pulsation of arteries in the peripheral parts of the limb is weakened or not determined.

Pathogenesis of long-term compartment syndrome

In a compression injury, one should distinguish between crushing and compression of tissues. When exposed to a large load, mechanical destruction (crushing, crushing) of both soft tissue and bones can occur. Such a mechanical injury leads primarily to the development of shock, which will determine its severity.

Although the remaining intact tissue will be subject to ischemia, the leading factor will still be mechanical injury. This is long-term crush syndrome.

When exposed to smaller loads, it is not mechanical damage that comes to the fore, but ischemia caused by tissue compression, the degree of which depends, among other things, on the time of compression. Of course, mechanical damage due to tissue compression can also occur and affect the severity of the victim’s condition.

However, if we keep in mind the specifics of pathogenetic changes, the features of the clinical picture and treatment tactics, in such cases the term “long-term compression syndrome” should be preferred. When local ischemia develops, the muscles are the first to suffer; skin and subcutaneous tissue are more resistant to hypoxia. In the clinical course of acute ischemic injury, two periods are distinguished: ischemia and reperfusion.

The period of ischemia is characterized by the cessation (or significant decrease) of local blood flow and the development of tissue hypoxia. The greatest pathogenetic significance during the period of ischemia is the pain factor (mechanical injury, ischemic increasing pain) and psycho-emotional stress.

A shock-like state develops with a drop in blood pressure, centralization of blood circulation, and the development of a deficit in circulating blood volume (CBV). After 3.5-4 hours, liquefaction necrosis of ischemic muscles occurs, toxic products of myolysis (myoglobin, creatinine, potassium and calcium ions, lysosomal enzymes, etc.) accumulate in the tissues.

The longer the ischemia lasts and the greater the mass of the affected tissue, the more toxic substances are released. At the same time, the effects of these endotoxins do not appear until they enter the general bloodstream, i.e. until the perfusion of the ischemic segment is restored. The period of ischemia does not pose an immediate danger to life; disorders of systemic blood flow are, as a rule, reversible. However, the severity of the next period and the final prognosis largely depend on the duration of the first period of ischemic injury. The reperfusion period is characterized by restoration of blood and lymph circulation. On the one hand, restoring perfusion is beneficial for ischemic tissues and makes it possible to stop the impact of the traumatic factor (ischemia) and reduce hypoxia.

On the other hand, the faster and more fully the perfusion is restored, the more actively the toxic substances formed during the period of ischemia enter the general bloodstream, causing life-threatening endogenous toxicosis. The speed of “washing out” toxins from the affected segment is very important. At a relatively low rate of their entry into the general bloodstream, the toxic effect is less pronounced due to the inclusion of detoxification mechanisms and adaptive reactions of the body. However, as a rule, blood flow is restored quickly (removal of the external compressive factor, restoration of the patency of the main vessel), and the so-called “volley” release of toxins occurs, which is the least favorable.

The severity of endogenous intoxication depends on the mass of affected tissue, the time and degree of ischemia.

Mass of fabrics.

When assessing the severity of a lesion in SDS, they usually talk not about mass, but about the area of compression. This is due to the fact that without special tables it is difficult to calculate the percentage of tissue mass of a particular segment, but the area can be determined quickly (rules of nines and palms). In fact, when talking about the area of compression, it is meant that the larger the area, the greater the mass of tissue that has been subjected to ischemia.

Ischemia time.

Even with complete ischemia, irreversible changes occur no earlier than 3.5-4.0 hours. This time is considered “threshold”, after exceeding which endogenous intoxication necessarily occurs due to ischemic cell breakdown.

Degree of ischemia.

If blood flow is not completely stopped and blood circulation is partially preserved, then the “threshold” time for the onset of irreversible ischemic changes can increase several times, reaching 12 hours or more.

After restoration of blood flow during the reperfusion period, tissue edema quickly develops. At its core, it has a rational biological meaning - a decrease in the activity of tissue perfusion of the affected segment, a kind of self-isolation of the toxic focus. At the same time, the rational adaptive response soon turns pathological, causing more harm than good and further exacerbating pathological changes. With rapidly growing swelling, the muscles compress themselves in intact fascial sheaths that do not have the ability to stretch (compartment syndrome, 8th tunnel syndrome). Secondary ischemia caused by edema develops, and ischemic tissue continues to die.

The ineffectiveness of systemic hemodynamics of vascular origin, caused by endogenous intoxication, as well as the direct impact of cytolysis products entering the bloodstream lead to numerous both functional and morphological disorders, which can be defined as multiorgan pathology, the leading place (both in terms of the timing of occurrence and mortality rates ) in which acute renal failure occurs.

Clinical course of prolonged compression

The clinical course of the reperfusion period can be divided into three stages:

Early stage(endogenous intoxication) lasts 1-2 days. Until blood flow is restored, the victim's condition may be relatively satisfactory, but then it begins to deteriorate. The victim, initially excited and in a state of euphoria, becomes lethargic while maintaining consciousness. Hemodynamic disorders are aggravated due to increasing intoxication (toxic shock), blood pressure drops. Pain impulses intensify, the compressed limb becomes cyanotic, the edema acquires a woody density (it is not even possible to form a dent when pressing on the skin) and spreads beyond the compressed area, blisters with serous or serous-hemorrhagic contents appear on the skin. Active movements in the joints of the limb are difficult, passive movements are painful. All types of skin sensitivity are affected. The rapid entry of cytolysis products into the bloodstream leads to severe hypercatecholemia and hyperkalemia with cardiac dysfunction. Endotoxicosis is increasing, but has not yet reached its maximum; detoxification mechanisms are working, but they are quickly depleted. In the kidneys, vascular stasis and thrombosis develop in both the cortex and medulla. The lumen of the tubules is filled with cell decay products due to toxic nephrosis. Myoglobin in an acidic environment turns into insoluble hydrochloric acid hematin, which, together with the desquamated epithelium, clogs the renal tubules and leads to increasing renal failure. At the early stage of the reperfusion period, despite the impairment of renal function (diuresis decreases, urine acquires a varnish-red color, high protein content, hematin, casts, blood detritus, myoglobin are determined in it), diuresis is still amenable to stimulation, the kidneys are still functioning.

