Emergency pre-hospital care for the syndrome of prolonged squeezing. How to provide first aid to victims of prolonged compression syndrome. The pathogenesis of the syndrome of prolonged compression

Prolonged compression syndrome (SDS) - (synonyms: crush syndrome, traumatic toxicosis, compression injury, crush syndrome - resulting from prolonged circulatory disorders (ischemia) of compressed soft tissues.

The reason is the compression of the limbs, less often the torso by heavy objects, fragments of buildings, rock. It occurs during earthquakes, landslides, as well as in traffic accidents, railway accidents.

Types of compression:
Long crush syndrome- soft tissues are crushed by fragments of buildings, structures, collapsed rock in mines, while there is a violation of skin damage, muscles - torn in places, saturated with blood.
Positional squeeze- compression of soft tissues by the weight of one's own body during a long forced position, accompanied by impaired blood circulation.
The pathogenesis of SDS:
painful irritation, causing a violation of the coordination of excitatory and inhibitory processes in the central nervous system;
traumatic toxemia, due to the absorption of decay products from damaged tissues (muscles) by myoglobin;
plasma loss, which occurs secondarily as a result of massive edema of damaged limbs.

We distinguish 3 periods:
1. Early (1-2 days) - traumatic shock
2. Intermediate (3-10 days) - acute renal failure
3. Late (10 days-2 months) - tissue necrosis, purulent complications
1. In the first period, there is: pain shock, general weakness, pallor of the skin, arterial hypotension and tachycardia.
2. In the intermediate period, it is noted: deep stunning, stupor, urine becomes brown, oligoanuria progresses, infectious complications develop.
3. In the late period, there is a gradual restoration of the function of damaged organs (kidneys, liver, lungs, etc.).

Clinic:

The damaged limb has a bluish tint, enlarged, edematous;
There are many abrasions, bruises, blisters containing fluid on the skin;
Immediately after removing the victim, you can see irregularities - "imprints" of the injured object;
Crushed muscles soaked in blood, torn in places. In the zone of necrosis, the muscles look like boiled meat;
All types of sensitivity are weakly expressed or absent. There is no pulse at the periphery of the limb.

First aid
1. Mandatory application of a tourniquet above the level of compression.
2. Release of the victim.
3. Then a quick tight bandage of the limb with an elastic or regular bandage, after which the tourniquet is removed.
4. Cold (ice wrapping) on the damaged area.
5. Immobilization of a limb in case of a suspected fracture using Kramer splints, vacuum splints. Pre-medical assistance can be actively used by any improvised means. The material for the tire can be a rolled up newspaper, a magazine, a piece of wood, plywood, etc. Place the splint in the same position on the broken limb as it is.
6. Treatment of wounds (using hydrogen peroxide) and the application of an aseptic bandage on abrasions, wounds, if any.
7. Anesthesia (promedol, morphine or analgin with diphenhydramine intramuscularly) or any painkillers antispasmodics (no-shpa, ketanal, analgin) before the arrival of a medical worker. Before the introduction of painkillers, it is necessary to clarify the allergic history.
8. Anti-shock measures (in / in infusion, hormones).
9. Abundant drinking in the absence of damage to the abdominal organs.
10. Oxygen therapy (access to fresh air, oxygen).
11. Transportation to a medical institution on a stretcher in the supine position.

Prolonged Compression Syndrome (SDS)- one of the most severe types of injuries that occur during various catastrophes and natural disasters as a result of blockages, destruction of buildings, landslides. It is known that after the atomic explosion over Nagasaki, about 20% of the victims had more or less pronounced clinical signs of the syndrome of prolonged compression or crushing. The development of a syndrome similar to the compression syndrome is observed after the removal of the tourniquet, imposed for a long time. This condition is called crash syndrome or prolonged compression syndrome.

When reading a large amount of educational literature, I noticed that a tourniquet or a twist (analogue of a tourniquet) is mentioned everywhere. I still don't recommend using a harness. Here is what our paramedic Elena Bednarskaya, who has extensive work experience, writes; and understanding all the difficulties of working with a tourniquet, for an unprepared person, or, even worse, thinking that he is already prepared for sure, but in fact - he just read the information on the Internet.

Note “Safety of Life. Territory of Russia.

Due to the fact that evil spirits attack and bomb exclusively residential buildings, people can be under the rubble. If a person is under a blockage, then the syndrome of prolonged compression is inevitable. This syndrome is considered one of the most severe types of injuries, it can also be complicated by fractures, bleeding, TBI (traumatic brain injury), and other "joys". Signs of the syndrome of prolonged compression: the injured limb swells strongly, has an atypical luster for healthy, cyanotic, cold to the touch, the skin may be covered with blisters, with prolonged compression the skin turns black. What to do if you find a person in the rubble? Firstly, the minimum number of people who can provide PHC (first aid) is two. Why two?! The algorithm for providing PMP in case of prolonged compression syndrome involves working in pairs. The algorithm itself is:

First aid is provided at the scene. Elimination of pain, reduction of psycho-emotional stress in victims in the focus of a disaster should be carried out as soon as possible, even before they are released from the squeezing factor. For the purpose of anesthesia, a 2% -1.0 solution of promedol, 50% - 2.0 analgin, sedatives are administered. In the absence of signs of damage to the abdominal organs, 40-70% alcohol is allowed to drink. The release of the victim, if possible, begins with the head, torso. At the same time, they fight against asphyxia (giving a comfortable position, cleaning the upper respiratory tract, artificial ventilation of the lungs). Take measures to stop external bleeding.