The main threat to life at the stage of endogenous intoxication is unstable hemodynamics.

When hemodynamics stabilize, a “bright period” may occur with a temporary subjective improvement in well-being without changes in blood counts, diuresis and urine composition.

Intermediate stage(acute renal failure) lasts from 3–4 days to 3–5 weeks. Multiple organ pathology develops with relatively stable hemodynamic parameters. By the 4th–6th day, the rejection of necrotic tissue begins with the development of wound infection. In conditions of depletion of the body's adaptive capabilities and suppression of the immune background, the wound process is very difficult with a tendency towards generalization of infection and the development of sepsis. A large array of necrotic tissue is a favorable environment for the development of anaerobic infection. On the 5th–7th day, pulmonary failure occurs due to pneumonia and interstitial pulmonary edema. Stress ulcers may appear in the stomach and intestines. 10 Acute renal failure continues to worsen, and stimulation of diuresis is no longer effective. Oligoanuria develops, urine becomes dark brown (a sign of myoglobinuria).

The main threat to life at the intermediate stage is acute renal failure.

When acute renal failure has already developed against the background of ischemic injury, the mortality rate reaches 25–30%, which is one of the highest rates in surgery. Subsequently, against the background of developing multiple organ pathology and the addition of liver failure, uremic syndrome with hyperazotemia develops. The level of urea can increase to 25 mmol/l or more, creatinine - up to 0.4-0.7 mmol/l. Some researchers distinguish this condition into a separate stage - azotemic intoxication.

Convalescence stage begins with short-term polyuria, which indicates resolution of acute renal failure. Homeostasis is gradually restored. However, signs of multiple organ pathology can persist for several years, or even a lifetime. As a result of extensive purulent-necrotic changes in soft tissues with damage to blood vessels and nerves, it is almost never possible to completely restore the function of the affected limb. Long-term orthopedic and rehabilitation treatment for osteomyelitis, contractures, neuritis, etc. is required.

Determining the severity of ischemic injury

The severity of ischemic injury depends primarily on the mass of the affected tissue and the duration of ischemia. Ischemia of a small segment (for example, the hand) can lead to severe local disorders, but does not pose a significant danger in terms of the development of the previously described general toxic complications.

A short time of even complete ischemia of the limb (less than 2 hours) does not lead to irreversible changes, and also cannot cause endogenous intoxication. It is believed that ischemic toxicosis is possible with ischemia of a tissue mass exceeding 1000 g (the approximate mass of the soft tissues of the hand and forearm) for at least 3–4 hours.

It should be noted that with short-term compression of tissues with significant force (fall of a heavy object, compression by a press), they are crushed (crushed), and not ischemic disorders, but mechanical damage come to the fore. Intoxication can develop not due to prolonged tissue ischemia, but due to their mechanical destruction, as well as the addition of a wound infection.

Thus, the severity of a victim’s condition during ischemic injury is assessed by the mass of ischemic tissue, ischemia time, and the presence of concomitant mechanical damage. The severity of ischemic limb injury can be fully determined only in a specialized hospital during dynamic observation with the use of additional (functional, laboratory) examination methods.

At the same time, it is very important to assess the severity of the lesion in the prehospital period, based on quickly and easily identified signs. Based on this task, in a prognostic assessment based on such characteristics as the area and time of ischemia, four degrees of severity of ischemic injury are distinguished.

Mild degree– ischemia of a small segment of the limb (lower leg, shoulder, forearm) for 3–4 hours. There is no immediate threat to life, ischemic toxicosis, as a rule, does not develop.

Average degree– ischemia of one or two limbs for 4 hours. Ischemic toxicosis develops, there is a threat of acute renal failure; cure without specialized medical care is impossible.

Severe degree– ischemia of one or two limbs for 7–8 hours. Severe ischemic toxicosis and threatening hemodynamic disorders occur. Acute renal failure develops in all victims who require intensive therapy and active detoxification in a specialized hospital. Extremely severe degree - complete ischemia of both lower extremities for more than 8 hours. Death, as a rule, occurs against the background of severe hemodynamic disturbances; acute renal failure simply does not have time to develop. Resuscitation measures aimed at restoring hemodynamics often do not lead to the desired effect.

It is fundamentally important that in case of ischemic damage to a limb, not only successful treatment, but also saving the life of the victim is possible only in a specialized hospital. Therefore, the main task of all types of medical care is to ensure the fastest possible evacuation to such a hospital.

At the same time, real emergency conditions do not always allow such evacuation, and therefore victims are sometimes delayed for quite a long time at the source of the lesion or in close proximity to it, without the possibility of receiving comprehensive medical care in a specialized hospital during this period.

When providing medical care in such situations, it is especially important to choose the most rational and effective tactics that can increase the victims’ chances of maintaining life and health.

When considering the algorithms of actions to provide assistance to victims with SDS in the affected area, two time intervals should be distinguished: Evacuation is possible within several hours. Evacuation is possible within 2–3 days. Evacuation is possible within 3 days.

Providing medical assistance if evacuation is possible within a few hours

With continued tissue compression or immediately after release from the press, the victim, as a rule, develops disorders characteristic of the period of ischemia and the first (initial) stage of the reperfusion period. At this time, the victim is provided, depending on the situation, with first, primary pre-medical or primary medical care. Since the main threat to life is shockogenic reactions with impaired hemodynamics, it is necessary to carry out the entire complex of anti-shock measures, taking into account, however, the specifics of ischemic injury.

Algorithm for providing medical care to victims with compression ischemic injury of the extremities at the source of the disaster

Analgesic and infusion therapy.

The introduction of analgesics (to all victims), vasopressors and cardiotonics (with a critical drop in blood pressure), sedatives (in the presence of agitation), the start of infusion therapy (saline and low molecular weight colloid solutions) and alkaline drinking should be performed as early as possible, sometimes (if there is such a possibility) until peripheral blood flow is restored and the limb is freed (if this is associated with a long-term extraction of the victim from the rubble during emergency rescue operations). After removing the victim from the rubble, infusion therapy should be continued, pursuing two main goals: compensation for hypovolemic disorders that develop against the background of rapidly increasing endotoxemia and redistribution shock, and achieving hemodilution, which helps reduce the concentration of endotoxins in the blood. Of great importance, especially in the first day (before the onset of acute renal failure), is the stimulation of diuresis to eliminate some of the toxins in the urine.

Perinephric block , is believed to improve micro-circulation and help the kidneys better resist toxic aggression. However, the degree of its effectiveness in case of SDS has not yet been conclusively determined, and performing such a blockade at the source of an emergency can lead to a large loss of time, as well as infectious complications. Therefore, if a quick evacuation is possible, it is better to refrain from such a blockade.

Elimination of the traumatic factor (i.e. ischemia) is to restore blood flow. During rescue operations, this is only possible when ischemia is caused by external compression. When eliminating external compression, it is important to try to avoid the “volley” release of toxins into the general bloodstream. To do this, a hemostatic rubber tourniquet is applied at the base of the limb. Then the limb is released from compression. The blood flow is not restored due to the applied tourniquet, which gives time to perform the main manipulation - bandaging the limb with an elastic bandage (preventing venous discharge through the superficial veins), and the bandaging should be carried out from the proximal to the distal part of the limb. If there are wounds or abrasions, they are covered with a protective bandage before applying an elastic bandage. Then the tourniquet is slowly released, restoring blood flow. If it was not possible to apply a tourniquet before freeing the limb, it is still necessary to perform elastic bandaging.

After releasing the limb from the obstruction, the degree of viability of the limb is assessed based on such signs as the presence or absence of movements in the joints of the limb and sensitivity.

The following types of ischemia are distinguished:

compensated (movements, tactile and pain sensitivity are preserved) - the limb is viable, there is no threat of massive necrosis;
decompensated (active movements are lost, tactile and pain sensitivity is reduced or lost) - the limb is conditionally viable, to save it it is necessary to urgently restore adequate blood flow;
irreversible (even passive movements are lost, rigor mortis of the muscles has set in) - the limb is not viable, its preservation is impossible, the only possible further tactic is its early amputation.

Having determined that ischemia is irreversible, it is necessary to leave or reapply a hemostatic tourniquet to the limb and transport the victim to the hospital with the tourniquet applied. The goal is to isolate as much as possible the obviously non-viable segment as a source of intoxication until amputation is performed. There is another situation in which it is permissible to transport the victim with a hemostatic tourniquet applied. This is a period of complete ischemia of the compressed segment of no more than 4–5 hours, combined with the possibility of delivering the victim to a specialized hospital within one hour. In this case, you can count on regional detoxification in the hospital, when, after removing the tourniquet, blood from the affected segment enters the general bloodstream through special sorbents. But one should remember the maximum permissible periods of complete tissue ischemia, which in no case should exceed 6 hours.

Increasing tissue resistance to hypoxia.

To increase tissue resistance to hypoxia, local hypothermia (ice, hypothermic bags, rescue blanket) is used. In addition, cold reduces the intensity of microcirculation, which also prevents the rapid entry of toxins into the bloodstream. However, when cooling a limb, one should remember the danger of frostbite, since with ischemic injury, the sensitivity of the skin (including temperature) is reduced.

Transport immobilization is absolutely necessary even in the absence of signs of mechanical damage: maximum rest promotes the survival of tissues subjected to ischemic injury. It is advisable to use pneumatic tires, which also serve as a tight elastic bandage. In their absence, other known immobilization techniques are used using improvised or standard means. It should, however, be remembered that the viability of soft tissues against the background of SDS is significantly reduced, which significantly increases the risk of developing pressure sores in places where the hard splint comes into contact with the tissues. Therefore, special attention should be paid to tire modeling and the use of soft pads.

Amputation of a limb in the hearth.

If it is not possible to free the limb from the blockage in a timely manner, and every extra hour reduces the victim’s chances of survival, in some exceptional cases it is permissible to perform guillotine amputation without releasing the limb. This operation, which already falls within the competence of emergency specialized medical care, is carried out strictly according to vital indications with the participation of a trauma surgeon, as well as an anesthesiologist, who provides adequate pain relief.