1. do not sharply raise the object, causing compression, raise its part and quickly bandage the limb with an elastic bandage, namely elastic, if not at all, only then with gauze, but this is much worse, i.e. the task is to release the limb in parts and, at the time of release, quickly bandage it. Why exactly? When squeezed, a huge amount of toxins accumulate in damaged tissues, blood supply is disturbed, etc. The object was abruptly removed: all these toxins flow into the muscles, shock develops just before our eyes, so correct and quick bandaging can save the victim.

2. apply cold to the injured limb, just bottles of cold water will do;

3. put soft under the limb(clothing, blanket, etc.);

4. during transportation, we look after the condition of the victim;

5. if the stomach is "soft", ie. there is no damage to the internal organs, we give the victim a plentiful warm drink with the addition of baking soda - this will save his kidneys. What is the difference between a soft belly and a hard belly? You just need to feel the stomach, if there are injuries to the internal organs, then the stomach will be very hard.

Experience shows that some can save their lives even after squeezing body parts for several days, while others die after a few hours.

After the release of the victim from under the rubble, it is necessary to determine the degree of violation of the blood supply to the tissues, on which the correctness of further actions to provide medical care depends. This is easy to do if you know the signs of the four degrees of ischemia.

First degree- compensated ischemia, which, despite prolonged compression, did not lead to impaired blood circulation and metabolism in the compressed limb. With such ischemia, active movements are preserved, i.e. the victim can independently move his fingers and other parts of the squeezed limb. There is tactile (the sense of touch) and pain sensitivity. We use elastic bandages.

Second degree- uncompensated ischemia. With such ischemia, tactile and pain sensitivity is not determined, there are no active movements, but passive ones are free, i.e. it is possible to bend and unbend the fingers and other parts of the injured limb with light efforts of the assisting hand. There is no rigor mortis of the muscles of the compressed limb. We use elastic bandages.

Third degree- irreversible ischemia. Tactile and pain sensitivity is also absent. The main symptom appears - the loss of passive movements, rigor mortis of the muscles of the compressed limb is noted. With such ischemia, the tourniquet cannot be removed.

fourth degree- necrosis (necrosis) of muscles and other tissues, which ends in gangrene. In this case, the tourniquet should not be removed either.

After the issue with the tourniquet is resolved, it is necessary to apply aseptic dressings to the existing wounds and immobilize the limb using standard splints or improvised material. If possible, cover the injured limb with ice packs or heating pads with cold water, warm the victim and give him an alkaline drink. After providing first aid, it is necessary to take all measures for the fastest evacuation of the victim to a medical institution. It is better to transport him lying on a stretcher, preferably accompanied by a medical worker.

REMEMBER! If within 15-20 minutes it was not possible to release the crushed limbs, then any attempts to release should be stopped and the rescue services should arrive.

REMEMBER! Before the arrival of rescuers and Ambulance, the limbs should be covered with ice or snow packs, tightly bandaged (if they have access) and provided with plenty of warm drinks.

IN NO EVENT IS IMPOSSIBLE!

Release pinched limbs

after 15-20 minutes after their compression

without the participation of rescue services.

UNACCEPTABLE!

Release the squeezed limb before applying protective tourniquets

and administering large amounts of fluid to the victim.

Warm crushed limbs.

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Syndrome of prolonged compression- symptoms and treatment

What is Prolonged Compression Syndrome? We will analyze the causes of occurrence, diagnosis and methods of treatment in the article of Dr. V. A. Nikolenko, a traumatologist with an experience of 10 years.

Definition of disease. Causes of the disease

Syndrome of long-term compression(crash syndrome, SDS) is a life-threatening condition that occurs due to prolonged compression of any part of the body and its subsequent release, causing traumatic shock and often leading to death.

Two conditions contribute to the occurrence of this syndrome:

These factors lead to the fact that after the release of the compressed part of the body, the injury goes beyond the damage and the local traumatic reaction.

In the compression zone, toxic products (free myoglobin, creatinine, potassium, phosphorus) are formed, which are not “washed out” by the liquid accumulated due to a mechanical obstacle to the circulation of its current. In this regard, after the elimination of the cause of compression, a systemic reaction of the body occurs - the products of destroyed tissues enter the bloodstream. So there is a poisoning of the body - toxemia.

A special form of crash syndrome is positional compression syndrome (SPS). In this situation, there is no traumatic factor from the outside, however, tissue compression arises from an unnatural and prolonged position of the body. Most often, SPS is characteristic of a person in a state of extreme intoxication: depression of consciousness and pain sensitivity, combined with a long immobile position, lead to critical ischemia (a decrease in blood supply in a separate part of the body). This does not mean at all that for positional compression a person must “rest” an arm or leg for hours. Tissue necrosis can be caused by maximum joint flexion, which is sufficiently long in time, which leads to squeezing of the vascular bundle and disruption of tissue blood supply. Concomitant shifts in homeostasis (self-regulation of the body), characteristic of the biochemistry of intoxication, accompany the described positional syndrome.