The time elapsed from the onset of ischemia to the start of comprehensive medical care is one of the most important factors influencing the prognosis. Ischemic injury in most cases poses a serious threat to life, and comprehensive medical care can only be provided in a specialized hospital.

Therefore, the sooner the victim is taken there, the greater his chances of survival. No therapeutic or diagnostic manipulations should cause a delay in transporting the victim to a specialized hospital. The algorithm of actions at the source of the disaster to provide medical care to victims with ischemic limb injury caused by external compression is shown in the figure. This algorithm is designed to ensure that evacuation is possible within the first 24 hours.

Providing medical care in cases of evacuation delay for 2-3 days and Providing medical care in cases of evacuation delay for more than 3 days in methodological recommendations.

Sequence of on-site first aid

1. Before releasing the limb from compression, apply a tourniquet above the place of compression.

2. After releasing the compression, without removing the tourniquet, bandage the limb from the base of the fingers to the tourniquet and only after that carefully remove the tourniquet.

3. An anesthetic is injected intramuscularly.

4. Provide warmth to the victim (wrap him in a blanket, give him a warm drink).

5. If there are wounds, an aseptic bandage is applied; if there are bone injuries, the limb is immobilized (immobilized) with splints.

6. The victim is urgently evacuated to a medical facility (on a stretcher).

7. If hospitalization is delayed, the limbs are given an elevated position by placing it on a pillow. The previously applied bandage is unbandaged and the limb is covered with ice. Give plenty of fluids (preferably mineral water), controlling the amount of urine excreted.

After the victim is freed from the rubble, the severity, danger and outcome depend on the duration of the compression of the limb:

up to 4 hours – mild severity;
up to 6 hours – average;
up to 8 hours or more – extremely severe.

As a result of exposure of a person's soft tissues to heavy objects for several hours, long-term compression syndrome begins to develop. In medical practice, this condition has several definitions: crash syndrome, traumatic toxicosis, positional syndrome or compression syndrome.

Long-term compression syndrome, for which first aid is of paramount importance, appears in people who have been in the area of earthquakes, rubble, collapses, and car accidents.

Positional compression is also distinguished, which develops due to a person’s prolonged stay under the influence of a compressive factor or the gravity of his own body in a state of sleep or unconsciousness. Most often, this condition occurs as a result of taking alcohol or drugs, when a person cannot control the level of danger.

A characteristic feature of SDS is the development of pathological changes after the removal of severity from the patient’s body. At this moment, active restoration of the stopped blood flow begins, in which tissue breakdown products have already accumulated.

Clinic and its manifestations

In case of long-term compression syndrome, the main criterion for the development of pathology is massive damage to muscle tissue, which occurs for the following reasons:

Damage and subsequent cell death due to the traumatic factor itself;
Lack of blood flow through the compressed muscle;
Cell hypoxia resulting from hemorrhagic shock.

Note!

At the moment of compression of the muscle, there is no crash syndrome. Their manifestations begin after the injured person is released from under heavy objects.

Constricted or crushed vessels and muscles, in which their decay products have accumulated, open up. All toxic substances rush through the bloodstream. Having reached the kidneys, a special muscle protein (myoglobin) blocks the tubules of the organ, preventing urine from being produced.

A few hours are enough for tubular necrosis to occur, and irreversible processes in the kidneys begin, the result of which will be.

First honey assistance will depend on the length of time the body remains under the rubble.

There are 3 stages of pathology development:

Early (characteristic symptoms appear in the first three days);
Intermediate (manifestations last one and a half months);
Late (time period until complete recovery).

Each of these periods has characteristic symptoms and features of their manifestation.

After properly provided emergency care for long-term compression syndrome in the late period, the body begins to independently reject dead tissue and restore the functioning of all vital organs.

In particularly severe cases, surgical removal of necrotic tissue is required.

The specifics of care for long-term compartment syndrome will depend on several other factors:

Type: crushing or squeezing;
Location: chest, pelvis, abdominal area, limbs;
Combination of injury with complications: violations of the integrity of internal organs, large vessels and nerves;
The severity and area of damage;
Combination with other injuries: poisoning, etc.

When providing primary care, it is mandatory to determine the severity of injuries.

Doctors distinguish 4 degrees:

Easy. The compression lasts no more than 3-4 hours. It has the most favorable prognosis, since renal dysfunction is insignificant.
Average. The duration of exposure to gravity is 5-6 hours. Fatalities are about 30%;
Heavy. Development of necrosis due to 7-8 hours of being under rubble. There are always serious complications. Mortality accounts for up to half of all cases.
Very severe degree is characterized by compression of large areas of the body for more than 9 hours. A fatal outcome is inevitable within a day after liberation from the rubble.

Specifics of urgent measures

First aid for long-term compartment syndrome has a number of characteristic features.

Note!

Its main feature is a categorical prohibition on releasing a person from under a heavy object without first applying a tourniquet or a pressure bandage.

Apply above the damaged area and only after that remove the weights. If this rule is violated, the released toxins will immediately begin to spread through the systemic bloodstream, causing irreversible damage to the kidneys and liver. Then there will be no need to provide medical care: the victim will die.

If the limbs are compressed, first aid consists of completely immobilizing them.

The general algorithm for providing first aid comes down to the following actions:

Secure the injured part with a tourniquet or bandage above the injury site;
Give to prevent painful shock (if possible, administer it intramuscularly);
Release the victim from the effects of heavy loads;
Cool the affected part of the body;
Open wounds will require disinfection;
Remove the tourniquet;
Apply a pressure bandage using the same principle;
Immobilize the limb;
If there are no signs of abdominal injury, the patient is given warm, generous fluids;
To prevent cardiovascular disorders, prednisolone can be given to the victim.

Note!

Long-term use of a tourniquet is allowed only in case of arterial bleeding or obvious signs of incipient gangrene.

Immediately after the actions taken, you need to write a note indicating the exact time of application of the device.

Further first aid for prolonged compression is provided in a health care facility, where the victim is taken on a stretcher.

Crash syndrome, or prolonged compression syndrome, is a traumatic toxicosis that develops in the tissues of the extremities when they are released after prolonged compression. The severity of this condition depends closely on how extensive the damage to the soft tissues was, as well as on the time the victim was under the rubble.

In medicine, there are three types of this compression: compression, positional compression and crushing, but in most cases there is a combination of several types of injuries.

In the article we will look at the main signs of this syndrome and ways to provide the necessary assistance after removing a person from under the weight pressing on him.

Main factors in the development of compartment syndrome

Crash syndrome was once described by researchers under different names: “release disease,” traumatic toxicosis, as well as compartment syndrome and myorenal syndrome. Doctors emphasized that in the development of this condition, three circumstances are of greatest importance:

painful effects that cause an imbalance between the processes of excitation and inhibition in the central nervous system;
traumatic toxemia, resulting from the penetration of decay products from damaged muscles and tissues;
plasma loss resulting from extensive swelling of injured limbs.

How does “release syndrome” develop?

If we consider the pathogenesis of crash syndrome, then the main cause of subsequent problems can be called ischemia (poor circulation) in a certain segment of the limb or in it as a whole, observed in combination with stagnation of venous blood.

At the same time, the nerve trunks are compressed and injured, which leads to corresponding neuro-reflex reactions. In addition, crash syndrome is also a mechanical damage to muscle tissue, which causes the release of large amounts of toxins (metabolic products).

Everything described above leads to traumatic shock, which develops in a unique way due to the occurrence of intoxication and renal failure.

What has the greatest influence on the development of the pathological condition?

Crash syndrome in all its manifestations is based to a large extent on the neuro-reflex component. Namely, on prolonged painful exposure, which causes respiratory spasms, disrupts blood circulation and, as a rule, entails thickening of the blood and inhibition of the process of urination.

Immediately after the victim is relieved of the object pressing on him (by the way, the same happens after removing a long-term compressive tourniquet), myoglobin and other toxic substances begin to enter the blood: histamine, potassium, protein breakdown products, creatine, adenosine and phosphorus . Against this background, the patient develops acute renal failure and symptoms reminiscent of traumatic shock.

Severity of the condition in crash syndrome

In medicine, there are 4 forms of clinical manifestations accompanying crash syndrome:

Lightweight. It occurs when the duration of compression does not exceed four hours.
Medium shape. Compression for 6 hours, usually of the entire limb. In this case, renal function is slightly impaired and there are no obvious hemodynamic disorders.
Heavy. It occurs after compression of an entire limb for 7-8 hours (by the way, most often we are talking about the leg). In this case, signs of renal failure clearly appear.
Extremely severe form. It is observed in the case of compression of both limbs for more than 6 hours. As a rule, victims die from manifestations of renal failure within the first three days after injury.

What do crash syndrome manifestations look like?

The symptoms accompanying crash syndrome directly depend on how long the compression lasted, over what area it extended, and whether there were concomitant damage to internal organs, bones, blood vessels and nerves.

After being freed from the rubble, most of the victims, as a rule, are in satisfactory condition. Patients complain mainly of nausea, weakness and pain in the injured limbs. The latter are pale colored and have traces of compression (dents). In the peripheral arteries, the pulsation in them is weakened.

Swelling of the extremities develops quickly - they greatly increase in volume and become woody to the touch, and pulsation due to vascular spasm disappears completely, causing the extremities to become cold. The growth of edema that accompanies crash syndrome (you can see a photo of it here) provokes a deterioration in the condition of the victim, who becomes weak, lethargic, and drowsy. His heart rate quickens, his blood pressure drops to critical levels, and the pain in his limbs increases.

How do signs of crash syndrome develop?

A sign of the early period of crash syndrome is oliguria (this is a process in which the patient’s urine output is greatly reduced). In this case, urine has a reddish color due to the presence of hemoglobin and myoglobin in it, an acidic reaction and high density.

If the treatment accompanying crash syndrome is timely, then on the 3rd day the patients feel better and the swelling decreases. But, unfortunately, on the 4th day nausea, vomiting, weakness and signs of uremia appear. The patient suffers from lower back pain and symptoms of renal failure. The condition worsens further, and on days 8-12 death may occur due to uremia.

But with proper treatment, by the 12th day the described symptoms subside and a period of gradual recovery begins. True, complete restoration of the limb, as a rule, does not happen - muscle atrophy and contracture are observed in it.

Crash syndrome: emergency care and treatment

In the treatment of crash syndrome, it is very important whether the necessary first aid was provided correctly to the person caught under the rubble. Immediately after its removal, the limb must be tied with a tourniquet above the injury site (i.e., closer to the body) and bandaged tightly to prevent swelling. It is also advisable to apply ice to it, which will help reduce the development of hyperkalemia and reduce the sensitivity of tissues to oxygen starvation.

Mandatory first aid accompanying crash syndrome is the administration of painkillers and sedatives.

It should be remembered that if there is the slightest doubt about the speed of delivery of the patient to a medical facility, the tourniquet must be removed immediately after tight bandaging and a cold compress - otherwise the process of tissue necrosis may begin.