Positional compression differs from true SDS by the rate of increase in toxemia and a rare frequency of irreversible organ damage.

Private and least destructive is neurological symptom. It occurs quite rarely and is a separate component of the crash syndrome. This symptom manifests itself in the form of damage or malfunction of a particular nerve (neuropathy). At the same time, there is no background chronic neurological disease or the fact of injury. This state is reversible.

If you experience similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

Symptoms of the syndrome of prolonged compression

The symptoms of crush syndrome are extensive and varied. It consists of local (local) and general manifestations, any of which in itself is a severe injury.

During the initial examination of the patient, local symptoms may be misinterpreted due to the non-obviousness of damage: the affected tissues in the early stages look healthier than they really are. Necrotic (dying) zones clearly appear only after a few days, and their demarcation can continue in the future.

The scale of local disturbances becomes apparent already at the stage of complications addition. This fact requires a special tactic from the surgeon - the implementation of a secondary revision (examination) of the victim.

Local symptoms are primarily represented by injuries encountered in everyday life, but their massiveness is more significant. SDS is characterized by combined and combined injuries, polytrauma. These include open and closed fractures, extensive wounds, skin detachments with fiber, crush injuries, traumatic limb amputations, torsion injuries (turning the bone around its axis).

With a crash syndrome, large areas of destruction (destruction), organ-destroying and irreversible injuries occur. In addition to skeletal injury and soft tissue injury, SDS is often accompanied by neurotrauma (damage to the nervous system), thoracic (chest injury), and abdominal (intra-abdominal) injuries. The condition of the victim can be aggravated by ongoing bleeding at the scene and infectious complications that arose earlier.

Local damage triggers such a general process as shock. Its appearance in SDS is due to multiple injuries, prolonged pain impulses, and a lack of blood supply to the compressed body segment.

Shock in crush syndrome is multicomponent: the mechanism of prolonged compression leads to the development of such types of stress in the body as hypovolemic (decrease in circulating blood volume), infectious-toxic and traumatic. Especially dangerous in SDS are the toxic components of shock, which are characterized by suddenness: after the release of the compressed part of the body, they immediately enter the bloodstream in large quantities. The combination of severe local damage and the toxic effect of one's own tissues determines the course of the disease and can lead to a fatal outcome.

The pathogenesis of the syndrome of prolonged compression

The human body has compensatory possibilities- the reaction of the body to damage, in which the functions of the affected area of the body are carried out by another organ. Against the background of a long stay of a person in conditions hypovolemia(decrease in the volume of circulating blood), intense pain, forced position and concomitant injuries of internal organs, such abilities of the body are at the limit or completely dry out.

Violation of the volume of erythrocytes in the blood and the flow of plasma into the interstitial space causes ischemia, slowing blood flow and increasing capillary permeability. The perspiration of plasma into the tissues and interstitial space also leads to the accumulation of myoglobin (a protein that creates oxygen stores in the muscles). The fall in blood pressure maintains hypoperfusion (insufficient blood supply), plasma loss, and increased tissue edema.

During the entire time of compression, the decay products of tissues entering the blood affect the kidneys. After the release of the victim, there is a sharp increase in the release of toxic substances and a massive "washout" of tissue detritus (destroyed cells) into the bloodstream. Released from block-compression, the blood flow resumes, inevitably filling the circulating blood volume with autotoxins that have arisen. This leads to the appearance acute renal failure, resulting in immediate autoimmune reactions: temperature crises, generalized violations of humoral regulation (metabolic processes).

Renal failure develops due to the blockage of the kidney tubules by myoglobin of destroyed muscles and the cessation of the vital process of reabsorption (reabsorption of water). This is greatly exacerbated by ionic disturbances. The decay products of tissues, additionally entering the blood, uncontrollably affect the diameter of the lumen of blood vessels. As a result, the vessels narrow, including in the filtration glomeruli of the kidneys, which leads to thrombosis and complete cessation of filtration.

Due to acute renal failure, the resulting decompensation is exacerbated by increasing ion imbalance (hyperkalemia). This leads to gross violations of the body's self-regulation and "acidification" of the internal environment - acidosis.

The phenomenon of mutual burdening (hypovolemia + pain impulses + toxemia) is now unfolding in full. Symptoms become maximally pronounced, cascading and growing, and the probability of their elimination by the forces of the body is impossible.

The described disorders are accompanied by a collapse of hemodynamics (blood flow through the vessels) due to blood loss and reflex hypotension (lowering blood pressure). This leads to a stepwise increase in severity and the formation of a vicious circle. It is possible to interrupt the pathological processes in the syndrome of prolonged compression only by medical intervention - timely, coordinated and competent.

Classification and stages of development of the syndrome of prolonged compression

The classification of the crush syndrome is based on the severity of the clinical manifestation, which depends on the area and duration of compression.

VTS Forms:

Due to the knowledge of the pathogenesis of the crash syndrome and the prognosis of each form of DFS, this classification is generally accepted and has remained unchanged for a long time. And although it is rather simplified, and it does not take into account the details of local injuries, this systematization proves its importance in the distribution of patient flows in a disaster, thereby increasing the efficiency of medical care.

by the predominant clinical component of shock;
according to the picture of toxinemia;
according to the ratio of local injuries, injuries of internal organs and the severity of the toxic-shockogenic component.