Treatment is carried out in the intensive care unit, from the very first hours the patient is transfused with large volumes of fresh frozen plasma, hemodez and saline solution. Heparin is injected under the skin of the abdomen, antibiotics, antiplatelet agents, Lasix and Trasylol are prescribed. If necessary, hemodialysis is performed. In the presence of complex edema, the patient is indicated for fasciotomy, and if gangrene develops, amputation of the limb is indicated.

LONG-TERM COMPRESSION SYNDROME.

Synonyms used to refer to this term are crash syndrome, traumatic endotoxicosis, tissue compression syndrome.

This syndrome is understood as the development of intravital tissue necrosis, causing endotoxemia due to prolonged compression of a body segment.

This phenomenon was first described by Dr. Corvisart, Napoleon's personal physician in 1810.

He noticed that when a horse was killed under a cuirassier, a horseman clad in metal armor, and he could not get out from under it on his own, after the battle and the release of his crushed lower limbs, he died quite quickly, although he had no injuries.

At that time, Corvisar did not find an explanation for this, but he described the fact itself.

PATHOGENESIS.

The leading pathogenetic factors of long-term compartment syndrome (PCS) are: traumatic toxemia, which develops due to the entry into the bloodstream of decay products of damaged cells that trigger intravascular coagulation; plasma loss as a result of severe edema of injured limbs; painful irritation leading to discoordination of the process of excitation and inhibition in the central nervous system.

The result of prolonged compression of the limbs is the occurrence of ischemia of the entire limb or its segment in combination with venous stagnation. Nerve trunks are also injured. Mechanical destruction of tissue occurs with the formation of a large number of toxic products of cell metabolism, primarily myoglobin. The combination of arterial insufficiency and venous congestion aggravates the severity of limb ischemia. Developing metabolic acidosis in combination with myoglobin entering the circulation leads to blockade of the kidney tubules, impairing their reabsorption capacity. Intravascular coagulation blocks filtration. Consequently, myoglobinemia and myoglobinuria are the main factors determining the severity of toxicosis in victims. Hyperkalemia, often reaching 7-12 mmol/l, significantly affects the patient’s condition. Toxemia is also aggravated by histamine, protein breakdown products, adenylic acid, creatinine, phosphorus, etc., coming from damaged muscles.

Already in the early period of DFS, blood thickening is observed as a result of plasma loss, and massive swelling of damaged tissues develops. In severe cases, plasma loss reaches 1/3 of the circulating blood volume.

The most severe complication observed in DFS is acute renal failure, which manifests itself differently at the stages of disease development.

CLASSIFICATION.

By type of compression:

crushing,

compression (direct, positional).

By localization:

isolated (one anatomical area),

multiple,

combined (with fractures, damage to blood vessels, nerves, traumatic brain injury).

By severity:

I Art. – mild (compression up to 4 hours),

II Art. – medium (compression up to 6 o’clock),

III Art. - severe (compression up to 8 hours),

IV Art. - extremely severe (compression of both limbs for 8 hours or more).

I degree – minor indurative swelling of soft tissues. The skin is pale, at the border of the lesion it bulges somewhat above the healthy skin. There are no signs of circulatory problems.

II degree – moderately expressed indurative swelling of soft tissues and their tension. The skin is pale, with areas of slight cyanosis. After 24-36 hours, blisters with transparent yellowish contents may form, which, when removed, reveal a moist, soft pink surface. Increased edema in subsequent days indicates a violation of venous circulation and lymphatic drainage, which can lead to the progression of microcirculation disorders, microthrombosis, increased edema and compression of muscle tissue.

III degree – pronounced indurative swelling and tension of soft tissues. The skin is cyanotic or “marbled” in appearance. Skin temperature is noticeably reduced. After 12-24 hours, blisters with hemorrhagic contents appear. Under the epidermis, a moist, dark red surface is exposed. Indurative edema and cyanosis quickly increase, which indicates gross disturbances of microcirculation, vein thrombosis, leading to a necrotic process.

IV degree – indurative edema is moderately expressed, the tissues are sharply tense. The skin is bluish-purple in color and cold. Individual epidermal blisters with hemorrhagic contents. After removal of the epidermis, a cyanotic-black, dry surface is exposed. In the following days, the swelling practically does not increase, which indicates deep microcirculation disorders, insufficiency of arterial blood flow, and widespread thrombosis of venous vessels.

I period – early (period of shock) – up to 48 hours after release from compression. This period can be characterized as a period of local changes and endogenous intoxication. At this time, the clinical manifestations of the disease are dominated by manifestations of traumatic shock: severe pain, psycho-emotional stress, hemodynamic instability, hemoconcentration, creatininemia; in the urine - proteinuria and cylindruria. After stabilization of the patient’s condition as a result of therapeutic and surgical treatment, a short clear period begins, after which the patient’s condition worsens and the second period of DDS develops - the period of acute renal failure. Lasts from 3-4 to 8-12 days. Swelling of the extremities, freed from compression, increases; blisters and hemorrhages are found on damaged skin. Hemoconcentration gives way to hemodilution, anemia increases, and diuresis sharply decreases down to anuria. Hyperkalemia and hypercreatininemia reach the highest numbers. Mortality in this period can reach 35%, despite intensive therapy.

From the 3-4th week of the disease, the third period begins - recovery. Kidney function, protein content and blood electrolytes are normalized. Infectious complications come to the fore. High risk of developing sepsis.

At the same time, the experience of disaster medicine has shown that the degree of compression and area of damage, the presence of concomitant damage to the internal organs of bones and blood vessels are of greatest importance in determining the severity of the clinical manifestations of SDS. The combination of even short-term compression of the limbs with any other injury (bone fractures, traumatic brain injury, ruptures of internal organs) sharply aggravates the course of the disease and worsens the prognosis.

The scope of treatment measures for SDS is determined by the severity of the victim’s condition.

One of the first pre-hospital necessary measures should be the application of a rubber tourniquet to the compressed limb, its immobilization, and the administration of narcotic analgesics (promedol, omnapon, morphine, morphilong) to relieve shock and emotional stress.

I period. After release from compression, it is necessary to carry out infusion (anti-shock and detoxification) therapy, including intravenous administration of fresh frozen plasma (up to 1 liter per day), polyglucin, rheopolyglucin, administration of saline solutions (acesol, disol), detoxification blood substitutes - hemodez, neohemodez, neocompensan. The sorbent – enterodesis – is applied orally.

Extracorporeal detoxification during this period is represented by plasmapheresis with the extraction of up to 1.5 liters of plasma.

II period. Infusion-transfusion therapy (volume of at least 2000 ml per day, transfusion media includes fresh frozen plasma 500-700 ml, 5% glucose with vitamins C and group B up to 1000 ml, albumin 5%-10% - 200 ml, 4% sodium bicarbonate solution - 400 ml, glucose-novocaine mixture 400 ml). The composition of transfusion media and the volume of infusions are adjusted depending on daily diuresis, acid-base balance data, degree of intoxication, and surgical procedures performed. Strict recording of the amount of urine excreted; if necessary, catheterization of the bladder.

Plasmapheresis is indicated for all patients who have obvious signs of intoxication, compression lasting more than 4 hours, and pronounced local changes in the injured limb (regardless of the area of compression).

Hyperbaric oxygenation sessions – 1-2 times a day to reduce the degree of tissue hypoxia.

Drug therapy: stimulation of diuresis by prescribing Lasix up to 80 mg per day and aminophylline 2.4% - 10 ml; heparin 2.5 thousand under the skin of the abdomen 4 times a day; chimes or trental for the purpose of disaggregation; retabolil 1.0 once every 4 days to enhance protein metabolism; cardiovascular drugs according to indications; antibiotics.

The choice of surgical tactics depends on the condition and degree of ischemia of the injured limb. Carrying out osteosynthesis is possible only after restoration of normal microcirculation, i.e. should be delayed.

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Long-term compartment syndrome(SDS) occurs in cases where the limbs or torso are pressed down for a long time (more than 2 hours) by some kind of weight (stones, earth).

In 80% of cases, the limbs are compressed, mainly the lower ones. In almost half of the victims, prolonged compartment syndrome is combined with fractures of the limbs and damage to other parts of the body. With compression of the chest, abdomen, face and head, if this does not lead to immediate death due to acute asphyxia, life can be preserved for a short time; with compression of the limbs - for several hours or more.

As a result of prolonged compression of the soft tissues of the limbs and cessation of blood flow, profound necrobiotic changes develop in the muscles, tissue and skin, up to complete necrosis of the limb. With prolonged exposure to rubble, even rigor mortis of the muscles of the limbs can occur. The development of deep necrobiotic changes in the muscles, accompanied by the release of myoglobin and other toxic products into the blood, is the cause of severe toxic shock. Subsequently, myoglobin settles in the renal tubules, which leads to their final blockade and severe renal failure. Victims die from shock in the early stages after injury, and from renal failure within the first 7-10 days. The severity of the manifestation of SDS depends on the amount of compression: compression of the distal parts of the limbs with a small number of muscles is not accompanied by such severe intoxication as compression of the thigh and lower leg, and can only result in amputation without the development of renal failure. Combined injuries are relatively rarely observed, most often when buildings collapse during a fire.

With prolonged compression syndrome, the limb is cold to the touch, the skin is raw, with hematomas and imbibition of blood, often with wounds that do not bleed. If there are fractures, there are their characteristic signs. With deep ischemia, there is no movement in the limb, tactile and pain sensitivity is sharply reduced or absent, the pulse in the distal parts of the limb is reduced or not detected. In a later period, swelling of the limb rapidly increases, and unbearable ischemic pain appears. Urine is varnish-red in color due to the admixture of myoglobin and hemoglobin, its amount is reduced.

When compression is released within less than 2 hours from the moment of injury, there are usually no general phenomena, blood flow in the limb is restored, ischemia is observed in the area of individual muscle groups in places of greatest compression.

In the daily practice of trauma departments, patients with long-term compression syndrome are very rare and are victims of industrial injuries - obstructions with earth and stones in trenches, crushing by a car during its repair, if the car falls off the jack, etc. These injuries can be called industrial injuries with a certain stretch , since victims with SDS did this work on their own, without following safety rules. However, in conditions of natural disasters, terrorist attacks and military operations, the SDS can take on the character of a mass catastrophe.

In the domestic literature, the greatest contribution to the development of the problem of long-term compartment syndrome was made by M.V. Kuzin, M.V. Grinev and G.M. Frolov (1994), Yu.V. Groshev et al. (2003), who led the provision of assistance during the catastrophic earthquakes in Ashgabat (1947) and Spitak (1988). A.L. Krichevsky and his school clinically and experimentally studied this syndrome in depth. Research Institute of Emergency Medicine named after. N.V. Sklifosovsky has extensive experience in treating SDS, since after the earthquake in Spitak a visiting team of specialists worked at the source, and then the most seriously injured were transported to Moscow and received further treatment at our institute. The results of this work were summarized by M.V. Zvezdina (1995).