However, these scales are of little use for a quick assessment of the condition of patients, as they slow down the provision of assistance by conducting laboratory and instrumental studies.

Before diagnosing and analyzing the clinical picture, it is important to assess which stage a particular DFS belongs to:

Early period- lasts less than three days from the moment the patient is removed from under the squeezing objects. This stage is characterized by the development of complications characteristic of shock, with the addition of acute renal failure.
Interim period- lasts 3-12 days. The clinic of acute renal failure unfolds completely, reaching the terminal stage. The overall clinical picture is expressed by clear zones of demarcation and the extent of damage.
Late period- lasts from 12 days to 1-2 months. It is a period of reparation (recovery): there were no violations of vital functions, the body mobilizes compensatory capabilities. The duration of the period up to two months is conditional - the duration depends on which structures and how seriously affected, as well as how adequate treatment is provided.

Complications of the syndrome of prolonged compression

The severity of the crash syndrome and the likelihood of its outcome depend on the complications that have arisen. The main complications of SDS include:

The chronology of complications plays a leading role in the syndrome of prolonged compression, explaining many clinical patterns.

Due to the severity of the damage, favorable ground arises for the development of the problems of "intensive separation":

distress syndrome (respiratory failure);
fatty, air and thromboembolism (blockages);
syndrome of disseminated intravascular coagulation;
nosocomial pneumonia.

These complications do not always occur with SDS, but their manifestation often causes the death of a large percentage of victims.

Also, with SDS, local complications of wounds occur:

wound infection with the addition of anaerobic flora;
destruction (destruction) of the anatomical structure: severe and poorly drained extensively scalped wounds, multiple "pockets", detachments, ischemic foci.

The local status of wounds in the syndrome of prolonged compression always causes concern and is unfavorable in terms of prognosis, even with the condition of full and timely surgical treatment. Healing of wounds, open fractures, injuries of internal organs proceeds with significant difficulties due to concomitant shock. The phenomenon of mutual burdening is pronounced.

Diagnosis of the syndrome of prolonged compression

The diagnosis of SDS is complex, that is, it can be established by adding and combining the components of the injury, taking into account its mechanism. Diagnostics of the crash syndrome is preventive - it has a warning character. The doctor, taking into account the circumstances and conditions of the injury, determines DFS as the expected diagnosis.

Despite the severity and variety of clinical manifestations, DFS can present a challenge for many experienced professionals. This is due to the rare occurrence of the syndrome in peacetime.

Diagnosis is greatly hampered if the history of injury is unknown. In this case, the only correct tactical decision of the surgeon is a cautious approach. It manifests itself in the assumption of SDS in the absence of contact with the patient, with polytrauma of unclear prescription, pronounced segmental damage with a compressive nature of the injury. Infected wounds, signs of compression of the extremities, discrepancy between the local manifestations of the injury and the general condition of the patient may also indicate the likelihood of a crash syndrome.

To detail the diagnosis, generally accepted research schemes are used: clarification of complaints, anamnesis, mechanism of injury, emphasis on the duration of compression and measures preceding release from compression.

When collecting a life history, attention is paid to past kidney diseases: glomerulonephritis, pyelonephritis, chronic renal failure, as well as nephrectomy (removal of a kidney or part of it).

When assessing the objective status, a close examination of the patient is shown in order to assess the massiveness of the damage. Clear consciousness, the insignificance of complaints, the patient's active position should not mislead the doctor, since it is possible that the examination is carried out during the "light" period, when the body is subcompensated, and symptoms do not appear.

Objective parameters are assessed: arterial and central venous pressure, heart rate, respiratory rate, saturation, diuresis (urine volume). Laboratory screening is underway.

The parameters of biochemical analyzes, "renal" markers are indicative: the concentration of creatinine, blood urea, creatinine clearance. Ionic blood shifts will become early informative indicators.

Revision of wounds and injuries as a result of tissue compression is performed primarily. It is a therapeutic and diagnostic manipulation that allows you to clarify the depth and extent of tissue destruction.

In order to exclude specialized injuries, narrow specialists are involved: urologists, neurosurgeons, abdominal surgeons, gynecologists.

X-ray, computed tomography and magnetic resonance imaging (optional) are also used for diagnosis. Patients are subject to continuous monitoring, even if their condition was stable at the time of admission.

Treatment of the syndrome of prolonged compression

Fundamental points in the treatment of crush syndrome are associated with the release and evacuation of the victim. The correctness of the actions of the doctor at the scene of the incident largely determines the success of inpatient treatment.

The preliminary and most effective care depends on the stage of DFS. And although the general therapy of crush syndrome is complex, the priority method of treatment also depends on the stage of this condition.

Immediately after detection, the victim is administered analgesics, including narcotic, antihistamine, sedative and vascular drugs proximal, that is, closer to the area of compression of the limb, and a tourniquet is applied. Without removing the tourniquet, the damaged segment is bandaged with an elastic bandage, immobilized and cooled. After completing this initial medical treatment, the tourniquet can be removed.