Depending on the area and duration of compression, as well as the force of compression, SDS is classified into mild, moderate and severe. With a mild degree of SDS, the compression period does not exceed 3 hours, the main blood flow of the limb is preserved during compression, and the volume of compression does not exceed the distal segment of the limb. After releasing the compressed part of the limb, there is no decrease in blood pressure, and renal function is slightly impaired in the future.

With a moderate degree of long-term compression syndrome, the lower or upper limb is usually crushed to the middle or upper third of the shoulder or thigh, the compression period is 3-6 hours, the compression force is significant with partial shutdown of the main blood flow. After the limb is released, a drop in SBP to 70-80 mm Hg is observed, and oliguria and other renal dysfunction develop within 1-2 weeks after the injury.

A severe degree of long-term compression syndrome occurs in cases where one or more limbs are completely compressed for more than 6 hours with a complete interruption of the main blood flow. In most cases, these patients die at the scene when the limb is released (tourniquet shock). If first aid is provided correctly and in full, then the victims are in severe shock, they quickly develop acute renal failure with anuria. Compressed limbs are usually non-viable, and to save the life of the victim it is necessary to perform amputations proximal to the border of the compression.

Treatment.

General treatment of long-term compartment syndrome is the prerogative of specialists in intensive care and renal failure and consists of correcting water-salt metabolism, primarily metabolic acidosis and hyperkalemia, maintaining vital functions, and in case of oligo- and anuria - artificial hemodialysis.

The tasks of a traumatologist at the resuscitation stage include surgical treatment of wounds, open fractures, stabilization (immobilization) of fractures, and resolving the issue of amputation and fasciotomy.

Wounds and open fractures are treated according to general surgical rules, without suturing and further wounds are kept open. Immobilization of fractures is performed only extrafocally - on the lower leg and forearm with Ilizarov apparatuses, on the thigh and shoulder - with rod ANF.

If there are clear signs of disruption of the main blood flow of the limb, which is observed in severe DFS, amputation is performed after stabilization of hemodynamics (SBP above 90 mm Hg, pulse below 12 per minute for at least 2 hours). The level of amputation is determined by angiography or by trial incisions, similar to what is done for anaerobic infection. Basically, you have to use the second method, since angiography is not available to most medical institutions, and if it is available, then in conditions of mass admission of victims there is simply no time and energy to perform it. The stump is always left open. If the limb is externally viable in the first period, then massive edema quickly develops, leading to compartment syndrome with the formation of necrosis of muscle tissue in the fascial spaces. The only chance in these cases to save the limb is early fasciotomy.

In the intermediate period of SDS (days 4-20), patients continue to be in the intensive care unit, which has hemodialysis facilities. At the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky, the most seriously injured from Armenia were treated in the laboratory of acute hepatic renal failure. During this period, the greatest risk of acute renal failure is observed with anuria, high levels of urea, creatinine and potassium in the blood plasma. Necrosis of muscle tissue, skin and fiber, suppuration of wounds and open fractures are formed locally. Infectious complications tend to generalize, resulting in sepsis and the formation of purulent foci in places where there are hematomas, crushed and necrotic tissue.

Necrosis in long-term compartment syndrome is distinguished by the fact that, in addition to the skin and fiber, it involves the underlying muscles. Often the focus of skin necrosis can be small, and the muscle is completely necrotic. Muscle necrosis occurs with intact fascia if fasciotomy has not been performed.

When necrosis forms, one should strive for early necrectomy, since necrotic tissue is an additional source of intoxication and contributes to increased renal failure. The optimal time for necrectomy is the first 7 days from the moment of injury. After excision of necrotic skin and tissue tissue, it is necessary to open the fascia and, if there is necrosis of the underlying muscles, excise them. If the muscle is located near the main vessel of the limb, the operation is performed together with an angiosurgeon.

In all cases, one should strive to preserve, if not the entire limb, then perhaps a more distal part of it. After excision, the wounds are kept open in a moist environment using gel dressings. Necrectomy has to be repeated in most patients. After cleaning the wounds and filling them with granulations, autodermoplasty is performed using a split flap. During treatment, contractures in the vicious position should be prevented, for which it is necessary to use Ilizarov apparatuses in most cases. Plaster casts are unsuitable because they exclude access to the wound, quickly become wet with pus and soften.

With the development of sepsis, the tasks of the traumatologist include timely diagnosis and opening of abscesses and phlegmons of the extremities. They form at the site of muscle necrosis, so large incisions are necessary to open the fascia to examine the muscles and remove necrotic areas (or the entire muscle). After this, the wound can be drained with double-lumen drainage from a separate puncture, sutured, and subsequently aspiration-washing treatment according to Kanshin.

With a favorable course, the condition of patients with long-term compartment syndrome gradually stabilizes, the level of creatinine and urea begins to decrease, and urine appears. The restoration of kidney function is preceded by a phase of polyuria, when the victim excretes up to 4-5 liters of low-concentrated urine per day. Once normal or slightly elevated urea and creatinine levels were achieved, the patient was usually transferred to the trauma unit, where the focus was on wound and fracture management and active rehabilitation. Some patients require correction of the deformed position of the limbs, most of them require restoration of movements in the joints, training in self-care techniques and walking.

V.A. Sokolov
Multiple and combined injuries