Then the toilet of wounds is carried out, aseptic dressings are applied. Permanent venous access (peripheral) is being established, infusions of solutions are carried out. Against the background of ongoing analgesia (removal of pain symptoms), the patient is transported to the hospital under the control of hemodynamic parameters (blood flow through the vessels). Effective treatment in the intensive care unit. Puncture and catheterization of the central vein, continuation of infusion-transfusion therapy (introduction of the necessary biochemical fluids) with transfusion of fresh frozen plasma, crystalloid and high-molecular solutions are shown. Plasmapheresis, hemodialysis (blood cleansing outside the body), oxygen therapy, hyperbaric oxygenation (high pressure oxygen treatment) are performed.

Based on the indications, symptomatic treatment is also carried out. Produce continuous monitoring of diuresis, heart rate, pulse, central venous pressure. Control the ionic composition of the blood.

The effectiveness of general measures directly depends on local surgical treatment. There are no universal schemes for the treatment of wounds and the management of the victim. Active prevention of compartment syndrome (edema and muscle compression in fascial sheaths) is performed, including early subcutaneous fasciotomy.

Assessing the viability of tissues during primary surgical treatment can be difficult: the lack of differentiation between healthy and damaged areas, borderline and mosaic perfusion disorders (bleeding through the tissues of the body) keep surgeons from radical actions.

In case of doubt, amputation of the limb is indicated with dissection of most fascial cases, additional accesses for adequate examination, drainage, delayed suturing or wound plugging.

The clinic of local injuries is scarce in the initial period of SDS. Therefore, there is a need for a secondary examination of the wound or revision of the limb after 24-28 hours. Such a tactic allows you to sanitize (clean) the resulting foci of necrosis against the background of secondary thrombosis of the capillaries, assess the viability of tissues and the segment as a whole, and correct the surgical plan.

Forecast. Prevention

The prognosis of SDS depends on the duration of compression and the area of compressed tissues. The number of deaths and the percentage of disability is predictably reduced depending on the quality of medical care, the experience of the surgical team, the equipment of the hospital and the capacity of the intensive care unit.

Knowledge of the pathogenesis and stages of the crush syndrome allows the doctor to choose a priority treatment method according to the situation. In a significant number of cases, with the exception of severe forms of the syndrome, this leads to functionally favorable outcomes.

Syndrome of prolonged compression (synonyms: crash syndrome, traumatic toxicosis, compression injury, crush syndrome, Bywaters syndrome) is a complex of specific symptoms resulting from the release of long-term crushed limbs. The essence of pathogenesis lies in a sharp surge in the general bloodstream of toxic elements accumulated below the squeezed area due to trophic insufficiency.

The mechanism of development of the syndrome of prolonged compression

The syndrome of prolonged compression is most common during times of war and natural disasters, when people, falling under the rubble of technical structures, are forced to wait for rescue for a long time. Often in these cases, some of the limbs are in a pressed state by separate structures, which causes the development of the pathological process.

The syndrome was first noticed by field surgeons during the First World War. When the legs of the officer, who had been waiting for rescue for a day, were released, he died within a few minutes.

The pathogenesis of the syndrome of prolonged compression is based on the compression effect on the nerve trunks and blood vessels of the limb.

The primary factor in triggering pathological processes is severe pain, in an attempt to defend against which the central nervous system blocks a large innervation in the pinched limb.

next step there will be ischemic phenomena in the area below the area of compression exposure. Reserve nutrients deposited in the muscles quickly run out, and fresh ones are not supplied with blood. In addition, due to the lack of blood circulation, its thickening and, as a result, clotting increases. Such a process is called plasma loss.

The subsequent reaction of the body will be the deposition of the total volume of blood circulating in the body, due to the lack of its need for a squeezed area. The higher to the center of the body is the area of compression, the greater the volume of blood accumulates in the liver and other organs that serve to store reserve blood volumes.

By the way, the total volume of circulating blood in an adult male decreases by 2-3 liters when squeezing one thoracic limb above the elbow joint and by 3-5 liters when squeezing the pelvic limb above the knee.

It is worth noting that the liquid part of the blood, plasma, is deposited mainly. The concentration of blood cells remains in a slightly changed state, which also causes blood clotting throughout the body. Total plasma loss is always tolerated by the body much harder than classical blood loss.

An important role in the development of the syndrome is played by general intoxication with metabolic products formed in the muscle tissues of the compressed area, i.e. toxemia. Venous stasis below the compression effect contributes to the accumulation of carbon dioxide and other metabolic products of muscle cells. When a limb is released, this toxic mass instantly enters the general bloodstream and triggers toxemic phenomena.

The strongest toxic effect has an increased content of potassium and muscle protein - myoglobin, which leads to blockage of the renal tubular system, and in the future - acute renal failure.
Large concentrations of carbon dioxide cause a decrease in the number of free erythrocytes capable of attaching oxygen, thereby providing respiratory dysfunction of the blood and general acidosis .
Degradation products such as biogenic amines and vasoactive polypeptides, the concentration of which increases in the general bloodstream, due to necrotic tissue processes at the site of compression, cause active autoimmune processes leading to severe allergic manifestations.
Renal failure, acidosis, autoimmune reactions, general tissue hypoxia lead to imbalance of the intestinal wall , thereby increasing its permeability, and dysfunctions of the protective barrier that keeps the pathological and toxic effects of microflora and digestive products located in the lumen of the intestinal tube.
Intestinal toxins and microflora , freely penetrating into the portal system of the liver, cause blocking of its antitoxic properties by suppressing mononuclear phagocytes - the most active cells that absorb toxic decay products.

Thus, the general intoxication of the body begins to reach its limits, causing a state close to coma with subsequent death. final touch leading to cardiac arrest and respiratory activity due to pathological effects on the central nervous system, is a sharp drop in blood pressure due to the appearance of vasopressor factors in the blood plasma and mass death of red blood cells.

The clinical picture of the syndrome of prolonged compression

The severity of the syndrome and subsequent complications depend on the adjacent traumatic factors obtained during the tragedy, as well as on the time of compression, its depth and area of compression.

There are several forms of compression, depending on the time of its impact.

Light form - squeezing for a period of no more 4 hours.
Middle form - up to 6 hours.
Severe form - up to 8 hours.
Extremely severe form more than 8 hours on one limb, up to 6 hours when squeezing two limbs, or up to 4 hours on three or more limbs.

Severe and extremely severe forms are characterized by a sudden lethal outcome when released without taking the necessary measures to save.

In other cases, the further course of the pathological condition is conditionally divided into three periods

Initial period

It is caused by focal changes in the place of compression and nearby tissues.
In addition, signs of endogenous intoxication begin to develop.
The duration of the period is 2-3 days after release.

As a rule, during the first few hours, the state of health and behavior of the victims does not cause concern, provided there are no serious associated injuries. Then the first visible disturbances begin to appear in the segment below the compression area - the skin becomes rough to the touch, its elasticity is lost. In the subcutaneous tissue, focal redness is formed, gradually flowing into generalized cyanosis. In a short period of time, swelling of the segment develops, the pulsation of the blood vessels is palpated weakly or is not detected at all.

In parallel with organic changes, emotional instability begins to develop, caused by traumatic shock and awareness of reality. Often, against this background, there are signs of acute heart failure and general pain syndrome.

The early stages of thrombohemorrhagic syndrome are launched.

Increasing the concentration of fibrinogen.
Immunity of blood plasma to heparin.

In addition, the number of white blood cells and the total volume of circulating blood are reduced - plasma loss. The density of urine increases, blood and protein appear in it.

Second Interim Period

The duration of the intermediate period is from 3 to 12 days, against the background of acute renal failure.

Puffiness increases injured limb segment.
appear on the skin large blisters with clear or hemorrhagic contents.
Begins generalized necrosis the entire injured limb.

In the blood, the number of red blood cells decreases due to their massive destruction, the daily urine output decreases, up to its complete absence, and the amount of potassium, residual nitrogen, and creatinine also increases. The general condition of the patient deteriorates sharply.

The overall body temperature rises.
The effects of lethargy, drowsiness and emotional dullness increase.
These symptoms occur against the general background of constant vomiting and thirst.
Mortality in this period, even taking into account intensive care, is about 35%.

The third period is recovery

It begins about a month after the exclusion of compression. It is characterized by the restoration of renal activity and the psychological state of the patient. The latter directly depends on the prognosis for the preservation of the damaged part of the limb, which, as a rule, is already known by this time.

Infectious lesions on the skin and tissues of the affected segment due to open wounds, including surgical ones, come to the fore.
Depending on the area of damage and the general state of the patient's immunity, sepsis may develop with characteristic clinical symptoms.
Soreness and swelling of the affected segments usually disappear.
As for anemia, low blood protein and, they have a very pronounced persistence and tend to change only after a month of hard work of specialists.

Reduced immunity and reduced bactericidal activity of the blood does not change its pathological conditions for several months after the injury.

A characteristic feature in the syndrome of prolonged compression is extensive blood contamination with bacteria such as:

clostridia;
enterobacteria;
anaerobic cocci.

That is, these are microorganisms that abundantly saturate the soil and enter the wounds due to their abundant contamination. Preventive measures against clostridial myonecrosis can be carried out for a month or more, due to the general weakness of the body's defenses and the resistance of microbes to therapeutic regimens.

What first aid should be provided to a person with suspected prolonged compression syndrome?

To reduce lethal risks due to the complex pathogenesis of the syndrome of prolonged compression, it is necessary to observe a number of measures that limit or prevent the development of pathological processes in the future. Based on this, the first medical aid provided at the scene of an accident plays an extremely important role and is carried out in a certain sequence.

First of all, before releasing the limb be sure to tightly apply a tourniquet in the area above the place of compression. This achieves minimal penetration into the blood of toxic elements that have arisen in the damaged segment immediately after release.
After that, the limb is released and tightly bandaged, the tourniquet is removed, a loading dose of painkillers is injected, usually of central action. Often, for these purposes, a case novocaine blockade is used above the compression area.
Also at the scene carry out mechanical cleaning of open wound surfaces apply antiseptic and dehydrating dressings.
Continue during the evacuation administration of painkillers and sedatives, carry out infusion therapy in combination with antibiotics.
Transportation should provide complete immobilization of the patient, especially his injured limb.

General treatment regimen and possible consequences of the syndrome

During the period of inpatient treatment, intensive anti-shock and therapeutic measures supporting blood purification are carried out. Large daily volumes of transfusion agents are widely used for these purposes - about 2000-4000 ml of intravenous infusions, the dosages of which are regulated hourly, depending on the indicators of daily diuresis and the state of homeostasis. The basis of transfusion intensive therapy is artificial blood plasma, physiological saline in combination with a set of necessary salts, as well as glucose in combination with vitamin and protein therapy.

It is obligatory to stimulate the formation of urine and reduce blood clotting, for which diuretics and drugs of the heparin group are used, respectively. The volume of urine excreted should be at least 30 ml per hour, which provides additional blood purification in a physiological way.

As a conservative therapy, drugs are used that support the functionality of the cardiovascular system and the level of the body's immune forces.

In the absence of the proper therapeutic effect, which occurs very often with extensive lesions of the limbs, a number of complex measures aimed at cleaning the blood of toxins are shown within 8-12 hours after the imputation of the scheme.

Plasmapheresis.
Cytapheresis.
Hyperbaric oxygenation to saturate tissues with oxygen.

If previous measures do not improve the condition, and the damaged segment of the limb is subjected to more and more extensive and deep necrotic processes, amputation of the limb is indicated with maximum economy of living areas.

Often, the separation of the damaged area is carried out in cases of massive additional damage in the form of crushed bone fractures, as well as ruptures and detachments of the muscle mass. That is, when the specialist comes to the conclusion that attempts at a therapeutic cure will not lead to a favorable prognosis.

As a rule, the completion of the intermediate stage of the pathogenesis of the syndrome of prolonged compression symbolizes a favorable prognosis in the subsequent periods of treatment and the post-hospital period.(No ratings yet)

Ksenia Skrypnik about the syndrome of prolonged compression, which occurs in victims during hostilities, during landslides, earthquakes, terrorist attacks, road accidents

The syndrome was first isolated as a separate disease in 1941 by the English physician Eric Bywaters, who treated people affected by the bombings in London during World War II. In patients who spent a long time under the rubble with compressed limbs, a special form of shock was observed. The peculiarity was that with not too severe injuries (internal organs in such patients, as a rule, were not injured), after a complex of therapeutic measures, the condition of the patients improved significantly, but then a sharp deterioration occurred. Most patients developed acute renal failure and soon died. There are several options for the names of this syndrome: compartment syndrome, compression injury, crash syndrome (from the English crush - “crushing, crushing”), traumatic toxicosis.

Bywaters was able to identify three successive stages leading to the development of the crash syndrome:

compression of the limb and subsequent tissue necrosis;
development of edema at the site of compression;
development of acute renal failure and ischemic toxicosis.

Pathogenesis

Bywaters syndrome occurs as a result of compression of the limb, damage to the main vessels and main nerves. Such an injury occurs in approximately 30% of people affected by natural or man-made disasters.

In the pathogenesis of this disease, three factors play a leading role: regulatory, associated with pain effects on the body, significant plasma loss, and, finally, tissue toxemia. It should be noted that such factors are observed to one degree or another in almost any injury, but with a crash syndrome they manifest themselves especially clearly. Each of these factors contributes to the clinical picture of the syndrome of prolonged compression.

Pain impact affects the person who has fallen under the rubble most strongly. There is a reflex spasm of the vessels of peripheral organs and tissues, which leads to disruption of gas exchange and subsequent tissue hypoxia. Vascular spasm and developing hypoxia cause dystrophic changes in the epithelium of the renal convoluted tubules, and glomerular filtration decreases significantly.

Plasma loss develops soon after injury and even after the cause of compression is eliminated.

Plasma loss is associated with an increase in capillary permeability against the background of injury, which leads to the release of blood plasma from the bloodstream.

The volume of circulating blood decreases, the viscosity increases, the transport of oxygen becomes more difficult. At the site of injury, edema develops, numerous hemorrhages, the outflow of blood from the squeezed limb is disturbed, since the edematous fluid leads to a narrowing of the lumen of the blood vessels up to their complete blockage. As a result, ischemia of the limb develops, the products of cellular metabolism intensively accumulate in the tissues, the amount of myoglobin, creatinine, potassium and calcium ions increases. An increase in the concentration of myoglobin in the circulating blood, developing metabolic acidosis have a detrimental effect on the functioning of the renal tubules. exacerbate toxemia and other protein factors that accumulate as a result of compression of the limb and damage to muscle tissue. After the restoration of blood circulation, they "in one gulp" begin to flow into the vascular bed. At this point, a number of symptoms characteristic of ischemic toxicosis appear.

Intoxication of the body is expressed the stronger, the greater the mass of compressed tissues and the duration of the compression effect.

The severity of the crash syndrome

Depending on the amount of damage and the duration of compression, there are 4 degrees of severity of the syndrome.

Light degree- compression of a small segment of the limb for no more than two hours. In this case, toxemia is mild, although acute renal failure and hemodynamic disturbances are noted. In most cases, with timely therapy, improvement occurs within a week.

Average degree occurs when the entire limb is compressed for four hours. This condition is characterized by intoxication, myoglobinuria and oliguria.

Prolonged compression of the limbs (4-7 hours) leads to the manifestation of symptoms characteristic of severe Bywaters syndrome. Significant hemodynamic disturbances are noted, symptoms of intoxication are expressed, acute renal failure develops rapidly.

Untimely and incorrect provision of medical care in most cases leads to death.

It is also important to act correctly and quickly if the patient is diagnosed with extremely severe degree crash syndrome. Such a diagnosis is made with compression of the lower extremities for 8 hours or more. Developing ischemic toxicosis will be detrimental to the patient soon after decompression. The mortality of such patients is extremely high even with timely treatment.

Treatment

The choice of approach to treatment begins with an assessment of the degree of compression and the duration of compression of the extremities. For professionals involved in rescue operations, it is important to try to release the maximum number of victims in the first two hours after the occurrence of an emergency. It is in this case that the prognosis will be favorable for most patients.

During the earthquake in Marmara (Turkey), which occurred in 1999, many children were affected. At that time, enormous experience was accumulated in eliminating the consequences of compression injury in young patients. The specificity of the treatment of Bywaters syndrome in children is due to the fact that their injuries are often much more severe than in adults.

It is more difficult to communicate with children during the rescue operation, so they often spend more time under the rubble than adults. The child's body is more susceptible to hypothermia and fluid loss, so special attention should be paid to rehydration immediately after the rescue of the child.

Regardless of the severity and age of the patient, anti-shock measures are taken: analgesics, cardiovascular drugs are administered to normalize blood pressure. In most cases, this is done even before the victim is removed from the rubble.

Treatment, begun even before the removal of the press, makes it possible to avoid the development of ischemic toxicosis. First of all, this applies to extensive compression injuries.

After the release of the injured limb, a tourniquet is applied to the place of compression, which helps to prevent a “volley” release of accumulated toxic substances into the bloodstream. This is an important feature of medical care for Bywaters syndrome. After moving the victim and removing the compression, the limb is bandaged with an elastic bandage, and only then the tourniquet is removed. Cooling of the injured limb is also recommended.

Following the sequence of steps in the treatment of patients with compression injuries is very important. Timely use of infusion therapy, understanding the pathogenesis of Byouters syndrome significantly increases the number of saved lives.

With a mild degree of the syndrome, surgical treatment is not carried out, often such patients are treated on an outpatient basis. With moderate severity, hemodynamic disturbances are quite pronounced: edema increases, microcirculation is disturbed, the number of microthromboses increases, however, surgical treatment in this case is not always indicated. Recommended infusion therapy, which allows you to prevent the development or progression of acute renal failure.

In cases of severe and extremely severe crush syndrome, conservative treatment is ineffective, and surgical treatment is necessary. A fasciotomy of the injured limb is performed, which helps to restore blood circulation and makes it possible to avoid complete necrosis of the limb. It is often necessary to amputate the distal limbs in order to save the patient.

At the same time, acute renal failure is being treated - a strict drinking regimen, hemodialysis, plasmapheresis and infusion therapy (introduction of glucose solutions, albumin, etc.) are prescribed.

In the rehabilitation period, attention should be paid to physiotherapy (for example, massage) and physiotherapy exercises, which contribute to a more effective recovery of the limb, minimizing muscle and nerve atrophy.

case from practice

As a result of a car accident, a 21-year-old young man spent 10 hours trapped in a damaged car. He was taken to a hospital in the city of Nizwa (Oman), being fully conscious. Examination showed that the chest, abdomen, back and pelvis were not damaged. At the same time, swelling of the right shoulder was observed, the right upper limb was immobilized. X-ray examination revealed a fracture of the right clavicle.

There was also swelling of the right lower limb, the skin was not damaged. There was diffuse edema on the left leg, affecting the lower leg and thigh, as well as deep abrasions. Both legs were practically motionless in the ankle joints, there were violations of sensitivity in the area of the legs. Doppler study showed a violation of venous blood flow in the foot and lower leg. Further observation revealed a rapid accumulation of creatinine, myoglobin, potassium in the blood serum, as well as myoglobinuria.

Conducted infusion therapy: saline, glucose, sodium bicarbonate. Despite this, the patient developed anuria, and the level of potassium in the blood continued to rise. The victim was prescribed hemodialysis and underwent fasciotomy of the left thigh and lower leg, as a result of which it was found that part of the femoral muscles was necrotic. On the 7th day of treatment, gram-negative bacteria were found in a swab from the wound - E. coli and bacteria of the genus Proteus. The patient was prescribed adequate antibiotic therapy, the wound was regularly treated with antiseptics. The patient's condition progressively worsened. Despite taking antibiotics, bacterial septicemia developed, in connection with which amputation of the left leg was recommended, which the patient and his family refused. They decided to continue treatment abroad, where the victim died of severe sepsis three days after arrival.

Summary

Bywaters syndrome was singled out as a nosological unit not so long ago - only in the middle of the 20th century. In the rescue and subsequent treatment of victims with severe compression injuries, coordinated actions of rescuers and doctors are important. Rapid extraction of people from the rubble and first aid even before the removal of the press minimizes the severe consequences of the syndrome of prolonged limb compression and helps to save the life of the patient.

2. Rudaev V.I. Krichevsky A.L., Galeev I.K. Crash syndrome in disaster conditions. - Methodological recommendations for resuscitation and anti-shock groups of the emergency medical unit, specialized teams of constant readiness of the Disaster Medicine Service and resuscitation ambulance teams. 1999.

3. Dario Gonzalez. crush syndrome. Crit Care Med. 2005 Vol. 33, no. 1 (Suppl.). S.34-41.

4.Dinesh Dhar, T. P. Varghese. Crush Syndrome Case Report and Literature Review. Macedonian Journal of Medical Sciences. 2010 Sep 15; 3(3):319-323.